Dataset Information

Transcriptomic analysis reveals insights into the response to Hop stunt viroid (HSVd) in sweet cherry (Prunus avium L.) fruits.

ABSTRACT: Hop stunt viroid (HSVd) is a member of the genus Hostuviroid of the family Pospiviroidae and has been found in a wide range of herbaceous and woody hosts. It causes serious dapple fruit symptoms on infected sweet cherry, notably inducing cherry tree decay. In order to better understand the molecular mechanisms of HSVd infection in sweet cherry fruit, transcriptome analysis of HSVd-infected and healthy sweet cherry fruits was carried out. A total of 1,572 differentially expressed genes (DEGs) were identified, involving 961 upregulated DEGs and 611 downregulated DEGs. Functional analysis indicated that the DEGs were mainly involved in plant hormone signal transduction, plant-pathogen interactions, secondary metabolism, and the MAPK signaling pathway. In addition, C2H2 zinc finger, MYB, bHLH, AP2/ERF, C2C2-dof, NAC and WRKY transcription factors can respond to HSVd infection. In order to confirm the high-throughput sequencing results, 16 DEGs were verified by RT-qPCR analysis. The results provided insight into the pathways and genes of sweet cherry fruit in response to HSVd infection.

SUBMITTER: Xu L

PROVIDER: S-EPMC7513744 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Transcriptomic analysis reveals insights into the response to Hop stunt viroid (HSVd) in sweet cherry (Prunus avium L.) fruits.

Xu Li L Zong Xiaojuan X Wang Jiawei J Wei Hairong H Chen Xin X Liu Qingzhong Q

PeerJ 20200921

Hop stunt viroid (HSVd) is a member of the genus Hostuviroid of the family Pospiviroidae and has been found in a wide range of herbaceous and woody hosts. It causes serious dapple fruit symptoms on infected sweet cherry, notably inducing cherry tree decay. In order to better understand the molecular mechanisms of HSVd infection in sweet cherry fruit, transcriptome analysis of HSVd-infected and healthy sweet cherry fruits was carried out. A total of 1,572 differentially expressed ge ...[more]

PMID: 33005494

Similar Datasets

Project description:BackgroundFruit color is one of the most important economic traits of the sweet cherry (Prunus avium L.). The red coloration of sweet cherry fruit is mainly attributed to anthocyanins. However, limited information is available regarding the molecular mechanisms underlying anthocyanin biosynthesis and its regulation in sweet cherry.Methodology/principal findingsIn this study, a reference transcriptome of P. avium L. was sequenced and annotated to identify the transcriptional determinants of fruit color. Normalized cDNA libraries from red and yellow fruits were sequenced using the next-generation Illumina/Solexa sequencing platform and de novo assembly. Over 66 million high-quality reads were assembled into 43,128 unigenes using a combined assembly strategy. Then a total of 22,452 unigenes were compared to public databases using homology searches, and 20,095 of these unigenes were annotated in the Nr protein database. Furthermore, transcriptome differences between the four stages of fruit ripening were analyzed using Illumina digital gene expression (DGE) profiling. Biological pathway analysis revealed that 72 unigenes were involved in anthocyanin biosynthesis. The expression patterns of unigenes encoding phenylalanine ammonia-lyase (PAL), 4-coumarate-CoA ligase (4CL), chalcone synthase (CHS), chalcone isomerase (CHI), flavanone 3-hydroxylase (F3H), flavanone 3'-hydroxylase (F3'H), dihydroflavonol 4-reductase (DFR), anthocyanidin synthase (ANS) and UDP glucose: flavonol 3-O-glucosyltransferase (UFGT) during fruit ripening differed between red and yellow fruit. In addition, we identified some transcription factor families (such as MYB, bHLH and WD40) that may control anthocyanin biosynthesis. We confirmed the altered expression levels of eighteen unigenes that encode anthocyanin biosynthetic enzymes and transcription factors using quantitative real-time PCR (qRT-PCR).Conclusions/significanceThe obtained sweet cherry transcriptome and DGE profiling data provide comprehensive gene expression information that lends insights into the molecular mechanisms underlying anthocyanin biosynthesis. These results will provide a platform for further functional genomic research on this fruit crop.

Project description:BACKGROUND AND AIMS: The cuticular membrane (CM) of Prunus avium (sweet cherry) and other fleshy fruit is under stress. Previous research indicates that the resultant strain promotes microscopic cuticular cracking. Microcracks impair the function of the CM as a barrier against pathogens and uncontrolled water loss/uptake. Stress and strain result from a cessation of CM deposition during early development, while the fruit surface continues to expand. The cessation of CM deposition, in turn, may be related to an early downregulation of CM-related genes. The aims of this study were to identify genes potentially involved in CM formation in sweet cherry fruit and to quantify their expression levels. METHODS: Fruit growth and CM deposition were quantified weekly from anthesis to maturity and rates of CM deposition were calculated. Sequences of genes expressed in the sweet cherry fruit skin (exocarp) were generated using high-throughput sequencing of cDNA and de novo assembly and analysed using bioinformatics tools. Relative mRNA levels of selected genes were quantified in the exocarp and fruit flesh (mesocarp) weekly using reverse transcriptase-quantitative real-time PCR and compared with the calculated CM deposition rate over time. KEY RESULTS: The rate of CM deposition peaked at 93 (±5) ?g per fruit d(-1) about 19 d after anthesis. Based on sequence analyses, 18 genes were selected as potentially involved in CM formation. Selected sweet cherry genes shared up to 100 and 98 % similarity with the respective Prunus persica (peach) and Arabidopsis thaliana genes. Expression of 13 putative CM-related genes was restricted to the exocarp and correlated positively with the CM deposition rate. CONCLUSIONS: The results support the view that the cessation of CM deposition during early sweet cherry fruit development is accounted for by a downregulation of genes involved in CM deposition. Genes that merit further investigation include PaWINA, PaWINB, PaLipase, PaLTPG1, PaATT1, PaLCR, PaGPAT4/8, PaLACS2, PaLACS1 and PaCER1.

Dataset Information

Transcriptomic analysis reveals insights into the response to Hop stunt viroid (HSVd) in sweet cherry (Prunus avium L.) fruits.

Publications

Transcriptomic analysis reveals insights into the response to <i>Hop stunt viroid</i> (HSVd) in sweet cherry (<i>Prunus avium</i> L.) fruits.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets