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SummaryChina is the origin and evolutionary centre of Oriental pears. Pyrus betuleafolia is a wild species native to China and distributed in the northern region, and it is widely used as rootstock. Here, we report the de novo assembly of the genome of P. betuleafolia‐Shanxi Duli using an integrated strategy that combines PacBio sequencing, BioNano mapping and chromosome conformation capture (Hi‐C) sequencing. The genome assembly size was 532.7 Mb, with a contig N50 of 1.57 Mb. A total of 59 552 protein‐coding genes and 247.4 Mb of repetitive sequences were annotated for this genome. The expansion genes in P. betuleafolia were significantly enriched in secondary metabolism, which may account for the organism's considerable environmental adaptability. An alignment analysis of orthologous genes showed that fruit size, sugar metabolism and transport, and photosynthetic efficiency were positively selected in Oriental pear during domestication. A total of 573 nucleotide‐binding site (NBS)‐type resistance gene analogues (RGAs) were identified in the P. betuleafolia genome, 150 of which are TIR‐NBS‐LRR (TNL)‐type genes, which represented the greatest number of TNL‐type genes among the published Rosaceae genomes and explained the strong disease resistance of this wild species. The study of flavour metabolism‐related genes showed that the anthocyanidin reductase (ANR) metabolic pathway affected the astringency of pear fruit and that sorbitol transporter (SOT) transmembrane transport may be the main factor affecting the accumulation of soluble organic matter. This high‐quality P. betuleafolia genome provides a valuable resource for the utilization of wild pear in fundamental pear studies and breeding.

Porcine epidemic diarrhea virus (PEDV) causes acute and devastating enteric disease in suckling piglets and results in huge economic losses in the pig industry worldwide. To establish productive infection, viruses must first circumvent the host innate immune response. In this study, we found that PEDV infection stimulated epidermal growth factor receptor (EGFR) activation, which has been linked to not only anticancer therapeutics, but also antiviral signaling. Therefore, we determined whether EGFR activation affected PEDV infection by using an activator or overexpression assay. The data showed that EGFR activation enhanced virus replication in both cases. We also found that specific inhibition of EGFR by either inhibitors or small interfering RNA (siRNA) led to a decrease in virus yields. Further analysis revealed that inhibition of EGFR produced augmentation of type I interferon genes. We next observed that the EGFR downstream cascade STAT3 was also activated upon PEDV infection. Similar to the case of EGFR, specific inhibition of STAT3 by either inhibitor or siRNA increased the antiviral activity of interferon and resulted in decreased PEDV RNA levels, and vice versa. The data on STAT3 depletion in combination with EGFR activation suggest that the attenuation of antiviral activity by EGFR activation requires activation of the STAT3 signaling pathway. Taken together, these data demonstrate that PEDV-induced EGFR activation serves as a negative regulator of the type I interferon response and provides a novel therapeutic target for virus infection. EGFR is a transmembrane tyrosine receptor that mediates various cellular events, as well as several types of human cancers. In this study, we investigated for the first time the role of EGFR in PEDV infection. We observed that PEDV infection induced EGFR activation. The role of EGFR activation is to impair the antiviral activity of type I interferon, which requires the involvement of the EGFR downstream signaling cascade STAT3. Our findings reveal a new mechanism evolved by PEDV to circumvent the host antiviral response, which might serve as a therapeutic target against virus infection.

Softening, a common phenomenon in many fruits, is a well coordinated and genetically determined process. However, the process of flesh softening during ripening has rarely been described in hawthorn. In this study, we found that ‘Ruanrou Shanlihong 3 Hao’ fruits became softer during ripening, whereas ‘Qiu JinXing’ fruits remained hard. At late developmental stages, the firmness of ‘Ruanrou Shanlihong 3 Hao’ fruits rapidly declined, and that of ‘Qiu JinXing’ fruits remained essentially unchanged. According to transmission electron microscopy, the middle lamella of ‘Qiu JinXing’ and ‘Ruanrou Shanlihong 3 Hao’ fruit flesh was largely degraded as the fruits matured. Microfilaments in ‘Qiu JinXing’ flesh were arranged close together and were deep in color, whereas those in ‘Ruanrou Shanlihong 3 Hao’ fruit flesh were arranged loosely, partially degraded and light in color. RNA-Seq analysis yielded approximately 46.72 Gb of clean data and 72,837 unigenes. Galactose metabolism and pentose and glucuronate interconversions are involved in cell wall metabolism, play an important role in hawthorn texture. We identified 85 unigenes related to the cell wall between hard- and soft-fleshed hawthorn fruits. Based on data analysis and real-time PCR, we suggest that β-GAL and PE4 have important functions in early fruit softening. The genes Ffase, Gns,α-GAL, PE63, XTH, and CWP, which are involved in cell wall degradation, are responsible for the different textures of hawthorn fruits. Thus, we hypothesize that the different textures of ‘Qiu JinXing’ and ‘Ruanrou Shanlihong 3 Hao’ fruits at maturity mainly result from cellulose/hemicelluloses degradation rather than from lamella degradation. Overall, we propose that different types of hydrolytic enzymes in cells interact to degrade the cell wall, resulting in ultramicroscopic Structure changes in the cell wall and, consequently, fruit softening. These results provide fundamental insight regarding the mechanisms by which hawthorn fruits acquire different textures and also lay a solid foundation for further research.

Tea tree oil (TTO), a volatile essential oil, has been widely used as an antimicrobial agent. However, the mechanism underlying TTO antifungal activity is not fully understood. In this study, a comprehensive metabolomics survey was undertaken to identify changes in metabolite production in Botrytis cinerea cells treated with TTO. Significant differences in 91 metabolites were observed, including 8 upregulated and 83 downregulated metabolites in TTO-treated cells. The results indicate that TTO inhibits primary metabolic pathways through the suppression of the tricarboxylic acid (TCA) cycle and fatty acid metabolism. Further experiments show that TTO treatment decreases the activities of key enzymes in the TCA cycle and increases the level of hydrogen peroxide (H2O2). Membrane damage is also induced by TTO treatment. We hypothesize that the effect of TTO on B. cinerea is achieved mainly by disruption of the TCA cycle and fatty acid metabolism, resulting in mitochondrial dysfunction and oxidative stress.

BackgroundA complete and hardened endocarp is a typical trait of drupe fruits. However, the ‘Liehe’ (LE) apricot cultivar has a thin, soft, cleavable endocarp that represents 60.39% and 63.76% of the thickness and lignin content, respectively, of the ‘Jinxihong’ (JG) apricot (with normal hardened-endocarp). To understand the molecular mechanisms behind the LE apricot phenotype, comparative transcriptomes of Prunus armeniaca L. were sequenced using Illumina HiSeq™ 2500.ResultsIn this study, we identified 63,170 unigenes including 15,469 genes >1000 bp and 25,356 genes with Gene Function annotation. Pathway enrichment and expression patterns were used to characterize differentially expression genes. The DEGs encoding key enzymes involved in phenylpropanoid biosynthesis were significantly down-regulated in LE apricot. For example, CAD gene expression levels, encoding cinnamyl alcohol dehydrogenase, were only 1.3%, 0.7%, 0.2% and 2.7% in LE apricot compared with JG cultivar at 15, 21, 30, 49 days after full bloom (DAFB). Furthermore, transcription factors regulating secondary wall and lignin biosynthesis were identified. Especially for SECONDARY WALL THICKENING PROMOTING FACTOR 1 (NST 1), its expression levels in LE apricot were merely 2.8% and 9.3% compared with JG cultivar at 15 and 21 DAFB, respectively.ConclusionsOur comparative transcriptome analysis was used to understand the molecular mechanisms underlie the endocarp-cleaving phenotype in LE apricot. This new apricot genomic resource and the candidate genes provide a useful reference for further investigating the lignification during development of apricot endocarp. Transcription factors such as NST1 may regulate genes involved in phenylpropanoid pathway and affect development and lignification of the endocarp.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-017-1023-5) contains supplementary material, which is available to authorized users.

To study the changes in sugar metabolism caused by fungal infection in post-harvest peaches, fruit from two cultivars (‘Baifeng’ and ‘Yulu’) was inoculated with Monilinia fructicola and stored at 10 °C. During disease development, soluble sugar content was monitored, as well as the activities and expression of selected enzymes. Disease progression was accompanied by a decrease in sucrose content and increases in reducing sugars and soluble solids, consistent with higher enzyme activities for acid invertase, neutral invertase and sucrose synthase-cleavage, and lower activities for sucrose synthase-synthesis and sucrose phosphate synthase. Activities of phosphofructokinase, hexokinase, and pyruvate kinase, which are related to hexose metabolism, also increased. These changes stimulate the Embden–Meyerhof–Parnas (EMP) pathway. We conclude that the fungal disease in peach fruit accelerates the decomposition of sucrose, thereby providing more glucose as a substrate to the EMP pathway.

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