Characterization of a knock-out mutation at the Gc2 locus in wheat
Characterization of a knock-out mutation at the Gc2 locus in wheat
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DOI：
10.1007/s00412-003-0234-8
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发表时间：
2003-05-01
期刊：
影响因子：
1.6
通讯作者：
Gill, BS
中科院分区：
文献类型：
--
作者：
Friebe, B;Zhang, P;Gill, BS
杀配子基因（Gc）是从山羊草属（Aegilops）近缘种引入普通小麦的一种自私的遗传因子，通过诱导染色体断裂来确保其优先传递。在这里，我们报告的Gc 2基因的敲除突变转移到小麦小麦小麦的小麦-沙荣山羊草T4 B-4S（sh）#1易位染色体的生产和表征。在半合子Gc 2/-条件下，缺乏Gc 2的配子体遭受染色体断裂并产生无功能配子，这导致孢子体半不育和Gc 2载体染色体的排他性传递。我们已经确定了一个假定的甲基磺酸乙酯（EMS）诱导的Gc 2突变体，恢复穗育性，并显示孟德尔分离。后代筛选将突变定位于Gc 2携带者染色体T4 B-4S（sh）#1。C-显带和荧光原位杂交分析表明，Gc 2功能的突变体中的损失是不是由于终端缺陷。对Gc 2（mut）/-植株的第一、二次花粉有丝分裂和测交后代的C-分带分析表明，突变体没有发生染色体断裂。没有配子体染色体断裂观察杂合Gc 2（突变体）/Gc 2植物，其中有完全可育穗。这些结果表明，Gc 2编码两种药物，一种引起缺乏Gc 2的配子体中的染色体断裂，另一种保护Gc 2载体免于断裂。EMS诱导的Gc 2突变体似乎是编码“破坏”剂的基因的敲除。这些数据是对Gc 2作用的分子理解的第一个关键步骤。
Gametocidal (Gc) genes, introduced into common wheat from related Aegilops species, are selfish genetic elements that ensure their preferential transmission by inducing chromosomal breaks. Here we report the production and characterization of a knock-out mutation of the Gc2 gene transferred to wheat as a wheat-Aegilops sharonensis T4B-4S(sh)#1 translocation chromosome. In hemizygous Gc2/- condition, gametophytes lacking Gc2 suffer chromosomal fragmentation and produce nonfunctional gametes, which leads to sporophytic semisterility and exclusive transmission of the Gc2-carrier chromosome. We have identified one putative ethyl methylsulfonate (EMS)-induced Gc2 mutant that restores spike fertility and shows Mendelian segregation. Progeny screening mapped the mutation to the Gc2-carrier chromosome T4B-4S(sh)#1. C-banding and fluorescence in situ hybridization analyses showed that the loss of Gc2 function in the mutant is not due to a terminal deficiency. Analysis of first and second pollen mitoses in Gc2(mut)/-plants and C-banding analysis of testcross progenies showed that no chromosomal breakage occurs in the mutant. No gametophytic chromosomal breakage was observed in heterozygous Gc2(mut)/Gc2 plants, which had fully fertile spikes. These results suggest that Gc2 encodes two agents, one causing chromosomal breaks in gametophytes lacking Gc2 and another that protects the Gc2 carrier from breakage. The EMS-induced Gc2 mutant appears to be a knock-out of the gene encoding the 'breaking' agent. These data are a first crucial step toward the molecular understanding of Gc2 action.