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Title: The mammalian Ced-1 ortholog MEGF10/KIAA1780 displays a novel adhesion pattern

Journal Article · · Experimental Cell Research
 [1];  [2]
  1. Department of Human Genome Research, Kazusa DNA Research Institute, 2-6-7, Kazusa-Kamatari, Kisarazu, Chiba 292-0818 (Japan)
  2. Department of Human Genome Research, Kazusa DNA Research Institute, 2-6-7, Kazusa-Kamatari, Kisarazu, Chiba 292-0818 (Japan) and Laboratory of Pharmacogenomics, Graduate School of Pharmaceutical Sciences, Chiba University, 2-6-7, Kazusa-Kamatari, Kisarazu, Chiba 292-0818 (Japan)

Ced-1 protein is a Caenorhabditis elegans cell surface receptor involved in phagocytosis of dead cells. The gene encoding the mammalian ortholog of Ced-1 is yet to be identified. Here, we describe a potential candidate: human MEGF10. MEGF10 has the overall domain organization of Ced-1, containing a signal peptide, a EMI domain, 17 atypical EGF-like repeats, a transmembrane domain, and a cytoplasmic domain with NPXY and YXXL motifs. MEGF10-EGFP fusion protein expressed in HEK293 cells produced an irregular, mosaic-like pattern on the surface of coated glass. Protruded MEGF10 bound tightly to the glass, in effect 'pinning' the cytoplasmic membrane firmly onto the glass, thereby restricting cell motility. These cells also took on a flat appearance. Although MEGF10-EGFP localized throughout the cytoplasmic membrane, no MEGF10-EGFP was found in lamellipodia. The MEGF10-EGFP signal was surrounded by a 1-2-{mu}m-wide dark strip lacking EGFP. Expression analyses of various MEGF10 deletion mutants revealed that the irregular, mosaic-like adhesion pattern characteristic of MEGF10 family members is due to concerted interactions between the EMI and 17 atypical EGF-like domains. Co-culturing of MEGF10-EGFP-expressing cells with apoptotic cells revealed that MEGF10 protein accumulated around the contact region during engulfment of apoptotic cells.

OSTI ID:
20955490
Journal Information:
Experimental Cell Research, Vol. 313, Issue 11; Other Information: DOI: 10.1016/j.yexcr.2007.03.041; PII: S0014-4827(07)00149-8; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English

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