https://mp.weixin.qq.com/s/JOjn1Fb1Aya-U4zHO-iVYQ

近日，上海交大尹若賀團隊在PBJ發(fā)表了題為《Characterization of a tomato chlh mis-sense mutant reveals a new function of ChlH in fruit ripening》的研究論文，揭示了番茄chlh錯義突變體的表征揭示了ChlH在果實成熟中的新功能。

番茄果實成熟是一個復雜的發(fā)育過程，對果實品質(zhì)和貨架期時間至關(guān)重要。許多因素，包括乙烯和幾個關(guān)鍵轉(zhuǎn)錄因子，已被證明在調(diào)節(jié)番茄果實成熟中發(fā)揮重要作用。然而，人們對番茄果實成熟的調(diào)控理解仍然有限。

在本研究中，作者描述了番茄突變體mut26，由EMS誘導，它在各種器官中表現(xiàn)出葉綠素缺乏表型，包括果實。

遺傳定位和功能分析揭示了在SlChlH（基因組解耦5，GUN5）中一個單一核苷酸置換和一個相應的Pro398->Ser錯義突變，導致了mut26突變體的表型，而該基因編碼的是鎂螯合酶的H亞基。

對許多SlPhANGs表達的轉(zhuǎn)錄分析表明，mut26在番茄果實成熟啟動期間的葉綠體逆行信號傳導中存在缺陷，即從成熟綠色到破裂階段的過渡。mut26表現(xiàn)出延遲的果實成熟進展特征，具體表現(xiàn)為果實乙烯排放減少、果實硬度增加、類胡蘿卜素含量降低以及從葉綠體到色素的轉(zhuǎn)化延遲。

鑒于果實成熟需要來自質(zhì)體的信號傳導到細胞核，這些數(shù)據(jù)支持GUN5介導的質(zhì)體逆行信號傳導促進番茄果實成熟的假設。作者進一步表明，mut26的延遲果實成熟不太可能是由葉綠素減少引起的。

綜上所述，作者確定了SlChlH在促進番茄果實成熟和乙烯生物合成方面的新功能，表明GUN5介導的質(zhì)體逆行信號傳導在番茄果實成熟中起著促進作用。

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.

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