| 172458 |
G5EEG9 |
HLH2_CAEEL |
Helix-loop-helix protein hlh-2 |
DISRUPTION PHENOTYPE |
RNAi-mediated knockdown in the early larval L1 stage causes both somatic gonadal progenitor (SGP) cells, Z1.ppp and Z4.aaa, to assume the ventral uterine precursor cell (VU) identity; whereas, if RNAi is applied during the late larval L1 stage, or at the larval L2 stage, both assume the anchor cell (AC) identity (PubMed:21784067, PubMed:14701877). RNAi-mediated knockdown applied at the time of the larval stage L1/L2 molt causes defects in invasion of the basement membrane by the AC (PubMed:21784067). RNAi-mediated knockdown causes the MI pharyngeal motorneuron to transform into an e3D-like epithelial cell (PubMed:21041366). RNAi-mediated knockdown reduces expression of alpha integrin ina-1 and of ADAMTS protease gon-1, and causes defects in migration of the gonadal distal tip cells (DTCs) (PubMed:25982859, PubMed:17588558). RNAi-mediated knockdown causes reduction in the number of hermaphrodites with DTCs, diminishes formation of elongated gonadal arms and reduces expression of lag-2 (PubMed:19376107). RNAi-mediated knockdown during larval stage L3 causes a subsequent three-fold reduction in germ cell number in the adult hermaphrodite gonad (PubMed:19376107). RNAi-mediated knockdown increases lifespan, reduces fertility, improves the response to proteotoxic stress, alters the response to reactive oxygen species (ROS) and reduces expression of arginine kinases such as argk-1 (PubMed:32203922). {ECO:0000269|PubMed:14701877, ECO:0000269|PubMed:17588558, ECO:0000269|PubMed:19376107, ECO:0000269|PubMed:21041366, ECO:0000269|PubMed:21784067, ECO:0000269|PubMed:25982859, ECO:0000269|PubMed:32203922}. |