Maize Dek407 Encodes the Nitrate Transporter 1.5 and Is Required for Kernel Development

The kernel serves as the storage organ and harvestable component of maize, and it plays a crucial role in determining crop yield and quality. Understanding the molecular and genetic mechanisms of kernel development is of considerable importance for maize production. In this study, we obtained a muta...

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Veröffentlicht in:International journal of molecular sciences 2023-12, Vol.24 (24), p.17471
Hauptverfasser: Wang, Hongqiu, Yan, Xiaolan, Du, Qingguo, Yan, Pengshuai, Xi, Jinjin, Meng, Xiaoruo, Li, Xuguang, Liu, Huijian, Liu, Guoqin, Fu, Zhongjun, Tang, Jihua, Li, Wen-Xue
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Sprache:eng
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Zusammenfassung:The kernel serves as the storage organ and harvestable component of maize, and it plays a crucial role in determining crop yield and quality. Understanding the molecular and genetic mechanisms of kernel development is of considerable importance for maize production. In this study, we obtained a mutant, which we designated defective kernel 407 ( ), through ethyl methanesulfonate mutagenesis. The mutant exhibited reduced kernel size and kernel weight, as well as delayed grain filling compared with those of the wild type. Positional cloning and an allelism test revealed that encodes a nitrate transporter 1/peptide transporter family (NPF) protein and is the allele of ( ) that was responsible for a poorly filled defective kernel phenotype. A transcriptome analysis of the developing kernels showed that the mutation of altered the expression of phytohormone-related genes, especially those genes associated with indole-3-acetic acid synthesis and signaling. Phytohormone measurements and analysis indicated that the endogenous indole-3-acetic acid content was significantly reduced by 66% in the kernels, which may be the primary cause of the defective phenotype. We further demonstrated that natural variation in is associated with kernel weight and kernel size. Therefore, is a potential target gene for improvement of maize yield.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms242417471