High impact information on lin-31

• 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 [1].
• A reduction-of-function mutation in ect-2 was isolated as a suppressor of the Multivulva phenotype of a lin-31 mutation [2].
• The Forkhead domain protein LIN-31 also acts positively on lin-39 in P6.p via this module [3].
• Mutations in lin-31 result in identical cell migration and spicule morphology defects [4].
• 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 [5].

Biological context of lin-31

• Two new genetic balancers for chromosome II of Caenorhabditis elegans were isolated and characterized. mIn1 was shown to be an inversion of a large central portion of the chromosome, extending from lin-31 to rol-1, that includes most of the genes on the chromosome [6].
• 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 [5].

References