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First published online January 26, 2007

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LINking neurobeachin to endocytosis

Vulval precursor cells (VPCs) of C. elegans have the potential, through reciprocal LIN-12/Notch and LET-23/EGFR signalling, to give rise to either vulval or nonvulval fates. In VPCs in which LET-23 is activated maximally, LIN-12 is endocytosed and degraded. Now on p. 691, Iva Greenwald and co-workers report the isolation of SEL-2, a C. elegans homologue of mammalian neurobeachin (which is required for neurotransmission at neuromuscular junctions) and LRBA (which positively regulates EGFR in cell culture). SEL-2, they show, is required for efficient endocytosis in epithelial cells and for maintaining LIN-12 in a steady state. LIN-12 is mislocalised basolaterally in sel-2 mutants and cannot be degraded in response to Ras activation. Moreover, endocytosis is compromised in the intestinal epithelium of these mutants, as revealed by the basolateral accumulation of a dye that marks endocytic vesicles. In VPCs, LIN-12 trafficking and stability, rather than its transcription, is modulated, and SEL-2's role may contribute to the mechanisms required for these processes and for cell fate specification.

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Related articles in Development:

SEL-2, the C. elegans neurobeachin/LRBA homolog, is a negative regulator of lin-12/Notch activity and affects endosomal traffic in polarized epithelial cells

Natalie de Souza, Laura G. Vallier, Hanna Fares, and Iva Greenwald
Development 2007 134: 691-702. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?