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首页> 外文期刊>The Journal of biological chemistry >Identification of a Pentatricopeptide Repeat Protein Implicated in Splicing of Intron 1 of Mitochondrial nad7 Transcripts
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Identification of a Pentatricopeptide Repeat Protein Implicated in Splicing of Intron 1 of Mitochondrial nad7 Transcripts

机译:鉴定致法的致法肽重复蛋白,其剪切线粒体NAD7转录物的Intron1

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Splicing of plant organellar transcripts is facilitated by members of a large protein family, the pentatricopeptide repeat proteins. We have identified a pentatricopeptide repeat protein in a genetic screen for mutants resistant to inhibition of root growth by buthionine sulfoximine (BSO), an inhibitor of glutathione synthesis and consequently named BIR6 (BSO-insensitive roots 6). BIR6 is involved in splicing of intron 1 of the mitochondrial nad7 transcript. Loss-of-function mutations in BIR6 result in a strongly reduced accumulation of fully processed nad7 transcript. This affects assembly of Complex I and results in moderate growth retardation. In agreement with disruption of Complex I function, the genes encoding alternative NADH oxidizing enzymes are induced in the mutant, and the mutant plants are less sensitive to mannitol and salt stress. Mutation in the BIR6 gene allowed normal root growth in presence of BSO and strongly attenuated depletion of glutathione content at these conditions. The same phenotype was observed with other mutants affected in function of Complex I, thus reinforcing the importance of Complex I function for cellular redox homeostasis.
机译:由大蛋白质家族的成员促进了植物细胞细胞素转录物的剪接,该肽肽重复蛋白质。我们已经在遗传筛网中鉴定了抗毒素抗突变体的五戊肽重复蛋白,抑制Buthionine磺酰胺(BSO),谷胱甘肽合成的抑制剂,并因此命名为Bir6(Bse-Isensite Roots 6)。 BIR6参与了线粒体NAD7转录物的内含子1的剪接。 BIR6中的功能突变突变导致完全加工的NAD7转录物的强烈积累。这会影响复杂的I的组装,并导致中等的生长延迟。在突变体中诱导编码替代的NADH氧化酶的基因,突变植物对甘露醇和盐胁迫敏感。 Bir6基因中的突变允许在BSO存在下均产生正常的根生长,并在这些条件下强烈衰减谷胱甘肽含量的耗尽。用络合物I的功能影响的其他突变体观察到相同的表型,从而加强了综合体掺杂剂对细胞氧化还原性稳态的重要性。

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