Xu Dawei, Lin Li, Liu Xiaorui, Wangzha MeLongying, Pang Xiaoqing, Feng Liping, Wan Bingbing, Wu Guo-Zhang, Yu Jingquan, Rochaix Jean-David, Grimm Bernhard, Yin Ruohe
School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Institute of Biology/Plant Physiology, Humboldt-Universität zu Berlin, Berlin, Germany.
Plant Biotechnol J. 2025 Mar;23(3):911-926. doi: 10.1111/pbi.14548. Epub 2024 Dec 19.
Tomato fruit ripening is a complex developmental process that is important for fruit quality and shelf life. Many factors, including ethylene and several key transcription factors, have been shown to play important roles in the regulation of tomato fruit ripening. However, our understanding of the regulation of tomato fruit ripening is still limited. Here, we describe mut26, an EMS-induced tomato (Solanum lycopersicum) mutant that exhibits chlorophyll-deficient phenotypes in various organs, including fruits. Genetic mapping and functional analyses revealed that a single-nucleotide substitution and a corresponding Pro398->Ser mis-sense mutation in SlChlH (GENOMES UNCOUPLED 5, GUN5), which encodes the H subunit of magnesium chelatase, are responsible for the defects in the mut26 strain. Transcript analyses towards the expression of many SlPhANGs revealed that mut26 is defective in plastid retrograde signalling during tomato fruit ripening initiation, namely the transition from mature green to breaker stage. mut26 exhibits delayed progression of fruit ripening characterized by reduced fruit ethylene emission, increased fruit firmness, reduced carotenoid content and delayed plastid conversion from chloroplast to chromoplast. Given that fruit ripening requires signalling from plastids to nucleus, these data support the hypothesis that GUN5-mediated plastid retrograde signalling promotes tomato fruit ripening. We further showed that the delayed fruit ripening of mut26 is not likely caused by reduced chlorophyll content. Taken together, we identified a new function of SlChlH in the promotion of tomato fruit ripening and ethylene biosynthesis, suggesting that GUN5-mediated plastid retrograde signalling plays a promotive role in tomato fruit ripening.
番茄果实成熟是一个复杂的发育过程，对果实品质和货架期至关重要。许多因素，包括乙烯和几个关键转录因子，已被证明在番茄果实成熟调控中发挥重要作用。然而，我们对番茄果实成熟调控的理解仍然有限。在此，我们描述了mut26，一种经甲基磺酸乙酯（EMS）诱变的番茄（Solanum lycopersicum）突变体，其在包括果实在内的各种器官中表现出叶绿素缺乏表型。遗传定位和功能分析表明，编码镁螯合酶H亚基的SlChlH（基因组解偶联5，GUN5）中的一个单核苷酸替换以及相应的Pro398→Ser错义突变是mut26突变体缺陷的原因。对许多SlPhANGs表达的转录分析表明，mut26在番茄果实成熟起始阶段，即从成熟绿果到破色期的转变过程中，质体逆行信号传导存在缺陷。mut26表现出果实成熟进程延迟，其特征为果实乙烯释放减少、果实硬度增加、类胡萝卜素含量降低以及质体从叶绿体向有色体的转变延迟。鉴于果实成熟需要从质体到细胞核的信号传导，这些数据支持了GUN5介导的质体逆行信号传导促进番茄果实成熟这一假说。我们进一步表明，mut26果实成熟延迟不太可能是由叶绿素含量降低引起的。综上所述，我们鉴定出SlChlH在促进番茄果实成熟和乙烯生物合成方面的新功能，表明GUN5介导的质体逆行信号传导在番茄果实成熟中起促进作用。
