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#embryonic development

100 public questions tagged with this topic.

Developmental biology Basics

The phenomenon of creating ordered form through coordinated cell actions is termed:

Morphogenesis encompasses cellular behaviors that generate ordered form and architecture. During gastrulation, neurulation, and organogenesis, cells migrate via chemotaxis guided by guidance cues, change shape through actin cytoskeleton and apical constriction, proliferate, and undergo programmed apoptosis to sculpt structures. Molecular drivers include cadherin-mediated adhesion, integrin matrix interactions, and signaling by BMP, Wnt, and Hedgehog coordinating cytoskeletal dynamics. This process transforms flat epithelial sheets into tubes, folds, branches. Differentiation provides cell identity while morphogenesis arranges cells into functional three-dimensional organization essential for organ patterning and body plan establishment.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 5: Morphogenesis and cell behaviors.

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Developmental biology Basics

Which of the following organisms exhibits meroblastic cleavage?

Meroblastic cleavage occurs in eggs with dense yolk concentrated at vegetal pole that prevents complete division. Only cytoplasmic disc at animal pole undergoes cleavage, forming blastoderm sitting on yolk mass. Birds such as chickens and reptiles possess telolecithal eggs with massive yolk for external development, necessitating meroblastic discoidal pattern. Mammals and frogs have holoblastic cleavage because isolecithal or mesolecithal eggs contain less yolk, allowing cleavage furrows to bisect entire egg. Holoblastic cleavage creates smaller equal or unequal blastomeres, while meroblastic supports large nutrient stores required for oviparous development.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 7: Cleavage patterns and yolk influence.

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Stem Cell -ll

The inner cell mass of a blastocyst is composed of:

Mouse blastocyst at embryonic day 3.5 consists of outer trophectoderm surrounding fluid cavity and inner cell mass clustered at embryonic pole expressing Oct4 and Nanog. Inner cell mass cells express Oct4, Nanog, Sox2, and are functionally pluripotent, capable of forming all somatic lineages and germ cells when tested by chimera contribution and teratoma assays, but do not generate trophoblast under normal development. After implantation, ICM diverges into epiblast and primitive endoderm. Cultured in LIF and 2i inhibitors, ICM outgrowths establish embryonic stem cell lines, confirming pluripotency not totipotency or lineage-restricted multipotency.

Ref: Evans & Kaufman, Nature 1981; Martin, PNAS 1981; Gilbert, Chapter 6: ICM pluripotency and ESC derivation.

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Stem Cell -lll

The inner cell mass (ICM) of a blastocyst contains cells that are:

Inner cell mass arises inside blastocyst at embryonic day 3.5 mouse, day 5 human, isolated from trophectoderm outer epithelium forming blastocoel. ICM cells express Oct4, Nanog, Sox2 pluripotency network, capable of differentiation into all three embryonic germ layers contributing to fetus but not efficiently to placenta, meeting pluripotency definition. Cultured ICM generates embryonic stem cells retaining pluripotency demonstrable via chimera and teratoma formation. Totipotent forms extraembryonic as well seen in zygote, multipotent limited to subset like blood, unipotent single lineage such as epidermal basal. ICM potency explains ES derivation.

Ref: Evans and Kaufman, Nature 1981, Pluripotency of Inner Cell Mass and ES Cells.

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Morphogen Induction-l

Which morphogen plays a key role in left-right axis determination?

Left-right asymmetry originates near embryonic node where motile cilia generate leftward fluid flow concentrating Nodal around left lateral plate mesoderm. Nodal, TGF-beta member, activates left-specific cascade including Pitx2 specifying left identity of heart looping and gut situs. Nodal antagonists Lefty2 and Cerberus restrict signal to left, while BMP and FGF modulate intensity. Mutations in Nodal or ciliary dynein cause situs inversus. Fibronectin matrix, Sox2 pluripotency factor and actin cytoskeleton lack instructive laterality information. Nodal gradient thus acts as critical left-right determinant linking ciliary flow to organ laterality and visceral patterning.

Ref: Shiratori and Hamada, Development 2006, Nodal and Left-Right Axis Determination.

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C-Elegans Development-l

Which type of cleavage is exhibited by C. elegans?

Rotational holoblastic cleavage characterizes C. elegans and mammals, diverging clearly from spiral or discoidal modes seen in mollusks and birds. The zygote first divides unequally into larger anterior AB founder and smaller posterior P1 stem cell. Subsequent divisions occur at right angles, with each P lineage division producing a somatic founder and continuing P cell. Founders AB, MS, E, C, D generate distinct tissues, while P4 becomes germline via Z2 and Z3 primordial cells. This invariant lineage enables precise fate mapping, unlike yolk-rich eggs where cleavage is restricted and incomplete.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Early C. elegans development - rotational holoblastic cleavage and founder cell lineages.

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Elegans -ll

What determines the default fate of EMS blastomere?

EMS blastomere default state without P2 signal is mesodermal MS fate. This is determined by nuclear POP-1 levels. In anterior MS daughter, high nuclear POP-1 binds and represses end-1 promoter together with histone deacetylases, allowing tbx-35 for pharynx and muscle. Low POP-1 permits endoderm. POP-1 repression defines default program: when Wnt signaling absent, both daughters maintain high POP-1 and become MS-like. SKN-1 provides competence for both MS and E, but fate choice gated by POP-1 differential. Therefore POP-1 concentration acts as binary switch establishing MS as ground state, repressed variant requiring Wnt input for E divergence.

Ref: Lin et al. 1995; Gilbert Chapter 4: POP-1 determines default fate of EMS blastomere as MS.

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Elegans -ll

Which factor ensures ABp fate specification?

ABp fate distinguishing dorsal versus ventral AB lineage derivatives depends on GLP-1 Notch receptor activation. GLP-1 protein segregates to all AB daughters but functionally active only in ABp due to contact with P2 ligands APX-1 and LAG-2. Activated GLP-1 ICD upregulates Notch target genes ref-1 family, promoting ABp-specific blastomere divisions generating dorsal epidermis and distinct pharyngeal cells. In glp-1 mutants ABp transforms to ABa, equalizing lineage. Therefore GLP-1 presence and selective activation is decisive intrinsic factor ensuring ABp identity, integrating positional signal from P2 to create anterior-posterior and dorsal-ventral pattern within early embryo ectoderm contribution.

Ref: Mango et al. 1994; Gilbert Chapter 4: GLP-1 Notch receptor ensures ABp fate specification in C. elegans.

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Elegans -ll

What happens in embryos lacking functional LAG-2?

LAG-2 encodes Delta-like ligand for LIN-12 and GLP-1 Notch receptors. In early embryo, ABa and MS express GLP-1 while P2 presents LAG-2 and APX-1 to activate GLP-1 in ABp for A-P patterning of pharynx. In gonad, Z1.ppp/Z4.aaa require LAG-2/LIN-12 interaction to decide anchor cell versus ventral uterine fate. Without functional LAG-2, GLP-1 and LIN-12 receptors remain unbound, NICD cleavage fails, downstream targets lag-1 dependent transcription silent. Consequently ABp to ABa transformation and AC/VU defects occur, but fundamentally LIN-12 remains inactive due to absent ligand triggering, revealing ligand-dependent activation mode of Notch signaling in nematode.

Ref: Henderson et al. 1994; Gilbert Chapter 4: LAG-2 loss - LIN-12 remains inactive due to ligand absence.

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Elegans -ll

What happens in embryos with a constitutively active LIN-12 receptor?

Constitutively active LIN-12 results from gain-of-function mutation deleting extracellular domain, making receptor ligand-independent. Normally LIN-12 Notch restricts primary fate via lateral signaling, promoting secondary fate in P5.p and P7.p. When all VPCs express activated LIN-12, Ras-MAPK mediated primary program blocked by LIN-12 targets lip-1 phosphatase that dephosphorylates MAPK, and lst inhibitors. Consequently even P6.p high LIN-3 cannot sustain primary, all P3.p-P8.p express secondary vulval markers and generate secondary lineages producing symmetrical vulval structures without central primary invagination. This phenotype parallels LIN-12 dominant mutants described by Greenwald showing all secondary fate adoption.

Ref: Greenwald et al. 1983; Gilbert Chapter 15: Constitutively active LIN-12 - all VPCs become secondary.

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Elegans -ll

Which pathway is involved in EMS fate specification?

EMS polarity relies heavily on Wnt signaling from P2. P2 expresses MOM-2 Wnt ligand and MOM-5 Frizzled, activating both canonical Wnt/beta-catenin asymmetry pathway and Src/MES-1 pathway in EMS. MOM-2 binding causes WRM-1 beta-catenin nuclear accumulation in E but not MS, along with reduction of POP-1 TCF, converting POP-1 to transcriptional activator with SYS-1 beta-catenin to induce end-1, end-3 endoderm genes. Mutations in mom-2, mom-5, wrm-1 cause both EMS daughters to become MS-like. Therefore EMS fate specification uses Wnt signal to establish E versus MS asymmetry downstream of initial SKN-1 competence input.

Ref: Rocheleau et al. 1997; Gilbert Chapter 4: Wnt pathway involved in EMS fate specification via MOM-2.

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Eye Lens Induction -l

Which of the following correctly describes the effect of Pax6 loss in vertebrates?

Pax6 serves as master control gene for eye morphogenesis across vertebrates. It sits at top of regulatory hierarchy, directly activating downstream genes including Sox2, Six3, Maf and crystallins in lens, retina and cornea. Null homozygous mutants in mice, rats and humans display anophthalmia or severely reduced eye rudiments because optic vesicle fails to maintain retinal identity and ectoderm cannot achieve lens competence. Even retina, iris and cornea development collapses. Dosage sensitivity explains why haploinsufficiency still permits small eye while complete loss eliminates entire eye field, not just lens alone.

Ref: NCBI Bookshelf, Molecular Biology of the Cell, Chapter 21: Pax6 master regulator - anophthalmia phenotype in mutants.

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