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The maintenance of neuromuscular function requires UBC-25 in Caenorhabditis elegans.

作者信息

Schulze Ekkehard, Altmann Maria E, Adham Ibrahim M, Schulze Bettina, Fröde Stephan, Engel Wolfgang

机构信息

Third Department of Zoology--Developmental Biology, Georg-August University, Göttingen, Humboldtallee 34 A, Göttingen D-37073, Germany.

出版信息

Biochem Biophys Res Commun. 2003 Jun 6;305(3):691-9. doi: 10.1016/s0006-291x(03)00824-6.

DOI:10.1016/s0006-291x(03)00824-6
PMID:12763049
Abstract

Caenorhabditis elegans gene ubc-25 encodes a novel type of an E2 ubiquitin transferase domain (UBCc) protein, which is highly conserved in multicellular animals, but which is not present in the genomes of fungi or plants. To identify the cellular localization of UBC-25 during the development of C. elegans, we used a ubc-25::gfp reporter gene construct. These experiments showed that ubc-25 expression starts during embryogenesis and that it is restricted to neurons and muscle cells in all later stages of development as well as in adult animals. RNA interference with ubc-25 caused late-onset paralysis of most muscular functions such as locomotion, egg laying, and defecation. We therefore propose that ubc-25 in C. elegans is required for the maintenance (homeostasis) of neuromuscular functions by contributing to a tissue specific protein modification pathway, and we speculate that the adult onset phenotype results from the accumulation of target proteins which fail to be degraded.

摘要

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