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#blastula

3 public questions tagged with this topic.

Specification Determination-ll

In sea urchin embryos, the removal of cells from an early blastula leads to normal development due to:

Sea urchin embryos exhibit remarkable regulative capacity after early blastomere removal because conditional specification dominates early patterning. Remaining cells sense altered neighbor relationships and remodel signaling landscapes, particularly nuclear beta-catenin localization, Delta-Notch activation and Nodal expression, to respecify toward missing micromere-derived lineages including skeletogenic mesenchyme. Intercellular communication and community effects restore correct proportion of endomesoderm and ectoderm, yielding normal albeit smaller pluteus larvae. If development relied solely on segregated determinants, compensation would be impossible. Regulative signaling ensures robustness against cell loss and experimental perturbation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Sea Urchin Regulative Development and Compensation.

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Sea Urchin -ll

Sea urchin blastula has how many cells at the blastula stage?

Sea urchin development features holoblastic cleavages generating relatively small coeloblastula. After successive divisions progressing through 16-cell, 32-cell and 60-cell stages, cells arrange as hollow epithelial sphere. By late blastula just before hatching, embryo contains approximately 120 cells arranged as single-layered epithelium surrounding blastocoel filled with blastocoelic fluid. Cells are ciliated and secrete hatching enzyme digesting fertilization envelope. Numbers vary slightly among species such as Lytechinus and Strongylocentrotus purpuratus, but classic morphological counts cite 120 cells comprising mesomeres, macromeres, small and large micromeres. This stage sets up primary mesenchyme ingression.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Blastula formation - cell numbers and epithelial organization.

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Fertilization in mammals-lll

Successful compaction from morula to blastula involves:

Compaction to form morula requires establishment of strong cell-cell adhesion mediated by E-cadherin, a calcium-dependent adhesion molecule. Extracellular calcium rigidifies cadherin repeats enabling trans-homophilic binding between blastomeres, intracellularly binding beta-catenin which links to alpha-catenin and actin cytoskeleton. Activation and clustering of this cadherin-catenin complex drives blastomere flattening, polarization, tighter apposition and induction of tight junction formation. Blockage of cadherin or removal of calcium prevents compaction, while calcium ionophores alone without cadherin function insufficient. Successful compaction therefore depends on coordinated calcium influx and functional cadherin-beta-catenin assembly orchestrating Hippo pathway mediated lineage segregation.

Ref: Maître JL et al., Nature Cell Biology 2015: E-cadherin beta-catenin regulation of compaction and Hippo mediated cell fate.

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