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EXPERIMENTS WITH DROSOPHILA AMPELOPHILA
CONCERNING EVOLUTION.

BY

FRANK E. LUTZ

WASHINGTON, D. C.
Published by the Carnegie Institution of Washington

1911

CARNEGIE INSTITUTION OF WASHINGTON, PUBLICATION No. 143

Paper No. 16 of the Station for Experimental Evolution at
Cold Spring Harbor, New York

3^iT^

Copies of
were first issued

MAR 14 1911

THE CORNMAN PRINTING CO.
CARLISLE, PA.

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

THE INHERITANCE OF ABNORMAL VENATION.

THE EFFECT OF SEXUAL SELECTION.

DISUSE AND DEGENERATION.

in

THE INHERITANCE OF ABNORMAL VENATION.

Practically all the experimental studies of inheritance have extended
through but few, rarely more than 6, generations and have been con-
cerned with pairs of non-intergrading characters. In the present work
more than 70 generations have been reared. This was possible for two
reasons: Drosophila ampelophila Loew has a very short life-history,
and it can be kept breeding throughout the year. The character
abnormal wing-venation, the inheritance of which was studied, may
be made to exhibit extreme variability, passing from less venation than
normal through normal to extra venation, so great that the additional
veins almost equal the normal in extent.

At the Boston (1907) meeting of the International Zoological Congress
a preliminary report was presented upon this subject, 6 generations
having been obtained. During the summer of 1908 a report upon the
work (covering about 25 generations) done at the Station for Experi-
mental Evolution was submitted to the Director, but I deferred publi-
cation because I wished to test more in detail certain points, especially
sexual selection and the further fate of the abnormal strains. This
additional work was done at the American Museum of Natural History.
Incidentally I obtained confirmation of the previous work, but for the
most part the present paper includes only the Cold Spring Harbor data
and the conclusions drawn are as given in the 1908 report, except where
otherwise indicated.

MATERIAL AND METHODS.

Drosophila ampelophila (the small red-eyed "pomace-fly") is very
common about cider-mills, ripe fruit, vinegar-barrels, and the like.
The larvae normally live in the pulp of rotting fruits, especially during
the acetic-acid stage of decay. They will, however, thrive on the side
of a tumbler containing fruit-juices, and I have reared them through
several generations on stale beer. At a temperature of 25° C. the eggs
hatch in 40 hours or less. The duration of the larval period is, on the
average, 5 days, and of the pupal period 4§ days. The adults become
sexually mature about 48 hours after emergence when kept at this tem-
perature. They live for about 3 weeks. The mean number of eggs is
close to 200. Copulation is repeated and frequent.

Most of the flies discussed in this paper were bred in an incubator,
where an average temperature of 25. 5° C. was maintained. A thermo-
graphic record was kept. Since the temperature of the incubator was so
nearly that of the working-room, absolute constancy was not obtained.
The amount of variation is shown in fig. 1, which gives the frequencies

l

2 EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

of the different degrees as found during four typical months from read-
ings of the thermogram at 3-hour intervals. For the purpose of these
experiments even this approximation to constancy does not seem neces-
sary, as variations of temperature were found to have no influence upon
the wing- venation. Therefore the incubator was not used in the latter
part of the work.

Class 18 33

Frequency o

Pig. 1.

Bananas were used as food. They were purchased while still quite
green and ripened in glass-stoppered bottles. In this way accidental
introduction of wild flies was rendered unlikely. Even had Drosophila
eggs been laid on the green banana, they would have hatched and the
larvae would have developed into plainly visible pupae before the banana
was used. Frequent control-cultures were kept and in no case was a
Drosophila found in them. The flies with their food were kept in care-
fully washed glassware and the instruments used in handling the food
were sterilized in an alcohol flame after every operation which could
possibly get eggs or larvae upon them. The importance of this caution
can not be too strongly urged upon those who carry out pedigree- work
with this insect.

An egg-laying female was given a fresh piece of banana every two days
and an effort was made to have all the banana of the same degree of
decay. Each piece was kept separate during the growth of the larvae.
This also is important, since, if one merely gives a large supply of food
to the female at the start of oviposition, and does not change it, the
early-born larvae will have very different food from those which are
born later. The pupae were picked out of the "larval dish" and placed

INHERITANCE OF ABNORMAL VENATION. 3

upon moist blotting-paper in a small vial, from which the adults could
readily be transferred to an etherizing vial as they emerged.

When mating was to be done the sexes were always separated before
they were a day old. Usually no female was used as a parent that was
more than 12 hours old before being isolated from the males. Numer-
ous tests showed that no females so treated laid fertile eggs. Only
rarely was there a difference of more than one day in the ages of the
parents, and they were usually mated before they were two days old.
For practical reasons, parents were killed after 50 to 100 offspring had
been secured. It was found that neither the percentage of abnormal
offspring nor the intensity of their abnormalities changed with the age
of their parents, so that this procedure was permissible.

In this paper only those families are considered which are in or close
to the main line of descent. I have not thought it worth while to include
any families having less than 40 offspring unless they were in this main
line. Typical data are given in table 36, page 31. I have tried to arrange
these so that they will be available for further work by those interested.
They should not, however, be used for more than they are worth. For
example, one can not study the inheritance of fecundity from them, as in
but few cases have I bred from a female until she died a natural death.

All individuals, both parents and offspring, have been kept for refer-
ence and are deposited in the American Museum of Natural History.
When of especial interest, the wings were mounted on glass slides in a
thin layer of paraffin. This was found to be an excellent method of
preservation. By all other methods which were tried the veins were
rendered more or less transparent. When, as in making matings, it
was desired to examine live flies, they were slightly etherized. They
completely revive in a few minutes. All examinations for abnormalities
in wing-venation must be made with a lens.

Occasionally the larvae were attacked by a disease ( ?) of unknown
origin which caused them to crawl out of the food, elongate, and die.
When this disorder appeared in a dish it was usually fatal to all the larvae
in that dish. Otherwise, Drosophila bears confinement very well. Prac-
tically all the larvae which hatch complete their development. My ex-
perience confirms the results reached by Castle (19066) that the closest
inbreeding may be practiced with this fly for generations with no injuri-
ous results. Such inbreeding was the rule in this work, being necessary
in long-continued breeding unless unpedigreed stock be used.

DESCRIPTION OF NORMAL VENATION.

The normal venation of Drosophila is extremely simple, as is shown
by fig. 2. The costal vein reaches to the fourth of the five longitudinal
veins. The auxiliary vein is incomplete or indistinct. The anal cell is
present. The discal and second basal cells are united and the first pos-
terior cell is not appreciably narrowed in the margin.

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

DESCRIPTION OF ABNORMAL VENATION.

It is probable that all insects occasionally show some abnormality of
wing-venation. In my experience with Drosophila ampelophila they
occur in one-third of 1 per cent of wild specimens. The data concern-
ing this point are given in table 1. In these the abnormalities consisted
of irregularities of the second longitudinal vein or small dashes near its
distal end (similar to figs. 3 to 10) . Only one of the 19 abnormal* wild
flies I have seen was abnormal in both wings.

Table 1. — Percentage of wild Drosophila ampelophila
which have extra veins in their wings.

Normal.

Abnor-
mal.

Percent-
age of
abnormal.

Bloomsburg, Pa

Huntington, N. Y. ...
Woods Hole, Mass....

1165

697

2083

1660

8
3
3
5

0.68
0.43
0.14
0.30

Total

5605

19

0.34

While rearing this insect for another purpose, several such abnormal
specimens were found in one family. My principal abnormal strain, in
which the variety and amount of abnormality is little short of astound-
ing, came from these. The various figures give a better conception of
what was obtained than would verbal description. There is the utmost
variation in the abnormal venation, not only in different flies, but in the
different wings of the same fly. The majority of the abnormalities are
in the distal portion of the marginal cell, but they have been found also
in the submarginal and a few in the first, second, and third posterior
cells, affecting all the longitudinal veins except the first.

CORRELATION BETWEEN THE RIGHT AND THE LEFT WINGS.

One wing may be abnormal, or both may be. In the latter case the
abnormality may be great in one wing, small in the other ; on one vein
in one wing and lacking on this vein but present on others in the other
wing (see figs. 44 to 46) . Nevertheless there is a correlation between
the intensity of the abnormality in the two wings, as is made clear by
tables 2 and 3. In drawing up these tables the range of variation of
the intensity of the abnormality was divided arbitrarily, since the char-
acter is not quantitatively measurable, into six classes: normal vena-
tion (or zero intensity of the abnormality), very slight (see figs. 3 to 7),
slight (see figs. 8 to 11), medium (see figs. 12 to 18), great (see figs.
19 to 24) , and very great (see figs. 25 to 35) . To which class a given
wing should be assigned is a matter of judgment ; but since when these
tables were made up it was thought that there was no correlation be-

*Unless otherwise stated "abnormal venation" means, throughout this paper,
"veins added."

INHERITANCE OF ABNORMAL VENATION.

tween the two wings with respect to the intensity of abnormality, the
personal equation which entered in would have tended to make the cor-
relation as shown by the tables too low rather than too high. The arabic

Table 2. — Correlation between right and left wings of males.
[For explanation see page 4.]

RIGHT.

N.

V. S.

S.

M.

G.

V. G.

N.

413

3U0

48
79

33

U6

34
58

3
17

531

V. S.

48
60

23

12

8
8

14

1
3

94

s.

23

15
9

9
9

15
8

9

2

71

M.

20

U7

14
10

17

7

14

9
2

74

G.

3
13

3

3

2
2

9

2

2

2

1

20

V. G.

1

1

1

507

103

69

86

25

1

791

Table 3. — Correlation between right and left wings of females.
[For explanation see page 4.]

RIGHT.

N.

V. S.

S.

M.

G.

V.G.

N.

226
150

43
51

37

57

47
73

1
18

•5

354

V. S.

42
46

22

16

21
17

20
25

3

•

1

2

109

s.

25

54

20

18

33
2i

37
26

12

7

1

2

128

M.

42

67

25
23

33
25

46
55

10

8

2

2

158

G.

9
21

7
7

6
8

13

10

11
5

4

1

50

V.G.

6

<?

2

5

5

6
1

4

15

344

117

130

168

43

12

814

numbers show the observed conditions ; the italics show the distribution
of frequencies which would have been expected had there been no cor-
relation. The fact that expectation is exceeded by observation in those
classes where the intensity is alike, or nearly so, in each wing, but is not

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

INHERITANCE OF ABNORMAL VENATION.

8

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

equaled in the classes where the two wings markedly differ, indicates a
definite positive correlation.

Furthermore, when one wing is abnormal the chances that the other
one will be abnormal also are 62 in 100 in the case of the males and 74
in 100 in the case of the females. This is an estimate based upon 4,000
pedigreed individuals. It will probably not hold for wild flies, since a
large part of the 4,000 were from the abnormal strain; hence the esti-
mated chances are larger than they would be in nature, because, as will
be shown shortly, there is a close relation between the percentage of
abnormal offspring in a family and the likelihood that an abnormal fly
will be abnormal in both wings. It does, however, give an idea of the
correlation which exists between the two wings with respect to the
presence or absence of abnormal venation when such abnormalities are
well fixed, and it brings out the further point that there is a sexual dif-
ference to be considered.

SEXUAL DIMORPHISM.

The females show a greater tendency to be abnormal than do the
males, and, when abnormal, their abnormalities are, on the average,
more intense than those of the males. The first of these points is illus-
trated in table 4 and fig. 51. Table 4 shows the percentage of abnor-
mal males and females in 200 families. It will be noted that as the
percentage of abnormal males increases the percentage of their sisters
which are abnormal increases until the latter have become practically
100 per cent abnormal. Then, since they can go no further, their
brothers gain on them in abnormality until we get families in which
100 per cent of both males and females are abnormal. In fig. 51 the
crosses show the position of the mean percentage of abnormal sisters for
each 10 per cent grade of abnormal brothers. A line is drawn to show
the condition when for each per cent of male abnormality the female
abnormality is 1.5 per cent. Thus, when 40 per cent of the males are
abnormal, 60 per cent of their sisters are abnormal. Corresponding to
60 per cent male abnormality, we get 90 per cent female abnormality.
Beyond that the females can go little further, hence the line becomes

INHERITANCE OF ABNORMAL VENATION.

9

Table 4. — Percentage of abnormal males and females in 200 families.

Females

.0

S.O

15.0

25.0

35.0

45.0

55.0

65.0

75.0

85.0

95.0

.o

31

II

1

43

5.0

2

10

7

2

21

15.0

1

2

3

5

1

12

25.0

3

2

3

4

12

35.0

3

3

2

3

2

1

1

IS

45.0

3

1

3

5

12

55.0

4

i

3

2

10

65-0

1

2

l

5

9

75.0

1

3

6

3

r3

65.0

3

e

8

95.0

1

43

44

33

22

10

8

10

7

6

12

10

17

65

200

Females

0

5

15

25 35 45

55

65

75 85

95

o

^v +

5

15

N.+

23

^\+

35

s. +

0

n
5

45
55

+

65

+

75

+

85
95

+

Fig. 51.— For explanation see p 8.

10

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

vertical,
relation

The close fit of this line to the observed data shows that the

Percentage of abnormal females = 1.5 X percentage of abnormal males

may be taken as approximately describing the average observed con-
dition.

Owing to the impossibility of describing the intensity of abnormality
in quantitative grades, we can not give a formula for showing its sexual
relation. Tables 2 and 3 show that there is such a relation. The ques-
tion as to whether both wings or only one shall be abnormal is also a
part of this same problem of the variation of the intensity of the abnor-
mality. We have seen that when a female is abnormal she will in 74
per cent of the cases be so abnormal that both wings will be affected,
while only 62 per cent of her abnormal brothers will be abnormal in both
wings.

THE RANGE OF VARIATION OF ABNORMALITY INCLUDES "NORMAL" VENATION.

One other point is to be noted. The intensity of abnormality ranges
all the way from cases in which there is almost as much abnormal vena-
tion as normal down to a barely discernible devia-
tion from normality. We have, then, in studying
the inheritance of abnormal venation, the serious
difficulty that a just indiscernible abnormality may
be present.* Such a fly would be recorded as nor-
mal. Table 5 suggests that they would be more like-
ly to occur in families in which the percentage of
abnormal offspring is low, for as such percentage
decreases the percentage of abnormal individuals
which are abnormal on both sides (C. S. ) decreases. In other words,
there is an increasing percentage of abnormal flies which have the abnor-
mality so reduced that in at least one wing it can not be seen. Hence,
presumably, there is an increasing percentage of flies which have the
abnormality reduced in both wings to a point just below visibility.
These will be more common among males than among females, because
the intensity of the abnormality is less in male than in female wings.
Whether this alone accounts for the fact that a smaller percentage of
brothers are visibly abnormal than of sisters is a question to which it is
difficult to give an answer.

*May not this be true also of the spotted condition in certain mammals? A guinea-
pig still behaves as a spotted animal even if the spots are reduced until only the eyes
remain affected. If the variation goes still further we would have an animal germi-
nally spotted, somatically spotless. We would then say that the spotted condition is
"latent."

Table 5.

Percentage of

abnormal flies

C. S.

per family.

lto 20...

20.9

21 to 40...

30.9

41 to 60...

50.6

61 to 80...

58.0

81 to 100...

83.1

INHERITANCE OF ABNORMAL VENATION. 11

HISTORY OF THE PEDIGREED STRAIN.

Before taking up the data concerning inheritance, it will be well to out-
line briefly the history of the chief pedigreed strains. Further details
are given in table 36. Mating 211 was the first family in these lines of
which a large number of offspring were described. Both parents were
abnormal in both wings . The wings of 177 offspring of this mating were
sketched. It was found that 31 per cent of the males were abnormal
and 65 per cent of the females. Successive generations after this,
breeding brother with sister, gave the following results: Abnormal
female by normal male (mating 257) , 70 per cent of each sex abnor-
mal; abnormal female by abnormal male (mating 284), 62 per cent of
the males and 96 per cent of the females abnormal; abnormal female
by normal male (mating 330), 96 per cent of the males and 91 per
cent of the females abnormal; abnormal female by normal male (mat-
ing 367) , 64 per cent of the males and 91 per cent of the females abnor-
mal. A number of matings were made from the offspring of No. 367.
Matings 405 and 408 are of especial interest.

In both of these matings both parents were abnormal in both wings.
Unfortunately there were a small number of offspring from each (25
and 29, respectively) , but all of the offspring of mating 405 were normal
and all those of mating 408 were abnormal. Three matings were made
from the offspring of 405. Of the 385 offspring of these, not a single
one showed the slightest trace of an abnormality, while of the 51
offspring of mating 440 (the parents being children of 408) only one, a
male, was free from abnormal venation. Mating 405, then, became the
starting-point of the "normal strain" and mating 408 the starting-point
of the "abnormal strain."

As can be seen from table 36, the various generations of the abnormal
strain gave approximately, sometimes actually, 100 per cent abnormal
flies, although normal individuals were far from rare. Furthermore,
the intensity of the abnormalities increased. The greatest abnormality
noticed before the fifth generation is shown in fig. 20. Up to that time
all abnormalities were confined to the second longitudinal vein. Begin-
ning with the sixth generation, abnormalities appeared on the third
longitudinal vein. They became frequent by the tenth generation. In
the fifteenth generation they were common and abnormalities began to
be noticed on the fourth longitudinal vein. These have, even yet, rarely
exceeded small spurs near the distal end. About this time the fifth
longitudinal vein also began to be affected, and specimens such as are
illustrated in figs. 30 and 32 were found. Meanwhile increasingly great
abnormalities on the second and third longitudinal veins occurred. (See
figs. 37 to 42 for examples. The condition shown in fig. 43 is unique. )

Turning now to the normal strain, three points should be borne in mind :
the parents in each generation were normal, it came from the same

12

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

ancestry as the abnormal strain, and about one- third of 1 per cent of
wild Drosophila ampelophila were found to be abnormal. For four
generations after branching from the abnormal strain (five, counting
mating 405) not a single abnormal individual was found, but in the next
generation 1 fly out of 216 (0.5 per cent) had a very slight abnormality.
In succeeding generations the percentage increased for a time, in spite
of artificial selection to the contrary, and then diminished to zero under
the same treatment. The abnormalities were all small, never greater
than "medium." Table 6 summarizes the history of this strain for 40
generations.

Table 6. — Fluctuation in percentage of abnormal individuals in a normal strain.

Generations

of normal

strain.

No. of
normal.

No. of
abnormal.

Percentage

of
abnormal.

Generations

of normal

strain.

No of
normal.

No. of
abnormal.

Percentage

of
abnormal.

1 and 2

3 4

5 6

7 8

9 10

11 12

13 14

15 16

17 18

19 20

21 22

418
235
575
594
336
471
183

79
110
234

56

0

0

1

7

31

45

14

2

5

14

2

0.0
0.0
0.2
1.2
8.4
8.7
7.1
2.5
4.3
5.6
3.4

23 and 24
25 26
27 28
29 30
31 32
33 34
35 36
37 38
39 40

Total

144
239
257
116
195
217
148
55
63

0
0

1

o

0
0
0
0
0

0.0
0.0
0.4
0.0
0.0
0.0
0.0
0.0
0.0

4,725

122

2.5

It is to be noted that the percentage of abnormal individuals is greater
in this strain artificially selected for normal venation than it is in nature.
At first thought one would say that this is an effect of the environment
to which they were subjected. If this be true, environment may have
played a part in the production of the abnormal strains. I think, how-
ever, that it is not true. A sufficient explanation seems to lie in the
fact that a form of selection exists in nature which is keener than the
artificial sort, even when the latter is carried out under a lens.

THE EEFECT OF SELECTION.

Of late years there has arisen considerable skepticism concerning the
cumulative effect of selection except as a means of isolating "pure
lines." Jennings (1908) says : "Certainly, therefore, until some one
can show that selection is effective within pure lines, it is only a state-
ment of fact to say that all experimental evidence is against this."
Whether or not the present material has a bearing upon the question
thus clearly put depends upon the definition of a pure line. If a pure
line be defined as one from which nothing else can be gotten by selec-
tion, further discussion is not necessary. On the other hand, if inbreed-
ing (for the most part, brother X sister) for 10 or 15 generations and
rigid selection (in this case, with respect to wing-venation) may be

INHERITANCE OF ABNORMAL VENATION. 13

reasonably supposed to have established as " pure " a line as exists in a
given case, the following facts may be of interest.

The abnormalities obtained, both in the direction of veins added and
of veins lacking, far surpass those found in nature in this or any other
insect with which I am familiar. Furthermore, they do not even remotely
suggest the venation of any of this fly's relatives. Something new has
been produced. In the strain whose early history has just been described
there was, at the start, no definite effort made to build up an abnormal
race as quickly as possible. Later I tried to do this from wild material
obtained from other localities.

Starting with an abnormal male and a normal female from Boston and
an abnormal male and female from Bloomsburg, Pennsylvania, I rigidly
selected for additional veins. The record for each successive set of two
generations was 8.8, 5.5, 11.5, 14.3, 30.3, 45.8, 85.9, and 100 per cent
abnormal. Thereafter mass-breeding was practiced and the abnormal
strain preserved for about a year by merely starting a fresh jar every
couple of weeks with the most abnormal individuals found at that time.

The abnormalities in this strain were of the same nature and extent
as in the one started from the Long Island material. It would seem
that this increase in the percentage of abnormal individuals up to 100
per cent and the subsequent increase of the intensity of the abnormalities
can not be due to the gradual weeding out of all units but the one or
several desired, because one quickly gets things which one can safely
say did not exist in the population with which we started, or, to be more
exact, which we do not see. Some can probably imagine that the "units"
for each successive grade of abnormality existed in the parents with
which we started, but that they were held in check by an equal number
of inhibiting "units " of corresponding powers, so that the result could
be explained by saying that in the selection we cut out step by step suc-
cessively stronger inhibiting units, thus allowing successively greater
abnormality-producing units to manifest themselves. On any other
hypothesis, it seems to me, we must admit the cumulative effect of
selection upon a "unit," i. e., within a pure line.

But, upon this hypothesis, how can we account for the occasional nor-
mal flies? Why do not the inhibiting units stay cut out after we have
once gotten rid of them so thoroughly that all the flies of several suc-
cessive generations show strong added veins? Perhaps they do stay
cut out and these occasional normals are merely fluctuating variations
in the abnormal unit. If so, and if selection does not have a cumula-
tive effect within a unit, it would be impossible to return to normality
from a series of inbred generations of abnormality. But it is possible.
Starting with a family which had one normal offspring in a total of 133
(99.2 per cent abnormal) and selecting to reduce the extra veins, the
percentage of abnormal offspring in successive generations was 81.8,
66.2, 32.9, 12.5, 17.0, 0.0, 0.0, 0.0, and so on, as a typical normal strain.

14 EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

The building up of an abnormal strain from a long-inbred normal one
was also nearly completed when it was stopped by accident. I did not
think it worth while to start it anew, as its accomplishment would prove
little, since it might be said that the normal strain was a "mixed general
population" due to normality (inhibiting) units masking all sorts of
latent abnormality units.

In nature a small percentage of flies have the fifth longitudinal vein
somewhat shortened (see fig. 47) . This variation also appears in the
experimental strains. Rather as a matter of curiosity, I selected for
shortened veins during a few generations and very quickly obtained such
specimens as are illustrated in figs. 48 to 50. One can not go further
in this direction without some special technique, because the wings,
lacking the support of the veins, droop and catch in the fly's food.
Probably breeding could be continued by cutting off the parent wings
when matings are made. I did not try it, as it was already very evident
that selection was just as effective in the negative as in the positive
direction.

On the other hand, all attempts to fix, by selection, some particular
type of abnormality utterly failed. It was thought possible that the
great variety of forms which the extra veins showed was due to a mix-
ture of a number of simple forms and that selection might isolate these
simple types. The most hopeful was a simple forking of the second
longitudinal vein (see fig. 10). Selection for this type was started sev-
eral times, but never went beyond the fifth generation, because, although
there were plenty of abnormal flies in each generation, there was no
increase in the number showing this particular type, and sooner or later
a generation would contain none of them from which to breed. The
same was true in the experiments aimed to fix the abnormality on, for
example, the third longitudinal vein, but to keep it off of the second.
It is easy to have all the abnormal flies abnormal only on the second
longitudinal vein, providing one be content with small abnormalities.
However, as soon as one increases greatly, by selection, the abnormality
on the second vein, the other veins begin to be abnormal.

These are the facts: Starting with slight extra veins, either in wild
material or in material selected and inbred for normal venation, we
can quickly get by selection 100 per cent abnormal offspring. In future
generations this strain can be quickly brought back again to its normal
condition by selection. Selection also quickly shortens the veins and
would probably largely do away with them, provided some technique
were adopted to keep the results of selection alive. But selection,
accompanied by the strictest inbreeding (brother X sister and parent X
child) failed to isolate any unit characterized by a given form or extent
of abnormality.

The interpretation of these facts would doubtless vary with varying
opinions as to unit-characters.

INHERITANCE OF ABNORMAL VENATION.

15

THE DATA CONCERNING INHERITANCE.

Without reference to the grandparents, the data are summarized in
table 7:

Table 7.

Crosses.

Average

p. ct. of

abnormal

offspring.

9.6
35.8
54.7
85.9

Abnormal male X normal female...
Normal male X abnormal female...

In this work a fly is counted as abnormal if there is the slightest trace
of abnormality in either wing. These results leave no room for doubt
concerning the heritability of the tendency toward extra veins.

Tables 8 to 19 show the relation between various ancestors and the
offspring. The coefficients of association found from these are given
below the respective tables. Although these coefficients are greater
than expectation on the basis of Pearson's Law of Ancestral Heredity,
they do not negative his conclusions. He was very careful to exclude
cases in which there is inbreeding or assortative mating. Both were
largely practiced in these experiments. These coefficients do show, how-
ever, that change of sex in the ancestry does not uniformly weaken in-
heritance. Thus, the average coefficient of association between father
and sons, and mothers and daughters (no change of sex) is 0.78 ; and
that between father and daughters, mothers and sons (one change of

Table 8.

SONS.

Table 9.

DAUGHTERS.

N.

A.

w
B

H
<

N.

A.

N.

2949

837

8786

N.

3011

1329

4340

A.

1341

1948

8189

A.

951

2763

3714

4190

2785

6975

3962

4092

8054

C. A. =0.694.

C. A. =0.736.

Table 10.

SONS.

Table 11.

DAUGHTERS.

N.

A.

§
a
g
o

N.

A.

N.

2801

465

3206

N.

2983

746

3729

A.

1389

2320

3709

A.

979

3346

4325

4190

2785

6975

3962

4092

8054

C. A. =0.819.

C. A. =0.864.

16

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

- H

Table 12.

SONS.

N.

A.

N.

2813

10T9

2892

A.

1329

1705

3034

4142

2784

6926

C. A. =0.540.

os a

IS

Table 13.

DAUGHTERS.

N.

A.

N.

2602

1855

4457

A.

1310

2228

3538

3912

4083

7995

C. A.=0.409.

Table 14.

SONS.

N.

A.

N.

2535

484

3019

A.

1607

2300

3907

4142

2784

0926

C. A. =0.765.

» OS

PS w

b h

H O

Table 15.

DAUGHTERS.

N.

A.

N.

2727

759

3486

A.

1185

3324

4509

3912

4083

7995

C. A. =0.820.

bs h

Kb
a*

Table 16.

SONS.

N.

A.

N.

2766

1015

3781

A.

1339

1761

3100

4105

2776

C881

'"BS

Table 17.

DAUGHTERS.

N.

A.

N.

2619

1768

4387

A.

1262

2296

3558

3881

4064

7945

C. A. =0.672.

C. A. =0.459.

-"bs'

W 03
B Eh

8»

Table 18.

SONS.

N.

A.

N.

2444

477

2921

A.

1661

2299

3960

4105

2776

6881

C. A. =0.753.

OS LJ

B H

go

Table 19.

DAUGHTERS.

N.

A.

N.

2630

741

3371

A.

1251

3323

4574

3881

4064

7945

C. A. =0.808.

sex) is also 0.78. Considering the grandparents, the average coefficient
of association between sons and father's father, and daughters and the
mother's mother (no change of sex) is 0.67, while that between sons
and the mother's father, and daughters and the father's mother (two
changes of sex) is 0.74. This result agrees with that of Blanchard
(1903) concerning the coat-color of horses and is not in harmony with
Pearson's (1900) and the writer's (1903) concerning the eye-color in man.

INHERITANCE OF ABNORMAL VENATION.

17

Table 20. — Relation between degree of
abnormality in parents and percent-
age of abnormal offspring.

It will be convenient in the present discussion to adopt the following
symbols: Ai denotes a fly that is abnormal in one wing only; A2, a fly
abnormal in both wings, and C. S.
(coefficient of symmetry) that per-
centage of a given lot of abnormal
flies which are abnormal in both
wings. Tables 20 and 21 may be
summarized as follows: Flies which
are so abnormal that both wings are
affected not only gave, on the aver-
age, a greater percentage of abnor-
mal offspring than flies abnormal in

only one wing, but the abnormal offspring of the former were more
likely to be abnormal in both wings than those of the latter. It must

Table 21. — Relation between parents and offspring with respect to one wing or both

being abnormal.

Parents.

P. ct. of

abnormal
offspring.

Parents .

P. Ct. Of

abnormal
offspring.

A-2 s\ A-2

A-2 ^ •"■!

1 AXX Ax

85.1
76.8
71.9

NX A2
NX A,

j NXN

45.8
35.1
13.8

Parents.

Offspring.

Parents.

Offspring,

Male.

Female.

Ai

A2

c. s.

Male.

Female.

A,

A2

c. s.

A2
A2
A2
A:
At

A2

Ai

N

A2

Ai

268
102
105
149
83

1271
178
118
428
158

0.83
0.64
0.52
0.74
0.66

Ai
N
N
N

N
A2
A,
N

55
122

57
285

61
198

53
160

0.53
0.62
0.48
0.36

Table 22. — Relation between parents and
offspring with respect to which wing
is abnormal.

[AR= Abnormal in right wing only; AL=Abnor-
mal in left wing only; A2=Abnormal in
both wings; Ai = Abnormal in one wing
only.]

be noted that this was only "on the average." Although it was an
exceptional case, we have seen that all the offspring of mating 405
were normal. The parents each had
"great" abnormality in both wings

From table 22 it seems evident
that a given asymmetry (abnormal
in the right wing only or abnormal
in the left wing only) is not inher-
ited. The offspring of a parent
which is abnormal in the left wing
only are as likely to be abnormal in
the right as in the left wing, and
vice versa. This is in accord with the
results obtained by Castle (1906a)
for polydactylism of guinea-pigs,
Larrabee (1906) for the reversed
optic chiasma of fishes, and Priz-
bram (1907) for eye-color of cats.

As was pointed out, all attempts
to fix any particular form of abnor-
mality by selection and inbreeding (pure lines?) have failed ; nor has

Parents.

Offspring.

AR

AL

A.R — AL

AX

A2 X A2
xi-2 X A.R

x*.2 /N. A-L

x\R /s An
AR X AL
ALX AL

NXA,
N X AL
N XN
NXA,

147
58
56
36
30
23
29
37
146
121

121
79
58
41
25
24
18
28
139
106

+0.10
-0.15
-0.02
-0.06
+0.09
-0.02
+0.23
+0.14
+0.02
+0.07

18 EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

there been any apparent tendency to settle down to any definite type. *
The "center of disturbance " has remained in the distal portion of the
marginal cell closely related to the second longitudinal vein. Next to
the second, the third vein has been the most affected, then the fifth;
but I have failed to fix the abnormalities in these veins. They are,
apparently, all the effects of the disturbing factor or factors, centered
on the second longitudinal vein in the marginal cell.

The hundreds of families studied showed that it is impossible to pre-
dict, from the character of the ancestors, what the form of the abnor-
mality will be in the offspring. The most that one can do is to give an
approximate estimate of the percentage of abnormal individuals and a
still less exact prediction of the average intensity of the abnormalities.

THE BEARING OF THESE DATA UPON PROPOSED LAWS OF HEREDITY.

In my former paper (1907) I considered that normal venation is more
or less dominant over abnormal in the Mendelian sense. Such was the
case in the early part of the work, although, as was pointed out, it was
the spirit only and not the letter of the law which was followed. When
a normal fly, having normal ancestors, was crossed with an abnormal
one, practically all the offspring were normal. The abnormalities which
did appear were slight, but there was no doubt about their presence.
Matings 318 to 322 (see table 36) illustrate such cases. The offspring
of matings 347 to 353 are second-generation hybrids from such a cross.
They show a condition not very divergent from the Mendelian expecta-
tion.

Since the number of offspring in most of the families considered here
is large, the Galtonian formula can be tested in single families, and it is
evidently not at all in accord with the data. Neither is Pearson's modi-
fication of it. The fact that normal X abnormal gave, in large families,
practically all normal completely negatives for these data all theories
which are founded on the hypothesis of equipotency of the two parental
characters.

On the other hand, while the results of certain matings accord with
Mendelian expectation, the fit is far from good in the majority even in
the early generations. For instance, we have seen that neither normal
nor abnormal breeds true. A Mendelian recessive would be expected to
do so ; therefore we can not consider either normality or abnormality
to be Mendelian unit-characters in that sense.

*Here again (see p. 10) the similarity to the experience of breeders of spotted ani-
mals is interesting. Castle (1905), for example, found that "one can by selection
progress in either direction through this series of changes, either increasing or de-
creasing the number and extent of the pigment patches, but it is impossible without
long-continued selection to fix the color-pattern at any particular stage in the series;
perhaps it is wholly impossible to do so, as Cuenot (1904) asserts on the basis of his
studies on mice, but this I very much doubt."

INHERITANCE OF ABNORMAL VENATION.

19

Fig. 52 shows graphically the results of the three sorts of matings :
normal X normal, normal X abnormal, and abnormal X abnormal. The
first should give one mode at zero abnormality and another at 25 per
cent abnormality on the assumption that normality is dominant in the
sense in which the term is now used in Mendelian literature. These
modes would represent the results of DD X DD and DR X DR, respec-
tively. They are present, but the curve runs all the way up to 65 per
cent abnormal. The second should give one mode at zero and another
at 50 per cent, representing the results of DDXRR and DRxRR, respec-
tively. The mode at 5 per cent is marked and might be explained as the

5 15 25 35 45 55 65 75

Percentage of abnormal individuals
Fig. 52.

result of "incomplete dominance," a thing which is itself badly in need
of a Mendelian explanation. At 50 per cent there is a drop in the curve
where there should be a mode. There is a strong mode at 75 per cent,
where there should be none. This is true both when the male is the
normal parent and when the male is the abnormal one (see fig. 53).
Abnormal X abnormal should have but a single mode, 100 per cent (or
95 per cent as the figure is drawn), representing the result of RR X RR.
Such a mode is pronounced in the curve, being chiefly made up of the
families of the abnormal strain after generation vil, but the curve
reaches all the way to zero.

These data are analyzed in tables 24 to 35, so that there is no need of
a further text description of them. They are taken from the early part

20 EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

of the work. The results of the seven crosses between the abnormal
and normal strains in the fifty-ninth generation— all that were made at
that time— are of interest in this connection and are shown in table 23.
Any theory applied to these data must accord with the following facts:
(1) Abnormalities occasionally appear in the venation of the wings
of wild Drosophila ampelophila. These are usually added veins. Since
evolution in the Diptera has been accompanied by a reduction in the
number of veins, these abnormalties are of the nature of " reversions."
The tendency to produce extra veins is inherited and has been increased
by selection. This is also true of the tendency to shortening of veins.

m

A Male abnormal x Female normal

^8 / . V --Male normal x. Female abnormal

I7 ' \

£6 / \

% * / ... \ .-•• \ ,••' / \ v-

fc3 // \ \ / \ ,-• / \

XJ o V '. V v^. »• / V

§ I .7 V \ K N. / N N

Z I — ^

0 5 15 25 35 45 55 65 75 85 95

Percentage of abnormal individuals
Fig. 53.

An examination of more than 50,000 abnormal wings has revealed an
immense diversity of forms which the abnormality assumes. Not only
are new forms being constantly discovered, but the intensity of the ab-
normality has constantly increased as long as selection for that end has
been kept up. The limit of the increase was apparently not reached, but
the extra veins have always been very crude, only rarely assuming a
form and position comparable to ordinary veins.

(2) A greater percentage of females than of males is abnormal. The
formula

Percentage of abnormal sisters = 1.5 X percentage of abnormal brothers

approximately describes the average condition in the various families.
Attempts to change significantly this relation have failed, and seem
destined to fail, for change of sex in the ancestry does not weaken
inheritance.

(3) The lower range in the variation of abnormality certainly includes
barely discernible deviations from normality and presumably just indis-
cernible deviations also. The latter would be considered normal.

(4) Frequently one wing of a fly is abnormal, the other not visibly so.
There is a direct relation between the percentage of abnormal offspring
of a given mating which are abnormal in both wings and the total per-
centage of abnormal offspring. Furthermore, on the average, parents
which are abnormal in both wings give a larger percentage of abnormal

INHERITANCE OF ABNORMAL VENATION. 21

offspring than those which are abnormal in one wing only. There is no
relation between parents and offspring with respect to the side upon
which asymmetrical abnormalities occur. There is a correlation between
the two wings of individual flies with respect to the intensity of the
abnormality.

(5) Normal male X abnormal female gives a greater percentage of
abnormal offspring than the reciprocal cross.

(6) Not only has the abnormality increased in the abnormal strain,
but, in spite of artificial selection to the contrary, an increasingly large
number of abnormal individuals appeared for a while in the normal strain
and then with the same treatment the percentage again decreased.
When the flies are allowed to choose their own mates the percentage of
abnormals is kept low even when abnormal flies are added from time
to time.

(7) Abnormality originally behaved somewhat like a Mendelian reces-
sive, but in the later generations departed, in its behavior, very far
from that theory as it is now understood.

There would be little profit in reviewing the various modifications of
the simple Mendelian formula and pointing out in detail why they are
not satisfactory in the present case. I have tried most, if not all, of
those which have been proposed and also a number of original hypothe-
ses involving two or more allelomorphs. All these attempts have been
failures with the exception of the idea of variation of potency (Lutz,
1907). If sufficiently elaborated this will "explain" each of the con-
ditions set forth above, and until quite recently I believed that the
inheritance of the abnormal venation followed this modification of the
Mendelian law. It seemed quite probable that there was a single pair
of allelomorphs involved— the abnormality-producing factor and its ab-
sence — but that the strength of the positive one varied, and that these
variations were inherited, making the problem a combination of the
inheritance of a fluctuation variate and of Mendelian segregation (Lutz,
1908) . In my report at the time of finishing the work at Cold Spring
Harbor I even constructed hypothetical curves for this variation. How-
ever, I have since realized that the "explanation " of conditions 6 and
7 was very weak. It was "that in selecting parents to continue the
normal strain I merely selected flies having no extra veins. For the
most of the time the work of describing offspring was unavoidably so
far behind the breeding- work that I did not know what percentage of
their brothers and sisters were abnormal. Hence I had no way of judg-
ing as to the germinal constitution of the parents. The normal strain
is probably a mixture of flies lacking the abnormal factor (might be
called NN's) and of flies which have it in hybrid condition of weak
allelomorphic strength (NA's). In generations VII to xxn I was prob-
ably unconsciously breeding from these NA's. This is an answer to
the first part of condition 6.

22

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

generation.

Mating
No.

Ab-
normal.

Total.

Per cent
abnormal.

2561
2562

43
42
65
47
21
19
14

113
126
130
79
28
27
24

38.1
33.3
50.0
59.5
75.0
70.4
58.3

2629

2630

2631

2633

2645

Total...

251

527

47.6

' We have, now, only to take up the fact that in inheritance these
abnormalities follow the spirit but not the letter of the Mendelian law
(condition 7). We might consider that the dominance of normal over
abnormal is merely due to the dilution of the abnormality-producing
factor in the NA's. If it is strong it may be potent enough to produce
abnormalities in spite of this dilu-
tion, thus giving incomplete domi- Tablle 23.— Results of seven crosses between
■n , ., . abnormal and normal strains in a late

nance. Even when it is pure
(AA), its fluctuation may give
individuals in which the zygotic
strength is not great enough to
produce abnormalities, thus ac-
counting for the normals in the
abnormal strain. Whether one
could so increase the strength of
the abnormality-producing factor
that when the selected flies are
mated with flies lacking the factor
all the offspring will be abnormal is not certain, but table 23 indicates
such a possibility."

If, however, we have, in carefully conducted experiments, many flies
somatically normal but germinally abnormal, and if by selection it is
easy to so weaken the abnormality-producing factor that from a strain
100 per cent abnormal we get and keep one 100 per cent somatically
normal (all presumably germinally abnormal, since they came from a
100 per cent abnormal strain) , must we not admit the possibility that all
somatically normal flies have the germinal possibilities of abnormality?
This makes the problem much simpler, as, leaving out the question of
Mendelian segregation, we have only to consider the inheritance of the
variations of an abnormality-producing factor, whatever that may be.
Let us take up the seven conditions which must be satisfied.

Condition 1. — All flies possess the abnormality-producing factor in the
germ. It is usually so weak that it has no visible effect upon the soma.
Occasionally, however, it is strong enough to do so, and its strength
can be so increased by selection that it always does so.

Condition 2. —It is necessary to suppose that it takes a greater strength
of the germinal factor to have a visible effect upon the male soma than
upon the female. This sexual difference of developmental physiology
is quite common and the hypothesis will doubtless be readily allowed
by most critics in this case. It is interesting to wonder whether the
possession of horns by certain male ungulates, while the females lack
them, is an extreme example of this same phenomenon.

Condition 3.— To be expected on this hypothesis.

Condition U. — The explanation here would differ according to different
notions of the mechanics of heredity. If we accept the apparently most

INHERITANCE OF ABNORMAL VENATION. 23

favored notion that there is some specific substance in the germ which
produces the character in question and which is divided at the cell-
division which separates the substances forming* the right side from
those forming the left side of the complete soma, it would be difficult to
believe the division is always, or in most cases, exactly even. If it is not
with respect to the abnormality-producing factor, it would give rise to
the phenomenon of asymmetry as to the extent of the abnormality.
Only when the factor is rather weak to start with would this deviation
from exact equality of division frequently result in the share going to
one wing being so small that that wing would be normal while the other
wing is abnormal; hence there would be a correlation between the
degree of the abnormality and the phenomenon of one wing being normal
while the other is abnormal (see p. 5) . The approximate equality of
the apportionment of the factor in division may be taken as the expla-
nation of the correlation in the intensity of the abnormality in the two
wings, and the degree of this correlation is a measure of the degree of
equality of the division. Since the going of a slightly greater strength
to the right side than to the left, or vice versa, is a mere accident in
development, it is not to be expected that there will be an inheritance
of a particular side getting the greater strength (see p. 17) . But since
flies abnormal in only one wing came from germs which had a weak
abnormality-producing factor, it is to be expected that the germs they
produce will be weak with respect to this factor, and so a smaller per-
centage of their offspring will be abnormal than of the offspring of
parents abnormal in both wings (see p. 17) .

Condition 5. — Since it takes a greater strength of the germinal factor
to produce abnormalities in the males than in the females, a male
somatically normal may be produced by and produce germs containing
as strong or stronger abnormality factors than a female which is somat-
ically abnormal. Hence, in the long run, normal male X abnormal
female will give more abnormal offspring than abnormal male X normal
female, because in the latter cross one of the parents (the female) neces-
sarily has the factor very weak.

Condition 6. — "In selecting parents to continue the normal strain, I
merely selected flies having no extra veins. For the most of the time
the work of describing offspring was unavoidably so far behind the
mating work that I did not know what percentage of their brothers and
sisters were abnormal. Hence I had no way of judging as to the ger-
minal constitution of the parents." Being unable, by examination of
the soma, to tell the exact strength of the germinal content, I uncon-
sciously used as parents flies in which the abnormality-producing factor
was relatively strong, and thus started and for a time maintained a
strain giving a relatively large number of abnormal flies. When the
flies were allowed to do their own selecting of mates they were more
successful (see p. 36) .

24 EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Condition 7. — From all we know of the inheritance of fluctuating
variations, the mating of one grade with another will give variations
about a mid-grade. If it takes a certain grade or strength of the germ-
inal factor to produce a somatic effect and we mate a low grade (somati-
cally normal) with one just sufficient to produce somatic abnormalities,
the variations about the mid-grade will, in most cases, be too low to
produce visible abnormalities. In other words, normality will dominate
over abnormality. If, however, the parents are such that the grades
of the offspring are about that required to produce somatic effects, the
dominance will be imperfect. The abnormality v/ill appear to be obey-
ing "the spirit of the Mendelian law," but it will naturally "pay little
attention to the letter of the simple law or any of the modifying clauses, "
especially in the latter generations, where the abnormal strain had the
germinal factor much strengthened by selection.

It seems to me, then, that if we accept the notion of some specific
factor in the germ which brings about the details of the characters of the
soma the facts here discussed may be considered to be the result of the
action of a factor present in all germs. The strength of this factor
varies, and when of a certain strength produces certain visible effects.
The partial dominance of normal over abnormal is due to the mean con-
dition of the factor in the offspring of

(flies with factor strong enough to produce extra veins) X (flies with factor weak)

usually being below the strength required to produce abnormality.

I have not taken up the resemblance of the behavior of these abnor-
malities to that of ' ' ever-sporting varieties, " because I feel that classing
these as such would not be a step toward an explanation. It would
merely be naming the difficulty. It is also not the intention to imply
that this hypothesis would apply to those other cases which are trouble-
some from a Mendelian standpoint and to which the principle of vary-
ing potency of Mendelian determiners has been applied (for example,
Davenport, 1910) . It seems not only possible but probable that many
apparently non-Mendelian cases may be explained as a combination of
alternative and blending inheritance (Lutz, 1908). But a simpler and
more probable explanation of these data, provided we accept the some-
what dubious "germinal factor " idea, seems to be that we are dealing
here solely with a fluctuating character — the strength of the abnormality-
producing factor— and that the study of its inheritance is made difficult,
if not largely impossible, by the fact that only in the upper part of its
range can we judge of the relative values of this variable, for in the
lower part its effects are invisible.

INHERITANCE OF ABNORMAL VENATION.

25

Table 24. —Percentage of abnormal offspring in 48 matings
ofNs (ex. Ns X iV?) X N2 (ex. Ns X N?).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

26

8

1

5

4

1

15

1

1

1

25

1

2

1

1

35

45

55

65

75

85

95

i

Table 25. — Percentage of abnormal offspring in 5 matings of
Ns (ex. As X Ai) X N<2 (ex. As X A?).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

3

5

1

1

15

25

35

45

55

65

75

85

95

26

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Table 26.— Percentage of abnormal offspring in 6 matings of
Ns (ex. As X 2V?) X N$ {ex. As X Nv).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

5

1

15

1

2

25

1

1

35

45

55

65

75

85

95

Table 27.— Percentage of abnormal offspring in 4 matings of
NS {ex. NS X A?) X N9 (ex.NS X A?).

FEMALES

0

5

15

25

35

45

55

65

75

85

95

0

1

t

5

15

25

35

1

1

45

1

55

65

75

85

95

INHERITANCE OF ABNORMAL VENATION.

27

Table 28. — Percentage of abnormal offspring in 5 matings of
Ns (ex. Ns X N<2) X Ai (ex. N$ X A2).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

1

5

1

1

15

25
85

1

45

1

55

65

75

85

ys

L..-

1

Table 29. —Percentage of abnormal offspring in 7 matings of
Ns (ex. NS X N$) X A2 (ex. As X A$).

FEMALES-

0 5

15

25

35

45

55

65

75

85

95

0

1

5

1

15

1

25

1

1

35

1

1

45

55

65

75

85

95

28

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Table 30. — Percentage of abnormal offspring in 13 matings
of Ns (ex. Ns X A$) X A? (ex. Ns X A?).

FEMALES.

0

5

15

25

35

■45

55

65

75

85

95

0

5

15

25

1

35

1

1

1

45

1

2

55

1

65

2

75

1

85

1

95

1

Table 31. —Percentage of abnormal offspring in 9 matings of
Ns (ex. AS X As) X A? (ex. As X A$).

FEMALES

0

5

15

25

35

45

55

65

75

85

95

0

5

15

25

35

45

1

55

1

65
75

1

1

85

1

95

4

INHERITANCE OF ABNORMAL VENATION.

29

Table 32. — Percentage of abnormal offspring in 6 matings of
As (ex. As X As) XN<Z (ex. Ns X 2V$).

FEMALES-

0

5

15

25

35

45

55

65

75

85

95

0

5

1

3

1

15

25

35

45

55

65

1

75

85

95

Table 33. — Percentage of abnormal offspring in 12 matings
of AS (ex. AS X N9) X N? (ex. As X JV9).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

1

5

1

1

15

1

25

1

35

1

45

55

1

65

1

75

2

1

1

85

95

30

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Table 34. — Percentage of abnormal offspring in 21 matings
of As {ex. Ns X A?) X A<Z (ex. Ns X A$).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

1

5

15

25

35

2

1

1

45

2

1

55

1

2

1

65

1

2

75

1

2

85

95

3

Table 35. — Percentage of abnormal offspring in 45 matings
of As (ex. As X A$) X Az (ex. As X A?).

FEMALES.

0

5

15

25

35

45

55

65

75

85

95

0

5

15

25

35

45

55

1

65

1

75

1

85

1

5

95

36

INHERITANCE OF ABNORMAL VENATION.

31

Table 36.-

-Percentage of abnormal offspring of20C

families.

Offspring.

Pare*1*

Mating
No.

Male.

Female.

Total

p. ct.

abnormal.

Father.

M other.

No.
recorded.

P. ct.
abnormal.

No.
recorded.

P. ct.

abnormal.

1
211

A 205

A 205

75

30.7

102

64.7

50.3

214

N205

N205

39

30.8

34

47.1

38.4

220

A 207

N207

11

0.0

8

0.0

0.0

226

A 205

A 205

69

46.4

77

80.5

64.4

230

A 205

A 210

38

84.2

27

85.2

84.6

233

A 210

A 210

31

71.0

25

76.0

73.2

238

A 210

A 210

22

36.4

23

52.2

44.4

239

N211

N210

29

51.7

29

69.0

60.3

241

N216

N216

61

0.0

69

0.0

0.0

242

N216

N216

55

0.0

63

3.2

1.7

243

N214

N214

64

28.1

57

36.8

32.2

245

N215

N215

20

20.0

14

42.9

29.4

246

N215

N215

27

25.9

31

32.3

29.3

247

N215

N215

37

29.7

27

40.7

34.4

253

N220

N220

13

0.0

16

0.0

0.0

257

N211

A 211

87

70.1

90

70.0

70.0

258

N211

A 211

47

93.6

63

96.8

95.5

259

N211

A 211

21

47.6

35

94.3

76.8

273

N242

N242

10

0.0

16

0.0

0.0

276

A 246

N246

18

11.1

23

34.8

24.4

278

N246

N246

16

25.0

17

58.8

42.4

280

N253

N253

10

0.0

20

0.0

0.0

281

N253

N253

37

2.7

52

1.9

2.2

283

A 257

A 257

47

38.3

54

83.3

62.4

284

A 257

A 257

77

62.3

91

95.6

80.4

285

N257

A 257

72

43.1

72

94.4

68.8

286

A 257

A 257

34

44.1

36

88.9

67.1

288

A 258

A 258

62

54.8

67

95.5

76.0

289

A 258

N258

43

46.5

38

97.4

70.4

291

A 258

A 258

44

65.9

66

93.9

82.7

292

A 258

A 258

16

37.5

27

92.6

72.1

294

N241

N241

16

0.0

19

0.0

0.0

297

N246

N241

34

2.9

57

10.5

7.7

298

N246

A 259

43

48.8

55

76.4

64.3

299

A 238

A 259

26

73.1

28

96.4

85.2

301

N257

N258

53

32.1

51

76.5

53.8

302

N257

A 258

56

51.8

41

92.7

69.1

305

N241

A 233

26

0.0

29

3.4

1.8

316

N276

N225

25

0.0

40

0.0

0.0

317

N225

A 289

25

16.0

25

4.0

10.0

318

A 288

N225

32

6.3

48

0.0

2.5

319

A 283

N225

30

3.3

42

7.1

5.6

320

A 284

N225

50

10.0

60

20.0

15.5

321

A 284

N225

27

7.4

39

2.6

4.5

322

A 284

N225

48

6.3

53

9.4

7.9

323

N297

N297

29

10.3

35

14.3

12.5

328

N284

A 284

28

92.9

26

96.2

94.4

330

N284

A 284

48

95.8

66

90.9

93.0

331

N284

A 284

33

78.8

28

82.1

80.3

333

A 285

A 285

27

59.3

26

84.6

71.7

338

A 285

A 285

26

53.8

29

62.1

58.2

339

N285

A 285

34

91.2

45

75.6

82.3

341

N288

A 288

20

90.0

25

92.0

91.1

342

N294

A 284

38

31.6

52

34.6

33.3

343

N297

A 284

35

25.7

47

44.7

36.6

344

N273

A 284

42

14.3

63

39.7

29.5

345

N273

A 288

58

37.9

41

48.8

42.4

347

N320

N320

32

28.1

55

i

23.6

25.3

32

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Table 36. — Percentage of abnormal offspring of 200 families— Continued.

Offspring.

Mating
No,

PaieLius.

Male.

Female.

Total

p. ct.

abnormal.

Father.

Mother.

No.
recorded.

P. ct.
abnormal.

No.
recorded.

P. ct.
abnormal.

348

N320

N320

31

19.4

37

21.6

20.6

349

A 320

N320

57

36.8

65

38.5

37.7

350

N320

N320

37 i

13.5

49

28.6

22.1

351

N320

A 320

36

19.4

32

31.3

25.0

353

N320

N320

37

10.8

24

16.7

13.1

354

A 284

N320

37

45.9

41

63.4

55.1

355

A 284

N321

44

2.3

51

21.6

12.6

356

A 284

N322

38

28.9

30

60.0

42.6

357

N318

N318

32

3.1

35

11.4

7.5

358

A 318

N322

28

0.0

48

2.1

1.3

359

A 318

N322

43

2.3

33

9.1

5.3

364

N317

N317

24

0.0

24

0.0

0.0

365

N345

A 345

44

36.4

52

67.3

53.1

366

N342

A 342

39

30.8

50

42.0

37.1

367

N330

A 330

42

64.3

80

91.3

81.9

368

N330

A 330

43

48.8

55

87.3

70.4

369

N339

A 339

32

34.4

42

76.2

58.1

372

N338

A 338

36

58.3

37

89.2

74.0

375

N344

A 344

29

t 24.1

36

52.8

40.0

377

N344

A 330

23

60.9

30

93.3

79.2

379

A 349

N349

68

70.6

58

70.7

70.6

380

A 349

N349

26

15.4

29

24.1

20.0

383

A 349

N349

35

25.7

37

59.5

43.1

384

A 349

N349

27

63.0

34

88.2

77.0

387

N368

A 368

32

84.4

36

83.3

83.8

388

A 349

N349

23

4.3

25

12.0

8.3

399

N367

A 367

20

50.0

23

95.7

74.4

401

A 367

A 367

52

92.3

61

93.4

92.9

402

A 367

A 367

103

76.7

90

94.4

85.0

404

A 367

A 367

66

60.6

67

64.2

62.4

405

A 367

A 367

9

0.0

16

0.0

0.0

406

A 367

A 367

56

58.9

76

86.8

75.0

408

A 367

A 367

13

100.0

16

100.0

100.0

409

A 367

A 367

51

43.1

49

93.9

68.0

411

A 367

A 367

23

78.3

39

82.1

80.6

414

N405

N405

56

0.0

69

0.0

o-o

415

N405

N405

75

0.0

74

0.0

0.0

417

N405

N405

38

0.0

73

0.0

0.0

418

A 379

N379

32

71.9

33

75.8

73 8

419

A 379

N379

35

77.1

22

100.0

83.0

433

N399

A 399

24

70.8

17

88.2

78.0

436

A 379

N379

20

75.0

36

88.9

83.9

439

A 408

A 408

54

85.2

53

81.1

83.2

440

A 408

A 408

25

96.0

26

i 100.0

98.0

453

Nwild

A 399

65

1.5

83

2.4

2.0

454

Nwild

A 399

49

0.0

52

0.0

0.0

455

Nwild

A 399

41

36.6

32

34.4

35.6

456

Nwild

A 399

42

4.8

59

10.2

7.9

459

A wild

Nwild

49

2.0

59

15.3

9.3

474

N414

N414

18

0.0

15

0.0

0.0

513

A 439

A 439

13

92.3

10

100.0

95.7

514

A 440

A 440

44

97.7

44

97.7

97.7

523

N474

N474

39

0.0

37

0.0

0.0

533

A 513

A 513

44

95.5

54

100.0

98.0

548

A 514

A 514

26

96.2

37

100.0

98.4

557

A 548

A 548

18

94.4

29

100.0

97.9

564

A 533

A 533

4

100.0

4

100.0

100.0

575

N523

N523

39

0.0

20

0.0

0.0

INHERITANCE OF ABNORMAL VENATION.

33

Table 36. — Percentage of abnormal offspring of 200 families — Continued.

Offspring.

T-*Q rpnto

Mating
No.

l.l! t;

Male.

Female.

Total

p. ct.

abnormal.

Father.

Mother.

No.
recorded.

P. ct.

abnormal.

No.
recorded.

P. ct.
abnormal.

576

N523

N523

52

0.0

48

0.0

0.0

582

N575

N575

28

0.0

37

0.0

0.0

584

N557

A 557

18

100.0

24

100.0

100.0

585

N576

A 557

48

4.2

45

24.4

14.0

587

N576

N576

29

0.0

21

4.8

2.0

588

N576

N576

55

0.0

46

0.0

0.0

589

A 564

A 564

24

100.0

20

100.0

100.0

590

N588

N582

48

0.0

55

0.0

0.0

591

N588

N588

1

0.0

3

0.0

0.0

592

N587

N582

32

0.0

33

0.0

0.0

593

N587

N582

39

0.0

36

0.0

0.0

594

N585

N585

73

41.1

69

62.3

51.4

600

N588

N588

55

0.0

58

0.0

0.0

602

A 589

A 589

21

100.0

25

100.0

100.0

605

A 584

A 585

30

40. 0

37

67.6

55.2

606

A 584

A 584

2

100.0

7

100.0

100.0

611

A 585

A"C"

45

17.8

50

38.0

28.4

613

N592

N592

38

0.0

53

1.9

1.1

614

N593

N590

38

0.0

50

2.1

1.1

622

N600

N591

19

0.0

45

4.4

3.1

623

N600

N591

24

0.0

35

0.0

0.0

626

A 602

A 594

53

32.1

60

53.3

43.4

632

A 606

A 606

22

100.0

19

100.0

100.0

633

A 602

A611

11

90.9

14

92.9

92.0

639

A 594

A 602

1

100.0

7

100.0

100.0

641

A 611

A 605

32

87.5

49

95.9

92.6

642

A 605

A 605

34

55.9

43

65.1

61.0

643

A 611

A 611

3

100.0

4

100.0

100.0

657

N614

N614

31

0.0

30

0.0

0.0

660

N622

N622

44

2.3

40

5.0

3.6

663

N623

N623

42

0.0

29

0.0

0.0

665

N613

N622

19

0.0

64

0.0

0.0

670

A 626

A 602

35

88.6

45

100.0

95.0

677

A 641

A 626

23

95.7

23

100.0

97.8

678

A 633

A 633

9

100.0

5

100.0

100.0

680

A 642

A 642

34

97.1

49

100.0

98.8

681

A 639

A 639

10

70.0

21

100.0

90.3

682

A 626

A 626

34

91.2

41

100.0

96.0

685

A 643

A 633

18

83.3

23

100.0

92.7

692

A 633

A 633

29

93.1

30

96.7

94.9

694

A 642

A 632

29

75.9

31

83.9

80.0

710

N660

N657

27

0.0

35

0.0

0.0

715

N665

N663

13

0.0

24

0.0

0.0

719

A 670

A 677

7

100.0

11

100.0

100.0

723

A 685

A 682

24

95.8

27

100.0

98.0

726

A 678

A 680

43

90.7

54

100.0

95.9

727

A 692

A 692

11

100.0

15

100.0

100.0

729

A 681

A 682

...

1

100. 0

100.0

737

A 694

A 694

9

88.9

7

100.0

93.8

752

A 726

A 719

45

100.0

56

100.0

100.0

753

A 726

A 723

27

92.6

27

100.0

96.3

763

A 727

A 727

12

100.0

13

100.0

100.0

764

A 726

A 727

29

96.6

29

100.0

98.3

765

A 726

A 729

46

97.8

50

100.0

99.0

767

A 737

A 737

20

80.0

27

100.0

91.5

785

N715

N715

63

20.6

83

20.5

20.5

799

A 753

A 753

17

88.2

38

92.1

90.9

802

N715

N710

40

0.0

44

0.0

0.0

34

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

Table 36. — Percentage of abnormal offspring of 200 families— Continued.

Offspring.

Pq tiAntu

Mating
No.

i til t:

Male.

Female.

Total

p. ct.

abnormal.

Father.

Mother.

No.
recorded.

P. ct.

abnormal.

No.
recorded.

P. ct.

abnormal

804

N710

N715

19

0.0

19

5.3

2.6

808

A 752

A 765

21

95.2

25

100.0

97.8

813

A 763

A 763

8

100.0

9

100.0

100.0

816

A 764

A 764

26

100.0

23

100.0

100.0

818

A 767

A 767

13

100.0

12

100.0

100.0

831

N804

N802

34

0.0

35

0.0

0.0

833

N802

N802

40

0.0

53

1.9

1.1

836

N785

N785

46

19.6

63

38.1

30.3

851

A 799

A 799

6

100.0

11

100.0

100.0

853

A 816

A 808

25

100.0

41

100.0

100.0

858

A 808

A 808

38

100.0

36

100.0

100.0

880

N836

N831

52

5.8

83

7.2

6.7

882

N833

N836

55

o.o

55

3.6

1.8

886

A 851

A 853

29

100.0

44

100.0

100.0

889

A 858

A 853

16

87.5

35

97.1

94.1

898

N857

N857

55

3.6

63

1.6

2.5

899

N857

N857

50

2.0

33

0.0

1.2

900

A 857

N857

38

2.6

44

13.6

8.5

902

A 886

A 889

28

100.0

36

97.2

98.4

907

A 886

A 886

37

100.0

27

100.0

100.0

908

A 886

A 886

42

100.0

55

100.0

100.0

917

A 886

A 886

39

100- 0

39

100.0

100.0

926

N880

N880

49

6.1

50

6.0

6.1

XXII

A 886

N882

20

65.0

27

74.1

70-2

943

A 902

A 902

59

98.3

74

100.0

99.2

946

A xxii

A xxii

44

40.9

62

62.9

53.8

947

A xxii

N xxii

50

52.0

78

66.7

60.9

948

N xxii

N xxii

54

25.9

59

40.7

36-9

953

N926

N926

40

0.0

58

13.8

8.2

954

N926

A 908

43

32.6

46

5S.7

46.1

955

N926

A 908

40

27.5

53

26.4

26.9

967

A xxii

A xxii

37

54.1

46

71.7

63.9

968

A xxii

A xxii

23

87.0

32

100.0

94.5

970

N xxii

N xxii

44

31.8

43

34.9

33.3

983

N946

N946

46

39.1

43

60.5

49.4

984

A 946

A 946

33

81.8

51

90.2

86.9

985

A 946

N946

41

56.1

41

78.0

67.1

986

N947

N947

29

24.1

36

38.9

32.3

989

A 947

N947

27

66.7

29

82.8

75.0

997

A 943

A 943

27

77.8

28

85.7

81.8

1006

A 930

N957

18

55.5

20

60.0

57.9

1017

N953

N953

7

0.0

8

12.5

7.3

1021

A 947

N947

21

47.6

22

45.5

46.5

1064

N997

A 997

30

50.0

38

78.9

66.2

1069

N1017

N1017

24

0.0

40

2.5

1.6

1071

A 981

N1006

4

0.0

7

14.3

9.1

1111

N1062

N1069

9

0.0

9

0.0

0.0

1117

N1064

N1064

19

26.3

18

4.4

35.1

1118

N1064

N1064

55

23.4

63

39.7

32.2

1123

N1069

N1069

52

0.0

65

0.0

0.0

1124

N1069

N1069

19

0.0

36

0.0

0.0

1141

2 A 1102

3 N 1071

39

10.3

58

8.6

9.3

1153

Nllll

Nllll

69

0.0

74

2.7

1.4

1154

Nllll

Nllll

51

2.0

47

6.4

4.1

1156

Nllll

Nllll

39

5 1

53

5.7

5.4

1158

N1117

N1118

2

0.0

6

16.7

12.5

1166

N1158

N1158

42

11.9

58

20.7

17.0

1172

N1156

N1156

37

8.1

42

21.4

15.2

1176

N1154

N1156

70

2.9

69

1.4

2.2

1177

N1154

N1156

53

7.5

59

13.6

10.7

INHERITANCE OF ABNORMAL VENATION.

35

Table 36. — Percentage of abnormal offspring of 200 families — Continued.

Offspring.

Po vpnto

Mating
No.

X <%l \

Male.

Female.

Total

p. ct.

abnormal.

Father.

Mother.

No.
recorded.

P. ct.
abnormal.

No.
recorded.

P. ct.

abnormal.

1181

A 1141

4 N 1141

39

10.3

70

22.9

18.3

1190

2 A 1141

4 N 1141

45

11.1

53

11.3

11.2

1192

N1177

N1177

39

2.6

28

17.9

9.0

1193

N1177

N1177

49

2.0

73

1.3

1.6

1197

N1176

N1176

61

0.0

53

1.9

0.9

1204

N1166

N1166

2

0.0

6

0.0

0.0

1208

A 1181

3 N 1181

49

8.2

53

11.3

9.8

1213

N1166

N1166

33

3.0

47

23.4

15.0

1217

3 A 1190

4 N 1190

28

21.4

29

41.4

31.6

1221

N1197

N1197

43

4.7

47

6.4

5.6

1226

N1193

N1193

29

0.0

21

9.5

4.0

1229

N1204

N1204

5

0.0

11

0.0

0.0

1254

N1229

N1229

23

0.0

21

0.0

0.0

1256

N1226

N1226

39

2.6

46

10.9

7.1

1266

N1254

N1254

25

4.0

26

3.8

3.9

1268

N1254

N1254

13

0.0

12

0.0

0.0

1269

N1254

N1254

4

0.0

9

0.0

0.0

1282

N1256

N1256

4

0.0

4

0.0

0.0

1286

N1269

N1269

27

0.0

29

0.0

0.0

1293

N1286

N1286

55

1.8

53

5.7

3.7

1300

N1282

N 1282

20

0.0

24

0.0

0.0

1309

N1293

N1293

12

0.0

14

0.0

0.0

1327

N1300

N 1300

52

0.0

48

0.0

0.0

1347

N1327

N1327

46

0.0

59

0.0

0.0

1394

N1347

N1347

61

0.0

73

0.0

0.0

1428

3 N 1394

3 N 1394

62

1.6

66

0.0

0.8

1454

N1428

N1428

65

0.0

64

0.0

o.o

1476

N1454

N1454

43

0.0

46

0.0

0.0

1533

N1476

N1476

34

0.0

33

0.0

0.0

1565

N1533

N1533

64

0.0

74

0.0

0.0

1587

* A 1498

* A 1498

37

24.3

40

15.0

19.5

1588

* A 1492

* A 1492

44

2.3

44

0.0

1.1

1626

N1565

N1565

25

0.0

32

0.0

o.o

1668

A 1587

A 1588

43

2.3

69

2.9

2.7

1687

A 1587

N1587

55

1.8

63

12..7

7.6

1701

N1626

N1626

77

0.0

68

0.0

0.0

1722

N1668

N1668

30

0.0

70

4.3

3.0

1785

N1687

A 1687

29

10.3

33

152

12.9

1787

N1701

N1701

32

0.0

40

0.0

.0

1788

A 1668

N1668

5

0.0

80

11.3

10.6

1830

N1787

N1787

45

0.0

88

0.0

0.0

1857

N1722

N1722

20

10.0

62

6.4

7.3

1859

A 1785

N1785

21

0.0

30

33.3

19.6

1890

N1830

N1830

7

0.0

8

0.0

0.0

1961

N1859

A 1859

49

16.3

44

9.1

12.9 1

2006

N1788

A 1788

18

5.6

40

25.0

19.0

2013

N1890

N1890

12

0.0

16

0.0

0.0

2084

A 1857

A 1857

8

12.5

23

8.7

9.7

2194

N2013

N2013

18

0.0

9

0.0

0.0

2224

A 1961

A 2006

13

15.4

28

39.3

31.7

2226

A 1961

A 2006

68

10.3

99

33.3

24.0

2296

A 2084

A 2084

25

28.0

10

30.0

28.6

2313

N2194

N2194

14

0.0

23

0.0

0.0

2366

A 2296

A 2224

8

50.0

16

43.8

45.8

2367

N2313

N2313

11

0.0

15

0.0

0.0

2458

N2367

N2367

24

0.0

21

0.0

0.0

2471

A 2366

A 2366

78

79.5

114

90.3

85.9

2503

N2458

N2458

53

0.0

46

0.0

0.0

2524

A 2471

A 2471

45

100.0

61

100.0

100.0

•From wild material (see page 13).

THE EFFECT OF SEXUAL SELECTION.*

It is relatively easy to get by artificial selection a strain of Drosophila
ampelophila in which practically all the individuals possess extra wing-
veins. Also, by selection one can reduce the amount of venation. The
latter strain is manifestly not fitted to maintain itself , because the wings,
deprived of the support of the veins, droop and catch in the food of the
insect, resulting in the insect's death. On the other hand, the wings
of the extra- veined race are strong, the individuals are vigorous and fer-
tile. What would be the fate of such a race if turned loose in nature
(a) where they would find plain-winged individuals with which to breed
and (6) where they were isolated from plain-winged individuals? Rea-
soning from the fate of most feral domestic races, one would expect
that in the former case they would soon disappear, although the reason
assigned for their disappearance would be the vague one that they
would be "swamped." In the latter case many would expect them to
keep the domestic characteristics.

Two cubic feet of space and a few decaying bananas form conditions
sufficiently feral for the purpose of testing what would happen. On
May 2 I released in a large battery-jar an equal number of flies from one
of my extra-veined strains and from one of my plain-winged strains.
This would clearly give the extra-veined an advantage, for not often will
a new form make up 50 per cent of the population. On May 19 only 26
per cent of the flies in the jar showed extra veins and these veins were
not as pronounced as those of the original 50 per cent. By May 26 the
number was reduced to 11 per cent. It was 7 per cent on June 9, and two
weeks later (June 23) only 1 per cent showed any trace of extra veins.

On February 19 I released in a similar jar a population of flies selected
from an extra-veined race on the basis of well-developed extra veins.
No plain-winged flies were introduced. However, after six weeks
(March 31) only 93 per cent showed extra veins and in none of these
cases were the extra veins very strong. On April 24 there were only
81 per cent; May 25, 72 per cent; June 23, 49 per cent; and by August
3 only 5 per cent showed any trace of extra veins.

As has been shown, plain-winged individuals occasionally turn up in
carefully-bred extra-veined races, but it was, at first, puzzling to see how
these occasional "reversions" could get such a foothold as to supplant
the extra-veined flies which were in the jar by the hundreds. The expla-
nation was found while testing the selective value of the prominent male
secondary sexual character on the anterior tibiae— the large tibial comb.

*Papsr read before the American Society of Naturalists, Boston meeting, 1909.
36

THE EFFECT OF SEXUAL SELECTION. 37

I cut them off of a plain-winged male and left them on a male of the
extra-veined race and vice versa. These two males were then given to
a female as mates. By a study of her offspring I could tell, in a rough
way, which mate she preferred. To my surprise she chose almost exclu-
sively the normal male, whether he had tibial adornments or not.

Then, without removing the tibial combs, I gave plain-winged and
extra-veined individuals the choice between mates which, as far as I
could determine, were alike in all particulars such as age, nutrition,
activity, and time since last copulation, but differed in that one had
extra veins while the other had not. I watched each experiment until
copulation had taken place. When the extra venation in one mate was
great, the chooser, whether male or female, normal or extra-veined,
chose the normal mate. I then tried weaker degrees of the character and
in 85 experiments, mostly with flies having the extra veins only very
slightly developed, 61 of the choices were in favor of the wild type.

The basis upon which these flies discriminate against extra-veined
individuals when choosing a mate is a matter for further study. There
is an elaborate "courtship," in which the flirting of the wings in front
of the prospective mate plays a large part. It seems as though a choice
were made on the basis of sight, but I doubt whether that is the case.
However, there is no doubt of the choice. It is a clear case of the
undoing of artificial selection by sexual selection.

DISUSE AND DEGENERATION.*

One of the several much-discussed but little-tested problems of the
theory of evolution is that of the inherited effects of disuse. I believe that
there is a pretty general idea that when a species no longer has need for
an organ that organ will degenerate. The explanations of this degener-
ation are varied, but the most popular seem to be the inheritance of
acquired characters, panmixia and selection. It is indisputable that in
the life of an individual many unused organs do degenerate, but it is far
from proven or even satisfactorily indicated that this ontogenetic degen-
eration is followed by a phylogenetic degeneration. There is no doubt
that many degenerate organs are not used in any way; but who can say
whether this disuse has preceded degeneration as a cause or merely fol-
lowed as a necessary consequence ? Before attempting to explain the
phylogenetic degeneration which follows disuse it seems desirable to find
a clear case of such a sequence, and this quest was the purpose of the
experiment with Drosophila ampelophila upon which I wish briefly to
report.

These insects are normally very good fliers, possessing wings which
are relatively quite large. In my experiments, however, they were con-
fined in glass vials barely large enough to contain the food. The only
opportunity they had to fly was when they were transferred from one
vial to another. This was done only three times a week. Such flight
could at most not be more than 5 cm., and was, as a matter of fact,
rarely made, as they usually walked.

The experiments are complicated by several facts which must be con-
sidered. These fall into two groups:

First, those which might explain the absence of degeneration in the
wings. Disuse does not affect, during the life of an individual, the
wing-dimensions, for after an insect's wings are expanded there is no
change in them and, of course, they are not subject to the effects of use
and disuse before they are expanded. However, the degeneration of
beetle-wings when the elytra are fused, of the wings of cave insects, of
parasites, and of the wings of many female Lepidoptera are used as stock
examples of disuse. Furthermore, if there be anything in the theory
of hormones (of which Cunningham has recently made so much) or the
various forms of the memory theory of inheritance, we would expect
phylogenetic degeneration because of the germ-plasm receiving the news
that the wings are not being used, providing the plasm is in condition to

*Paper read before the American Society of Zoologists, Baltimore meeting, 1908.
38

DISUSE AND DEGENERATION. 39

receive and act upon such a stimulus. In certain insects the germ-cells
are all practically matured before or by the time the wings are expanded
and ready for use. This, however, is not the case with Drosophila.
Not only are the germ-cells not all matured by the time it becomes adult,
but they are in all stages of development and continue to mature, a few
at a time, for a month thereafter. In these experiments I rarely used
as parents the individuals coming from first-laid eggs, so that there were
strong chances of my using affected germ-plasm if such exists. Any
experiment, such as this, is always open to the criticism that it has not
been sufficiently long continued, but I am sure that most will agree
that 43 generations, combined with microscopic measurements and the
delicacy of biometric analysis, ought to give a satisfactory indication of
what is taking place.

The second set of considerations might explain any observed degen-
erations without reference to the disuse. Excessive inbreeding was
practiced, sister usually being bred to brother. This was necessary for,
if I had planned to stop at this point and had wished to entirely avoid
inbreeding, I would have needed more than 8 trillion flies with which to
start the work. Inbreeding is supposed to lead to degeneration and might
thus be solely accountable for degeneration, or it might assist disuse.
Unnatural conditions might have adversely affected thefflies. Confine-
ment itself, apart from the entailed disuse, might at least help to bring
about degeneration. Furthermore, I kept the insects breeding winter
and summer, with no rest for hibernation and with no change of food.
There was no conscious selection favoring perfect and large wings, as
all measurements of this strain were made quite recently and the vari-
ations in wing-dimensions are not readily appreciable, hence the removal
of selection in favor of good wings might result in panmixia and conse-
quent degeneration. Finally, I was constantly on the lookout for signs
of degeneration, as I hoped and still do hope to produce a wingless Dro-
sophila. My desire might have influenced my actions and an unconscious
selection on my part might have reduced the size of the wings without
disuse playing a part.

The only necessary answer to this second set of considerations is that,
in spite of the possibility of the degenerating effect of disuse being helped
by inbreeding, unnatural conditions, panmixia, or selection, there has
been no degeneration.

Evidence of degeneration was sought for by carefully measuring the
expanded wings of the individuals belonging to successive stages of the
experiment. In making these measurements one may not mix the sexes
because of the sexual difference in size. Therefore the females alone
were used, since among insects it is more commonly the females which
have degenerate wings. The results are shown in table 37, where 33
units of length equal 1 mm.

40

EXPERIMENTS WITH DROSOPHILA AMPELOPHILA.

TABLE 37. — Mean tving-dimensions at various periods of continued disuse.

Generations of disuse.

Length of wing.

Breadth of wing.

Length X breadth.

1st to 3rd

67.00 ±0.12
66.50 ±0.11
64.91 ±0.12
67.67 ±0.18

32.55 ±0.07
33.60 ±0.06
31.98 ±0.06
34.06 ±0.08

2223.12 ± 8.85
2281.12 ± 7.41
2115.44 ± 7.42
2358.94 ± 11.46

17th to 19th

33rd to 35th

41st to 43rd

If the experiment had stopped at the end of the thirty-fifth generation
it would have appeared from this table that the wings were actually
getting smaller, since the area, as judged by length X breadth, was
smaller in the second lot than in the first, and still smaller in the third —
the difference being nearly ten times the expected error. However, this
would have been a hasty conclusion. The fourth lot is as much larger
than the first as the third is smaller. So we must conclude that there
is no evidence that the constant disuse of the wings during more than
40 generations has had any effect.

BIBLIOGRAPHY.

Blanchard, N.

1903. On the inheritance in thoroughbred horses. Biometrika, II, 229-234.
Castle, W. E.

1905. Heredity of coat characters in guinea-pigs and rabbits. Carnegie Institu-

tion of Washington, Publication No. 23.
1906a. The origin of a polydactylous race of guinea-pigs. Carnegie Institution

of Washington, Publication No. 49.
19066. Inbreeding, cross-breeding, and sterility in Drosophila. Science, n. s. ,

xxill, No. 578. (See also Proc. Am. Acad., xli, No. 33.)
Cu£not, L.

1904. L'he're'dite de la pigmentation chez les souris. ( 3me note. ) Arch. Zool.

Exper. et Gen., se*r. 4, torn. 2, Notes et Revue, pp. xlv-lvi.

Davenport, C. B.

1910. The imperfection of dominance and some of its consequences. Amer. Nat.
XLIV, No. 519.
Jennings, H. S.

1908. Heredity, variation, and evolution in Protozoa. II. Proc. Am. Phil. Soc,
xlvii, No. 190, p. 523.
Larrabee, A. P.

1906. The optic chiasma of Teleosts : A study of inheritance. Proc. Am. Acad.

XLII, No. 12.
Lutz, F. E.

1903. Note on the influence of change in sex on the intensity of heredity. Bio-
metrika, H, pp. 237-240.

1907. Paper read at the Seventh International Zoological Congress.

1908. Combinations of alternative and blending inheritance. Science, n. s.,

xxvili, No. 714.
Pearson, Karl.

1900. On the inheritance of characters not capable of exact quantitative measure-
ment. Phil. Trans., A., cxcv, pp. 115-117.
Prizbram, Hans.

1907. Vererbungsversuche uber asymmetrische Augenfarbung bein Angorakat-
zen. Archiv f. Entwicklungsmechanik, xxv, 260-265.

3 4- 6 f

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