RESUMO
The evolution of viviparity requires eggshell thinning to bring together the maternal uterus and extraembryonic membranes to form placentae for physiological exchanges. Eggshell thinning likely involves reduced activity of the uterine glands that secrete it. We tested these hypotheses by comparing the uterine and eggshell structure and histochemistry among oviparous and viviparous water snakes (Helicops) using phylogenetic methods. Eggshell thinning occurred convergently in all three origins of viviparity in Helicops and was accomplished by the loss of the mineral layer and thinning of the shell membrane. Uterine glands secrete the shell membrane in both oviparous and viviparous Helicops. These glands increase during vitellogenesis regardless of the reproductive mode, but they always reach smaller sizes in viviparous forms. As there is no phylogenetic signal in eggshell thickness and gland dimensions, we conclude that interspecific differences are related to reproductive mode and not phylogeny. Therefore, our results support the hypothesis that eggshell thinning is associated with the evolution of viviparity and that such thinning result from a reduction in gland size in viviparous taxa. Interestingly, the shell membrane thickness of viviparous females of the reproductively bimodal Helicops angulatus is intermediate between their oviparous and viviparous congeners. Thus, although eggshell thinning is required by the evolution of viviparity, a nearly complete loss of this structure is not. However, uterine gland dimensions are similar across viviparous Helicops. Fewer glands or their functional repurposing may explain the thinner shell membrane in viviparous species of Helicops in comparison to viviparous females of the bimodal H. angulatus.
RESUMO
We used immunofluorescent confocal microscopy and scanning electron microscopy to quantify uterine vascularity and to describe uterine surface morphology during gestation in pregnant females of the lecithotrophic lizard Niveoscincus coventryi. As uterine angiogenesis and epithelial cell morphology are thought to be under progesterone control, we studied the effect of a progesterone receptor antagonist (mifepristone) on uterine and chorioallantoic microvasculature and features of the uterine epithelial surfaces. Although intussuceptive angiogenesis was observed in both, uterine and chorioallantoic, vascular beds during gestation, the only significant increases were in the diameters of the uterine vessels. An ellipsoid vessel-dense area grows in the mesometrial hemisphere of the developing conceptus, which parallels the expansion of the allantois to form the chorioallantoic placenta. Uterine surface topography changed during gestation. In particular, uterine blood vessels bulge over the luminal surface to form marked ridges on the uterine embryonic hemisphere, especially during the last stage of pregnancy, and ciliated cells are maintained in the embryonic and abembryonic hemispheres but disappear in both the mesometrial and antimesometrial poles. This distinct regionalization of uterine ridges and ciliated cells in the uterine surface and in the shape of the epithelial component of the chorion might be related to the function of both chorioallantoic and yolk sac placentae during gestation. There was no significant difference between females treated with or without mifepristone, which may be related to the partial function of mifepristone as a progestin antagonist and/or with the function and time of action of progesterone in the uterus during gestation in N. coventryi. Differences in the pattern of angiogenesis and uterine surface morphology during gestation among squamates may be related to the functional diversity of the uterine component of the different placentae and probably reflect its diverse evolutionary history.