膜蛋白的损伤与修复：叶绿体膜中失活的32千道尔顿多肽的去除与替换
Membrane protein damage and repair: removal and replacement of inactivated 32-kilodalton polypeptides in chloroplast membranes.
作者信息
Ohad I, Kyle D J, Arntzen C J
出版信息
J Cell Biol. 1984 Aug;99(2):481-5. doi: 10.1083/jcb.99.2.481.
Abstract
Incubation of Chlamydomonas reinhardii cells at light levels that are several times more intense than those at which the cells were grown results in a loss of photosystem II function (termed photoinhibition). The loss of activity corresponded to the disappearance from the chloroplast membranes of a lysine-deficient, herbicide-binding protein of 32,000 daltons which is thought to be the apoprotein of the secondary quinone electron acceptor of photosystem II (the QB protein). In vivo recovery from the damage only occurred following de novo synthesis (replacement) of the chloroplast-encoded QB protein. We believe that the turnover of this protein is a normal consequence of its enzymatic function in vivo and is a physiological process that is necessary to maintain the photosynthetic integrity of the thylakoid membrane. Photoinhibition occurs when the rate of inactivation and subsequent removal exceeds the rate of resynthesis of the QB protein.
摘要
莱茵衣藻细胞在比其生长时的光照强度高几倍的条件下培养，会导致光系统II功能丧失（称为光抑制）。活性丧失与叶绿体膜上一种分子量为32000道尔顿、缺乏赖氨酸且能结合除草剂的蛋白质的消失相对应，该蛋白质被认为是光系统II的次级醌电子受体（QB蛋白）的脱辅基蛋白。只有在叶绿体编码的QB蛋白重新合成（替换）后，体内损伤才能恢复。我们认为，这种蛋白质的周转是其在体内酶功能的正常结果，是维持类囊体膜光合完整性所必需的生理过程。当QB蛋白的失活和随后的去除速率超过其重新合成速率时，就会发生光抑制。
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Molecular Basis of Herbicide Resistance in Amaranthus hybridus.苋菜抗除草剂的分子基础。
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