Abstract
The membrane trafficking events that regulate unicellular tube formation and maintenance are not well understood. Here, using an RNAi screen, we identified the small GTPase ARF1 homolog ARF-1.2 as a regulator of excretory tube formation in Caenorhabditis elegans. RNAi-mediated knockdown and knockout of the arf-1.2 gene resulted in the formation of large intracellular vacuoles at the growth sites (varicosities) of the excretory canals. arf-1.2 mutant animals were sensitive to hyperosmotic conditions. arf-1.2 RNAi affected the localization of the anion transporter SULP-8, which is expressed in the basal plasma membrane of the excretory canals, but did not affect the expression of SULP-4, which is expressed in the apical membrane. The phenotype of arf-1.2 mutants was suppressed by mutation of the small Rho GTPase CDC-42, a regulator of apical/basal traffic balance. These results suggest that ARF-1.2 plays an essential role in basal membrane traffic to regulate the formation of the unicellular excretory tube.
Highlights
Epithelial tubes that enable nutrition uptake and fluid transport are essential in all metazoans
We previously reported that a H +/myo-inositol transporter (HMIT) gene, hmit-1.2, was selectively expressed in the excretory cell and the sheath glia in C. elegans [17]
To identify the gene(s) that participates in membrane traffic of the unicellular tubes, we carried out an RNA interference (RNAi) screen for clone(s) that affect the morphology of the excretory cell
Summary
Epithelial tubes that enable nutrition uptake and fluid transport are essential in all metazoans. We identified the small GTPase ARF-1.2 as a regulator of basal trafficking in the excretory tube of C. elegans. To identify the gene(s) that participates in membrane traffic of the unicellular tubes, we carried out an RNAi screen for clone(s) that affect the morphology of the excretory cell.
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