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An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.Membrane tension plays an inhibitory role in clathrin-mediated endocytosis (CME) by impeding the transition of flat plasma membrane to hemispherical clathrin-coated structures (CCSs). Membrane tension also impedes the transition of hemispherical domes to omega-shaped CCSs. However, CME is not completely halted in cells under high tension conditions. Here we find that epsin, a membrane bending protein which inserts its N-terminus H0 helix into lipid bilayer, supports flat-to-dome transition of a CCS and stabilizes its curvature at high tension. This discovery is supported by molecular dynamic simulation of the epsin N-terminal homology (ENTH) domain that becomes more structured when embedded in a lipid bilayer. In addition, epsin has an intrinsically disordered protein (IDP) C-terminus domain which induces membrane curvature via steric repulsion. Insertion of H0 helix into lipid bilayer is not sufficient for stable epsin recruitment. Epsin's binding to adaptor protein 2 and clathrin is critical for epsin's association with CCSs under high tension conditions, supporting the importance of multivalent interactions in CCSs. Together, our results support a model where the ENTH and unstructured IDP region of epsin have complementary roles to ensure CME initiation and CCS maturation are unimpeded under high tension environments.Due to large and complex genomes of Triticeae species, skim sequencing approaches have cost and analytical advantages for detecting genetic markers and building linkage maps. Here, we develop a high-density linkage map and identify quantitative trait loci (QTLs) for recombinant inbred lines of Aegilops tauschii, a D-genome donor of bread wheat, using the recently developed genotyping by Random Amplicon Sequencing-Direct (GRAS-Di) system, which facilitates skimming of the large and complicated genome and generates a large number of genetic markers. The deduced linkage groups based on the GRAS-Di genetic markers corresponded to the chromosome number of Ae. tauschii. We successfully identified stable QTLs for flowering time and spikelet shape-related traits. Genotype differences of RILs at the QTL-linked markers were significantly associated with the trait variations. In particular, one of the QTL-linked markers for flowering time was mapped close to VRN3 (also known as FLOWERING LOCUS T), which controls flowering. The GRAS-Di system is, therefore, an efficient and useful application for genotyping and linkage mapping in species with large and complex genomes, such as Triticeae species.The commensal microbiome is known to influence a variety of host phenotypes. Microbiome profiling followed by differential abundance analysis has been established as an effective approach to study the mechanisms of host-microbiome interactions. Pexidartinib However, it is challenging to interpret the collective functions of the resultant microbe-sets due to the lack of well-organized functional characterization of commensal microbiome. We developed microbe-set enrichment analysis (MSEA) to enable the functional interpretation of microbe-sets by examining the statistical significance of their overlaps with annotated groups of microbes that share common attributes such as biological function or phylogenetic similarity. We then constructed microbe-set libraries by query PubMed to find microbe-mammalian gene associations and disease associations by parsing the Disbiome database. To demonstrate the utility of our novel MSEA methodology, we carried out three case studies using publicly available curated knowledge resource and microbiome profiling datasets focusing on human diseases. We found MSEA not only yields consistent findings with the original studies, but also recovers insights about disease mechanisms that are supported by the literature. Overall, MSEA is a useful knowledge-based computational approach to interpret the functions of microbes, which can be integrated with microbiome profiling pipelines to help reveal the underlying mechanism of host-microbiome interactions.We prepared a novel adsorbent functionalized by bagasse magnetic biochar (BMBC). To study the removal behaviors and mechanisms of Cr(VI) by BMBC, batch adsorption experiments were conducted by modifying variables, such as pH, adsorption time, BMBC dosages, initial Cr concentration, co-existing ions, and ionic strength, and characterizing BMBC before and after Cr(VI) adsorption. BMBC was primarily composed of Fe2O3 and Fe3O4 on bagasse boichar with an amorphous structure. The specific surface area of BMBC was 81.94 m2 g-1, and the pHpzc of BMBC was 6.2. The fabricated BMBC showed high adsorption performance of Cr(VI) in aqueous solution. The maximum Cr(VI) adsorption capacity of BMBC was 29.08 mg g-1 at 25 ºC, which was much higher than that of conventional biochar sorbents. The adsorption process followed pseudo-second-order kinetics and could be explained by the involvement of the Langmuir isotherm in monolayer adsorption. The crystalline structure of Fe3O4 in the BMBC changed slightly during the adsorption process; Fe3O4 improved the adsorption of Cr(VI) on BMB. The desorption capacity of Cr(VI) was 8.21 mg g-1 when 0.2 mol L-1 NaOH was used as the desorption solution. After being reused three times, the removal efficiency is still as high as 80.36%.The tendency of brain cells to undergo apoptosis in response to exogenous events varies across neural development, with apoptotic threshold dependent on proliferation state. Proliferative neural progenitors show a low threshold for apoptosis, while terminally differentiated neurons are relatively refractory. To define the mechanisms linking proliferation and apoptotic threshold, we examined the effect of conditionally deleting Bcl2l1, the gene that codes the antiapoptotic protein BCL-xL, in cerebellar granule neuron progenitors (CGNPs), and of co-deleting Bcl2l1 homologs, antiapoptotic Mcl-1, or pro-apoptotic Bax. We found that cerebella in conditional Bcl2l1-deleted (Bcl-xLcKO) mice were severely hypoplastic due to the increased apoptosis of CGNPs and their differentiated progeny, the cerebellar granule neurons (CGNs). Apoptosis was highest as Bcl-xLcKO CGNPs exited the cell cycle to initiate differentiation, with proliferating Bcl-xLcKO CGNPs relatively less affected. Despite the overall reduction in cerebellar growth, SHH-dependent proliferation was prolonged in Bcl-xLcKO mice, as more CGNPs remained proliferative in the second postnatal week.

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