The mismatch repair (MMR) pathway promotes genome stability by controlling the fidelity of replication and recombination. The first step of the pathway involves recognition of the mismatch by heterodimers composed of MutS homologs (MSH). Although MSH6 has been well characterized in yeasts and humans, the role of the plant protein has not been extensively studied. We first analyzed gene expression in Arabidopsis thaliana. The use of transgenic plants expressing the β-glucuronidase (GUS) reporter gene under the control of approximately 1-kb region upstream of the start codon of the AtMSH6 gene demonstrated that MSH6 is preferentially expressed in undifferentiated cells with an intense cell division rate. We then examined protein function in meiotic and somatic recombination. Suppression of AtMSH6 did not affect the rate of meiotic recombination, but increased the frequency of recombination between two homeologous repeats of a marker gene by 3-fold relative to wild-type plants. Expression of the AtMSH6 gene under the control of its own promoter in msh6 homozygous mutant plants rescued the altered somatic recombination phenotype. We conclude that MSH6 shows a functional conservation across different biological kingdoms and a functional specificity in plants.

中文翻译：

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错配修复蛋白MSH6调节拟南芥中的体细胞重组。

错配修复（MMR）途径通过控制复制和重组的保真度来促进基因组稳定性。该途径的第一步涉及由MutS同源物（MSH）组成的异二聚体识别错配。尽管MSH6已在酵母和人类中得到很好的表征，但尚未广泛研究植物蛋白的作用。我们首先分析了拟南芥中的基因表达。在AtMSH6基因起始密码子上游大约1kb区域的控制下，使用表达β-葡萄糖醛酸苷酶（GUS）报告基因的转基因植物表明，MSH6优先在未分化的细胞中以强烈的细胞分裂速率表达。然后，我们检查了减数分裂和体细胞重组中的蛋白质功能。AtMSH6的抑制不影响减数分裂重组的速率，但相对于野生型植物，标记基因的两个同源重复序列之间的重组频率增加了3倍。AtMSH6基因在其自身启动子的控制下在msh6纯合突变植物中的表达挽救了改变的体细胞重组表型。我们得出的结论是，MSH6显示了跨不同生物学界的功能保守性和植物中的功能特异性。