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首页> 外文期刊>Acta Societatis Botanicorum Poloniae >Downregulation of chloroplast protease AtDeg5 leads to changes in chronological progression of ontogenetic stages, leaf morphology and chloroplast ultrastructure in Arabidopsis
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Downregulation of chloroplast protease AtDeg5 leads to changes in chronological progression of ontogenetic stages, leaf morphology and chloroplast ultrastructure in Arabidopsis

机译:叶绿体蛋白酶AtDeg5的下调导致拟南芥个体发育阶段,叶片形态和叶绿体超微结构的时间顺序变化

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摘要

The chloroplast protein AtDeg5 is a serine-type protease peripherally attached to thylakoid membrane at its lumenal side. Since reliable data regarding the role of AtDeg5 in controlling the course of growth and developmental processes are extremely limited, two independent T-DNA insertional lines with different extent of AtDeg5 reduction were prepared and ontogenesis stage-based analysis performed. Both mutant lines displayed a compensatory overaccumulation of AtDeg8. The repression of AtDeg5 protease altered a range of phenotypic features in at least one of the mutants, with the most prominent being changes in chronological progression of development and growth of individual rosette leaves, flower production and silique ripening as well as in the area of fully expanded leaves and chloroplast ultrastructure. By analyzing the results of parallel-mutant screening we conclude that AtDeg8 overdose may rescue 23% of AtDeg5 deficiency with regard to some AtDeg5-controlled traits; alternatively AtDeg5 may have catalytic sites in excess so that these traits might remain unaltered when AtDeg5 pool is reduced by 23%. For some other AtDeg5-dependent traits the absence of excessive amount of AtDeg5 catalytic sites, lack of AtDeg5 dosage effect and inability of AtDeg8 to compensate deficiency or absence of AtDeg5 occurred.
机译:叶绿体蛋白AtDeg5是一种丝氨酸型蛋白酶,在其管腔侧周围附着在类囊体膜上。由于有关AtDeg5在控制生长和发育过程中作用的可靠数据非常有限,因此准备了两条具有不同AtDeg5还原程度的独立T-DNA插入系,并进行了基于成瘤阶段的分析。两条突变株系都显示出AtDeg8的补偿性过度积累。 AtDeg5蛋白酶的抑制改变了至少一个突变体中的一系列表型特征,最突出的是单个莲座丛叶的发育和生长的时序变化,花的产生和长角果成熟以及整个区域的变化。叶片扩张和叶绿体超微结构。通过分析平行突变筛选的结果,我们得出结论,就某些AtDeg5控制的性状而言,过量服用AtDeg8可以挽救23%的AtDeg5缺乏症。或者,AtDeg5可能具有过量的催化位点,因此当AtDeg5库减少23%时,这些性状可能保持不变。对于某些其他依赖于AtDeg5的性状,发生了过量的AtDeg5催化位点缺失,缺乏AtDeg5剂量效应以及无法补偿AtDeg5缺乏或缺乏的AtDeg8。

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