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#LIN-12

3 public questions tagged with this topic.

C-Elegans Development-l

What happens if both Z1.ppp and Z4.aaa fail to express LIN-12?

Two gonadal precursors Z1.ppp and Z4.aaa use Notch-mediated lateral inhibition to single out anchor cell required for uterus-vulva connection. Each expresses LIN-12 receptor and LAG-2 ligand competing for fate. When both lack LIN-12 functional receptor due to null mutation or RNA interference, negative feedback and transcriptional repression fails; neither cell receives inhibitory Notch signal to adopt ventral uterine fate and express uterine genes. Consequently both differentiate as anchor cells, each secreting LIN-3 EGF and invading basement membrane via fos-1a. This leads to double induction, duplicated vulval invaginations and disorganized egg-laying.

Ref: Seydoux & Greenwald, Cell: LIN-12 loss leads to two anchor cells due to failed lateral inhibition.

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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 of the following describes the function of LIN-12?

LIN-12 encodes one of two C. elegans Notch receptors, homologous to Drosophila Notch. It is expressed in ventral uterine precursors and vulval precursor cells, where binding of ligands LAG-2, APX-1, DSL-1 from anchor cell or primary VPC triggers proteolytic cleavage by ADAM and gamma-secretase, releasing NICD that translocates to nucleus with LAG-1 CSL transcription factor to activate secondary vulval genes lst and lip-1. This lateral signaling restricts primary fate and ensures correct patterning of uterine versus anchor cell decisions and secondary VPC fates, representing canonical Notch activation pathway in nematode development.

Ref: Greenwald 1998; Gilbert Chapter 15: LIN-12 activates Notch signaling in C. elegans vulval and AC/VU decisions.

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