Large intergenic noncoding RNA regulator of reprogramming (Linc‐RoR) was first identified as a regulator to increase the emergence of induced pluripotent stem cells through reprogramming differentiated cells and is abnormal expression in a variety of malignant tumors. However, the function of Linc‐RoR in pancreatic cancer progression needs further clarification. The data from this study demonstrated that Linc‐RoR knockdown suppressed cell proliferative capacity and colony formation, while Linc‐RoR overexpression promoted these behaviors. In particular, Linc‐RoR overexpression promoted the level of mesenchymal markers, inhibited the expression of epithelial markers, as well as enhanced pancreatic cancer cells migration and invasion, whereas Linc‐RoR knockdown inhibited the expression of mesenchymal markers, promoted the expression of epithelial markers, as well as weakened pancreatic cancer cells migration and invasion. Further study revealed that Linc‐RoR knockdown brought about a significant fall in YAP phosphorylation and a rise in total YAP, while Linc‐RoR overexpression produced the opposite results. Specifically, Linc‐RoR promoted YAP in the cytoplasm into the nucleus. Taken together, we conjectured that Linc‐RoR promoted proliferation, migration, and invasion of pancreatic cancer cells by activating the Hippo/YAP pathway. YAP might be an underlying target of Linc‐RoR and mediate epithelial‐mesenchymal transition (EMT) in pancreatic cancer (PC); thus, Linc‐RoR might be a very meaningful biomarker for PC.

Many important crops (e.g., tuber, root, and tree crops) are cross-pollinating. For these crops, no inbred lines are available for genetic study and breeding because they are self-incompatible, clonally propagated, or have a long generation time, making the identification of agronomically important genes difficult, particularly in crops with a complex autopolyploid genome. In this study, we developed a method, OutcrossSeq, for mapping agronomically important loci in outcrossing crops based on whole-genome low-coverage resequencing of a large genetic population, and designed three computation algorithms in OutcrossSeq for different types of outcrossing populations. We applied OutcrossSeq to a tuberous root crop (sweet potato, autopolyploid), a tree crop (walnut tree, highly heterozygous diploid), and hybrid crops (double-cross populations) to generate high-density genotype maps for the outcrossing populations, which enable precise identification of genomic loci underlying important agronomic traits. Candidate causative genes at these loci were detected based on functional clues. Taken together, our results indicate that OutcrossSeq is a robust and powerful method for identifying agronomically important genes in heterozygous species, including polyploids, in a cost-efficient way. The OutcrossSeq software and its instruction manual are available for downloading at www.xhhuanglab.cn/tool/OutcrossSeq.html.

SummaryHeterosis, or hybrid vigour, is a predominant phenomenon in plant genetics, serving as the basis of crop hybrid breeding, but the causative loci and genes underlying heterosis remain unclear in many crops. Here, we present a large‐scale genetic analysis using 5360 offsprings from three elite maize hybrids, which identifies 628 loci underlying 19 yield‐related traits with relatively high mapping resolutions. Heterotic pattern investigations of the 628 loci show that numerous loci, mostly with complete–incomplete dominance (the major one) or overdominance effects (the secondary one) for heterozygous genotypes and nearly equal proportion of advantageous alleles from both parental lines, are the major causes of strong heterosis in these hybrids. Follow‐up studies for 17 heterotic loci in an independent experiment using 2225 F2 individuals suggest most heterotic effects are roughly stable between environments with a small variation. Candidate gene analysis for one major heterotic locus (ub3) in maize implies that there may exist some common genes contributing to crop heterosis. These results provide a community resource for genetics studies in maize and new implications for heterosis in plants.

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SLC47A2 encodes MATE 2-K in the kidney, which mediates the secretion of certain endogenous and exogenous compounds. SLC47A2 was dramatically repressed in patients with renal cell carcinoma (RCC), and a lower level of SLC47A2 might act as a negative prognostic marker, although the mechanism is not well understood. In this study, we aimed to investigate the mechanism via which SLC47A2 is downregulated in RCC. Based on the annotation information of the SLC47A2 locus available in the UCSC genome browser database, we identified a novel lncRNA, which is transcribed from the SLC47A2 locus and named it SANT1. Overexpression and knock-down assays were performed to investigate the effects of SANT1 on cis-regulation of SLC47A2. We verified the direct binding between SANT1 and SFPQ/E2F1/ HDAC1 using the cross-linking and immunoprecipitation (CLIP) assay. Chromatin immunoprecipitation was performed to confirm the molecular mechanism via which SANT1 activates the transcription of the SLC47A2 coding region. We observed that SANT1 can cis-regulate its own genetic locus. In tumouradjacent tissues, the SLC47A2 locus highly expresses SANT1, which can remove the regulatory SFPQ/ E2F1/HDAC1 suppressor complex from the promoter region, thereby significantly increasing the levels of the H3K27ac modification and RNAPII binding. Owing to a low SANT1 level, the binding of this inhibitory complex in the promoter region is upregulated in RCC, which results in silencing of the SLC47A2 coding region. In conclusion, we identified a novel lncRNA and elucidated the mechanism via which it regulates SLC47A2 expression in RCC.