
The retromer protein ZmVPS29 regulates maize kernel morphology likely through an auxin‐dependent process(es)
Author(s) -
Chen Lin,
Li YongXiang,
Li Chunhui,
Shi Yunsu,
Song Yanchun,
Zhang Dengfeng,
Wang Haiyang,
Li Yu,
Wang Tianyu
Publication year - 2020
Publication title -
plant biotechnology journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.525
H-Index - 115
eISSN - 1467-7652
pISSN - 1467-7644
DOI - 10.1111/pbi.13267
Subject(s) - biology , auxin , microbiology and biotechnology , retromer , process (computing) , morphology (biology) , botany , endosome , gene , biochemistry , genetics , computer science , intracellular , operating system
Summary 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 , qKM 4.08 , 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 LV 28 (slender kernel). Positional cloning and transgenic analysis revealed that qKM 4.08 encodes Zm VPS 29, a retromer complex component. Compared with the Zm VPS 29 HZS allele, the Zm VPS 29 LV 28 allele showed higher expression in developing kernels. Overexpression of Zm VPS 29 conferred a slender kernel morphology and increased the yield per plant in different maize genetic backgrounds. Sequence analysis revealed that Zm VPS 29 has been under purifying selection during maize domestication. Association analyses identified two significant kernel morphology‐associated polymorphic sites in the Zm VPS 29 promoter region that were significantly enriched in modern maize breeding lines. Further study showed that Zm VPS 29 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 Zm VPS 29 regulates kernel morphology, most likely through an auxin‐dependent process(es).