Sweet cherry (Prunus avium) is an economically significant fruit species in the genus Prunus. However, in contrast to other important fruit trees in this genus, only one draft genome assembly is available for sweet cherry, which was assembled using only Illumina short-read sequences. The incompleteness and low quality of the current sweet cherry draft genome limit its use in genetic and genomic studies. A high-quality chromosome-scale sweet cherry reference genome assembly is therefore needed. A total of 65.05 Gb of Oxford Nanopore long reads and 46.24 Gb of Illumina short reads were generated, representing ~190x and 136x coverage, respectively, of the sweet cherry genome. The final de novo assembly resulted in a phased haplotype assembly of 344.29 Mb with a contig N50 of 3.25 Mb. Hi-C scaffolding of the genome resulted in eight pseudochromosomes containing 99.59% of the bases in the assembled genome. Genome annotation revealed that more than half of the genome (59.40%) was composed of repetitive sequences, and 40,338 protein-coding genes were predicted, 75.40% of which were functionally annotated. With the chromosome-scale assembly, we revealed that gene duplication events contributed to the expansion of gene families for salicylic acid/jasmonic acid carboxyl methyltransferase and ankyrin repeat-containing proteins in the genome of sweet cherry. Four auxin-responsive genes (two GH3s and two SAURs) were induced in the late stage of fruit development, indicating that auxin is crucial for the sweet cherry ripening process. In addition, 772 resistance genes were identified and functionally predicted in the sweet cherry genome. The high-quality genome assembly of sweet cherry obtained in this study will provide valuable genomic resources for sweet cherry improvement and molecular breeding.

Fruit 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. In 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). The 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.

Phytoplasmas are cell wall-less bacteria that induce abnormal plant growth and various diseases, causing severe economic loss. Phytoplasmas are highly dependent on nutrients imported from host cells because they have lost many genes involved in essential metabolic pathways during reductive evolution. However, metabolic crosstalk between phytoplasmas and host plants and the mechanisms of phytoplasma nutrient acquisition remain poorly understood. In this study, using metabolomics approach, sweet cherry virescence (SCV) phytoplasma-induced metabolite alterations in sweet cherry trees were investigated. A total of 676 metabolites were identified in SCV phytoplasma-infected and mock inoculated leaves, of which 187 metabolites were differentially expressed, with an overwhelming majority belonging to carbohydrates, fatty acids/lipids, amino acids, and flavonoids. Available omics data of interactions between plant and phytoplasma were also deciphered and integrated into the present study. The results demonstrated that phytoplasma infection promoted glycolysis and pentose phosphate pathway activities, which provide energy and nutrients, and facilitate biosynthesis of necessary low-molecular metabolites. Our findings indicated that phytoplasma can induce reprograming of plant metabolism to obtain nutrients for its own replication and infection. The findings from this study provide new insight into interactions of host plants and phytoplasmas from a nutrient acquisition perspective.

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.

We conducted a small RNA sequencing of Sweet cherry (Prunus avium L. cv. Red-lamp) exhibiting mosaic symptoms for virus screening. After sequencing data analysis, Cherry virus A, Prunus necrotic ringspot virus, Little cherry virus 1 and Citrus leaf blotch virus were detected. The partial sequence of this CLBV was sequenced and analyzed with other members of Betaflexiviridae. We conclude that this virus from sweet cherry is a novel strain of CLBV. To our knowledge, this is the first report of CLBV infection in sweet cherry trees in the world.