Unfolded protein response followed by induction of cell death in cultured tobacco cells treated with tunicamycin
Unfolded protein response followed by induction of cell death in cultured tobacco cells treated with tunicamycin
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DOI：
10.1007/s00425-004-1479-z
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发表时间：
2005-03-01
期刊：
影响因子：
4.3
通讯作者：
Koizumi, N
中科院分区：
文献类型：
--
作者：
Iwata, Y;Koizumi, N
当内质网（ER）中蛋白质的正确折叠被阻止时，细胞会做出反应来克服未折叠蛋白质的积累。这种细胞反应，包括内质网伴侣的诱导，被称为未折叠蛋白反应（UPR）。虽然UPR与细胞凋亡之间的联系已经在哺乳动物细胞中报道过，但对植物细胞中的这一机制知之甚少。蛋白质的天冬酰胺(N)连接糖基化对内质网中的蛋白质折叠至关重要；tunicamycin是一种有效的n -链糖基化抑制剂，可诱导UPR。tunicamycin对培养的烟草细胞有抑制生长作用。在加入tunicamycin后的24小时内观察到细胞死亡和Hsr203J（程序性细胞死亡的标志物）的诱导，随后在2小时内开始UPR。这些结果表明，植物细胞中UPR与程序性细胞死亡之间存在密切联系。
When correct folding of protein in the endoplasmic reticulum (ER) is prevented, cells respond to overcome the accumulation of unfolded proteins. This cellular response, which includes the induction of ER chaperones, is called an unfolded protein response (UPR). Although a link between the UPR and apoptosis has been reported in mammalian cells, little is known about this mechanism in plant cells. Asparagine (N)-linked glycosylation of proteins is critical for protein folding in the ER; and tunicamycin, a potent inhibitor of N-linked glycosylation, induces UPR. Growth arrest was observed in cultured tobacco cells treated with tunicamycin. Cell death and induction of Hsr203J, a marker for programmed cell death, were observed in the 24-h period after addition of tunicamycin, following UPR that started within 2 h. These results indicate a strong link between UPR and programmed cell death in plant cells.