Wiedmann B, Silver P, Schunck W H, Wiedmann M
Cellular Biochemistry and Biophysics Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.
Biochim Biophys Acta. 1993 Dec 12;1153(2):267-76. doi: 10.1016/0005-2736(93)90415-v.
High expression of microsomal cytochrome P-450 CYP52A3 from Candida maltosa induces the formation of membrane stacks in Saccharomyces cerevisiae. Membrane proliferation is accompanied by coinduction of the ER proteins KAR2p and SEC61p and accumulation of precursor forms of proteins that have to translocate across the ER membrane (KAR2p, alpha factor). Cytosolic proteins (SSA1p and 2p) and mitochondrial proteins (CYT c1p and F1 beta p) are not affected. N-terminal truncated P-450 proteins remain in the cytoplasm and fail to induce membrane proliferation, KAR2p/SEC61p expression, and precursor accumulation. Membrane and precursor protein accumulation are typical features of sec mutants. We assume that the high amounts of P-450p block one or more factor(s) of the transport machinery and thereby cause the observed phenomena.
来自麦芽糖假丝酵母的微粒体细胞色素P-450 CYP52A3的高表达诱导酿酒酵母中膜堆叠的形成。膜增殖伴随着内质网蛋白KAR2p和SEC61p的共诱导以及必须跨内质网膜转运的蛋白质前体形式的积累（KAR2p、α因子）。胞质蛋白（SSA1p和2p）和线粒体蛋白（CYT c1p和F1βp）不受影响。N端截短的P-450蛋白保留在细胞质中，无法诱导膜增殖、KAR2p/SEC61p表达和前体积累。膜和前体蛋白积累是sec突变体的典型特征。我们假设大量的P-450p阻断了转运机制的一个或多个因子，从而导致了观察到的现象。
