E plus subgroup PPR protein defective kernel 36 is required for multiple mitochondrial transcripts editing and seed development in maize and Arabidopsis
E plus subgroup PPR protein defective kernel 36 is required for multiple mitochondrial transcripts editing and seed development in maize and Arabidopsis
复制标题
玉米和拟南芥中多个线粒体转录本编辑和种子发育需要 E+ 亚组 PPR 蛋白缺陷籽粒 36
DOI:
10.1111/nph.14507
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发表时间:
2017
期刊:
影响因子:
9.4
通讯作者:
Song Rentao
中科院分区:
文献类型:
--
作者:
Wang Gang;Zhong Mingyu;Shuai Bilian;Song Ji;ong;Zhang Jie;Han Liang;Ling Huiling;Tang Yuanping;Wang Guifeng;Song Rentao
Mitochondria are semi‐autonomous organelles that are the powerhouse of the cells. Plant mitochondrial RNA editing guided by pentatricopeptide repeat (PPR) proteins is essential for energy production.We identify a maize defective kernel mutantdek36, which produces small and collapsed kernels, leading to embryos and/or seedlings lethality. Seed filling indek36is drastically impaired, in line with the defects observed in the organization of endosperm transfer tissue. Positional cloning reveals thatDEK36, encoding a mitochondria‐targeted E+ subgroup PPR protein, is required for mitochondrial RNA editing atatp4‐59,nad7‐383 andccmFN‐302, thus resulting in decreased activities of mitochondrial complex I, complex III and complex IV indek36.Loss‐of‐function of its Arabidopsis ortholog At DEK36 causes arrested embryo and endosperm development, leading to embryo lethality.At_dek36also has RNA editing defects inatp4,nad7,ccmFN1andccmFN2, but at the nonconserved sites. Importantly, efficiency of all editing sites inccmFN1,ccmFN2andrps12is severely decreased inAt_dek36, probably caused by the impairment of their RNA stabilization.These results suggest that the DEK36 orthologue pair are essential for embryo and endosperm development in both maize and Arabidopsis, but through divergent function in regulating RNA metabolism of their mitochondrial targets.