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Histone chaperones and the Rrm3p helicase regulate flocculation in S. cerevisiae.
Epigenetics & Chromatin ( IF 3.9 ) Pub Date : 2019-09-23 , DOI: 10.1186/s13072-019-0303-8
Hollie Rowlands 1 , Kholoud Shaban 1 , Barret Foster 1 , Yannic Proteau 1 , Krassimir Yankulov 1
Affiliation  

Biofilm formation or flocculation is a major phenotype in wild type budding yeasts but rarely seen in laboratory yeast strains. Here, we analysed flocculation phenotypes and the expression of FLO genes in laboratory strains with various genetic backgrounds. We show that mutations in histone chaperones, the helicase RRM3 and the Histone Deacetylase HDA1 de-repress the FLO genes and partially reconstitute flocculation. We demonstrate that the loss of repression correlates to elevated expression of several FLO genes, to increased acetylation of histones at the promoter of FLO1 and to variegated expression of FLO11. We show that these effects are related to the activity of CAF-1 at the replication forks. We also demonstrate that nitrogen starvation or inhibition of histone deacetylases do not produce flocculation in W303 and BY4742 strains but do so in strains compromised for chromatin maintenance. Finally, we correlate the de-repression of FLO genes to the loss of silencing at the subtelomeric and mating type gene loci. We conclude that the deregulation of chromatin maintenance and transmission is sufficient to reconstitute flocculation in laboratory yeast strains. Consequently, we propose that a gain in epigenetic silencing is a major contributing factor for the loss of flocculation phenotypes in these strains. We suggest that flocculation in yeasts provides an excellent model for addressing the challenging issue of how epigenetic mechanisms contribute to evolution.

中文翻译:

组蛋白伴侣和Rrm3p解旋酶调节酿酒酵母中的絮凝。

生物膜形成或絮凝是野生型发芽酵母中的主要表型,但在实验室酵母菌株中很少见。在这里,我们分析了具有不同遗传背景的实验室菌株中的絮凝表型和FLO基因的表达。我们显示,组蛋白伴侣,解旋酶RRM3和组蛋白脱乙酰基酶HDA1中的突变能抑制FLO基因并部分重构絮凝。我们证明,压抑的丧失与几个FLO基因的表达升高,在FLO1启动子处的组蛋白乙酰化增加以及FLO11的多样化表达相关。我们表明,这些影响与复制叉处CAF-1的活性有关。我们还证明了氮饥饿或组蛋白脱乙酰基酶的抑制作用不会在W303和BY4742菌株中产生絮凝,但会在染色质维持受损的菌株中产生絮凝。最后,我们将FLO基因的抑制与亚端粒和交配型基因位点的沉默丧失相关联。我们得出的结论是,染色质维持和传递的失调足以重构实验室酵母菌株中的絮凝。因此,我们提出表观遗传沉默的获得是这些菌株中絮凝表型丧失的主要促成因素。我们建议酵母中的絮凝为解决表观遗传机制如何促进进化这一具有挑战性的问题提供了一个极好的模型。我们将FLO基因的去抑制与亚端粒和交配型基因位点的沉默丧失联系起来。我们得出的结论是,染色质维持和传递的失调足以重构实验室酵母菌株中的絮凝。因此,我们提出表观遗传沉默的获得是这些菌株中絮凝表型丧失的主要促成因素。我们建议酵母中的絮凝为解决表观遗传机制如何促进进化这一具有挑战性的问题提供了一个极好的模型。我们将FLO基因的抑制与亚端粒和交配型基因位点的沉默丧失联系起来。我们得出的结论是,染色质维持和传递的失调足以重构实验室酵母菌株中的絮凝。因此,我们提出表观遗传沉默的获得是这些菌株中絮凝表型丧失的主要促成因素。我们建议酵母中的絮凝为解决表观遗传机制如何促进进化这一具有挑战性的问题提供了一个极好的模型。我们提出表观遗传沉默的增加是这些菌株絮凝表型丧失的主要因素。我们建议酵母中的絮凝为解决表观遗传机制如何促进进化这一具有挑战性的问题提供了一个极好的模型。我们提出表观遗传沉默的增加是这些菌株絮凝表型丧失的主要因素。我们建议酵母中的絮凝为解决表观遗传机制如何促进进化这一具有挑战性的问题提供了一个极好的模型。
更新日期:2020-04-22
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