| 181759 | Q22782 | RAB6B_CAEEL | Ras-related protein rab-6.2 | DISRUPTION PHENOTYPE | Grinder formation defects, whereby the grinder is formed, but it is small (PubMed:23792950). Animals have a fragile cuticle phenotype, which is prone to rupturing at random positions along the body (PubMed:30665892). This phenotype is intensified in response to hypotonic shock (PubMed:30665892). Due to a compromised cuticle barrier, which increases permeability to exogenous chemicals, all animals become paralyzed in response to acetylcholine agonist tetramisole or the GABA agonist piperazine (PubMed:30665892). Resistant to infection by the bacterium M. nematophilum and does not exhibit a deformity at the anal region phenotype (also known as a dar phenotype), which is possibly indicative of cuticle glycosylation defects (PubMed:30665892). Reduces spontaneous reversal rate and mechanosensitivity (PubMed:22213799). Disrupts the localization of glr-1, and there is a decreased number of glr-1-positive puncta along the ventral cord dendrites (PubMed:22213799, PubMed:26891225). The reduced number of glr-1-positive puncta along the ventral cord dendrites phenotype is suppressed in an unc-11 e47 mutant background (PubMed:22213799). The number of glr-1-positive puncta is further reduced in a rab-6.1 RNAi-mediated knockdown in glr-1 expressing neurons (PubMed:26891225). RNAi-mediated knockdown results in delayed growth and grinder formation defects (PubMed:23792950). RNAi-mediated knockdown disrupts seam cell division and alae formation (PubMed:33826611). RNAi-mediated knockdown suppresses the seam cell division and alae formation defects in the tbc-11 ok2576 mutant (PubMed:33826611). {ECO:0000269|PubMed:22213799, ECO:0000269|PubMed:23792950, ECO:0000269|PubMed:26891225, ECO:0000269|PubMed:30665892, ECO:0000269|PubMed:33826611}. |