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The retromer protein ZmVPS29 regulates maize kernel morphology likely through an auxin‐dependent process(es)

Kernel size and morphology are two important yield‐determining traits in maize, but their molecular and genetic mechanisms are poorly characterized. Here, we identified a major QTL,qKM4.08, which explains approximately 24.20% of the kernel morphology variance in a recombinant population derived from...

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Detalles Bibliográficos
Autores principales: Chen, Lin, Li, Yong‐Xiang, Li, Chunhui, Shi, Yunsu, Song, Yanchun, Zhang, Dengfeng, Wang, Haiyang, Li, Yu, Wang, Tianyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061865/
https://www.ncbi.nlm.nih.gov/pubmed/31553822
http://dx.doi.org/10.1111/pbi.13267
Descripción
Sumario:Kernel size and morphology are two important yield‐determining traits in maize, but their molecular and genetic mechanisms are poorly characterized. Here, we identified a major QTL,qKM4.08, which explains approximately 24.20% of the kernel morphology variance in a recombinant population derived from two elite maize inbred lines, Huangzaosi (HZS, round kernel) and LV28 (slender kernel). Positional cloning and transgenic analysis revealed that qKM4.08 encodes ZmVPS29, a retromer complex component. Compared with the ZmVPS29 HZS allele, the ZmVPS29 LV28 allele showed higher expression in developing kernels. Overexpression of ZmVPS29 conferred a slender kernel morphology and increased the yield per plant in different maize genetic backgrounds. Sequence analysis revealed that ZmVPS29 has been under purifying selection during maize domestication. Association analyses identified two significant kernel morphology‐associated polymorphic sites in the ZmVPS29 promoter region that were significantly enriched in modern maize breeding lines. Further study showed that ZmVPS29 increased auxin accumulation during early kernel development by enhancing auxin biosynthesis and transport and reducing auxin degradation and thereby improved kernel development. Our results suggest that ZmVPS29 regulates kernel morphology, most likely through an auxin‐dependent process(es).