The maize CMS-C fertility restore gene ZmRf4b encodes a SPL transcription factor that represses ZmMAP1D-mediated co-translational turnover of mitochondrial toxic ATP6C protein.

Authors

Bing Li, Huaisheng Zhang, Runbo Zhang, Shicheng Feng, Fanli Yang, Congnian Ding, Xuyuan Shen, Keke Shao, Lu Yang, Yanan Lin, Dong Ding, Quancan Hou, Hongwei Xue, Huili Yang, Jihua Tang, Yadong Xue

Published in

Molecular plant. Aug 20, 2026. Epub Aug 20, 2026.

Abstract

The promising CMS-C/Rf system has not been applied on a large scale in maize hybrid breeding due to the unclear restoration mechanism for the primary restorer ZmRf4b. In CMS-C maize, the mitochondrial chimeric gene atp6c encodes a cytotoxic variant of ATP6 that over-accumulates and disrupts the assembly of mitochondrial complex V, leading to male sterility. Here, we report the map-based cloning and functional characterization of ZmRf4b, which encodes a SQUAMOSA promoter-binding protein-like (SPL) transcription factor. Through DAP-seq and yeast two-hybrid screening, we identified ZmMAP1D, a mitochondrion-targeted methionine aminopeptidase, as a direct downstream target of ZmRf4b. ZmRf4b functions as a transcriptional repressor that directly binds the ZmMAP1D promoter; in the restorer line, the relatively low expression level of ZmRf4b weakens its repression of ZmMAP1D, permitting moderate ZmMAP1D accumulation. ZmMAP1D is then imported to mitochondria, where it co-translationally removes the N-terminal methionine of ATP6C, thereby targeting excess ATP6C for degradation. The reduction of ATP6C to normal levels restores mitochondrial complex V assembly, alleviates reactive oxygen species accumulation and tapetal programmed cell death, and ultimately restores male fertility. This study reveals a previously unrecognized fertility restoration mechanism operating through co-translational protein turnover-rather than transcriptional or translational suppression of the CMS gene-providing new insights into nucleus-mitochondria communication and mitochondrial protein homeostasis.

PMID:
42625368
Bibliographic data and abstract were imported from PubMed on 21 Aug 2026.

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