新疆北部石炭纪—二叠纪孢粉组合的植物区系性质初步探讨

新疆北部石炭纪—二叠纪孢粉植物群总体上属亚安加拉区,但其形成、发展经历了若干阶段,即由 C_1(Tournaisian-Visean)的泛世界性+欧美型+安加拉土著分子→C_2早期(Bashkirian早期)安加拉型为主+欧美型成分→亚安加拉区形成(Bashkirian晚期—Moscovian)、扩张(Stephani-an—P_1)→P_2—T_1欧美色彩成分和泛世界性成分增加的过程。从巴什基尔晚期起混生有冈瓦纳色彩成分,但目前难以找到合理的解释;与华夏植物群关系微弱。     

沙冬青属的细胞学研究

沙冬青属(Ammopiptanthus)植物仅两个种,即蒙古沙冬青(A.mongolicus)和新疆沙冬青(A.nanus),为第三纪残遗种,是中亚荒漠唯一的常绿阔叶植物,因珍稀,临危而被列为国家重点保护植物”。国内外对该属两个种的染色体数目的记载存在着差异。本文对沙冬青属两种植物的染色体数目和核型进行了分析研究,旨在为探讨该属植物的发生和系统发育,以及开展植物多样性保护和合理开发利用积累资料。     

嗜酸乳杆菌及其制剂对大鼠血脂代谢的影响

本实验表明,口服嗜酸乳杆茵及其制剂,能升高大鼠ADL—C和HDL—C/T比值及降低[VLDL LDL]—C的浓度。这一作用对于防止动粥发生显然是十分有利的。若将嗜酸乳杆菌及其制剂,与其它降血脂药物配伍,用于高血脂症的辅助治疗,将会产生良好的效果。     

中国瘿螨亚科四新种记述（蜱螨亚纲：瘿螨总科）

本文记述中国瘿螨亚科４新种,它们是为害桃树的昌吉瘤瘿螨Ａｃｅｒｉａ ｃｈａｎｇｊｉｅｎｓｉｓ Ｋｕａｎｇ ｅｔ Ｐａｎｇ;为害垂柳的青海瘤瘿螨Ａｃｅｒｉａ ｑｉｎｇｈａｉｅｎｓｉｓ Ｋｕａｎｇ,垂柳刺子瘿螨Ａｃｕｌｏｄｅｓ ｓａｌｉｃｉｓＫｕａｎｇ和兰州狭点瘿螨Ｓｔｅｎａｃｉｓ ｌａｎｚｈｏｕｅｎｓｉｓ Ｋｕａｎｇ。模式标本保存在南京农业大学植物保护系。     

Crucial role of the C-terminus of PTEN in antagonizing NEDD4-1-mediated PTEN ubiquitination and degradation

PTEN (phosphatase and tensin homologue deleted on chromosome 10), a potent tumour suppressor and multifunctional signalling protein, is under intricate regulation. In the present study, we have investigated the mechanism and regulation of PTEN ubiquitination catalysed by NEDD4-1 (neural-precursor-cell-expressed, developmentally down-regulated 4-1), a ubiquitin ligase for PTEN we identified recently. Using the reconstituted assay and cellular analysis, we demonstrated that NEDD4-1-mediated PTEN ubiquitination depends on its intact HECT (homologous to E6-associated protein C-terminus) domain. Instead of using its WW domains (protein-protein interaction domains containing two conserved tryptophan residues) as a protein interaction module, NEDD4-1 interacts with PTEN through its N-terminal region containing a C2 domain as well as the HECT domain. Strikingly, we found that a C-terminal truncated PTEN fragment binds to NEDD4-1 with higher affinity than the full-length PTEN, suggesting an intrinsic inhibitory effect of the PTEN C-terminus on PTEN-NEDD4-1 interaction. Moreover, the C-terminal truncated PTEN is more sensitive to NEDD4-1-mediated ubiquitination and degradation. Therefore the present study reveals that the C-terminus of PTEN plays a critical role in stabilizing PTEN via antagonizing NEDD4-1-induced PTEN protein decay; conversely, truncation of the PTEN C-terminus results in rapid NEDD4-1-mediated PTEN degradation, a possible mechanism accounting for attenuation of PTEN function by certain PTEN mutations in human cancers.     

植物NAC转录因子家族研究概况

植物特有的NAC家族转录因子数量众多,广泛分布于陆生植物中。NAC转录因子涉及多个生长发育和胁迫应答过程,功能多样而重要,从发现至今一直是研究的热点。ANAC019蛋白三维结构的解析和一系列NAC基因功能的揭示可以帮助我们更全面地了解NAC家族,包括它们的起源与分类、生物学功能、表达调控规律以及结构与功能的关系。该文较为详尽地阐述了NAC家族转录因子的研究现状,并展望其未来的研究方向。     

Evolutionary genomics reveals lineage-specific gene loss and rapid evolution of a sperm-specific ion channel complex: CatSpers and CatSperbeta

The mammalian CatSper ion channel family consists of four sperm-specific voltage-gated Ca2+ channels that are crucial for sperm hyperactivation and male fertility. All four CatSper subunits are believed to assemble into a heteromultimeric channel complex, together with an auxiliary subunit, CatSperbeta. Here, we report a comprehensive comparative genomics study and evolutionary analysis of CatSpers and CatSperbeta, with important correlation to physiological significance of molecular evolution of the CatSper channel complex. The development of the CatSper channel complex with four CatSpers and CatSperbeta originated as early as primitive metazoans such as the Cnidarian Nematostella vectensis. Comparative genomics revealed extensive lineage-specific gene loss of all four CatSpers and CatSperbeta through metazoan evolution, especially in vertebrates. The CatSper channel complex underwent rapid evolution and functional divergence, while distinct evolutionary constraints appear to have acted on different domains and specific sites of the four CatSper genes. These results reveal unique evolutionary characteristics of sperm-specific Ca2+ channels and their adaptation to sperm biology through metazoan evolution.     

Induction of Autophagy by a Novel Small Molecule Improves Aβ Pathology and Ameliorates Cognitive Deficits

Growing evidence has demonstrated a neuroprotective role of autophagy in Alzheimer’s disease (AD). Thus, autophagy has been regarded as a potential therapeutic target, attracting increasing interest in pharmaceutical autophagy modulation by small molecules. We designed a two-cycle screening strategy on the basis of imaging high-throughout screening (HTS) and cellular toxicity assay, and have identified a novel autophagy inducer known as GTM-1. We further showed that GTM-1 exhibits dual activities, such as autophagy induction and antagonism against Aβ-oligomer toxicity. GTM-1 modulates autophagy in an Akt-independent and mTOR-independent manner. In addition, we demonstrated that GTM-1 enhances autophagy clearance and reverses the downregulation of autophagy flux by thapsigargin and asparagine. Furthermore, administration of GTM-1 attenuated Aβ pathology and ameliorated cognitive deficits in AD mice.     

Ubiquitination regulates PTEN nuclear import and tumor suppression

The PTEN tumor suppressor is frequently affected in cancer cells, and inherited PTEN mutation causes cancer-susceptibility conditions such as Cowden syndrome. PTEN acts as a plasma-membrane lipid-phosphatase antagonizing the phosphoinositide 3-kinase/AKT cell survival pathway. However, PTEN is also found in cell nuclei, but mechanism, function, and relevance of nuclear localization remain unclear. We show that nuclear PTEN is essential for tumor suppression and that PTEN nuclear import is mediated by its monoubiquitination. A lysine mutant of PTEN, K289E associated with Cowden syndrome, retains catalytic activity but fails to accumulate in nuclei of patient tissue due to an import defect. We identify this and another lysine residue as major monoubiquitination sites essential for PTEN import. While nuclear PTEN is stable, polyubiquitination leads to its degradation in the cytoplasm. Thus, we identify cancer-associated mutations of PTEN that target its posttranslational modification and demonstrate how a discrete molecular mechanism dictates tumor progression by differentiating between degradation and protection of PTEN.