Rab GTPases are master regulators of intracellular transport. We previously showed that a rab-6.2 deletion leads to a compromised cuticle, glycosylation defects, and increased axon regeneration. Mammalian orthologs of rab-6.2 and rab-33 have been shown to mediate Golgi trafficking of cargo in mammalian cells, including that of glycosyltransferase enzymes. We engineered a novel STOP-IN putative null allele of rab-33 ( axr2 ) to determine if loss of function of rab-33 phenocopies the phenotypes seen in rab-6.2 ( ok2254 ). Our results suggest that rab-33 is not required for cuticle integrity.
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