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#EMS fate

2 public questions tagged with this topic.

Elegans -ll

Which pathway is involved in EMS fate specification?

EMS polarity relies heavily on Wnt signaling from P2. P2 expresses MOM-2 Wnt ligand and MOM-5 Frizzled, activating both canonical Wnt/beta-catenin asymmetry pathway and Src/MES-1 pathway in EMS. MOM-2 binding causes WRM-1 beta-catenin nuclear accumulation in E but not MS, along with reduction of POP-1 TCF, converting POP-1 to transcriptional activator with SYS-1 beta-catenin to induce end-1, end-3 endoderm genes. Mutations in mom-2, mom-5, wrm-1 cause both EMS daughters to become MS-like. Therefore EMS fate specification uses Wnt signal to establish E versus MS asymmetry downstream of initial SKN-1 competence input.

Ref: Rocheleau et al. 1997; Gilbert Chapter 4: Wnt pathway involved in EMS fate specification via MOM-2.

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Elegans -ll

If P2 is removed from the 4-cell stage embryo, what happens to EMS fate?

EMS fate specification integrates maternal SKN-1 and signal from neighboring P2 cell via MOM-2 Wnt pathway. P2 secretes MOM-2 and expresses MES-1, activating Src and Wnt cascades that lower nuclear POP-1 in posterior EMS daughter, allowing E fate. Anterior MS retains high POP-1. When P2 is ablated or removed at 4-cell stage, no Wnt signal reaches EMS, POP-1 remains high in both daughters, repressing endoderm program. Both progeny differentiate as MS-like cells producing mesoderm and pharynx, no intestine. This demonstrates inductive requirement for E patterning despite autonomous SKN-1 presence, showing P2-dependent polarization.

Ref: Goldstein 1993; Gilbert Developmental Biology Chapter 4: P2 removal effect - EMS produces two MS cells.

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