SignificanceWe sequenced the genome and transcriptomes of the wild olive (oleaster). More than 50,000 genes were predicted, and evidence was found for two relatively recent whole-genome duplication events, dated at about 28 and 59 million years ago. Whole genome sequencing, as well as gene expression studies, provide further insights into the evolution of oil biosynthesis, and will aid future studies aimed at further increasing the production of olive oil, which is a key ingredient of the healthy Mediterranean diet and has been granted a qualified health claim by FDA. 5 AbstractHere, we present the genome sequence and annotation of the wild olive tree (Olea europaea var. sylvestris), called oleaster, which is considered an ancestor of cultivated olive trees. More than 50,000 protein-coding genes were predicted, a majority of which could be anchored to 23 pseudo-chromosomes obtained through a newly constructed genetic map. The oleaster genome contains signatures of two Oleaceae-lineage specific paleopolyploidy events, dated at approximately 28 and 59 million years ago. These events contributed to the expansion and neofunctionalization of genes and gene families that play important roles in oil biosynthesis.The functional divergence of oil biosynthesis pathway genes, such as FAD2, SACPD, EAR and ACPTE, following duplication, has been responsible for the differential accumulation of oleic and linoleic acids produced in olive compared to sesame, a closely related oil crop. Duplicated oleaster FAD2 genes are regulated by a short-interfering RNA (siRNA) derived from a transposable element-rich region, leading to suppressed levels of FAD2 gene expression.Additionally, neofunctionalization of members of the SACPD gene family has led to increased expression of SACPD2, 3, 5 and 7, consequently resulting in an increased desaturation of steric acid. Taken together, decreased FAD2 expression and increased SACPD expression likely explain the accumulation of exceptionally high levels of oleic acid in olive. The oleaster genome thus provides important insights into the evolution of oil biosynthesis and will be a valuable resource for oil crop genomics. 6 /bodyAs a symbol of peace, fertility, health and longevity, the olive tree (Olea europaea L.) is a socio-economically important oil crop that is widely grown in the Mediterranean Basin.Belonging to the Oleaceae family (order Lamiales), it can biosynthesize essential unsaturated fatty acids and other important secondary metabolites, such as vitamins and phenolic compounds (1). The olive tree is a diploid (2n = 46) allogamous crop that can be vegetatively propagated and live for thousands of years (2). Paleobotanical evidence suggests that olive oil was already produced in the Bronze Age (3). It has been thought that cultivated varieties were derived from the wild olive tree, called oleaster (O. europaea var. sylvestris), in Asia Minor, which then spread to Greece (4). Nevertheless, the exact domestication history of the olive tree is unknown (5). Due to their longevity, oleaster...

BackgroundAccumulating evidence has highlighted the potential role of long non-coding RNAs (lncRNAs) in the biological behaviors of glioblastoma stem cells (GSCs). Here, we elucidated the function and possible molecular mechanisms of the effect of lncRNA-SOX2OT on the biological behaviors of GSCs.ResultsReal-time PCR demonstrated that SOX2OT expression was up-regulated in glioma tissues and GSCs. Knockdown of SOX2OT inhibited the proliferation, migration and invasion of GSCs, and promoted GSCs apoptosis. MiR-194-5p and miR-122 were down-regulated in human glioma tissues and GSCs, and miR-194-5p and miR-122 respectively exerted tumor-suppressive functions by inhibiting the proliferation, migration and invasion of GSCs, while promoting GSCs apoptosis. Knockdown of SOX2OT significantly increased the expression of miR-194-5p and miR-122 in GSCs. Dual-luciferase reporter assay revealed that SOX2OT bound to both miR-194-5p and miR-122. SOX3 and TDGF-1 were up-regulated in human glioma tissues and GSCs. Knockdown of SOX3 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and decreased TDGF-1 mRNA and protein expression through direct binding to the TDGF-1 promoter. Over-expression of miR-194-5p and miR-122 decreased the mRNA and protein expression of SOX3 by targeting its 3’UTR. Knockdown of TDGF-1 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and inhibited the JAK/STAT signaling pathway. Furthermore, SOX3 knockdown also inhibited the SOX2OT expression through direct binding to the SOX2OT promoter and formed a positive feedback loop.ConclusionThis study is the first to demonstrate that the SOX2OT-miR-194-5p/miR-122-SOX3-TDGF-1 pathway forms a positive feedback loop and regulates the biological behaviors of GSCs, and these findings might provide a novel strategy for glioma treatment.Electronic supplementary materialThe online version of this article (10.1186/s12943-017-0737-1) contains supplementary material, which is available to authorized users.

Growing evidence demonstrates that long noncoding RNAs (lncRNAs) are involved in the progression of various cancers including glioma. Nuclear enriched abundant transcript 1 (NEAT1), an essential lncRNA for the formation of nuclear body paraspeckles, was not fully explored in glioma. We aimed to determine the expression, roles, and functional mechanisms of NEAT1 in the progression of glioma. By real-time PCR, we suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. RNA immunoprecipitation assay combined with luciferase reporter assay confirmed miR-449b-5p-specific binding to NEAT1. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met. This regulation menchaism promotes glioma pathogenesis and may provide a potential target for the prognosis and treatment of glioma.