کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10934298 | 1093889 | 2005 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dd-Alix, a conserved endosome-associated protein, controls Dictyostelium development
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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![عکس صفحه اول مقاله: Dd-Alix, a conserved endosome-associated protein, controls Dictyostelium development Dd-Alix, a conserved endosome-associated protein, controls Dictyostelium development](/preview/png/10934298.png)
چکیده انگلیسی
We have characterized the Dictyostelium homolog of the mammalian protein Alix. Dd-Alix is encoded by a single gene and is expressed during vegetative growth and multicellular development. We showed that the alx null strain fails to complete its developmental program. Past the tight aggregate stage, morphogenesis is impaired, leading to markedly aberrant structures containing vacuolated and undifferentiated cells but no mature spores. The developmental defect is cell-autonomous as most cells remain of the PstB type even when mixed with wild-type cells. Complementation analysis with different Alix constructs allowed the identification of a 101-residue stretch containing a coiled-coil domain essential for Alix function. In addition, we showed that the protein associates in part with vesicular structures and that its distribution on a Percoll gradient overlaps that of the endocytic marker Vamp7. Dd-Alix also co-localizes with Dd-Vps32. In view of our data, and given the role of Vps32 proteins in membrane protein sorting and multivesicular body formation in yeast and mammals, we hypothesize that the developmental defects of the alx null strain result from abnormal trafficking of cell-surface receptors.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental Biology - Volume 279, Issue 1, 1 March 2005, Pages 99-113
Journal: Developmental Biology - Volume 279, Issue 1, 1 March 2005, Pages 99-113
نویسندگان
Sara Mattei, W. Jonathan Ryves, Béatrice Blot, Rémy Sadoul, Adrian J. Harwood, Michel Satre, Gérard Klein, Laurence Aubry,