A Maize Necrotic Leaf Mutant Caused by Defect of Coproporphyrinogen III Oxidase in the Porphyrin Pathway

被引:14
作者
Zhao, Yan [1 ,2 ]
Xu, Wei [2 ]
Wang, Lijing [3 ]
Han, Shuai [2 ]
Zhang, Yongzhong [2 ]
Liu, Qingzhi [2 ]
Liu, Baoshen [2 ]
Zhao, Xiangyu [1 ]
机构
[1] Shandong Agr Univ, Coll Life Sci, State Key Lab Crop Biol, Tai An 271018, Shandong, Peoples R China
[2] Shandong Agr Univ, Coll Agron, State Key Lab Crop Biol, Tai An 271018, Shandong, Peoples R China
[3] Zhou Univ, Coll Life Sci, Dezhou 253023, Peoples R China
基金
中国国家自然科学基金;
关键词
maize; necrotic lesions; coproporphyrinogen III oxidase; light; temperature; LESION MIMIC MUTANTS; CELL-DEATH; REPEAT PROTEIN; GENE; DEFENSE; ACCUMULATION; RESPONSES; ENCODES; RICE;
D O I
10.3390/genes13020272
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Lesion mimic mutants provide ideal genetic materials for elucidating the molecular mechanism of cell death and disease resistance. The maize necrotic leaf mutant (nec-t) is a recessive mutant with necrotic spots and yellow-green leaves. In this study, we found that nec-t was a light and temperature-dependent mutant. Map-based cloning and the allelic test revealed that nec-t was a novel allelic mutant of the Necrotic4 gene. Necrotic4 encodes the coproporphyrinogen III oxidase (CPX1), a key enzyme in the tetrapyrrole pathway, catalyzing coproporphyrinogen III oxidate to protoporphyrinogen IX. Subcellular localization showed that the necrotic4 protein was localized in the chloroplast. Furthermore, RNA-seq analysis showed that the Necrotic4 mutation caused the enhanced chlorophyll degradation and reactive oxygen species (ROS) response. The mechanism of plant lesion formation induced by light and temperature is not clear. Our research provides a basis for understanding the molecular mechanism of necrosis initiation in maize.
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页数:14
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