Chromosome segment duplications in Neurospora crassa and their effects on repeat-induced point mutation and meiotic silencing by unpaired DNA.

IF 5.1 3区 生物学 Genetics Pub Date : 2006-03-01 Epub Date: 2005-12-15 DOI:10.1534/genetics.105.050468
Meenal Vyas, C Ravindran, Durgadas P Kasbekar
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引用次数: 16

Abstract

The size and extent of four Neurospora crassa duplications, Dp(AR17), Dp(IBj5), Dp(OY329), and Dp(B362i), was determined by testing the coverage of RFLP markers. The first three duplications were all > approximately 350 kb and have been shown in earlier studies to act as dominant suppressors of repeat-induced point mutation (RIP) in gene-sized duplications, possibly via titration of the RIP machinery. Dp(B362i), which is only approximately 117 kb long, failed to suppress RIP. RIP suppression in gene-sized duplications by large duplications was demonstrated using another test gene, dow, and supposedly applies generally. Crosses homozygous for Dp(AR17) or Dp(IBj5) were as barren as heterozygous crosses. Barrenness of the heterozygous but not the homozygous crosses was suppressible by Sad-1, a semidominant suppressor of RNAi-dependent meiotic silencing by unpaired DNA. A model is proposed in which large duplications recessively suppress semidominant Sad-1 mutations. The wild-isolated Sugartown strain is hypothesized to contain a duplication that confers not only dominant suppression of RIP but also a barren phenotype, which is linked (9%) to supercontig 7.118 in LG VII.

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粗神经孢子虫染色体片段复制及其对重复诱导点突变和非配对DNA减数分裂沉默的影响。
通过检测RFLP标记覆盖率,确定4个粗神经孢子虫重复序列Dp(AR17)、Dp(IBj5)、Dp(OY329)和Dp(B362i)的大小和范围。前三个重复都>大约350 kb,并且在早期的研究中被证明是重复诱导点突变(RIP)在基因大小重复中的显性抑制因子,可能是通过RIP机制的滴定。日志含义Dp(B362i)报文抑制RIP失败,该报文长度约为117kb。使用另一种测试基因(dow)证明了大重复对基因大小重复的RIP抑制作用,并且可能普遍适用。Dp(AR17)或Dp(IBj5)纯合子的不育性与杂合子的不育性相同。杂合子而非纯合子的不育性可被Sad-1抑制,Sad-1是rnai依赖性减数分裂沉默的半显性抑制因子。提出了一个大重复隐性抑制半显性Sad-1突变的模型。假设野生分离的Sugartown菌株含有一个重复,该重复不仅赋予RIP显性抑制,而且还具有贫瘠表型,这与LG VII的超contig 7.118相关(9%)。
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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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