| 172826 |
G5EDR3 |
2AB1_CAEEL |
Serine/threonine-protein phosphatase 2A regulatory subunit sur-6 (Serine/threonine-protein phosphatase 2A 55 kDa regulatory subunit sur-6) (Serine/threonine-protein phosphatase 2A regulatory subunit B sur-6) (SUR-6/B55) (SUR-6/PR55) |
DISRUPTION PHENOTYPE |
RNAi-mediated knockdown causes severe embryonic lethality (PubMed:10521400). In mutants, during the first embryonic divisions, P1 cell initiates division prior to AB cell, spindles appear abnormal or collapse during anaphase and chromatin bridges and supernumerary centrosomes are often detected (PubMed:14724126). In addition, RNAi-mediated knockdown causes a partial defect in centriole duplication during the first embryonic divisions where 24% of spindles are monopolar and 47% have asymmetric spindles, a decrease in the spindle protein sas-5 levels and occasional bridging of chromatin with no obvious defects in cell cycle progression or mitotic exit (PubMed:21497766). The few surviving animals of RNAi-mediated knockdown lack a vulva resulting from defects in vulva cell induction, vulva precursor cell (VPC) generation and in vulval execution lineage, and are slightly uncoordinated (PubMed:10521400). In L4 larvae mutants, somatic mpk-1/ERK phosphorylation is also severely reduced (PubMed:14724126). In intestinal epithelial cells, RNAi-mediated knockdown causes an accumulation of SNARE proteins including snb-1, snap-29 and syx-4 (PubMed:24192838). RNAi-mediated knockdown at the L1 larval stage in the exocyst component exoc-8 (ok2523) mutant background results in lethality (PubMed:24192838). {ECO:0000269|PubMed:10521400, ECO:0000269|PubMed:14724126, ECO:0000269|PubMed:21497766, ECO:0000269|PubMed:24192838}. |