Abstract
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.
Highlights
Necrotic or lesion mimic mutants exhibit spontaneous necrotic lesions on the leaves or stems without pathogen attack
Over the past several decades, many LMM genes have been cloned, and it has been found that chlorophyll synthesis, fatty acid, lipid biosynthesis, riboflavin biosynthesis, and kinase signaling pathways are closely related to the formation of necrotic spots [3,12,13]
Necrotic Lesion Formation in NEC-T Depends on Light and High Temperature
Summary
Necrotic or lesion mimic mutants (lmms) exhibit spontaneous necrotic lesions on the leaves or stems without pathogen attack. Their phenotype is similar to the hypersensitive response (HR), which induces visible morphological variations through local programmed cell death (PCD) or cell necrosis [1,2]. Over the past several decades, many LMM genes have been cloned, and it has been found that chlorophyll synthesis, fatty acid, lipid biosynthesis, riboflavin biosynthesis, and kinase signaling pathways are closely related to the formation of necrotic spots [3,12,13]. The heredity of plant lesion mimics obeys Mendel’s law, a large number of studies have found that its phenotype is susceptible to the influence of environmental factors and genetic background [14,15]. Identifying more lesion mutants and cloning-related genes is vital to elucidate how cell death is regulated and executed in plants
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