No abstract

Parthenogenesis, embryonic development of an unfertilized egg, occurs naturally in turkey, chicken, and quail species. In fact, parthenogenesis in turkeys and chickens can be increased by genetic selection. However, it is unknown if genetic selection for parthenogenesis is effective in quail or if selection for parthenogenesis affects egg production. Therefore, the objectives of this study were to determine if the incidence of parthenogenesis in quail could be increased by genetic selection and if selection for this trait affects egg production. To prevent fertilization, 1,090 females were caged separately from males at 4 wk of age and then caged individually at 6 wk of age to monitor egg production. Eggs were collected daily, labeled, and stored for 0 to 3 d. After 10 d of incubation, 20 unfertilized eggs from each hen were examined for the occurrence of parthenogenesis and embryonic growth. In the parent (P) generation and subsequent generations (1 to 4), hens laying eggs containing parthenogenetic development and males whose sisters or mothers exhibited parthenogenesis were used for breeding. There was a linear increase in the percentage of hens exhibiting parthenogenesis as generation of selection increased. With each successive generation, there was a quadratic response in the percentage of eggs positive for parthenogenesis. When compared with the P generation, parthenogenesis was almost 3 times greater for eggs laid by the fourth generation (4.6 to 12.5%, respectively). Even when only hens exhibiting parthenogenesis were examined, the percentage of eggs demonstrating embryonic development responded quadratically with generation of selection. The embryonic size at 10 d of incubation was greater for each subsequent generation when compared with the P generation. There was a linear decrease in both egg production and the average position of an egg in a clutch as generation of selection increased. In conclusion, genetic selection for parthenogenesis increased the incidence of parthenogenesis and embryonic size but decreased egg production and average position of an egg in a clutch as generations of selection increased.

Recent experiments, in which barriers were inserted between anterior and posterior tissues of the chick wing bud, resulted in deletion of structures anterior to the barrier (Summerbell, 1979). From these data it was concluded that blockage of morphogen from the polarizing zone by the barrier resulted in the observed failure of specification of anterior structures. We suggest an alternative interpretation, viz. the interruption of the apical ridge by the barrier caused the deletions. This hypothesis was tested by removal of increasing lengths of ridge. This was done beginning at either the anterior or posterior junction of the wing bud with the body wall and proceeding posteriorly or anteriorly, respectively, to each half-somite level between 16/17 and 19/20. With removal of progressively greater lengths of anterior ridge, more anterior limb elements failed to develop. These data were used to construct a map of the ridge responsible for each digit. To test our hypothesis we removed posterior sections of apical ridge, as described above. Removal of posterior ridge to a level which was expected to allow outgrowth of digits anterior to the level of removal resulted in wings without digits in the majority of cases. An exception occurred when ridge posterior to the mid-19 somite level was removed. In almost half of these cases digits 2 and 3 did develop. In most cases the retention of only a half-somite piece of ridge with all other ridge removed, also resulted in deletion of all digits. Again the exception occurred when ridge posterior to somite level mid-19 and anterior to level 18/19 was removed, leaving only that ridge between somite level 18/19 and mid-19. In many of these cases digit 3 did develop. We conclude from these data that, in the wing bud, ridge anterior to the mid-19 somite level must be connected to more posterior ridge to function. The leg ridge does not exhibit the asymmetrical, low anterior, high posterior configuration, which appears in the wing. Because the leg ridge is symmetrically high anteriorly and posteriorly, we questioned whether or not leg would also require a continuity between anterior and posterior ridge for anterior ridge to function. It did not. When posterior ridge was removed, structures developed under remaining anterior ridge and the elements which developed were complementary to those which developed after anterior ridge removal to the same somite level. Those leg elements, which failed to develop, were truncated at the appropriate proximodistal levels as indicated by the fate map we have constructed for the leg. The data reported here do not rule out a role for the polarizing zone in specification of anterior structures. It is apparent that posterior ridge removal in the wing results in loss of structures anterior to the removal. However, this is not true for the leg.

Currently the chick leg bud or its components are being used extensively to study questions in development. Although fate maps of the leg, similar to that developed by Saunders (1948) for the wing, have been available (Hampé, 1957a, 1959), no study of the proximodistal sequence of the specification of leg structures exists. Such a sequence developed fot the wing by removal of the apical ectodermal ridge at successive stages (Saunders, 1948; Summerbell, 1974), has proven useful to the study of wing development. In this paper, we present a similar proximodistal sequence for the chick leg including the same developmental stage range as that of the wing sequence.

Impermeable barriers were inserted into the stage-20 to -21 leg bud to test whether or not such an interruption of diffusion of the proposed morphogen from the polarizing zone would result in failure of leg elementsto develop anterior to the barrier. Tantalum foil was placed at somite levels 30/31 or mid-31 through thedorsoventral extent of the leg bud separating anterior from posterior mesoderm and ectodermal ridge. In the resulting legs, structures developed anterior to the level of the barrier. For example, legs with foil at the 30-/31-somite level developed digits 1 and 2. We conclude that either the barrier is not an effective block of diffusion of polarizing zone morphogen or that the influence of the polarizing zone is not required fordetermination of leg structures at these stages.