Skip to content

#P6.p

2 public questions tagged with this topic.

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.

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.