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#embryo development

7 public questions tagged with this topic.

What happens in embryos lacking PAL-1 function?

PAL-1 is Caudal-like homeodomain transcription factor maternally deposited posteriorly via post-transcriptional control by MEX-3 RNA-binding protein, MEX-5/6 and SPN-4 regulating translation efficiency. It activates posterior program genes including tbx-8/9 T-box and elt-3 in EMS descendants C and D blastomeres producing body wall muscle, hypodermis, intestine-associated muscle. C blastomere generates hypodermis and muscle, D generates muscle only. In pal-1 mutants or RNAi knockdown, posterior blastomeres transform to anterior-like EMS fates, lacking muscle myosin MYO-3 and COL cuticle markers, causing embryonic arrest with absent C and D lineages.

Ref: Hunter & Kenyon, Cell 1996: PAL-1 Caudal homolog required for C and D blastomere specification.

Which of the following correctly describes the effect of glp-1 mutation in C. elegans embryos?

GLP-1 encodes C. elegans Notch receptor essential for AB lineage distinction. After first cleavage, P2 Delta signals via APX-1/LAG-2 activate GLP-1 only in ABp because ABa contact with P2 is minimal. This induces ABp-specific gene expression, including repression of LAG-2 in ABa. In glp-1 loss-of-function embryos, Notch signaling absent in ABp, so ABp defaults to ABa program, producing two ABa-like lineages with duplicated anterior pharynx cells and loss of dorsal ventral patterning. EMS division unaffected but overall embryo fails pharyngeal asymmetry. Thus transformation is ABp to ABa, classic Notch lineage conversion evidence.

Ref: Priess 2005; Gilbert, Developmental Biology 12th ed., Chapter 4: glp-1 mutation - ABp transforms into ABa.

β-catenin accumulation in sea urchin micromeres leads primarily to formation of:

Vegetal micromeres in sea urchin inherit high levels of Dishevelled and consequently nuclear beta-catenin due to vegetal cortex localization established before fertilization. Beta-catenin activates endomesoderm gene regulatory network including Pmar1, which represses HesC repressor, allowing expression of Wnt8, blimp1b, krox, and Delta ligand. These cells become primary mesenchyme producing larval skeleton and act as organizers inducing adjacent macromeres to become endoderm forming gut and secondary mesenchyme pigment cells. Without beta-catenin accumulation, embryos become animalized ciliated balls lacking mesodermal skeleton and endodermal gut, demonstrating requirement for mesoderm and endoderm induction.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 10: Beta-catenin in micromeres induces mesoderm endoderm.

Disheveled protein in sea urchin embryos is localized initially in:

Dishevelled protein acts as key adaptor upstream of beta-catenin in Wnt pathway hierarchy. In sea urchin oocytes before fertilization, Dishevelled protein and mRNA are anchored to vegetal cortex via interactions with actin-associated proteins, cortically localized vesicles, and cytoskeletal scaffolds. This pre-fertilization localization establishes asymmetry inherited by micromeres after fourth unequal cleavage. Vegetal cortical Dishevelled locally inhibits GSK-three, permitting beta-catenin accumulation vegetally and activating endomesoderm genes. If Dishevelled were localized animally or in blastocoel, vegetal specification would fail, animalizing embryo and altering endomesoderm patterning strongly.

Ref: Davidson, Sea Urchin GRN, Chapter: Dishevelled localized in vegetal cortex before fertilization.

Blastocyst formation marked by formation of:

Blastocyst stage is defined by formation of fluid-filled blastocoel cavity segregating embryonic lineages. After compaction outer cells polarize, establish E-cadherin-mediated adherens junctions and tight junctions sealing intercellular spaces. Basolaterally positioned Na/K ATPase pumps sodium into intercellular clefts, water follows osmotically via aquaporins causing intercellular spaces to coalesce into single cavity. Expansion of blastocoel positions inner cell mass at embryonic pole and trophectoderm surrounding cavity. Cavity formation marks preparation for hatching, implantation competency, lineage differentiation essential for survival, nutrient exchange and epithelial transport functions.

Ref: NCBI Bookshelf, Early Development Chapter: Blastocoel formation and Na/K ATPase-driven cavitation in blastocyst development.

First cleavage in mammalian embryos occurs in:

In mammals fertilization occurs in ampulla of fallopian tube and first mitotic cleavage initiates during embryonic transit toward uterus. Zygote undergoes cleavage divisions within oviductal lumen bathed in fluid secreted by epithelial cells providing pyruvate, lactate and growth factors, while still enclosed by zona pellucida. No contact with uterine epithelium occurs yet. Morula reaches uterus after three to four days. Thus oviduct supplies protected, nutritive microenvironment sustaining genome activation, compaction, cavitation preparation before implantation becomes possible inside uterine cavity and decidualization begins for pregnancy establishment.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Early cleavage and embryonic transit within oviductal environment.