P45 Forms a Complex with FADD and Promotes Neuronal Cell Survival Following Spinal Cord Injury

Fas-associated death domain (DD) adaptor (FADD), a member of the DD superfamily, contains both a DD and a death effector domain (DED) that are important in mediating FAS ligand-induced apoptotic signaling. P45 is a unique member of the DD superfamily in that it has a domain with sequence and structural characteristics of both DD and DED. We show that p45 forms a complex with FADD and diminishes Fas-FADD mediated death signaling. The DED of FADD is required for the complex formation with p45. Following spinal cord injury, transgenic mice over-expressing p45 exhibit increased neuronal survival, decreased retraction of corticospinal tract fibers and improved functional recovery. Understanding p45-mediated cellular and molecular mechanisms may provide insights into facilitating nerve regeneration in humans.     

Identification of FAAP24, a Fanconi anemia core complex protein that interacts with FANCM

The Fanconi anemia (FA) core complex plays a crucial role in a DNA damage response network with BRCA1 and BRCA2. How this complex interacts with damaged DNA is unknown, as only the FA core protein FANCM (the homolog of an archaeal helicase/nuclease known as HEF) exhibits DNA binding activity. Here, we describe the identification of FAAP24, a protein that targets FANCM to structures that mimic intermediates formed during the replication/repair of damaged DNA. FAAP24 shares homology with the XPF family of flap/fork endonucleases, associates with the C-terminal region of FANCM, and is a component of the FA core complex. FAAP24 is required for normal levels of FANCD2 monoubiquitylation following DNA damage. Depletion of FAAP24 by siRNA results in cellular hypersensitivity to DNA crosslinking agents and chromosomal instability. Our data indicate that the FANCM/FAAP24 complex may play a key role in recruitment of the FA core complex to damaged DNA.     

Identification of a newly isolated erythritol-producing yeast and cloning of its erythritol reductase genes

A new erythritol-producing yeast (strain BH010) was isolated in this study. Analysis of the D1/D2 domain of the 26S rDNA sequence, the ITS/5.8S rDNA sequence, and the 18S rDNA sequence allowed the taxonomic position of strain BH010 to be discussed and it was identified and named Moniliella sp. BH010. Physiological characteristics were described. Scanning electron micrography clearly indicated that the cells were cylindrical to elliptical with an average size of 5?×?10?μm when growing in liquid medium, and that pseudohyphae and blastoconidia were observed when cultivated in agar plates. The erythritol reductase genes were cloned, sequenced, and analyzed. BLAST analysis and multiple sequence alignment demonstrated that erythritol reductase genes of Moniliella sp. BH010 shared very high homology with that of Trichosporonoides megachiliensis SNG-42 except for the presence of introns. The deduced amino acid sequences showed high homology to the aldo–keto reductase superfamily.     

黑曲霉催化雄甾-4-烯-3,17-二酮16β-羟基化

为进一步确定黑曲霉菌株TCCC41650的生物转化能力,以雄甾-4-烯-3,17-二酮(Androstenedione)为底物,利用黑曲霉菌株TCCC41650进行催化,产物经纯化、重结晶后,通过单晶衍射鉴定为16β-羟基雄甾-4-烯-3,17-二酮。转化条件为:培养液pH 6.0,乙醇添加量为2%,投料浓度为1‰时,72 h转化率为85.8%。目前甾体研究领域对于C16β-羟基化的微生物转化未见报道,研究结果为C16β-羟基甾体药物的研发奠定了基础。     

USP52 inhibits cell proliferation by stabilizing PTEN protein in non-small cell lung cancer

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer. Ubiquitination is closely related to the development of lung cancer. However, the biological importance of newly discovered ubiquitin-specific peptidase (USP) 52 (USP52) in NSCLC remained unclear. Here, our findings identify USP52 as a novel tumor suppressor of NSCLC, the low expression of USP52 predicts a poor prognosis for NSCLC patients. The present study demonstrates that USP52 inhibits cancer cell proliferation through down-regulation of cyclin D1 (CCND1) as well as AKT/mTOR signaling pathway inhibition. Meanwhile, USP25 also suppresses NSCLC progression via enhancing phosphatase and tensin homolog (PTEN) stability in cancer cells, which further indicates the significance/importance of USP52 in NSCLC suppression.     

短期增温对中亚热带杉木人工幼林土壤氮磷耦合作用的影响

全球变暖引起陆地生态系统和整个生物圈一系列生态问题,未来全球平均气温的持续增加将使这些问题进一步加剧。目前增温、氮沉降和森林更新方式对中亚热带土壤氮磷等养分的影响已有部分研究,但增温对亚热带森林的氮磷耦合作用的影响仍然未知。以中亚热带杉木(Cunninghamia lanceolate)幼苗为研究对象,设置埋设电缆以加热土壤增温实验(增温幅度(5±0.5)℃),研究短期增温对土壤含水量、微生物生物量氮(MBN)、微生物生物量磷(MBP)、土壤氮磷养分,以及氮(N)、磷(P)耦合作用的影响。结果表明:短期增温对全氮、全磷无显著影响;增温第1年显著提高了有效氮、铵态氮(NH_4~+)和有效磷的含量,显著降低了MBN含量。增温第2年,土壤中有效磷、NH_4~+和MBP含量显著下降;短期增温虽然对土壤全N/P,有效N/P的影响不显著,但是增温使铵态氮/硝态亚硝态氮(NH_4~+/(NO_3~-+NO_2~-))显著降低;此外,增温显著降低了MBN/MBP,缓解了微生物对磷的限制。相关性分析表明,耦合作用不仅受N和P之间相互作用的影响,也受土壤温度、水分含量等其他因素的影响。研究表明,短期增温并未对中亚热带杉木人工幼林土壤氮磷耦合作用产生显著影响,但增温后降低了有效氮、有效磷的含量。因此,在未来全球变暖背景下,研究结果为中亚热带森林生态系统的的健康发展和科学管理提供重要的理论依据。     

生态系统服务功能与景观格局耦合协调度研究——以武陵山区退耕还林工程为例

生态系统服务功能与景观格局演变关系极为密切,研究生态系统服务功能与景观格局的耦合协调度对于区域发展具有重要意义。以武陵山区退耕还林工程为例,参照国家标准和行业标准,采用分布式测算方法、景观格局指数分析和耦合协调度模型等方法,旨在揭示武陵山区退耕还林工程生态系统服务功能与景观格局二者耦合协调关系。结果表明:(1)2005—2017年间武陵山区退耕还林工程各项生态服务功能物质量均以15倍左右速度增长,生态系统服务空间分布格局最佳区域由西部地区逐渐向东南扩大;(2)武陵山区景观演变存在时空差异,1995—2005年景观格局变化更为明显,变化区域集中在中西部地区,2005—2015年与之相比,景观格局变化空间上更为分散;(3)武陵山区退耕还林工程生态系统服务与景观格局演变存在较高水平的耦合以及高水平的协调性。研究结果可为武陵山区土地利用规划及退耕还林工程进一步实施提供科学依据。