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#cell fate specification

2 public questions tagged with this topic.

Which morphogen gradient determines primary and secondary vulval cell fates?

Anchor cell LIN-3 forms graded spatial distribution across P3.p-P8.p equivalence group functioning as classic morphogen. High concentration at P6.p activates strong EGFR MAPK output surpassing threshold for primary 1° fate via egl-17 FGF and lin-39 targets inducing vulE vulF toroids. Lower concentration plus lateral LIN-12 Notch activation induced by DSL ligands APX-1, LAG-2 from P6.p induces secondary 2° fate in P5.p and P7.p expressing lip-1 phosphatase and lst repressors. Absence leads to tertiary 3° hypodermal fate. Dosage experiments displacing anchor cell demonstrate dose-dependent switching.

Ref: Greenwald & Kovall, Genetics: LIN-3/EGF morphogen gradient patterning primary and secondary vulval fates.

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.