The genome of the mesopolyploid crop species Brassica rapaThe Brassica rapa Genome Sequencing Project Consortium 1 Abstract:The Brassicaceae family which includes Arabidopsis thaliana, is a natural priority for reaching beyond botanical models to more deeply sample angiosperm genomic and functional diversity. Here we report the draft genome sequence and its annoation of Brassica rapa, one of the two ancestral species of oilseed rape. We modeled 41,174 protein-coding genes in the B. rapa genome. B. rapa has experienced only the second genome triplication reported to date, with its close relationship to A. thaliana providing a useful outgroup for investigating many consequences of triplication for its structural and functional evolution. The extent of gene loss (fractionation) among triplicated genome segments varies, with one copy containing a greater proportion of genes expected to have been present in its ancestor (70%) than the remaining two (46% and 36%). Both a generally rapid evolutionary rate, and specific copy number amplifications of particular gene families, may contribute to the remarkable propensity of Brassica species for the development of new morphological variants. The B. rapa genome provides a new resource for comparative and evolutionary analysis of the Brassicaceae genomes and also a platform for genetic improvement of Brassica oil and vegetable crops.2

Two-dimensional nanosheets have attracted tremendous attention because of their promising practical application and theoretical values. The atomic-thick nanosheets are able to not only enhance the intrinsic properties of their bulk counterparts but also give birth to new promising properties. Herein, we highlight an available pathway to prepare the ultrathin graphitic-phase C(3)N(4) (g-C(3)N(4)) nanosheets by a "green" liquid exfoliation route from bulk g-C(3)N(4) in water for the first time. The as-obtained ultrathin g-C(3)N(4) nanosheet solution is very stable in both the acidic and alkaline environment and shows pH-dependent photoluminenscence (PL). Compared to the bulk g-C(3)N(4), ultrathin g-C(3)N(4) nanosheets show enhanced intrinsic photoabsorption and photoresponse, which induce their extremely high PL quantum yield up to 19.6%. Thus, benefiting from the inherent blue light PL with high quantum yields and high stability, good biocompatibility, and nontoxicity, the water-soluble ultrathin g-C(3)N(4) nanosheet is a brand-new but promising candidate for bioimaging application.

Summary Glioblastomas are lethal cancers characterized by florid angiogenesis promoted in part by glioma stem cells (GSCs). As hypoxia regulates angiogenesis, we examined hypoxic responses in GSCs. We now demonstrate that hypoxia-inducible factor HIF2α and multiple HIF-regulated genes are preferentially expressed in GSCs in comparison to nonstem tumor cells and normal neural progenitors. In tumor specimens, HIF2α co-localizes with cancer stem cell markers. Targeting HIFs in GSCs inhibits self-renewal, proliferation and survival in vitro, and attenuates tumor initiation potential of GSCs in vivo. Analysis of a molecular database reveals that HIF2A expression correlates with poor glioma patient survival. Our results demonstrate that GSCs differentially respond to hypoxia with distinct HIF induction patterns and HIF2α may represent a promising target for anti-glioblastoma therapies. Significance Recent evidence supports the presence of cancer stem cell populations that contribute to tumor progression through preferential resistance to radiation and chemotherapy, and promotion of tumor angiogenesis, invasion, and metastasis. Therefore, the elucidation of molecular regulators of cancer stem cells may translate into improved anti-neoplastic therapies. Our work demonstrates that cancer stem cells derived from glioblastomas differentially respond to hypoxia with a distinct induction of HIF2α. We find that HIFs are critical to cancer stem cell maintenance and angiogenic drive, and that expression of HIF2α is significantly associated with poor glioma patient survival. These data further suggest that anti-angiogenic therapies can be designed to target cancer stem cell specific molecules involved in neoangiogenesis, including HIF2α and its regulated factors.