| 172249 |
G5EDT1 |
LIN35_CAEEL |
Retinoblastoma-like protein homolog lin-35 (Abnormal cell lineage protein 35) (Synthetic multivulva protein lin-35) |
DISRUPTION PHENOTYPE |
Viable, but with a reduced fertility and brood size (PubMed:11684669, PubMed:15328017, PubMed:15280233, PubMed:17417969). Low penetrance defects including reduced integrity of the proximal gonad, a low percentage of endomitotic oocytes, distal tip cell migration defects and abnormalities in vulval morphology (PubMed:17417969). Some studies demonstrate aberrant intestinal nuclear divisions, with increased intestinal nuclei in growing larvae (PubMed:17466069). In addition there is increased sensitivity to RNA-induced gene silencing by RNAi (PubMed:16507136, PubMed:17417969). RNAi-mediated knockdown results in increased survival in response to ER stress inducer tunicamycin as compared to wild-type animals (PubMed:24715729). RNAi-mediated knockdown results in larval arrest at 25 degrees Celsius in an xpn-1 mutant background (PubMed:15649460). RNAi-mediated knockdown in a ced-1 mutant background results in reduced somatic cell apoptosis (PubMed:27650246). Double knockout with the synthetic multivulva class B protein lin-15A results in a multiple vulva (Muv) phenotype (PubMed:16624904, PubMed:26100681). Double knockout with either cdk-4 or cyd-1 rescues the cell cycle progression defect in the single cdk-4 and cyd-1 mutants (PubMed:11684669, PubMed:25562820). Double knockout with xnp-1 results in 43% embryonic lethality (PubMed:15328017). Surviving animals develop slowly, are small, sterile and display male and female gonad developmental defects characterized by shorter gonadal arms, fewer germ cells, an everted vulva phenotype, and failed formation of sheath and spermathecal cells (PubMed:15328017). Double knockout with spr-1 or zfp-2 results in defects in growth, vulval morphogenesis, somatic gonad development and fertility (PubMed:17417969, PubMed:17070797). Double knockout with the programmed cell death regulator mcd-1 results in 100% lethality during the L1 stage of larval development (PubMed:17237514). Programmed cell death defect in a ced-3 n2427 mutant background (PubMed:17237514). Knockout with RNAi-mediated knockdown of psa-1, ham-3, swsn-2.2, swsn-3 or swsn-6 (components of the SWI/SNF complex) results in larval arrest during larval development (PubMed:15280233). Knockout with RNAi-mediated knockdown of pha-1 (developmental protein), snfc-5 or swsn-8 (additional SWI/SNF complex components) results in sterility and/or a protruding vulva phenotype (PubMed:15196946, PubMed:15280233). Double knockout with slr-2 results in early larval arrest due to mis-regulation of intestinal specific gene expression, which results in starvation-induced growth arrest (PubMed:18437219, PubMed:22542970). {ECO:0000269|PubMed:11684669, ECO:0000269|PubMed:15196946, ECO:0000269|PubMed:15280233, ECO:0000269|PubMed:15328017, ECO:0000269|PubMed:15649460, ECO:0000269|PubMed:16507136, ECO:0000269|PubMed:16624904, ECO:0000269|PubMed:17070797, ECO:0000269|PubMed:17237514, ECO:0000269|PubMed:17417969, ECO:0000269|PubMed:17466069, ECO:0000269|PubMed:18437219, ECO:0000269|PubMed:22542970, ECO:0000269|PubMed:24715729, ECO:0000269|PubMed:25562820, ECO:0000269|PubMed:26100681, ECO:0000269|PubMed:27650246}. |