MutS HOMOLOG1 silencing mediates ORF220 substoichiometric shifting and causes male sterility in Brassica juncea.
MutS HOMOLOG1 silencing mediates ORF220 substoichiometric shifting and causes male sterility in Brassica juncea.
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MutS HOMOLOG1 沉默介导 ORF220 亚化学计量变化并导致芥菜雄性不育
DOI：
10.1093/jxb/erv480
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发表时间：
2016-01
影响因子：
6.9
通讯作者：
Zhang M
中科院分区：
文献类型：
--
作者：
Zhao N;Xu X;Wamboldt Y;Mackenzie SA;Yang X;Hu Z;Yang J;Zhang M
MSH 1通过介导线粒体基因组ORF 220亚化学计量转移和改变芥菜花药发育相关基因的表达参与育性恢复和雄性不育。细胞质雄性不育（CMS）一直与由基因组重排引起的线粒体开放阅读框（ORF）的表达相关。在几个案例中已经观察到CMS的自发育性逆转，但对受核遗传影响控制的育性逆转缺乏清晰的认识。在这里，我们确定了芥菜CMS细胞质中的线粒体基因组经历了亚化学计量转换（SSS），以抑制ORF 220拷贝数的自发可育回复系。我们将ORF 220（有或没有线粒体靶向前序列）置于拟南芥中CaMV 35 S和AP 3启动子的控制下，以确认ORF 220在位于生殖道时导致雄性不育。我们发现，在抑制MSH 1的条件下，ORF 220基因的拷贝数发生了改变，MSH 1是一种控制植物线粒体中非法重组的核基因。与野生型相比，ORF 220拷贝数增加的MSH 1-RNAi株系雄性不育。我们发现，在回复突变体和MSH 1-RNAi株系中，参与花药发育的广泛基因分别上调和下调。我们已经开发的系统提供了宝贵的未来洞察MSH 1和SSS在CMS诱导和生育力逆转中的相互作用，作为核线粒体串扰的介质。
MSH1 participates in fertility reversion and male sterility by mediating mitochondrial genomic substoichiometric shifting of ORF220 and altering expression of anther development-associated genes in Brassica juncea. Cytoplasmic male sterility (CMS) has consistently been associated with the expression of mitochondrial open reading frames (ORFs) that arise from genomic rearrangements. Spontaneous fertility reversion in CMS has been observed in several cases, but a clear understanding of fertility reversion controlled by nuclear genetic influences has been lacking. Here, we identified spontaneous fertile revertant lines for Brassica juncea CMS cytoplasm in which the mitochondrial genome has undergone substoichiometric shifting (SSS) to suppress ORF220 copy number. We placed ORF220, with or without a mitochondrial targeting presequence, under the control of the CaMV35S and AP3 promoters in Arabidopsis to confirm that ORF220 causes male sterility when mitochondrially localized. We found that copy number of the ORF220 gene was altered under conditions that suppress MSH1, a nuclear gene that controls illegitimate recombination in plant mitochondria. MSH1-RNAi lines with increased ORF220 copy number were male sterile compared with wild type. We found that a wide range of genes involved in anther development were up- and down-regulated in revertant and MSH1-RNAi lines, respectively. The system that we have developed offers valuable future insight into the interplay of MSH1 and SSS in CMS induction and fertility reversion as a mediator of nuclear–mitochondrial crosstalk.