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Trimethylated histone H3 lysine 27 (H3K27me3) regulates gene repression, cell-fate determination and differentiation. We report that a conserved bromo-adjacent homology (BAH) module of BAHCC1 (BAHCC1BAH) 'recognizes' H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and integrated chromatin immunoprecipitation-sequencing-based analyses demonstrate that direct readout of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-L-lysine-binding 'cage' formed by BAHCC1BAH, mediating colocalization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is highly expressed in human acute leukemia and interacts with transcriptional corepressors. In leukemia, depletion of BAHCC1, or disruption of the BAHCC1BAH-H3K27me3 interaction, causes derepression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to suppression of oncogenesis. In mice, introduction of a germline mutation at Bahcc1 to disrupt its H3K27me3 engagement causes partial postnatal lethality, supporting a role in development. This study identifies an H3K27me3-directed transduction pathway in mammals that relies on a conserved BAH 'reader'.

The dynamic nature of formamidine lead iodide quantum dots (FAPbI3 QDs) limits their practical application by causing the appearance of ionic vacancy defects on the surface of QDs, which would then allow for significant trap-assisted non-radiative recombination of charge carriers. Herein, we explore a feasible surface modification strategy for passivating vacancy defects. Different lead salts are employed in the post-treatment procedure of quantum dot films. Based on both experimental and theoretical findings, Pb(NO3)2 passivation comprises Pb2+ and FA+. On the quantum dot surface, the O atoms from NO −3 form strong chemical bonds with FA+, and the O–C⋯O–N structure, defined by a dual-anchored configuration, contributes to the establishment of a stable crystal structure by exhibiting optimal bond lengths (3.486 Å and 3.775 Å, respectively) and a higher binding energy (10.51 eV). Finally, FAPbI3 quantum dot solar cells simultaneously achieve both exceptional environmental stability and a champion photoelectric conversion efficiency of 12.11%. This work provides valuable insights into surface chemical engineering of quantum dots, paving the way for high-performing photovoltaic devices. [ABSTRACT FROM AUTHOR]

It is unclear whether neurogenesis occurs in the adult mammalian enteric nervous system (ENS). Neural crest-derived cells capable of forming multilineage colonies in culture, and neurons and glia upon transplantation into chick embryos, persist throughout adult life in the mammalian ENS. In this study we sought to determine the physiological function of these cells. We discovered that these cells could be identified based on CD49b expression and that they had characteristics of enteric glia, including p75, GFAP, S100B, and SOX10 expression. To test whether new neurons or glia arise in the adult gut under physiological conditions, we marked dividing progenitors with a thymidine analog in rodents under steady-state conditions, or during aging, pregnancy, dietary changes, hyperglycemia, or exercise. We also tested gut injuries including inflammation, irradiation, benzalkonium chloride treatment, partial gut stenosis, and glial ablation. We readily observed neurogenesis in a neurogenic region of the central nervous system, but not reproducibly in the adult ENS. Lineage tracing of glial cells with GFAP-Cre and GFAP-CreERT2 also detected little or no adult ENS neurogenesis. Neurogenesis in the adult gut is therefore very limited under the conditions we studied. In contrast, ENS gliogenesis was readily observed under steady-state conditions and after injury. Adult enteric glia thus have the potential to form neurons and glia in culture but are fated to form mainly glia under physiological conditions and after the injuries we studied., INTRODUCTION In the 1960s Altman and Das administered tritiated thymidine to adult rats to label dividing cells and demonstrated that neurogenesis occurs in the dentate gyrus and the olfactory bulb [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.01.020 Byline: Shenghui He (a), Toshihide Iwashita (a), Johanna Buchstaller (a), Anna V. Molofsky (a), Dafydd Thomas (b), Sean J. Morrison (a) Keywords: Stem cell; Bmi-1; Transgenic mouse; Over-expression; Central nervous system (CNS); Glioma; Glioblastoma; Tumorigenesis Abstract: The polycomb gene Bmi-1 is required for the self-renewal of stem cells from diverse tissues, including the central nervous system (CNS). Bmi-1 expression is elevated in most human gliomas, irrespective of grade, raising the question of whether Bmi-1 over-expression is sufficient to promote self-renewal or tumorigenesis by CNS stem/progenitor cells. To test this we generated Nestin-Bmi-1-GFP transgenic mice. Analysis of two independent lines with expression in the fetal and adult CNS demonstrated that transgenic neural stem cells formed larger colonies, more self-renewing divisions, and more neurons in culture. However, in vivo, Bmi-1 over-expression had little effect on CNS stem cell frequency, subventricular zone proliferation, olfactory bulb neurogenesis, or neurogenesis/gliogenesis during development. Bmi-1 transgenic mice were born with enlarged lateral ventricles and a minority developed idiopathic hydrocephalus as adults, but none of the transgenic mice formed detectable CNS tumors, even when aged. The more pronounced effects of Bmi-1 over-expression in culture were largely attributable to the attenuated induction of p16.sup.Ink4a and p19.sup.Arf in culture, proteins that are generally not expressed by neural stem/progenitor cells in young mice in vivo. Bmi-1 over-expression therefore has more pronounced effects in culture and does not appear to be sufficient to induce tumorigenesis in vivo. Author Affiliation: (a) Howard Hughes Medical Institute, Life Sciences Institute, Department of Internal Medicine, Center for Stem Cell Biology, University of Michigan, 5435 Life Sciences Institute, 210 Washtenaw Ave., Ann Arbor, MI 48109-2216, USA (b) Department of Pathology, University of Michigan, Ann Arbor, MI 48109-2216, USA Article History: Received 28 May 2008; Revised 24 December 2008; Accepted 15 January 2009

Compound mutant mice that lack Bmi-1 is generated to test whether Ink4a deletion rescues stem cells frequency or neural development in Bmi-1(super -/-) mice, and whether p19(super Arf) also mediates part of the effect of Bmi-1 on stem cell function or neural development. Bmi-1 is required for the post-natal maintenance of stem cells in multiple tissues including the central nervous system (CNS) and peripheral nervous system (PNS).

Mammalian ageing is associated with reduced regenerative capacity in tissues that contain stem cells. It has been proposed that this is at least partially caused by the senescence of progenitors with age; however, it has not yet been tested whether genes associated with senescence functionally contribute to physiological declines in progenitor activity. Here we show that progenitor proliferation in the subventricular zone and neurogenesis in the olfactory bulb, as well as multipotent progenitor frequency and self-renewal potential, all decline with age in the mouse forebrain. These declines in progenitor frequency and function correlate with increased expression of p16INK4a, which encodes a cyclin-dependent kinase inhibitor linked to senescence. Ageing p16INK4a-deficient mice showed a significantly smaller decline in subventricular zone proliferation, olfactory bulb neurogenesis, and the frequency and self-renewal potential of multipotent progenitors. p16INK4a deficiency did not detectably affect progenitor function in the dentate gyrus or enteric nervous system, indicating regional differences in the response of neural progenitors to increased p16INK4a expression during ageing. Declining subventricular zone progenitor function and olfactory bulb neurogenesis during ageing are thus caused partly by increasing p16INK4a expression. [ABSTRACT FROM AUTHOR]

Formamidinium lead triiodide quantum dot (FAPbI 3 QD) exhibits substantial potential in solar cells due to its suitable band gap, extended carrier lifetime, and superior phase stability. However, despite great attempts toward reconfiguring the surface chemical environment of FAPbI 3 QDs, achieving the optimal efficiency of charge carrier extraction and transfer in cells remains a challenge. To circumvent this problem, we selectively introduced Au/FAPbI 3 Schottky heterojunctions by reducing Au + to Au 0 and subsequently anchoring them on the surface of FAPbI 3 QDs, which acts as a light-harvesting layer and establishes high-speed electron transfer channels (Au dot ↔ Au dot). As a result, the champion photoelectric conversion efficiency of solar cells reached 13.68%, a significant improvement over 11.19% of that of FAPbI 3 -based solar cells. The enhancement is attributed to efficient and directed electron transfer as well as a more aligned energy level arrangement. This work constructed Au/FAPbI 3 QD Schottky heterojunctions, providing a viable strategy to enhance QD electron coupling for high-performance optoelectronic applications.

Formamidinium lead triiodide (FAPbI 3 ) perovskite quantum dot has outstanding durability, reasonable carrier lifetime, and long carrier diffusion length for a new generation of highly efficient solar cells. However, ligand engineering is a dilemma because of the highly ionized and dynamic characteristics of quantum dots. To circumvent this issue, herein, we employed a mild solution-phase ligand-exchange approach through adding short-chain amino acids that contain amino and carboxyl groups to modify quantum dots and passivate their surface defects during the purification process. As a result, the photoelectric conversion efficiency of FAPbI 3 perovskite quantum dot solar cells (PQDSCs) increased from 11.23 to 12.97% with an open-circuit voltage of 1.09 V, a short-circuit current density of 16.37 mA cm -2 , and a filling factor of 72.13%. Furthermore, the stability of the device modified by amino acids retains over 80% of the initial efficiency upon being exposed to 20-30% relative humidity for 240 h of aging treatment. This work may offer an innovative concept and approach for surface ligand treatment to improve the photovoltaic performance of PQDSCs toward large-scale manufacture.

Self-renewal is the process by which stem cells divide to make more stem cells, perpetuating the stem cell pool throughout life. Self-renewal is division with maintenance of the undifferentiated state. This requires cell cycle control and often maintenance of multipotency or pluripotency, depending on the stem cell. Self-renewal programs involve networks that balance proto-oncogenes (promoting self-renewal), gate-keeping tumor suppressors (limiting self-renewal), and care-taking tumor suppressors (maintaining genomic integrity). These cell-intrinsic mechanisms are regulated by cell-extrinsic signals from the niche, the microenvironment that maintains stem cells and regulates their function in tissues. In response to changing tissue demands, stem cells undergo changes in cell cycle status and developmental potential over time, requiring different self-renewal programs at different stages of life. Reduced stem cell function and tissue regenerative capacity during aging are caused by changes in self-renewal programs that augment tumor suppression. Cancer arises from mutations that inappropriately activate self-renewal programs.