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#SKN-1

5 public questions tagged with this topic.

C-Elegans Development-l

Which phenotype results from a loss-of-function mutation in SKN-1?

SKN-1 specifies mesendodermal progenitors central to nematode gastrulation and gut formation. Maternal SKN-1 accumulates in EMS nucleus where it directly binds promoters of med-1,2 GATA factors, which activate end-1,3 and tbx-35 to segregate endoderm versus mesoderm lineages differentially. Null skn-1 alleles lack pharynx derived from MS, body wall muscle from MS, intestine derived from E, causing embryonic lethality with excess skin, neurons but no gut markers. Rescue shows autonomous requirement in EMS not P2. Thus loss mirrors mesendoderm deletion rather than vulval defects highlighting master regulator role.

Ref: Bowerman et al., Cell 1992: SKN-1 mutants lack mesoderm and endoderm derivatives from EMS lineage.

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C-Elegans Development-l

Which transcription factor is required for EMS blastomere fate in C. elegans?

SKN-1 is bZip transcription factor related to mammalian Nrf2, maternally provided and enriched in EMS and P2 via post-translational regulation and Wnt asymmetry. In EMS blastomere, SKN-1 directly activates MED-1,2 GATA factors and END-1,3 endoderm determinants leading to mesendoderm specification and tbx-35 muscle regulator. Nuclear entry depends on phosphorylation and redox sensing. Loss abolishes MS-derived pharynx, anterior body muscle, plus E-derived intestine causing embryonic lethality. It integrates maternal polarity, MET-2, and P2 inductive inputs ensuring EMS produces both mesoderm and endoderm lineages.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: SKN-1 transcription factor specifying EMS mesendoderm fate.

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Elegans -ll

Which protein is essential for E cell fate in C. elegans?

E cell, posterior daughter of EMS, requires combinatorial inputs from SKN-1, MED-1/2 and Wnt-modified POP-1 to activate end-1 and end-3 GATA factors specifying intestine. Maternal SKN-1 activates med genes broadly in EMS lineage; Wnt signal from P2 causes reduction of POP-1 in E, converting it from repressor to coactivator with SYS-1 beta-catenin. Modified POP-1 together with SKN-1 induced MEDs binds endoderm enhancers, driving END-1/3 expression. POP-1 null causes both EMS daughters to become E-like, revealing essential role in distinguishing MS versus E. Hence POP-1 essential for activating E fate in cooperation with Wnt signaling pathway.

Ref: Maduro et al. 2005; Gilbert Chapter 4: POP-1 essential for E cell fate specification in C. elegans endoderm.

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Elegans -ll

Which of the following occurs in skn-1 mutant embryos?

SKN-1 is maternally deposited transcription factor required for EMS blastomere descendant fates. In skn-1 null or strong loss-of-function embryos generated by RNAi, transcriptional activation of med-1, med-2 fails, so cascade leading to end-1, end-3, tbx-35, ceh-51 not induced. EMS produces daughters that do not form pharynx mesoderm from MS or intestine from E, instead adopts C-like muscle fate producing excess body wall muscle, while overall embryo arrests. Hence loss of EMS-derived lineages including intestinal, pharyngeal and body wall muscle subsets normally sourced from MS and E leads to failure of gut formation and embryonic lethality with phenotype lacking endoderm.

Ref: Bowerman et al. 1993; Gilbert Chapter 4: skn-1 mutant embryos loss of EMS-derived lineages.

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Elegans -ll

Which of the following statements correctly describes SKN-1 function?

SKN-1, maternally provided bZIP transcription factor related to Nrf, accumulates in P1 and later EMS blastomere due to PAR polarity and SKR-mediated regulation. It directly binds promoters of med-1, med-2 GATA factors, initiating mesendoderm program that subsequently activates end-1, end-3 and tbx-35 for E versus MS divergence. skn-1 mutants lack pharynx and intestine derived from EMS, with EMS transforming to C-like muscle fate. It does not regulate LIN-39 or vulval signaling, but serves as earliest zygotic activator connecting maternal polarity to zygotic endomesoderm specification, upstream of Wnt-modified POP-1 decision mechanism.

Ref: Bowerman et al. 1992; Gilbert Chapter 4: SKN-1 regulation of EMS fate via MED factors.

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