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首页> 外文期刊>Journal of bacteriology >Both linked and unlinked mutations can alter the intracellular site of synthesis of exported proteins of Escherichia coli.
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Both linked and unlinked mutations can alter the intracellular site of synthesis of exported proteins of Escherichia coli.

机译：连锁突变和非连锁突变均可改变大肠杆菌输出蛋白合成的胞内位点。

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It previously has been demonstrated that synthesis of the periplasmic maltose-binding protein (MBP) and alkaline phosphatase (AP) of Eschericha coli predominantly occurs on membrane-bound polysomes. In this study, signal sequence alterations that adversely affect export of MBP and AP, resulting in their cytoplasmic accumulation as unprocessed precursors, were investigated to determine whether they have an effect on the intracellular site of synthesis of these proteins. Our findings indicate that export-defective MBP and AP are not synthesized or are synthesized in greatly reduced levels on membrane-bound polysomes. In some instances, a concomitant increase in the amount of these proteins synthesized on free polysomes was clearly discerned. We also determined the site of synthesis of MBP and AP in strains harboring mutations thought to alter the cellular secretion machinery. It was found that the presence of a prlA suppressor allele partially restored synthesis of export-defective MBP on membrane-bound polysomes. On the other hand, the absence of a functional SecA protein resulted in the synthesis of wild-type MBP and AP predominantly on free polysomes.
机译：先前已证明，大肠杆菌的周质麦芽糖结合蛋白（MBP）和碱性磷酸酶（AP）的合成主要发生在膜结合的多核糖体上。在这项研究中，研究了对MBP和AP的输出产生不利影响的信号序列改变，导致它们作为未加工的前体在细胞质中积累，以确定它们是否对这些蛋白质合成的胞内位点有影响。我们的发现表明，出口缺陷型MBP和AP在膜结合多核糖体上未合成或合成程度大大降低。在某些情况下，清楚地看出在游离多核糖体上合成的这些蛋白质的数量随之增加。我们还确定了携带突变的菌株中MBP和AP的合成位点，这些突变被认为可以改变细胞分泌机制。已经发现，prlA抑制等位基因的存在部分恢复了膜结合多核糖体上出口缺陷型MBP的合成。另一方面，缺少功能性SecA蛋白导致野生型MBP和AP的合成主要在游离多核糖体上进行。

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