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黄果表型是由 yft1 突变体番茄中 YFT1 等位基因 5'UTR 的 573bp 插入引起的。

Yellow-fruited phenotype is caused by 573 bp insertion at 5' UTR of YFT1 allele in yft1 mutant tomato.

机构信息

Department of Plant Science, School of Agriculture and Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China; Joint Tomato Research Institute, School of Agriculture and Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.

Department of Plant Science, School of Agriculture and Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.

出版信息

Plant Sci. 2020 Nov;300:110637. doi: 10.1016/j.plantsci.2020.110637. Epub 2020 Aug 16.

DOI:10.1016/j.plantsci.2020.110637
PMID:33180715
Abstract

The yft1 tomato mutant has a yellow-fruited phenotype controlled by a recessive gene of YFT1 allele, which has been shown by map-based cloning to be a homolog of ETHYLENE INSENSITIVE 2 (EIN2). Genetic lesion of YFT1 allele in yft1 is attributed to a 573 bp DNA fragment (IF) insertion at 1,200 bp downstream of the transcription start site. Transcriptomic analysis revealed that YFT1 lesion resulted in 5,053 differentially expressed genes (DEGs) in yft1 pericarp compared with the M82 wild type cultivar. These were annotated as being involved in ethylene synthesis, chromoplast development, and carotenoid synthesis. The YFT1 lesion caused a reduction in its own transcript levels in yft1 and impaired ethylene emission and signal transduction, delayed chromoplast development and decreased carotenoid accumulation. The molecular mechanism underlying the downregulated YFT1 allele in yft1 was examined at both RNA and DNA levels. The IF event appeared to introduce two negative regulatory sequences located at -272 to -173 bp and -172 to -73 bp in the YFT1 allele promoter, causing alterative splicing due to introduction of aberrant splicing sites, and breaking upstream open reading frames (uORF) structure in the 5'-UTR. Those results a new provided insight into molecular regulation of color formation in tomato fruit.

摘要

yft1 番茄突变体的果实呈黄色,受 YFT1 等位基因隐性基因控制,该基因已通过图谱克隆被证明是 ETHYLENE INSENSITIVE 2(EIN2)的同源物。yft1 中 YFT1 等位基因的遗传缺陷归因于转录起始位点下游 1200bp 处的 573bp DNA 片段(IF)插入。转录组分析显示,与 M82 野生型品种相比,yft1 果皮中 YFT1 损伤导致 5053 个差异表达基因(DEGs)。这些基因被注释为参与乙烯合成、质体发育和类胡萝卜素合成。YFT1 损伤导致 yft1 中自身转录水平降低,抑制乙烯的排放和信号转导,延迟质体发育,减少类胡萝卜素的积累。在 RNA 和 DNA 水平上检查了 yft1 中下调的 YFT1 等位基因的分子机制。IF 事件似乎在 YFT1 等位基因启动子中 -272 到 -173bp 和 -172 到 -73bp 处引入了两个负调控序列,由于引入了异常剪接位点,导致选择性剪接,并破坏了 5'-UTR 中的上游开放阅读框(uORF)结构。这些结果为番茄果实颜色形成的分子调控提供了新的见解。

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