Poteryaev D, Spang A
Friedrich Miescher Laboratory of the Max Planck Society, Spemannstrasse 39, Tuebingen D-72076, Germany.
Biochem Soc Trans. 2005 Aug;33(Pt 4):606-8. doi: 10.1042/BST0330606.
Caenorhabditis elegans has recently been used as an attractive model system to gain insight into mechanisms of endocytosis in multicellular organisms. A combination of forward and reverse genetics has identified a number of new membrane trafficking factors. Most of them have mammalian homologues which function in the same transport events. We describe a novel C. elegans gene sand-1, whose loss of function causes profound endocytic defects in many tissues. SAND-1 belongs to a conserved family of proteins present in all eukaryotic species, whose genome is sequenced. However, SAND family has not been previously characterized in metazoa. Our comparison of C. elegans SAND-1 and its yeast homologue, Mon1p, showed a conserved role of the SAND-family proteins in late steps of endocytic transport.
秀丽隐杆线虫最近已成为一种有吸引力的模型系统,用于深入了解多细胞生物中的内吞作用机制。正向遗传学和反向遗传学相结合已鉴定出许多新的膜运输因子。它们中的大多数都有在相同运输事件中起作用的哺乳动物同源物。我们描述了一个新的秀丽隐杆线虫基因sand-1,其功能丧失会在许多组织中导致严重的内吞缺陷。SAND-1属于所有已测序真核物种中存在的一个保守蛋白家族。然而,SAND家族以前在后生动物中尚未得到表征。我们对秀丽隐杆线虫SAND-1及其酵母同源物Mon1p的比较表明,SAND家族蛋白在内吞运输的后期步骤中具有保守作用。