Caenorhabditis elegans


CELE_C06G1.4, C06G1.4
ain-1 encodes an unfamiliar protein synergistically required, with LIN-31, for the normal timing of vulval differentiation, independently of LET-60/RAS, and parallel to or downstream of LIN-14/LIN-28/HBL-1; AIN-1 is expressed in cytoplasmic foci (that are probably P bodies) in several tissues, including vulval precursor cells and neurons; AIN-1 coimmunoprecipitates with DCR-1 and ALG-1, also binds ALG-1 in vitro, and does not require DNA or RNA for its binding; in vivo, AIN-1 targets ALG-1 to cytoplasmic foci, in which it colocalizes with DCAP-2; AIN-1 is likely to be a RISC component, since anti-AIN-1 antibodies precipitate 29 different miRNAs, including mir-2, mir-52, mir-58, mir-71, mir-77, and mir-239a; ain-1(ku322) mutants are essentially wild-type, except for sporadically gapped alae and excess seam cell nuclei arising from retarded seam cell fusion; more prominently, ain-1(ku322) suppresses the multivulva phenotype of lin-31(n1053) mutations, while strongly enhancing lin-31(n1053)'s egg-laying defect; the cellular basis of lin-31(n1053);ain-1(ku322) phenotypes is a delay in vulval development in L4 larvae not seen with either mutation alone; ain-1(ku322) has no effect on let-60(n1046) or lin-3(e1275) mutations; ain-1(ku322) suppresses the precocious vulval development of lin-14(RNAi), lin-28 mutants, and hbl-1(RNAi); alg-1 or alg-1 ain-1 mutant alae resemble ain-1 alae, indicating that ALG-1 and AIN-1 act in a common genetic pathway; AIN-1 is homologous to Brugia malayi 14748.m00068, 14052.m00191, and 14963.m01790, and paralogous to C. elegans B0041.2; AIN-1 and its nematode homologs have weak similarity to human TNRC6A (GW182; OMIM:610739) and Drosophila GAWKY.

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