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E+ subgroup PPR protein defective kernel 36 is required for multiple mitochondrial transcripts editing and seed development in maize and Arabidopsis
Author(s) -
Wang Gang,
Zhong Mingyu,
Shuai Bilian,
Song Jiandong,
Zhang Jie,
Han Liang,
Ling Huiling,
Tang Yuanping,
Wang Guifeng,
Song Rentao
Publication year - 2017
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14507
Subject(s) - endosperm , pentatricopeptide repeat , biology , arabidopsis , rna editing , mitochondrial dna , rna , mutant , microbiology and biotechnology , mitochondrion , genetics , embryo , gene
Summary 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 mutant dek36 , which produces small and collapsed kernels, leading to embryos and/or seedlings lethality. Seed filling in dek36 is drastically impaired, in line with the defects observed in the organization of endosperm transfer tissue. Positional cloning reveals that DEK 36 , encoding a mitochondria‐targeted E+ subgroup PPR protein, is required for mitochondrial RNA editing at atp4‐ 59, nad7‐ 383 and ccm F N ‐ 302, thus resulting in decreased activities of mitochondrial complex I, complex III and complex IV in dek36 . Loss‐of‐function of its Arabidopsis ortholog At DEK 36 causes arrested embryo and endosperm development, leading to embryo lethality. At_dek36 also has RNA editing defects in atp4 , nad7 , ccm F N1 and ccm F N2 , but at the nonconserved sites. Importantly, efficiency of all editing sites in ccm F N1 , ccm F N2 and rps12 is severely decreased in At_dek36 , probably caused by the impairment of their RNA stabilization. These results suggest that the DEK 36 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.