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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Constitutive Mutations of the Saccharomyces cerevisiae MAL-Activator Genes MAL23, MAL43, MAL63, and mal64
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Constitutive Mutations of the Saccharomyces cerevisiae MAL-Activator Genes MAL23, MAL43, MAL63, and mal64

机译:啤酒酵母MAL激活基因MAL23,MAL43,MAL63和mal64的组成性突变

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We report the sequence of several MAL -activator genes, including inducible, constitutive, and noninducible alleles of MAL23, MAL43, MAL63, and mal64. Constitutive alleles of MAL23 and MAL43 vary considerably from inducible alleles in their C-terminal domain, with many of the alterations clustered and common to both alleles. The 27 alterations from residues 238–461 of Mal43-C protein are sufficient for constitutivity, but the minimal number of alterations needed for the constitutive phenotype could not be determined. The sequence of mal64, a nonfunctional homologue of MAL63, revealed that Mal64p is 85% identical to Mal63p. Two mutations that activate mal64 and cause constitutivity are nonsense mutations resulting in truncated proteins of 306 and 282 residues. We conclude that the C-terminal region of the MAL -activator, from residues 283–470, contains a maltose-responsive negative regulatory domain, and that extensive mutation or deletion of the entire region causes loss of the negative regulatory function. Additionally, certain sequence elements in the region appear to be necessary for efficient induction of the full-length Mal63 activator protein. These studies highlight the role of ectopic recombination as an important mechanism of mutagenesis of the telomere-associated family of MAL loci.
机译:我们报告了几种MAL激活基因的序列,包括MAL23,MAL43,MAL63和mal64的诱导型,组成型和非诱导型等位基因。 MAL23和MAL43的组成型等位基因在其C端结构域中与诱导型等位基因相差很大,并且许多改变都聚集在两个等位基因中且共有。 Mal43-C蛋白残基238-461的27个改变足以构成,但无法确定构成表型所需的最小改变数。 mal64的序列是MAL63的一种非功能性同源物,显示Mal64p与Mal63p具有85%的同一性。激活mal64并导致组成性的两个突变是无意义的突变,导致306和282个残基的蛋白被截短。我们得出的结论是,MAL激活剂的C末端区域(来自残基283-470)包含一个麦芽糖反应性负调控域,并且整个区域的广泛突变或缺失导致负调控功能的丧失。另外,该区域中的某些序列元件似乎对于有效诱导全长Mal63激活蛋白是必需的。这些研究强调了异位重组作为诱变端粒相关的MAL基因座家族的重要机制的作用。

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