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乙醛酸循环在乙酸盐上生长加速的突变体中的去阻遏作用。

Derepression of the glyoxylate cycle in mutants of accelerated for growth on acetate.

作者信息

Chaure P T, Connerton I F

机构信息

Department of Microbiology, University of Reading, Whiteknights, PO Box 228, Reading RG6 2AJ, UK.

Institute of Food Research, Protein Engineering Department, Earley Gate, Whiteknights Road, Reading RG6 2EF, UK.

出版信息

Microbiology (Reading). 1995 Jun;141(6):1315-1320. doi: 10.1099/13500872-141-6-1315.

Abstract

Two spontaneous allelic mutations have been isolated with the unusual semi-dominant phenotype of faster-than-wild-type growth on acetate as sole carbon source. The mutants were designated (accelerated acetate growth) and mapped on linkage group II. Upon re-isolation of both the alleles from repeated back-crosses to wild-type, between 1 and 6% of the progeny were found to be (acetate non-utilizing) mutants. Ten of these were selected for heterokaryon complementation analysis with known mutants; nine proved to be new alleles of (deficient in acetyl-CoA synthetase), and one was a new acetate non-utilizing class, designated . Although the mutants clearly have no acetate-growth-related enzyme deficiencies, they did exhibit significant constitutive enzyme levels for acetyl-CoA synthetase and the glyoxylate cycle enzymes (isocitrate lyase and malate synthase) on the non-inducing carbon source, sucrose. The derepression was restricted to these enzymes, as representative enzymes from other carbon-assimilatory pathways remained repressed and subject to carbon catabolite repression. Northern blot analysis of the mRNA levels of acetyl-CoA synthetase and the glyoxylate cycle enzymes from the mutants demonstrated the derepression to occur at the level of transcription. These data suggest that the physiological explanation for the accelerated acetate growth phenotype lies in the standing levels of the acetate-assimilatory enzymes, which enable the mutants to forgo some of the normal time required for adaption to growth on acetate.

摘要

已经分离出两个自发等位基因突变体,它们具有不寻常的半显性表型,即在以乙酸盐作为唯一碳源时,其生长速度比野生型快。这些突变体被命名为(乙酸盐生长加速),并定位在连锁群II上。当从与野生型的重复回交中重新分离出这两个等位基因时,发现1%至6%的后代是(乙酸盐不利用)突变体。其中十个被选用于与已知的突变体进行异核体互补分析;九个被证明是(乙酰辅酶A合成酶缺陷)的新等位基因,一个是新的乙酸盐不利用类别,命名为。尽管突变体显然没有与乙酸盐生长相关的酶缺陷,但它们在非诱导性碳源蔗糖上确实表现出乙酰辅酶A合成酶和乙醛酸循环酶(异柠檬酸裂解酶和苹果酸合酶)的显著组成型酶水平。这种去阻遏作用仅限于这些酶,因为来自其他碳同化途径的代表性酶仍然受到阻遏,并受到碳分解代谢物阻遏。对突变体中乙酰辅酶A合成酶和乙醛酸循环酶的mRNA水平进行Northern印迹分析表明,去阻遏作用发生在转录水平。这些数据表明,乙酸盐生长加速表型背后的生理学解释在于乙酸盐同化酶的持续水平,这使得突变体能够省去适应乙酸盐生长所需的一些正常时间。

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