DNA mismatch repair (MMR) is a highly conserved biological pathway that improves the fidelity of DNA replication and recombination. MMR is initiated when MutS proteins recognize mismatches and small loops of unpaired nucleotides. Arabidopsis thaliana and other plants encode MutS protein homologs (MSH) conserved among other eukaryotic organisms, but also encode an extra MSH polypeptide (MSH7). In order to better understand the role of MSH7 in vivo, a full set of phenotypic parameters that covered the development of the plant from seed imbibition to flowering and seed maturation was analyzed in A. thaliana harboring two different msh7 alleles. Plants deficient in MSH7 show statistically significant faster germination rates, longer primary roots during the juvenile vegetative phase, and higher cauline leaf and axillary and lateral inflorescence numbers compared with wild type. We also quantified number, length and area of siliques and seed number per silique. Disruption of MSH7 resulted in a higher number of smaller siliques than wild type. There were no differences in seed number per silique between genotypes. These findings suggest that mutant plant growth appears to be caused by an impaired cell cycle checkpoint that allows cell division without adequate DNA repair. This increase in proliferation activity demonstrates a functional and temporal link between DNA repair and cell cycle regulation.

中文翻译：

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拟南芥中AtMSH7突变体的生长和发育。

DNA错配修复（MMR）是高度保守的生物途径，可提高DNA复制和重组的保真度。当MutS蛋白识别错配和未配对核苷酸的小环时，会启动MMR。拟南芥和其他植物编码在其他真核生物中保守的MutS蛋白同源物（MSH），但也编码额外的MSH多肽（MSH7）。为了更好地了解MSH7在体内的作用，在带有两个不同msh7等位基因的拟南芥中分析了涵盖植物从种子吸取到开花和种子成熟的整个发育过程的全套表型参数。缺乏MSH7的植物在幼年营养期显示出显着的更快发芽率，更长的初生根，与野生型相比，茎生叶和腋生和侧生花序数更高。我们还量化了角果的数量，长度和面积，以及每个角果的种子数量。与野生型相比，MSH7的断裂导致了更多的较小的小角果。基因型之间每个长角果的种子数量没有差异。这些发现表明，突变植物的生长似乎是由细胞周期检查点受损导致的，该检查点允许细胞分裂而没有适当的DNA修复。增殖活性的增加证明了DNA修复与细胞周期调节之间的功能和时间联系。基因型之间每个长角果的种子数量没有差异。这些发现表明，突变植物的生长似乎是由细胞周期检查点受损导致的，该检查点允许细胞分裂而没有适当的DNA修复。增殖活性的增加证明了DNA修复与细胞周期调节之间的功能和时间联系。基因型之间每个长角果的种子数量没有差异。这些发现表明，突变植物的生长似乎是由细胞周期检查点受损导致的，该检查点允许细胞分裂而没有适当的DNA修复。增殖活性的增加证明了DNA修复与细胞周期调节之间的功能和时间联系。