#gastrulation

Sea Urchin -ll

The first structure formed during sea urchin gastrulation is:

In sea urchins gastrulation begins with ingression of primary mesenchyme cells derived from large micromeres entering blastocoel. Vegetal plate then invaginates to form primitive gut archenteron, and opening at vegetal pole where invagination occurs becomes blastopore surrounded by circumblastoporal cells. Since deuterostome fate dictates blastopore persists as anus, initial blastopore remains as larval anus while mouth forms secondarily where archenteron contacts stomodeum. Therefore among early gastrula landmarks, anus represents first functional structure derived directly from blastopore, reflecting ancestral deuterostome patterning principles.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Gastrulation in sea urchins - blastopore fate and deuterostomy.

View Details

amphibian Development-l

During amphibian development, archenteron forms from:

During amphibian gastrulation, invagination at dorsal blastopore lip pulls vegetal endoderm and mesoderm inside blastocoel cavity. As involution progresses, expanding cavity lined by endoderm becomes primitive gut or archenteron. Its roof consists of involuted chordamesoderm that will become notochord, floor and side walls are endoderm destined for gut epithelium. Blastocoel is displaced and ultimately obliterated as archenteron enlarges posteriorly. This new cavity later connects to exterior at blastopore forming anus and mouth secondarily, establishing digestive tract anlage that later differentiates into foregut, midgut, hindgut, and associated organs.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Archenteron formation via gastrula invagination amphibians.

View Details

amphibian Development-l

Gastrulation involves which primary cell movement?

Amphibian gastrulation integrates three movements: epiboly expands animal cap ectoderm over entire embryo via radial intercalation; involution rolls marginal zone mesoderm inside over blastopore lip; invagination and involution driven by bottle cells create archenteron cavity. Convergent extension of dorsal mesoderm narrows and elongates body axis through mediolateral intercalation regulated by non-canonical Wnt planar cell polarity pathway. These coordinated morphogenetic events occur without large growth, reshaping blastula into gastrula with internalized mesoderm and endoderm and dorsal organizer positioned for subsequent neural induction and patterning of body plan.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Gastrulation movements epiboly involution invagination convergent extension.

View Details

amphibian Development-l

Gastrulation results in formation of:

Gastrulation converts radially symmetrical blastula into triploblastic gastrula through morphogenetic movements epiboly, emboly, involution, invagination, and convergent extension that reorganize cells without net growth. Animal cap ectoderm spreads over embryo, marginal zone mesoderm rolls inside over blastopore lip, and vegetal endoderm internalizes to line archenteron cavity. Molecularly BMP, Nodal, Wnt, and FGF pathways pattern germ layer identities before movements, with Nodal highest vegetally. End result is establishment of three definitive germ layers ectoderm, mesoderm, endoderm positioned appropriately for organogenesis, with dorsal mesoderm forming organizer inducing neural tissue via inhibition of BMP signaling.

Ref: Alberts, Molecular Biology of the Cell, 6th ed., Chapter 21: Gastrulation forms three germ layers.

View Details

amphibian Development-l

Gastrulation in amphibians begins at:

Amphibian gastrulation initiates specifically where dorsal determinants have accumulated before cleavage. Following cortical rotation, gray crescent region opposite sperm entry acquires high nuclear beta-catenin, expresses organizer genes siamois and goosecoid, and forms bottle cells by apical constriction. This site becomes dorsal lip of blastopore, first point of marginal zone involution and archenteron initiation. Involution spreads laterally and ventrally around blastopore forming lateral and ventral lips. Initiation at gray crescent ensures chordamesoderm internalizes dorsally to form notochord beneath ectoderm where it secretes BMP antagonists inducing neural plate formation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Amphibian gastrulation begins at gray crescent.

View Details

amphibian -ll

The primary embryonic induction process involves:

Primary embryonic induction defined by Spemann and Mangold as organizer dorsal mesoderm inducing overlying ectoderm to become neural plate rather than epidermis, mediated by BMP antagonists Chordin, Noggin. This mesoderm-ectoderm interaction is archetypal induction: dorsal mesoderm secreting inhibitors instructs competent ectoderm whose fate changes upon contact requiring time for transcription. Secondary inductions like lens or limb involve similar principles. Although endoderm and blastocoel form earlier and neural crest arises later via Wnt and BMP border signals, fundamental conceptual breakthrough concerned mesoderm signaling to ectoderm generating central nervous system and body pattern.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 10: Primary embryonic induction - mesoderm-ectoderm interactions in neural induction.

View Details

amphibian -ll

Dorsal mesoderm during organizer formation specifically induces:

Dorsal mesoderm from Spemann organizer involutes as chordamesoderm: anterior prechordal plate induces forebrain, while posterior notochordal and paraxial dorsal mesoderm secretes Wnt antagonists Frzb plus FGF and retinoic acid gradients that posteriorize overlying neural ectoderm, converting default anterior neural fate to hindbrain rhombomeres expressing Krox20 and spinal cord trunk expressing HoxB9. Experiments grafting dorsal mesoderm beneath animal caps induced Krox20-positive hindbrain and HoxB9 trunk markers. Ventral mesoderm and epidermis lack this caudalizing ability, confirming dorsal mesoderm induces hindbrain and trunk, essential for AP neural patterning.

Ref: Wolpert, Principles of Development, 5th ed., Chapter 6: Dorsal mesoderm patterning hindbrain and trunk neural tissue.

View Details

amphibian -ll

The pharyngeal endoderm and prechordal plate induce formation of:

Anterior endomesoderm consisting of pharyngeal endoderm and prechordal plate mesoderm involutes early and underlies anterior neuroectoderm. These cells secrete antagonists Cerberus, Dkk1 and Frzb inhibiting Wnt and BMP, plus IGF signals, creating permissive anterior condition suppressing caudalization. They induce Otx2, Six3 and BF1 expression specifying forebrain and midbrain identity. Posterior hindbrain and spinal cord require later chordamesoderm producing Wnt, FGF and retinoic acid to caudalize neural plate via Hox activation. Hence head organizer activity localized in pharyngeal endoderm and prechordal plate determines anterior brain regionalization.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 11: Head induction - pharyngeal endoderm and prechordal plate inducing forebrain and midbrain.

View Details

amphibian -ll

The dorsal lip of the blastopore forms due to:

After cortical rotation, vegetal endoderm undergoes vegetal rotation where large yolky dorsal marginal cells move inward and upward, forming wedge thrust pushing dorsal marginal mesoderm outward creating lip. This movement of bottle cells and involution starts at gray crescent region, generating dorsal blastopore lip visible as pigment-free arc. Rotation driven by Brachyury and Wnt11 dependent cell intercalation and apical constriction via Shroom3. Animal pole elongation not involved. Process establishes site of gastrulation and marks organizer region preparing for mesoderm involution and archenteron formation during amphibian gastrulation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Vegetal rotation and formation of dorsal blastopore lip.

View Details

chick development-l

Gastrulation in chicks primarily occurs through:

Due to enormous yolk mass preventing circular blastopore formation, chick gastrulation utilizes linear primitive streak as blastopore equivalent. Epiblast cells converge via Wnt-PCP mediated mediolateral intercalation toward posterior midline, undergo EMT, ingress through streak to generate definitive endoderm displacing hypoblast and mesoderm layers. Hensen's node at anterior tip contributes chordamesoderm forming notochord. Molecularly driven by Nodal, Wnt3a, Brachyury and FGF signaling. This ingression mechanism efficiently internalizes mesoderm around yolk while keeping blastoderm flat. Blastocoel, neural tube and hypoblast not gastrulation portals but products or separate processes.

Ref: Wolpert, Principles of Development, 5th ed., Chapter 5: Gastrulation through primitive streak in chick and amniotes.

View Details

chick development-l

Primitive streak formation in chick is initiated at:

Koller's sickle is thickened crescent of epiblast cells plus polyingressing mesenchymal cells at posterior edge of area pellucida, expressing Vg1/GDF1, Nodal and FGF4. Experimental fate mapping shows it acts as avian Nieuwkoop-like center, secreting TGF-beta signals inducing adjacent epiblast to express Brachyury and form primitive streak. Posterior marginal zone overlying sickle provides Wnt8c permissive signal. Together they organize streak initiation, maintaining high beta-catenin and Nodal activity posteriorly. Removal or anterior transplantation abolishes or relocates streak, confirming Koller's sickle as essential streak initiator for gastrulation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Koller's sickle, posterior marginal zone and primitive streak induction.

View Details

Chick development-ll

Epiblast cell ingression through primitive streak forms:

Gastrulation ingression in chick is EMT event regulated by FGF and Wnt signals inducing Snail2, downregulating tight junction proteins. Epiblast cells at streak lose basement membrane, ingress through primitive groove as individual mesenchymal cells. Early ingressors displace hypoblast forming definitive endoderm of gut, later ingressors occupy middle layer forming embryonic mesoderm including chordamesoderm, paraxial, intermediate, lateral plate and extraembryonic mesoderm, while remaining epiblast becomes ectoderm. Neural crest delaminates later after neurulation, neural plate remains ectodermal, demonstrating ingression forms mesoderm and endoderm rather than ectoderm. This illustrates conserved developmental logic of morphogen gradients patterning embryonic axes through Wnt and BMP antagonism.

Ref: Gilbert, Developmental Biology 12th ed., Chapter 12: Fate of cells ingressing through primitive streak.

View Details