Silique length (SL) and seed weight (SW) are two important yield-related traits controlled by quantitative trait loci (QTL) in oilseed rape (Brassica napus L.). The genetic bases underlying these two traits are largely unknown at present. In this study, we conducted QTL analyses for SL and SW using 186 recombinant inbred lines (RILs) derived from a cross between S1, an EMS mutant with extremely long siliques and large seeds, and S2, an inbred line with regular silique length and seed size. RILs were grown in Wuhan in the 2008/09 (SS09) and 2009/10 (SS10) growing seasons, and mean SL and SW for each line were investigated. Ten non-redundant QTL were identified for SL. Of these, a major QTL, cqSLA9, consistently explained as much as 53.4% of SL variation across environments. The others are minor QTL and individually explained less than 10% of the SL variation. Nine non-redundant QTL were identified for SW. Of which, one major QTL, cqSWA9, explained as much as 28.2% of the total SW variation in the SS09 and SS10 environments. In addition, three additive by additive interactions with small effects were detected for SL, and no interactions were detected for SW. Interestingly, the two major QTL, cqSLA9 for SL and cqSWA9 for SW colocalized in the same chromosomal region and were integrated into a unique QTL, uqA9. The S1 allele at this locus increases both SL and SW, suggesting that uqA9 has pleiotropic effects on both SL and SW. The existence and effect of uqA9 was confirmed in genetically different RILs derived from the cross between S1 and No2127, a resynthesized DH line having regular silique length and seed size. Individuals in one residual heterozygous line for cqSLA9 showed significant difference in silique length. The results in this study revealed that silique length in the S1 mutant is mainly controlled by the cqSLA9 locus, which will be suitable for fine mapping and marker-assisted selection in rapeseed breeding for high yield.

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To determine the effects of plant density and row spacing on the mechanical harvesting of rapeseed (Brassica napus L.), field experiments were conducted. Higher plant density produced fewer pods and reduced the yield per plant. Wider row spacing at higher plant densities increased seeds per pod and the 1000-seed weight, resulting in a higher yield per plant. The highest yields were achieved at a density of 45 × 104 plants ha−1 (D45) in combination with 15 cm row spacing (R15) because mortality associated with competition increased as both the plant density and row spacing increased. The leaf area index (LAI) and pod area index (PAI) showed similar relations to the yield per hectare, and they were positively correlated with the percentage of intercepted light, whereas the radiation use efficiency (RUE) was positively correlated with population biomass. Reduced plant height and increased root/shoot ratios led to a decreased culm lodging index. Improved resistance to pod shattering was also observed as plant density and row spacing increased. The angle of the lowest 5 branches decreased as row spacing increased under D30 and D45. All of these structural changes influenced the mechanical harvesting operations, resulting in the highest yield of mechanically harvesting rapeseed under D45R15.

Long non-coding RNAs (lncRNAs) have a critical role in cancer initiation and progression, and thus may mediate oncogenic or tumor suppressing effects, as well as be a new class of cancer therapeutic targets. We performed high-throughput sequencing of RNA (RNA-seq) to investigate the expression level of lncRNAs and protein-coding genes in 30 esophageal samples, comprised of 15 esophageal squamous cell carcinoma (ESCC) samples and their 15 paired non-tumor tissues. We further developed an integrative bioinformatics method, denoted URW-LPE, to identify key functional lncRNAs that regulate expression of downstream protein-coding genes in ESCC. A number of known onco-lncRNA and many putative novel ones were effectively identified by URW-LPE. Importantly, we identified lncRNA625 as a novel regulator of ESCC cell proliferation, invasion and migration. ESCC patients with high lncRNA625 expression had significantly shorter survival time than those with low expression. LncRNA625 also showed specific prognostic value for patients with metastatic ESCC. Finally, we identified E1A-binding protein p300 (EP300) as a downstream executor of lncRNA625-induced transcriptional responses. These findings establish a catalog of novel cancer-associated functional lncRNAs, which will promote our understanding of lncRNA-mediated regulation in this malignancy.

Purpose: Heterogeneous sensitivity of melanoma cells to tumor necrosis factor^related apoptosis-inducing ligand (TRAIL)^induced apoptosis may lead to outgrowth ofTRAIL-resistant cells and limit successful treatment by TRAIL. The present study aims to better understand the biological characteristics of melanoma cells resistant toTRAIL-induced apoptosis. Experimental Design: We generated TRAIL-resistant melanoma cells by prolonged exposure to TRAIL and characterized the cells in terms of their sensitivity to killing induced by a panel of cytotoxic agents using biological and biochemical methods. Results: TRAIL-resistant melanoma cells are cross-resistant to apoptosis induced by another death ligand FasL, the DNA-damaging agent cisplatin, the histone deacetylase inhibitor suberic bishydroxamate, and the antimicrotubule Vinca alkaloid, vincristine. The apoptotic signaling seemed to be inhibited upstream of mitochondrial apoptotic events and was associated with decreased expression of multiple apoptotic mediators, including pro-caspase-8, Fas-associated death domain, Bid, Bim, p53, and the products of its proapoptotic target genes. Despite being resistant to apoptosis,TRAIL-resistant melanoma cells were more vulnerable to cisplatin-induced nonapoptotic cell death. This was characterized by lack of DNA fragmentation, delayed externalization of phosphatidylserine, caspase and p53 independence, and severe mitochondrial disruption, and was preceded by poly(ADP)ribose polymerase (PARP) activation and depletion of intracellularATP, indicative of necrotic cell death. Inhibition of PARP activity partially converted the mode of cell death from necrosis to apoptosis. Conclusions:TRAIL-resistant melanoma cells are cross-resistant to apoptosis induced by various apoptotic stimuli but are more sensitive to nonapoptotic cell death induced by cisplatin. Exploration of chemotherapy-induced nonapoptotic cell death may provide an alternative strategy in overcoming resistance of melanoma cells toTRAIL-induced apoptosis.