lin-31
abnormal cell LINeage 31
Knowledge Graph Relationships
Outgoing (11)
Incoming (11)
Evidence (24 claims)
We used these constructs to show that at the time of vulval induction both lin-39::GFP reporters are upregulated in P6.p, indicating that the accumulation of high levels of LIN-39 protein detected previously corresponds to transcriptional upregulation of lin-39 expression.
From our analysis we conclude: (1) the null phenotype of lin-31 is the phenotype displayed by almost all of the existing alleles, (2) the DNA-binding domain plays a critical role in LIN-31 function, and (3) direct screens for multivulva and vulvaless mutants will probably yield only null (or strong) alleles of lin-31.
Phosphorylation of LIN-31 by MPK-1 disrupts the LIN-1/LIN-31 complex, relieving vulval inhibition.
LIN-31 is a vulval-specific effector of MPK-1, while LIN-1 acts as a general effector.
The Forkhead domain protein LIN-31 also acts positively on lin-39 in P6.p via this module.
LIN-31 binds to LIN-1, and the LIN-1/LIN-31 complex inhibits vulval induction.
We show that lin-31 acts downstream of the ras homolog let-60 and that lin-31 encodes a member of the HNF-3/fork head family of DNA-binding transcription factors. lin-31 regulates how vulval precursor cells choose their fate; in lin-31 mutants, these cells do not properly choose which fate to express and therefore adopt any one of the three possible vulval cell fates in a deregulated fashion.
We show that lin-31 acts downstream of the ras homolog let-60 and that lin-31 encodes a member of the HNF-3/fork head family of DNA-binding transcription factors. lin-31 regulates how vulval precursor cells choose their fate; in lin-31 mutants, these cells do not properly choose which fate to express and therefore adopt any one of the three possible vulval cell fates in a deregulated fashion.
We show that MPK-1 directly regulates both the LIN-31 winged-helix and the LIN-1 Ets transcription factors to specify the vulval cell fate. lin-31 and lin-1 act genetically downstream of mpk-1, and both proteins can be directly phosphorylated by MAP kinase.
LIN-31 is a vulval-specific effector of MPK-1, while LIN-1 acts as a general effector.
These results argue that while Cbr-lin(gu167) may act upstream of Cbr-lin-3/EGF, the other three genes influence the EGF pathway downstream or in parallel to Cbr-lin-3.
The lin-31 gene is required for the proper specification of vulval cell fates in the nematode Caenorhabditis elegans and encodes a member of the winged-helix family of transcription factors.
We found that the LIN-1/Ets and LIN-31/FoxB transcription factors promote expression of CKI-1, a member of the p27 family of cyclin-dependent kinase inhibitors (CKIs).
DNA sequencing of 13 lin-31 alleles revealed six nonsense mutations and two missense mutations within the DNA-binding domain, plus three deletions, one transposon insertion, and one frameshift mutation that all cause large-scale disruptions in the gene.
Furthermore, lin-31, which specifies cell fates during vulval induction and encodes a putative transcription factor similar to HNF-3/fork head, acts in the Pn.p cells.
Phosphorylated LIN-31 may also act as a transcriptional activator, promoting vulval cell fates.
Phosphorylation of LIN-31 by MPK-1 disrupts the LIN-1/LIN-31 complex, relieving vulval inhibition.
We show that MPK-1 directly regulates both the LIN-31 winged-helix and the LIN-1 Ets transcription factors to specify the vulval cell fate. lin-31 and lin-1 act genetically downstream of mpk-1, and both proteins can be directly phosphorylated by MAP kinase.
We show that MPK-1 directly regulates both the LIN-31 winged-helix and the LIN-1 Ets transcription factors to specify the vulval cell fate. lin-31 and lin-1 act genetically downstream of mpk-1, and both proteins can be directly phosphorylated by MAP kinase.
We show that lin-31 acts downstream of the ras homolog let-60 and that lin-31 encodes a member of the HNF-3/fork head family of DNA-binding transcription factors. lin-31 regulates how vulval precursor cells choose their fate; in lin-31 mutants, these cells do not properly choose which fate to express and therefore adopt any one of the three possible vulval cell fates in a deregulated fashion.