SKD1 AAA ATPase-dependent endosomal transport is involved in autolysosome formation
SKD1 AAA ATPase-dependent endosomal transport is involved in autolysosome formation
复制标题
DOI：
10.1247/csf.27.29
复制
发表时间：
2002-02-01
影响因子：
1.5
通讯作者：
Yoshimori, T
中科院分区：
文献类型：
--
作者：
Nara, A;Mizushima, N;Yoshimori, T
小鼠SKD 1 AAA ATP酶参与从内体的分选和转运;过表达显性阴性突变体SKD 1（E235 Q）的细胞在向质膜和溶酶体的内体转运方面存在缺陷（Yoshimori et al，2000）。在本研究中，我们证明了使用腺病毒递送系统过度表达SKD 1（E235 Q）会导致自噬依赖的大量蛋白质降解缺陷。形态学观察表明，这种抑制自噬的结果从自溶酶体形成的损害。SKD 1（E235 Q）过表达还抑制了从内体到自噬体的转运，这是一种通常发生在与溶酶体融合之前的事件。这些结果表明，SKD 1依赖性内体膜运输是形成自体溶酶体所必需的。
Mouse SKD1 AAA ATPase is involved in the sorting and transport from endosomes; cells overexpressing a dominant-negative mutant, SKD1(E235Q) were defective in endosomal transport to both the plasma membranes and lysosomes (Yoshimori et al, 2000). In the present study, we demonstrated that overexpression of SKD1(E235Q) using an adenovirus delivery system caused a defect in autophagy-dependent bulk protein degradation. Morphological observations suggested that this inhibition of autophagy results from an impairment of autolysosome formation. SKD1(E235Q) overexpression also inhibited transport from endosomes to autophagosomes, an event normally occurring prior to fusion with lysosomes. These results indicate that SKD1-dependent endosomal membrane trafficking is required for formation of autolysosomes.