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调控叶绿素生物合成和早期叶绿体发育的黄绿叶基因的特征和精细定位。

Characterization and Fine Mapping of a Yellow-Virescent Gene Regulating Chlorophyll Biosynthesis and Early Stage Chloroplast Development in .

机构信息

Oil Crops Research Institute of the Chinese Academy of Agricultural Sciences/The Key Laboratory of Biology and Genetic Improvement of Oil Crops, The Ministry of Agriculture and Rural Affairs, Wuhan 430062, China.

National Key Laboratory of Crop Genetic Improvement, National Center of Rapeseed Improvement, Huazhong Agricultural University, Wuhan 430070, China.

出版信息

G3 (Bethesda). 2020 Sep 2;10(9):3201-3211. doi: 10.1534/g3.120.401460.

DOI:10.1534/g3.120.401460
PMID:32646913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7466985/
Abstract

Chlorophyll biosynthesis and chloroplast development are crucial to photosynthesis and plant growth, but their regulatory mechanism remains elusive in many crop species. We isolated a yellow-virescent leaf () mutant, which exhibited yellow-younger-leaf and virescent-older-leaf with decreased chlorophyll accumulation and delayed chloroplast development. We mapped locus to a 70-kb interval between molecular markers yvl-O10 and InDel-O6 on chromosome A03 in BCF population using whole genome re-sequencing and bulked segregant analysis. The mutant had a 'C' to 'T' substitution in the coding sequence of , which encodes putative H subunit of Mg-protoporphyrin IX chelatase (CHLH). The mutation resulted in an imperfect protein structure and reduced activity of CHLH. It also hampered the plastid encoded RNA polymerase which transcribes regulatory genes of photosystem II and I. Consequently, the chlorophyll a/b and carotenoid contents were reduced and the chloroplast ultrastructure was degraded in mutant. These results explain that a single nucleotide mutation in impairs PEP activity to disrupt chloroplast development and chlorophyll biosynthesis in .

摘要

叶绿素生物合成和叶绿体发育对光合作用和植物生长至关重要,但在许多作物物种中,其调控机制仍不清楚。我们分离到一个黄绿叶突变体(),该突变体表现为嫩叶黄化和老叶返绿,叶绿素积累减少,叶绿体发育延迟。我们利用全基因组重测序和混池分离分析,将该突变体定位在 BCF 群体中分子标记 yvl-O10 和 InDel-O6 之间的 70kb 区间内。该突变体在编码 Mg-原卟啉 IX 螯合酶(CHLH)的 H 亚基的编码序列中有一个'C'到'T'的取代,导致该蛋白结构不完整,CHLH 活性降低。它还阻碍了质体编码的 RNA 聚合酶,该酶转录 II 和 I 型光合系统的调节基因。因此,突变体中的叶绿素 a/b 和类胡萝卜素含量降低,叶绿体超微结构降解。这些结果表明,突变体中一个核苷酸的突变破坏了 PEP 活性,从而破坏了叶绿体的发育和叶绿素的生物合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/7be5f9726105/3201f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/a99264a159c9/3201f5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/7be5f9726105/3201f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/97df75efffd8/3201f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/00557e275d8e/3201f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e100/7466985/7be5f9726105/3201f7.jpg

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