Phenolic compounds in tea plant [Camellia sinensis (L.)] play a crucial role in dominating tea flavor and possess a number of key pharmacological benefits on human health. The present research aimed to study the profile of tissue-specific, development-dependent accumulation pattern of phenolic compounds in tea plant. A total of 50 phenolic compounds were identified qualitatively using liquid chromatography in tandem mass spectrometry technology. Of which 29 phenolic compounds were quantified based on their fragmentation behaviors. Most of the phenolic compounds were higher in the younger leaves than that in the stem and root, whereas the total amount of proanthocyanidins were unexpectedly higher in the root. The expression patterns of 63 structural and regulator genes involved in the shikimic acid, phenylpropanoid, and flavonoid pathways were analyzed by quantitative real-time polymerase chain reaction and cluster analysis. Based on the similarity of their expression patterns, the genes were classified into two main groups: C1 and C2; and the genes in group C1 had high relative expression level in the root or low in the bud and leaves. The expression patterns of genes in C2-2-1 and C2-2-2-1 groups were probably responsible for the development-dependent accumulation of phenolic compounds in the leaves. Enzymatic analysis suggested that the accumulation of catechins was influenced simultaneously by catabolism and anabolism. Further research is recommended to know the expression patterns of various genes and the reason for the variation in contents of different compounds in different growth stages and also in different organs.

HighlightThe identification of three UDP-glycosyltransferases involved in the biosynthesis of galloylated catechins and glycosylated flavonols which are astringent taste compounds in tea.

R2R3-MYB, bHLH, and WD40 proteins have been shown to control multiple enzymatic steps in the biosynthetic pathway responsible for the production of flavonoids, important secondary metabolites in Camellia sinensis. Few related transcription factor genes have been documented. The presence of R2R3-MYB, bHLH, and WD40 were statistically and bioinformatically analyzed on 127,094 C. sinensis transcriptome unigenes, resulting in identification of 73, 49, and 134 genes, respectively. C. sinensis phylogenetic trees were constructed for R2R3-MYB and bHLH proteins using previous Arabidopsis data and further divided into 27 subgroups (Sg) and 32 subfamilies. Motifs in some R2R3-MYB subgroups were redefined. Furthermore, Sg26 and Sg27 were expanded compared to Arabidopsis data, and bHLH proteins in C. sinensis were grouped into nine subfamilies. According to the functional annotation of Arabidopsis, flavonoid biosynthesis in C. sinensis was predicted to include R2R3-MYB genes in Sg4 (6), Sg5 (2), and Sg7 (1), as well as bHLH genes in subfamily 2 (2) and subfamily 24 (5). The wide evolutionary gap prevented phylogenetic analysis of WD40s; however, a single gene, CsWD40-1, was observed to share 80.4 % sequence homogeny with AtTTG1. Analysis of CsMYB4-1, CsMYB4-2, CsMYB4-3, CsMYB4-4, CsMYB5-1, and CsMYB5-2 revealed the interaction motif [DE]Lx2[RK]x3Lx6Lx3R, potentially contributing to the specificity of the bHLH partner in the stable MYB-bHLH complex. Full-length end-to-end polymerase chain reaction (PCR) and quantitative reverse transcriptase (qRT)-PCR were used to validate selected genes and generate relative expression ratio profiles in C. sinensis leaves by developmental stage and treatment conditions, including hormone and wound treatments. Potential target binding sites were predicted.

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Extranodal natural killer T-cell lymphoma (nasal type; NKTCL) is an aggressive malignancy strongly associated with Epstein-Barr virus (EBV) infection. However, the role of EBV in NKTCL development is unclear, largely due to the lack of information about EBV genome and transcriptome in NKTCL. Here, using high-throughput sequencing, we obtained whole genome (n = 27) and transcriptome datasets (n = 18) of EBV derived from NKTCL tumor biopsies. We assembled 27 EBV genomes and detected an average of 1,152 single nucleotide variants and 44.8 indels (<50 bp) of EBV per sample. We also identified frequent focal EBV genome deletions and integrated EBV fragments in the host genome. Moreover, Phylogenetic analysis revealed that NKTCL-derived EBVs are closely clustered; transcriptome analysis revealed less activation of both latent and lytic genes and larger amount of T-cell epitope alterations in NKTCL, as compared with other EBV-associated cancers. Furthermore, we observed transcriptional defects of the BARTs miRNA by deletion, and the disruption of host NHEJ1 by integrated EBV fragment, implying novel pathogenic mechanisms of EBV. Taken together, we reported for the first time global mutational and transcriptional profiles of EBV in NKTCL clinical samples, revealing important somatic events of EBV and providing insights to better understanding of EBV’s contribution in tumorigenesis.