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Persimmon fruits accumulate a large amount of condensed tannins(proanthocyanidins,PAs)in the vacuole during development.PAs cause astringency,which is a dry or puckering sensation due to the coagulation with oral proteins.Persimmon cultivars are categorized into pollination constant non-astringent(PCNA)and non-PCNA types.PCNA type can lose the astringency on the tree,which comprises Chinese PCNA(C-PCNA)and Japanese PCNA(J-PCNA).Thedilution effectare responsible for J-PCNA natural astringency removal,while it is not adequate for explaining the astringency loss mechanism in C-PCNA.A coagulation process that converting soluble tannin into insoluble need to be elucidated during late stage of fruit development in C-PCNA.The RNAs from the key stages of natural astringency removal(10 and 20 WAB)and the 40 ℃ water treated fruits were sampled for de novo assemble and annotate the transcriptome of the Eshi 1(C-PCNA).A total of 36.5 billion clean nucleotides were generated with 135,999 unigenes assembled.The genes involved in PAs synthesis were significantly down-regulated in both natural and artificial deastringency process.9,692 common down-regulated unigenes were enrichment of GO terms which were mainly related to PAs biosynthesis.In addition,the shared down-regulated genes were also enrichment in Plant Cell Way related terms.Meanwhile,403 common up-regulated genes were mainly related to glucose metabolism GO term and glycolysis pathway.In this study,we propose a possible model on natural deastringency for C-PCNA genotype.The insolubilization of tannins occurred by interacting with pectin,cell wall,soluble sugar,and acetaldehyde in the fruit vacuole during the late stage of fruit development in C-PCNA.Thus we hypothesis that coagulation effect should be responsible for natural lose astringency in C-PCNA.