Overexpression of tomato SlNAC1 transcription factor alters fruit pigmentation and softening.
Overexpression of tomato SlNAC1 transcription factor alters fruit pigmentation and softening.
复制标题
番茄 SlNAC1 转录因子的过度表达改变果实色素沉着和软化
DOI：
10.1186/s12870-014-0351-y
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发表时间：
2014-12-10
影响因子：
5.3
通讯作者：
Meng Q
中科院分区：
文献类型：
--
作者：
Ma N;Feng H;Meng X;Li D;Yang D;Wu C;Meng Q
果实的成熟和成熟是基因调控的过程，涉及植物激素、生长调节剂以及多种生物和环境因素的复杂相互作用。番茄（Solanum lycopersicum）已被用作调节特定成熟途径（包括乙烯、类胡萝卜素和细胞壁代谢）的生物学和遗传学研究的模型。该模型还用于研究上游信号传导和转录调节因子的功能。迄今为止，已经报道了许多影响果实发育和成熟的成熟相关转录因子。 NAC转录因子是植物特有的，在植物生长发育的许多阶段发挥着重要作用，如侧根形成、次生细胞壁合成以及胚胎、花器官、营养器官和果实发育。通过实时定量PCR进行的组织特异性分析表明，SlNAC1在未成熟的绿色果实中高度积累； SlNAC1的表达量随着果实成熟而增加，在破粒期后7 d达到最高水平。 SlNAC1的过度表达通过改变类胡萝卜素途径通量和减少主要由system-2乙烯生物合成基因表达减少介导的乙烯合成而导致类胡萝卜素减少，从而导致黄色或橙色成熟果实。酵母单杂交实验结果表明，SlNAC1可以与番茄红素和乙烯合成相关基因的调控区域相互作用。这些结果还表明，SlNAC1 通过影响 SlNAC1 过表达株系中的乙烯合成和类胡萝卜素积累来抑制果实成熟。此外，SlNAC1的过表达降低了果实的硬度和果皮的厚度，并产生更多的脱落酸，导致果实提前软化。因此，在SlNAC1过表达株系中，乙烯依赖性和脱落酸依赖性途径均受到果实成熟调控网络中SlNAC1的调节。 SlNAC1 对番茄果实成熟具有广泛影响，并通过乙烯依赖性和脱落酸依赖性途径调节 SlNAC1 过表达番茄果实成熟。因此，这项研究为当前番茄果实成熟调控网络模型提供了新的见解。本文的在线版本 (doi:10.1186/s12870-014-0351-y) 包含补充材料，可供授权用户使用。
Fruit maturation and ripening are genetically regulated processes that involve a complex interplay of plant hormones, growth regulators and multiple biological and environmental factors. Tomato (Solanum lycopersicum) has been used as a model of biological and genetic studies on the regulation of specific ripening pathways, including ethylene, carotenoid and cell wall metabolism. This model has also been used to investigate the functions of upstream signalling and transcriptional regulators. Thus far, many ripening-associated transcription factors that influence fruit development and ripening have been reported. NAC transcription factors are plant specific and play important roles in many stages of plant growth and development, such as lateral root formation, secondary cell wall synthesis, and embryo, floral organ, vegetative organ and fruit development. Tissue-specific analysis by quantitative real-time PCR showed that SlNAC1 was highly accumulated in immature green fruits; the expression of SlNAC1 increased with fruit ripening till to the highest level at 7 d after the breaker stage. The overexpression of SlNAC1 resulted in reduced carotenoids by altering carotenoid pathway flux and decreasing ethylene synthesis mediated mainly by the reduced expression of ethylene biosynthetic genes of system-2, thus led to yellow or orange mature fruits. The results of yeast one-hybrid experiment demonstrated that SlNAC1 can interact with the regulatory regions of genes related lycopene and ethylene synthesis. These results also indicated that SlNAC1 inhibited fruit ripening by affecting ethylene synthesis and carotenoid accumulation in SlNAC1 overexpression lines. In addition, the overexpression of SlNAC1 reduced the firmness of the fruits and the thickness of the pericarp and produced more abscisic acid, resulting in the early softening of fruits. Hence, in SlNAC1 overexpression lines, both ethylene-dependent and abscisic acid-dependent pathways are regulated by SlNAC1 in fruit ripening regulatory network. SlNAC1 had a broad influence on tomato fruit ripening and regulated SlNAC1 overexpression tomato fruit ripening through both ethylene-dependent and abscisic acid-dependent pathways. Thus, this study provided new insights into the current model of tomato fruit ripening regulatory network. The online version of this article (doi:10.1186/s12870-014-0351-y) contains supplementary material, which is available to authorized users.