The atroviolacea Gene Encodes an R3-MYB Protein Repressing Anthocyanin Synthesis in Tomato Plants.
The atroviolacea Gene Encodes an R3-MYB Protein Repressing Anthocyanin Synthesis in Tomato Plants.
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DOI：
10.3389/fpls.2018.00830
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发表时间：
2018
影响因子：
5.6
通讯作者：
Gonzali S
中科院分区：
文献类型：
--
作者：
Colanero S;Perata P;Gonzali S
花色素苷的生物合成途径在植物中得到了很好的表征。而番茄（Solanum lycopersicum L.）对它的管理仍然缺乏详尽的了解。在果实或营养组织中显示出较高水平的花色素苷的番茄突变体，例如花色素苷果实（Aft）或紫丁香（atv），已经被广泛地利用以试图阐明该过程。然而，只有候选基因已被提出负责这些表型。隐性atv突变可能代表了从野生茄属物种渗入番茄中的基因的等位基因变体。我们进行了atv/atv植物的基因组测序，然后进行候选基因分析，并确定了编码R3-MYB蛋白的突变基因。当过表达时，这种蛋白质通过沉默该途径的关键调控因子和生物合成基因来消除番茄幼苗和植物中的花青素产生。对该蛋白的功能分析清楚地表明，它可以负干扰由内源MYB-bHLH-WDR（MBW）复合物介导的花青素生物合成途径的激活。特别地，该R3-MYB蛋白可以直接结合作为MBW复合物的一部分的bHLH因子，因此充当竞争性抑制剂。因此，这里描述的R3-MYB蛋白参与反馈机制，一旦被内源性或外源性刺激激活，该反馈机制就抑制花青素苷的产生。atv突变导致R3-MYB因子的截短版本的产生，其不能保留抑制MBW复合物的全部潜力，从而导致花青素苷的组成性更高的产生。
The anthocyanin biosynthetic pathway is well characterized in plants. However, in tomato (Solanum lycopersicum L.) an exhaustive knowledge of its regulation is still lacking. Tomato mutants showing higher levels of anthocyanins in fruits or vegetative tissues, such as Anthocyanin fruit (Aft) or atroviolacea (atv), have been extensively exploited in the attempt to clarify the process. Nevertheless, only candidate genes have been proposed as responsible for such phenotypes. The recessive atv mutation likely represents an allelic variant of a gene introgressed in tomato from wild Solanum species. We performed genome sequencing of atv/atv plants followed by candidate gene analysis, and identified a mutated gene encoding an R3-MYB protein. When overexpressed, this protein abolished anthocyanin production in tomato seedlings and plants, by silencing key regulators and biosynthetic genes of the pathway. The functional analysis of the protein clearly showed that it can negatively interfere with the activation of the anthocyanin biosynthetic pathway mediated by the endogenous MYB-bHLH-WDR (MBW) complexes. In particular, this R3-MYB protein can directly bind the bHLH factors which are part of the MBW complexes, therefore acting as a competitive inhibitor. The R3-MYB protein here described is therefore involved in a feedback mechanism that dampens the production of anthocyanins once activated by endogenous or exogenous stimuli. The atv mutation causes the production of a truncated version of the R3-MYB factor that cannot retain the full potential to inhibit the MBW complexes, thus leading to a constitutively higher production of anthocyanins.
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影响因子：
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