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First published online 17 July 2007
doi: 10.1242/jcs.03474

Journal of Cell Science 120, 2741-2751 (2007)
Published by The Company of Biologists 2007
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Research Article

C. elegans Disabled is required for cell-type specific endocytosis and is essential in animals lacking the AP-3 adaptor complex

Alex Holmes1, Aileen Flett1, Damien Coudreuse2, Hendrik C. Korswagen2 and Jonathan Pettitt1,*

1 Cell and Developmental Biology Program, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK
2 Hubrecht Lab/NIOB, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands

* Author for correspondence (e-mail: j.pettitt{at}abdn.ac.uk)

Accepted 24 May 2007

Disabled proteins are a conserved family of monomeric adaptor proteins that in mammals are implicated in the endocytosis of lipoprotein receptors. Previous studies have shown that the sole Caenorhabditis elegans Disabled homologue, DAB-1, is involved in the lipoprotein receptor-mediated secretion of a fibroblast growth factor. We show here that DAB-1 is essential for the uptake of yolk protein by developing oocytes, and for the localisation of the yolk receptor RME-2. The localisation of DAB-1 in oocytes is itself dependent upon clathrin and AP2, consistent with DAB-1 acting as a clathrin-associated sorting protein during yolk protein endocytosis. DAB-1 is also required for the endocytosis of molecules from the pseudocoelomic fluid by the macrophage-like coelomocytes, and is broadly expressed in epithelial tissues, consistent with a general role in receptor-mediated endocytosis. We also show that dab-1 mutations are synthetic lethal in combination with loss-of-function mutations affecting the AP-1 and AP-3 complexes, suggesting that the reduced fluid and membrane uptake exhibited by dab-1 mutants sensitises them to defects in other trafficking pathways.

Key words: Receptor-mediated endocytosis, C. elegans, Disabled, CLASP


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© The Company of Biologists Ltd 2007