linguistic:paraphrasing, structural:scholar_edition, structural:expansion, linguistic:translation
Embryonic development

Snake embryonic development initially follows similar steps as any vertebrate embryo. The snake embryo begins as a zygote, undergoes rapid cell division, forms a germinal disc, also called a blastodisc, then undergoes gastrulation, neurulation, and organogenesis. Cell division and proliferation continues until an early snake embryo develops and the typical body shape of a snake can be observed. Multiple features differentiate the embryologic development of snakes from other vertebrates, two significant factors being the elongation of the body and the lack of limb development.

The elongation in snake body is accompanied by a significant increase in vertebra count (mice have 60 vertebrae, whereas snakes may have over 300). This increase in vertebrae is due to an increase in somites during embryogenesis, leading to an increased number of vertebrae which develop. Somites are formed at the presomitic mesoderm due to a set of oscillatory genes that direct the somitogenesis clock. The snake somitogenesis clock operates at a frequency 4 times that of a mouse (after correction for developmental time), creating more somites, and therefore creating more vertebrae. This difference in clock speed is believed to be caused by differences in Lunatic fringe gene expression, a gene involved in the somitogenesis clock.

There is ample literature focusing on the limb development/lack of development in snake embryos and the gene expression associated with the different stages. In basal snakes, such as the python, embryos in early development exhibit a hind limb bud that develops with some cartilage and a cartilaginous pelvic element, however this degenerates before hatching. This presence of vestigial development suggests that some snakes are still undergoing hind limb reduction before they are eliminated. There is no evidence in basal snakes of forelimb rudiments and no examples of snake forelimb bud initiation in embryo, so little is known regarding the loss of this trait. Recent studies suggest that hind limb reduction could be due to mutations in enhancers for the SSH gene, however other studies suggested that mutations within the Hox Genes or their enhancers could contribute to snake limblessness. Since multiple studies have found evidence suggesting different genes played a role in the loss of limbs in snakes, it is likely that multiple gene mutations had an additive effect leading to limb loss in snakes