The color of tomato fruit is mainly determined by carotenoids and flavonoids. Phenotypic analysis of an introgression line (IL) population derived from a cross between Solanum lycopersicum 'Moneyberg' and the wild species Solanum chmielewskii revealed three ILs with a pink fruit color. These lines had a homozygous S. chmielewskii introgression on the short arm of chromosome 1, consistent with the position of the y (yellow) mutation known to result in colorless epidermis, and hence pink-colored fruit, when combined with a red flesh. Metabolic analysis showed that pink fruit lack the ripening-dependent accumulation of the yellow-colored flavonoid naringenin chalcone in the fruit peel, while carotenoid levels are not affected. The expression of all genes encoding biosynthetic enzymes involved in the production of the flavonol rutin from naringenin chalcone was down-regulated in pink fruit, suggesting that the candidate gene underlying the pink phenotype encodes a regulatory protein such as a transcription factor rather than a biosynthetic enzyme. Of 26 MYB and basic helix-loop-helix transcription factors putatively involved in regulating transcription of genes in the phenylpropanoid and/or flavonoid pathway, only the expression level of the MYB12 gene correlated well with the decrease in the expression of structural flavonoid genes in peel samples of pink- and red-fruited genotypes during ripening. Genetic mapping and segregation analysis showed that MYB12 is located on chromosome 1 and segregates perfectly with the characteristic pink fruit color. Virus-induced gene silencing of SlMYB12 resulted in a decrease in the accumulation of naringenin chalcone, a phenotype consistent with the pink-colored tomato fruit of IL1b. In conclusion, biochemical and molecular data, gene mapping, segregation analysis, and virus-induced gene silencing experiments demonstrate that the MYB12 transcription factor plays an important role in regulating the flavonoid pathway in tomato fruit and suggest strongly that SlMYB12 is a likely candidate for the y mutation.

中文翻译：

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粉红色番茄的生化和分子分析：编码转录因子 SlMYB12 的基因表达失调导致番茄果实呈粉红色。


番茄果实的颜色主要由类胡萝卜素和类黄酮决定。对源自番茄‘Moneyberg’和野生物种 Solanum chmielewskii 杂交的基因渗入系 (IL) 群体的表型分析揭示了三种具有粉红色果实颜色的 IL。这些品系在 1 号染色体短臂上有纯合 S. chmielewskii 渗入，与已知导致无色表皮的 y（黄色）突变的位置一致，因此当与红色果肉结合时会产生粉红色的果实。代谢分析表明，粉红色水果缺乏果皮中黄色类黄酮柚皮素查耳酮的成熟依赖性积累，而类胡萝卜素水平不受影响。在粉红色水果中，编码参与从柚皮素查尔酮生产黄酮醇芦丁的生物合成酶的所有基因的表达均下调，这表明粉红色表型背后的候选基因编码调节蛋白，例如转录因子，而不是生物合成酶。在 26 个 MYB 和碱性螺旋-环-螺旋转录因子中，推测参与调节苯丙素和/或类黄酮途径中基因的转录，只有 MYB12 基因的表达水平与果皮中结构类黄酮基因表达的减少密切相关。成熟过程中粉色和红色果实基因型的样本。遗传图谱和分离分析表明，MYB12 位于 1 号染色体上，与特有的粉红色果实颜色完美分离。病毒诱导的 SlMYB12 基因沉默导致柚皮素查尔酮积累减少，这种表型与 IL1b 的粉红色番茄果实一致。 总之，生化和分子数据、基因图谱、分离分析和病毒诱导的基因沉默实验表明，MYB12 转录因子在调节番茄果实中的类黄酮途径中发挥着重要作用，并强烈表明 SlMYB12 可能是番茄果实中黄酮类化合物途径的候选者。 y 突变。