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#protein inhibition

2 public questions tagged with this topic.

C-Elegans Development-l

Which protein prevents LIN-3 signaling in tertiary vulval precursor cells?

Tertiary vulval precursor cells must avoid responding to low LIN-3 despite molecular competence maintained by LIN-39. LIN-12 Notch activity in P3.p, P4.p, P8.p and induced cells modulates EGFR sensitivity by cross-inhibition. LIN-12 signaling upregulates LIP-1 dual-specificity MAPK phosphatase, LST-1-4 inhibitors, DPY-23 adaptin dampening LET-23/MAPK cascade and Ras output. Additionally, LIN-12 promotes expression of synMuv B genes including lin-35 retinoblastoma antagonizing EGF induction via chromatin remodeling. This reciprocal inhibition between RTK and Notch ensures only P6.p attains high MAPK, distal VPCs remain hypodermal despite low LIN-3.

Ref: Sternberg, WormBook Vulval development: LIN-12 Notch inhibits MAPK via LIP-1 and lst to block tertiary response.

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Elegans -ll

Which protein prevents LIN-3 activation in tertiary VPCs?

Lateral inhibition ensures tertiary fate protection. After induction, P6.p primary cell expresses LAG-2 ligands activating LIN-12 Notch in P5.p and P7.p, specifying secondary fate. Secondary cells also secrete DSL signals that activate LIN-12 in more distant P3.p, P4.p, P8.p. LIN-12 activation induces transcriptional repressors that prevent activation of LET-23 EGFR pathway by low LIN-3 and promotes hyp7 fusion via inhibition of egl-17 and vulval genes. Thus LIN-12 prevents LIN-3 activation from specifying vulval fate in tertiary cells, ensuring correct 3-2-1-2-3 pattern by restricting EGFR responsiveness through Notch-mediated lateral inhibition mechanism.

Ref: Sternberg WormBook Vulval Development: LIN-12 prevents LIN-3 activation in tertiary VPCs via lateral inhibition.

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