VIMa and paternal-specifically expressed VIMb are involved in regulating DNA methylation and endosperm development in maize

Clicks: 3
ID: 316322
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #299 of 310 articles by views in The Plant cell

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 310 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Abstract Kernel development is a pivotal determinant of grain yield in maize (Zea mays), a cereal crop that is fundamentally important for global food security. Here, we elucidated the essential role of VIM family genes in maize endosperm development by characterizing a miniature seed9 (mn9) mutant, in which the kernel size is reduced. Through map-based cloning, we demonstrated that the mn9 phenotype is caused by the concurrent disruption of two homologous genes, VIMa and VIMb. Notably, VIMa is broadly expressed and follows Mendelian segregation, whereas VIMb is an endosperm-specific imprinted gene with near-exclusive paternal expression. In maize, there exists another broadly expressed non-imprinted VIM family gene, VIMc, which is closest to VIMa in terms of expression pattern and sequence similarity, and we were unable to obtain vima;vimc double mutants. Single mutants of VIMa, VIMb, or VIMc exhibited no visible phenotypes or alterations in DNA methylation levels, whereas simultaneous loss of VIMa and VIMb function induced a reduction in genome-wide CG methylation specifically in the endosperm. In addition, we found that endoreduplication is impaired in vima;vimb mutant endosperm, leading to reduced endosperm cell ploidy, decreased cell size, and consequently diminished kernel weight. In summary, our results reveal that loss of VIMa and VIMb causes endosperm-specific CG hypomethylation, defective endoreduplication and reduced kernel size, and provide a systematic characterization of VIM family functions in maize endosperm development.
Reference Key
openalex_W7163804211 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Xiangde Hong, Zijian Wang, Yang Cui, Liangliang Huang, Xianguan Zhi, Xin Yi, Y Q Zhou, Weibin Song, Jinsheng Lai, Qiujie Liu, Jian Chen
Journal The Plant cell
Year 2026
DOI
10.1093/plcell/koag158
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.