在細胞質雄性不育植物中,線粒體與細胞核的協調是決定育性的關鍵。通過酵母單雜交篩選,我們鑑定了一個在大液泡期,不育小孢子中高度表達的轉錄因子 ZmDREB1.7,並激活了 CMS 基因 orf355在線粒體中的表達。
該基因是 ZmDREB1.7啟動子的弱等位基因,由於缺失 UPR 基因的關鍵序列,部分恢復了玉米 CMS-S 的雄性育性。
ZmDREB1.7的表達在抗黴素 a 治療後迅速增加,但在 pro 等位基因存在時這種反應減弱。
我們進一步發現,線粒體中 orf355的表達激活了線粒體逆行信號,從而誘導了 ZmDREB1.7的表達。
這些研究結果表明,在雄性不育決定中,核調節因子和線粒體 CMS 基因之間存在正反饋轉錄調控,為研究植物細胞核-線粒體之間的通訊提供了依據。
Activation of Mitochondrial orf355 Gene Expression by A Nuclear-Encoded DREB Transcription Factor Causes Cytoplasmic Male Sterility in Maize
1 State Key Laboratory of Plant Cell and Chromosome Engineering, Innovative Academy of Seed Design, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
2 University of Chinese Academy of Sciences, Beijing 100864, China
3 Beijing Key Laboratory of Maize DNA Fingerprinting and Molecular Breeding, Maize Research Center, Beijing Academy of Agriculture and Forestry Sciences, Beijing, 100097, China
Abstract:
Coordination between mitochondria and nucleus is crucial for fertility determination in cytoplasmic male sterility (CMS) plant. Using yeast one-hybrid screening, we identified a transcription factor ZmDREB1.7 that is highly expressed in sterile microspores at the large vacuole stage and activates CMS gene orf355 expression in mitochondria. Δpro, a weak allele of ZmDREB1.7 promoter due to the loss of key UPR motif, partially restores male fertility of CMS-S maize. ZmDREB1.7 expression increases rapidly in response to antimycin A treatment, but this response is attenuated in the present of Δpro allele. We further show that expression of orf355 in mitochondria activates mitochondrial retrograde signal, which in turn induces ZmDREB1.7 expression. These findings demonstrate a positive feedback transcriptional regulation between nuclear regulator and mitochondrial CMS gene in male sterility determination and provide insight into nucleus-mitochondria communication in plants.
版權作品,未經PaperRSS書面授權,嚴禁轉載,違者將被追究法律責任。
PaperRSS,關注生命科學,高校院所科研進展。