由非同形序列和减数分裂沉默控制的十字花科神经孢子(Neurospora crassa)重组热点。

IF 3.3 3区 生物学
Genetics Pub Date : 2023-12-20 DOI:10.1093/genetics/iyad213
P Jane Yeadon, Frederick J Bowring, David E A Catcheside
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引用次数: 0

摘要

早在 20 世纪 60 年代,就有人描述了调节克拉斯神经孢子(Neurospora crassa)特定染色体区间重组的基因,但其机制至今仍不清楚。对于 rec-1、rec-2 和 rec-3 基因中的每一个基因,单个拷贝的假定显性等位基因(例如在圣劳伦斯 OR74 A 野生型中发现的 rec-2SL)会减少该基因特定染色体区域的重组。然而,当我们对隐性等位基因 rec-2LG(来源于 Lindegren 1A 野生型)进行测序时,发现 rec-2SL 株系中的 10 kb 区域被一个 2.7 kb 的非相关序列所取代,从而使 "等位基因 "成为非等位基因。当我们在杂合的 rec-2SL/rec-2LG 中引入 sad-1 时,它是一种缺乏 RNA 依赖性 RNA 聚合酶的突变体,而这种 RNA 依赖性 RNA 聚合酶能在减数分裂过程中沉默未配对的编码区。与此相一致的是,通过 RIP(重复诱导点突变)对 rec-2LG 进行突变,产生了一个在预测的 rec-2 基因中含有多个终止密码子的等位基因,它不促进重组,是 rec-2LG 的隐性基因。在 rec-1 等位基因杂交和 rec-3 等位基因杂交中,Sad-1 也解除了对相关目标区域重组的抑制。我们的结论是,对于所有三个已知的 rec 基因来说,其中一个等位基因出现显性,只是因为减数分裂沉默阻止了活性 "隐性 "等位基因的产物在减数分裂过程中刺激重组。此外,拟议的 REC-2 氨基酸序列表明,神经孢子中的重组调控与目前已知的任何机制都不同。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Recombination hotspots in Neurospora crassa controlled by idiomorphic sequences and meiotic silencing.
Genes regulating recombination in specific chromosomal intervals of Neurospora crassa were described in the 1960s but the mechanism is still unknown. For each of the rec-1, rec-2 and rec-3 genes, a single copy of the putative dominant allele, for example rec-2SL found in St Lawrence OR74 A wild type, reduces recombination in chromosomal regions specific to that gene. However, when we sequenced the recessive allele, rec-2LG (derived from the Lindegren 1A wild type) we found that a 10 kb region in rec-2SL strains was replaced by a 2.7 kb unrelated sequence, making the "alleles" idiomorphs. When we introduced sad-1, a mutant lacking the RNA-dependent RNA polymerase that silences unpaired coding regions during meiosis into crosses heterozygous rec-2SL/rec-2LG, it increased recombination, indicating that meiotic silencing of a gene promoting recombination is responsible for dominant suppression of recombination. Consistent with this, mutation of rec-2LG by RIP (Repeat-Induced Point mutation) generated an allele with multiple stop codons in the predicted rec-2 gene, which does not promote recombination and is recessive to rec-2LG. Sad-1 also relieves suppression of recombination in relevant target regions, in crosses heterozygous for rec-1 alleles and in crosses heterozygous for rec-3 alleles. We conclude that for all three known rec genes, one allele appears dominant only because meiotic silencing prevents the product of the active, "recessive", allele from stimulating recombination during meiosis. In addition, the proposed amino acid sequence of REC-2 suggests that regulation of recombination in Neurospora differs from any currently known mechanism.
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来源期刊
Genetics
Genetics 生物-遗传学
CiteScore
6.20
自引率
6.10%
发文量
177
期刊介绍: GENETICS is published by the Genetics Society of America, a scholarly society that seeks to deepen our understanding of the living world by advancing our understanding of genetics. Since 1916, GENETICS has published high-quality, original research presenting novel findings bearing on genetics and genomics. The journal publishes empirical studies of organisms ranging from microbes to humans, as well as theoretical work. While it has an illustrious history, GENETICS has changed along with the communities it serves: it is not your mentor''s journal. The editors make decisions quickly – in around 30 days – without sacrificing the excellence and scholarship for which the journal has long been known. GENETICS is a peer reviewed, peer-edited journal, with an international reach and increasing visibility and impact. All editorial decisions are made through collaboration of at least two editors who are practicing scientists. GENETICS is constantly innovating: expanded types of content include Reviews, Commentary (current issues of interest to geneticists), Perspectives (historical), Primers (to introduce primary literature into the classroom), Toolbox Reviews, plus YeastBook, FlyBook, and WormBook (coming spring 2016). For particularly time-sensitive results, we publish Communications. As part of our mission to serve our communities, we''ve published thematic collections, including Genomic Selection, Multiparental Populations, Mouse Collaborative Cross, and the Genetics of Sex.
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