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沙门氏菌噬菌体P22中的基因表达调控。II. 晚期功能表达的调控。

Regulation of gene expression in Salmonella phage P22. II. Regulation of expression of late functions.

作者信息

Prell H H

机构信息

Abteilung für Molekulare Genetik, Institut für Mikrobiologie der Gesellschaft für Strahlen- und Umweltforschung mbH München, Göttingen, Federal Republic of Germany.

出版信息

Mol Gen Genet. 1975;136(4):351-60. doi: 10.1007/BF00341719.

Abstract

Transactivation experiments were performed involving the genetically related Salmonella phages P22, L and Px1 in order to find out if more than one positively acting regulatory product is engaged in the expression of vegetative gene functions of each of these phages. The results obtained with Px1- and L-lysogenic cells superinfected with P22 suggest the following conclusions: 1. The expression of the early genes 12 and 23 and of the late gene 19 (lysozyme synthesis) is positively regulated by two different regulatory products, since P22 transactivates in prophage Px1 both early and late genes (Prell, 1973), in prophage L only late genes. 2. The transactivation by P22 of the lysozyme gene of prophage L takes place in the presence of L repressor. This conclusion is suggested, since the superinfecting P22 does not derepress early gene expression (see 1.), and is confirmed by demonstration of replication inhibition for L phage in L lysogenic cells doubly superinfected with L and P22 phages (Thomas-Bertani-experiment). 3. The late gene regulatory protein seems to be synthesized by gene 23, as transactivation experiments with both L- and Px1 prophages suggest. 4. The expression of gene 23 itself is turned on by an early regulatory product. The gene which codes for it is still unidentified. However its product seems to by highly specific, since it is active on Px1- but not on L-prophage.

摘要

进行了涉及基因相关的沙门氏菌噬菌体P22、L和Px1的反式激活实验,以查明是否有不止一种正向作用的调节产物参与这些噬菌体各自营养基因功能的表达。用P22超感染Px1和L溶原性细胞所获得的结果提示了以下结论:1. 早期基因12和23以及晚期基因19(溶菌酶合成)的表达受两种不同调节产物的正向调节,因为P22在原噬菌体Px1中能反式激活早期和晚期基因(Prell,1973),而在原噬菌体L中只能反式激活晚期基因。2. P22对原噬菌体L的溶菌酶基因的反式激活是在L阻遏物存在的情况下发生的。这一结论是基于超感染的P22不会解除早期基因表达(见1.)而提出的,并通过对L和P22噬菌体双重超感染的L溶原性细胞中L噬菌体复制抑制的证明得到证实(Thomas-Bertani实验)。3. 晚期基因调节蛋白似乎是由基因23合成的,因为对L和Px1原噬菌体的反式激活实验都提示了这一点。4. 基因23自身的表达由一种早期调节产物开启。编码该产物的基因仍未确定。然而其产物似乎具有高度特异性,因为它对Px1原噬菌体有活性,而对L原噬菌体无活性。

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