Patients with retinitis pigmentosa (RP) typically develop night blindness early in life due to loss of rod photoreceptors. The remaining cone photoreceptors are the mainstay of their vision; however, over years or decades, these cones slowly degenerate, leading to blindness. We created transgenic pigs that express a mutated rhodopsin gene (Pro347Leu). Like RP patients with the same mutation, these pigs have early and severe rod loss; initially their cones are relatively spared, but these surviving cones slowly degenerate. By age 20 months, there is only a single layer of morphologically abnormal cones and the cone electroretinogram is markedly reduced. Given the strong similarities in phenotype to that of RP patients, these transgenic pigs will provide a large animal model for study of the protracted phase of cone degeneration found in RP and for preclinical treatment trials.

Pine wilt disease caused by pine wood nematode (Bursaphelenchus xylophilus, PWN) is a severe forest disease of the genus Pinus. Masson pine as an important timber and oleoresin resource in South China, is the major species infected by pine wilt disease. However, the underlying mechanism of pine resistance is still unclear. Here, we performed a transcriptomics analysis to identify differentially expressed genes associated with resistance to PWN infection. By comparing the expression profiles of resistant and susceptible trees inoculated with PWN at 1, 15, or 30 days post-inoculation (dpi), 260, 371 and 152 differentially expressed genes (DEGs) in resistant trees and 756, 2179 and 398 DEGs in susceptible trees were obtained. Gene Ontology enrichment analysis of DEGs revealed that the most significant biological processes were “syncytium formation” in the resistant phenotype and “response to stress” and “terpenoid biosynthesis” in the susceptible phenotype at 1 and 15 dpi, respectively. Furthermore, some key DEGs with potential regulatory roles to PWN infection, including expansins, pinene synthases and reactive oxidation species (ROS)-related genes were evaluated in detail. Finally, we propose that the biosynthesis of oleoresin and capability of ROS scavenging are pivotal to the high resistance of PWN.

Gastric cancer remains the third leading cause of cancer-related mortality worldwide, and proliferation of gastric cancer represents the major reason for its poor prognosis. Recent evidence indicates that long non-coding RNAs play crucial roles in development and progression of gastric cancer. Long non-coding RNA differentiation antagonizing non-protein coding RNA is upregulated in hepatic cell carcinoma, but the role of lncRNA differentiation antagonizing non-protein coding RNA in gastric cancer has not been explored. In this article, we found that differentiation antagonizing non-protein coding RNA is also upregulated in gastric cancer. Experiments revealed that silencing differentiation antagonizing non-protein coding RNA significantly inhibited gastric cancer cell proliferation in vitro and in vivo. Overexpression of differentiation antagonizing non-protein coding RNA notably increases gastric cancer cell proliferation. From RNA-seq and gene ontology annotations, we found that differentiation antagonizing non-protein coding RNA influences the gene expression programs in cell metabolic and cycle process. Taken together, our findings suggest that the long non-coding RNA differentiation antagonizing non-protein coding RNA promotes the proliferation of gastric cancer and is a potential prognostic biomarker and therapeutic target in gastric cancer.

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