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Gastrulation in the frog embryo occurs in four main steps: invagination, involution, convergent extension and epiboly.

Invagination of the frog embryo occurs opposite the site of sperm. The cells regulating invagination, called bottle cells, undergo apical constriction where the apical-facing aspect of the cell tightens "like a purse string" and promotes an inward buckling of the membrane. Experimentally, researchers noted the ability of cells from the dorsal blastopore lip to induce invagination when transplanted into regions of the embryo that do not undergo invagination during normal development.

Involution of the frog embryo occurs when involuting marginal cells migrate along the outer animal hemisphere cells, effectively "towing" a string of cells towards the interior of the embryo. These leading edge cells propel their migration by traveling upon extracellular matrix proteins.

Convergent extension follows involution, occurring when cells at the blastopore lip merge together in a manner similar to cars merging during traffic. The process of numerous, small individual cell movements causes a dramatic overall lengthening of the forming archenteron. Molecularly, convergent extension operates through lamellipodia extensions regulated by PCP and Disheveled signaling.

Lastly, epiboly occurs when animal cap cells and non-involuting cells spread out over the exterior of the embryo. This process is mediated by the flattening of cells such that cells transition from a cuboidal to a squamous shape.
The patterns of embryonic cleavage differ dramatically between amphibian, avian and mammalian embryos.

Cleavage of the amphibian embryo is holoblastic, meaning that the cleavage furrow divides the cells completely during each division. Initial division of the amphibian embryo is radially symmetrical; and while division of the yolk is not as dramatic as is seen in fish or avian embryos, the yolk is divided unequally between cells.

Cleavage of the avian embryo occurs in the oviduct prior to encasing of the embryo in an eggshell. Division of the embryo is telolecithal, meaning that the cleavage furrow does not completely divide the cells during division. Initial cleavage is discoidal, with a large yolk cell forming the base of the embryo, and several, rapidly dividing animal pole cells comprise a disc that sits atop the yolk. At this time, some blastoderm cells absorb water to form the subgerminal cavity, which later helps to form the area pellucida where most of the actual embryo is formed.

The mammalian embryo undergoes holoblastic rotational cleavage, where the second cleavage has one cell divide equitorally and the other cell divide meridionally. Several characteristics of mammalian cleavage are unique. Specifically, the timing of division is significantly slower than observed in other animals, and cells do not divide synchronously. Additionally, the mammalian embryo undergoes compaction, where cell adhesion proteins (cadherins) are expressed promoting the tight grouping of cells.
BMP signaling plays important roles in both the induction of neural crest cells and in the initial dispersal of neural crest cells from the neural tube.

Based on the previously studied role of bmp signaling in amphibian axis specification, researchers suspected that bmp signaling might play a role in the specification of neural tube. Researchers determined that a gradient of bmp signaling specifies neural crest cells - specifically high levels of bmp and non-existent bmp signaling do not specify neural crest cell development, while low, "Goldilocks-levels" of bmp signaling specify neural crest cell development. Experimentally, researchers discovered that embryos that artificially overexpressed bmp failed to develop neural crest cells, while embryos that expressed limited amounts of bmp developed neural crest cells throughout the embryo.

During the initial dispersal of neural crest cells, the regulation of bmp expression plays a critical role in the timing of dispersal. Researchers have determined that, while bmp is dispersed throughout the embryo, a variety of other factors are localized to neural crest cells. These factors act to regulate the activity of bmp, which ultimately promotes dispersal of neural crest cells. Specifically, somatic cells inhibit that activity of noggin, which in turn inhibits the activity of bmp. Therefore activation of somatic cells activates bmp activity in neural crest cells by preventing noggins inhibition of bmp. After activation, bmp activates an unidentified protease enzyme that degrades N-cadherin, which under normal circumstances acts as a cell adhesion molecule to attach neural crest cells to the neural tube. In sum: somatic cells activate bmp by inhibiting noggin activity. And bmp facilitates the dispersal of neural crest cells by degrading their N-Cadherin mediated attachment to the neural tube.