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异常10号染色体上的四个基因座导致玉米减数分裂驱动。

Four loci on abnormal chromosome 10 contribute to meiotic drive in maize.

作者信息

Hiatt Evelyn N, Dawe R Kelly

机构信息

Department of Genetics, University of Georgia, Athens 30602, USA.

出版信息

Genetics. 2003 Jun;164(2):699-709. doi: 10.1093/genetics/164.2.699.

Abstract

We provide a genetic analysis of the meiotic drive system on maize abnormal chromosome 10 (Ab10) that causes preferential segregation of specific chromosomal regions to the reproductive megaspore. The data indicate that at least four chromosomal regions contribute to meiotic drive, each providing distinct functions that can be differentiated from each other genetically and/or phenotypically. Previous reports established that meiotic drive requires neocentromere activity at specific tandem repeat arrays (knobs) and that two regions on Ab10 are involved in trans-activating neocentromeres. Here we confirm and extend data suggesting that only one of the neocentromere-activating regions is sufficient to move many knobs. We also confirm the localization of a locus/loci on Ab10, thought to be a prerequisite for meiotic drive, which promotes recombination in structural heterozygotes. In addition, we identified two new and independent functions required for meiotic drive. One was identified through the characterization of a deletion derivative of Ab10 [Df(L)] and another as a newly identified meiotic drive mutation (suppressor of meiotic drive 3). In the absence of either function, meiotic drive is abolished but neocentromere activity and the recombination effect typical of Ab10 are unaffected. These results demonstrate that neocentromere activity and increased recombination are not the only events required for meiotic drive.

摘要

我们对玉米异常10号染色体(Ab10)上的减数分裂驱动系统进行了遗传分析,该系统导致特定染色体区域优先分离到生殖大孢子中。数据表明,至少有四个染色体区域对减数分裂驱动有贡献,每个区域提供不同的功能,这些功能在遗传和/或表型上可以相互区分。先前的报道表明,减数分裂驱动需要在特定串联重复序列阵列(着丝粒节)处有新着丝粒活性,并且Ab10上的两个区域参与反式激活新着丝粒。在这里,我们证实并扩展了数据,表明只有一个新着丝粒激活区域足以移动许多着丝粒节。我们还证实了Ab10上一个位点/多个位点的定位,该定位被认为是减数分裂驱动的先决条件,它促进结构杂合子中的重组。此外,我们鉴定出减数分裂驱动所需的两个新的独立功能。一个是通过对Ab10的缺失衍生物[Df(L)]的表征鉴定出来的,另一个是作为新鉴定的减数分裂驱动突变(减数分裂驱动抑制因子3)。在没有任何一种功能的情况下,减数分裂驱动被消除,但新着丝粒活性和Ab10典型的重组效应不受影响。这些结果表明,新着丝粒活性和重组增加不是减数分裂驱动所需的唯一事件。

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