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#vulval development

11 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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C-Elegans Development-l

Which of the following describes the fate of P6.p in vulval development?

P6.p receives maximal LIN-3/EGF signal due to proximity directly underneath gonadal anchor cell, activating high MAPK MPK-1 and inhibiting LIN-1 repressor via phosphorylation. This induces primary lineage: three rounds of division generating eight cells forming central vulval rings vulE and vulF creating precise lumen for egg passage. Descendants express egl-17 fibroblast growth factor, cdh-3 cadherin, zmp-1 metalloprotease. P6.p also expresses DSL ligands APX-1, LAG-2, DSL-1 to activate LIN-12 Notch in neighboring P5.p and P7.p promoting secondary fate and preventing adjacent primaries, acting as organizer.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: P6.p primary vulval fate and central vulval lineages.

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C-Elegans Development-l

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.

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C-Elegans Development-l

What happens when there is a loss-of-function mutation in LIN-3?

Loss-of-function lin-3 eliminates anchor cell inductive cue essential for vulvogenesis. In wild type, anchor cell expresses lin-3 at early L3 stage, activating LET-23/MAPK cascade in VPCs through SEM-5, LET-60, LIN-45, MEK-2, MPK-1 phosphorylation of transcription factors. Mutants lacking LIN-3 fail to trigger Ras signaling, so P5.p-P7.p never adopt vulval fates and fuse with hypodermis via EFF-1, remaining epidermal. Result is vulvaless animals unable to lay eggs, exhibiting bag-of-worms phenotype where larvae hatch inside mother. Rescue by heat-shock lin-3 restores induction confirming indispensable inductive role.

Ref: Sternberg, WormBook, Chapter Vulval development: LIN-3 loss-of-function causes vulvaless phenotype and egg-laying defective.

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C-Elegans Development-l

Which of the following proteins is essential for specifying VPCs in C. elegans?

LIN-39 is Sex Combs Reduced-like Hox protein expressed in central body region P3.p-P8.p controlling vulval precursor competence and central patterning. LIN-39 maintains LET-23 EGFR expression, prevents premature fusion of VPCs with hyp7 syncytium during L1-L2 via repression of eff-1 fusogen. Without LIN-39, all six VPCs fuse and become refractory to LIN-3 induction, causing vulvaless phenotype despite normal anchor cell signaling and positioning. LIN-39 cooperates with Wnt effectors BAR-1 beta-catenin, LIN-31 forkhead, and other Hox genes, linking anteroposterior patterning to tissue competence.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: LIN-39 Hox gene and vulval precursor cell competence.

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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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Elegans -ll

Which cells contribute to anchor cell formation in C. elegans?

Somatic gonad precursors define anchor cell formation. In early L2, gonadal cells Z1 and Z4 divide to generate somatic and germline lineages. Their somatic daughters Z1.ppp and Z4.aaa retain equipotential, undergoing Notch-mediated lateral competition via LIN-12 and LAG-2. One cell maintains high LIN-12 activity becoming ventral uterine precursor, other downregulates LIN-12 becoming anchor cell expressing lag-2 and lin-3. Ablation studies show either Z1.ppp or Z4.aaa can become AC, demonstrating equivalence. VPCs and AB lineages do not contribute. This bipotential origin ensures single AC to induce vulva and later fuse for uterine-vulval connection.

Ref: Kimble & Hirsh 1979; WormBook Gonad Development: Anchor cell formation from Z1.ppp and Z4.aaa cells.

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Elegans -ll

Which gene is required for primary vulval precursor cell fate?

LIN-39, C. elegans HOX5 ortholog, specifies vulval precursor cell competence and primary fate potential. It is expressed in central body region P3.p-P8.p during L1-L2, preventing fusion with hypodermal syncytium and promoting vulval competence by activating egl-17 and repressing fusion genes eff-1. Without LIN-39, all VPCs fuse prior to anchor cell signaling, yielding vulvaless phenotype even if LIN-3 present. LIN-39 also cooperates with Ras-MAPK to drive primary fate in P6.p by enhancing lin-3 responsiveness. LIN-12 Notch instead promotes secondary fate, and SKN-1 is embryonic factor, making LIN-39 central to VPC competence.

Ref: Clark et al. 1993; Gilbert Chapter 15: LIN-39 required for primary vulval precursor cell fate competence.

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Elegans -ll

Which morphogen gradient influences primary and secondary vulval cell fates?

Primary and secondary vulval fates are graded by LIN-3/EGF morphogen secreted from anchor cell. LIN-3 forms diffusion gradient highest at P6.p overlying AC, intermediate at P5.p and P7.p, low at distant P3.p, P4.p, P8.p. High concentration surpasses threshold activating LET-23 EGFR to MAPK to LIN-1 inhibition, driving primary genes egl-17. Lower LIN-3 combined with lateral LIN-12 Notch activation specifies secondary fate expressing secondary markers. Experimental expression of LIN-3 under heat-shock promoter induces ectopic primary cells proportional to dose, demonstrating morphogen interpretation. Therefore LIN-3 gradient patterns 3-2-1-2-3 array in competent group.

Ref: Katz et al. 1995; WormBook: LIN-3 EGF morphogen gradient influencing VPC fates.

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Elegans -ll

What happens in a C. elegans lin-3 loss-of-function mutant?

LIN-3 encodes nematode EGF-like growth factor secreted from anchor cell, activating LET-23 receptor tyrosine kinase EGFR. Loss-of-function lin-3 mutants lack inductive signal, so vulval precursor cells receive no Ras-MAPK activation, fail to express LIN-39 dependent vulval genes, instead fuse with hyp7 syncytium via eff-1 fusogen and adopt tertiary hypodermal fate. Resulting adult is vulvaless, unable to lay eggs, exhibiting egg-laying defective phenotype. Gain-of-function conversely yields multivulva because ectopic LIN-3 overinduces. Thus LIN-3 essential for vulval induction, its absence produces vulvaless phenotype similar to let-23 or let-60 Ras mutants.

Ref: Hill & Sternberg 1992; Gilbert Chapter 15: lin-3 loss-of-function vulvaless phenotype in C. elegans.

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Elegans -ll

What is the fate of P6.p in normal vulval development?

Vulval precursor cells P3.p-P8.p form competence group in central ventral epidermis. During mid-L3, anchor cell positioned over P6.p secretes LIN-3 EGF, activating LET-23 EGFR Ras-MAPK cascade highest in P6.p. This high signal induces primary vulval fate defined by lineage generating central invagination forming vulval tube and connection to uterus. P6.p daughters divide three times producing cells vulE and vulF that attach to anchor cell and utse. In wild type, P6.p invariably generates central vulval lineage, while neighbors become secondary and outer cells fuse to hypodermis, ensuring single vulva positioned correctly.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 15: Fate of P6.p as central vulval lineage in C. elegans.

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