滇金丝猴（Rhinopithecusbieti）现状及其保护对策研究

滇金丝猴（Ｒｈｉｎｏｐｉｔｈｅｃｕｓｂｉｅｔｉ）是我国特有的珍稀濒危动物,生活在海拔３８００～４３００ｍ的原始冷杉林中,但有时也会在４３００～４７００ｍ的低矮灌丛、草甸和流石滩上活动达数小时之久,甚至能跨越近千米的无林高海拔地带,因而它们是海拔分布最高的非人灵长类。松萝是它们的主要食物,取食松萝的时间占总取食时间的９１％。猴群活动范围可达近百平方公里。笔者在历时８年的野外考察中,已查明这一物种的全部现存自然种群只有１３个,分布在云南的德钦、兰坪、潍西、丽江和西藏的芒康这五县境内,其现存种群数量为１０００～１５００只;所有现存自然种群几乎均处在相互隔离的状态,群间已不可能进行基因交流,充分表明它们已到达灭绝边缘。然而其栖息地内的商业伐木规模仍在继续扩大,周围的人口压力正在不断增加,各猴群均面临不同程度的偷猎压力。这一现状委实令人担忧。如何拯救这一“国宝”应引起我国保护学家和各级政府有关职能部门的重视     

Genomic insights into speciation history and local adaptation of an alpine aspen in the Qinghai–Tibet Plateau and adjacent highlands

Natural selection serves as an important agent to drive and maintain interspecific divergence. Populus rotundifolia Griff. is an alpine aspen species that mainly occurs in the Qinghai–Tibet Plateau (QTP) and adjacent highlands, whereas its sister species, P. davidiana Dode, is distributed across southwest and central to northeast China in much lower altitude regions. In this study, we collected genome resequencing data of 53 P. rotundifolia and 42 P. davidiana individuals across their natural distribution regions. Our population genomic data suggest that the two species are well delimitated in the allopatric regions, but with hybrid zones in their adjacent region in the eastern QTP. Coalescent simulations suggest that P. rotundifolia diverged from P. davidiana in the middle Pleistocene with following continuous gene flow since divergence. In addition, we found numerous highly diverged genes with outlier signatures that are likely associated with high-altitude adaptation of these alpine aspens. Our finding indicate that Quaternary climatic changes and natural selection have greatly contributed to the origin and distinction maintenance of P. rotundifolia in the QTP.     

ProBDNF collapses neurite outgrowth of primary neurons by activating RhoA

Background

Neurons extend their dendrites and axons to build functional neural circuits, which are regulated by both positive and negative signals during development. Brain-derived neurotrophic factor (BDNF) is a positive regulator for neurite outgrowth and neuronal survival but the functions of its precursor (proBDNF) are less characterized.

Methodology/Principal Findings

Here we show that proBDNF collapses neurite outgrowth in murine dorsal root ganglion (DRG) neurons and cortical neurons by activating RhoA via the p75 neurotrophin receptor (p75NTR). We demonstrated that the receptor proteins for proBDNF, p75NTR and sortilin, were highly expressed in cultured DRG or cortical neurons. ProBDNF caused a dramatic neurite collapse in a dose-dependent manner and this effect was about 500 fold more potent than myelin-associated glycoprotein. Neutralization of endogenous proBDNF by using antibodies enhanced neurite outgrowth in vitro and in vivo, but this effect was lost in p75NTR^−/− mice. The neurite outgrowth of cortical neurons from p75NTR deficient (p75NTR^−/−) mice was insensitive to proBDNF. There was a time-dependent reduction of length and number of filopodia in response to proBDNF which was accompanied with a polarized RhoA activation in growth cones. Moreover, proBDNF treatment of cortical neurons resulted in a time-dependent activation of RhoA but not Cdc42 and the effect was absent in p75NTR^−/− neurons. Rho kinase (ROCK) and the collapsin response mediator protein-2 (CRMP-2) were also involved in the proBDNF action.

Conclusions

proBDNF has an opposing role in neurite outgrowth to that of mature BDNF. Our observations suggest that proBDNF collapses neurites outgrowth and filopodial growth cones by activating RhoA through the p75NTR signaling pathway.     

Rottlerin-Mediated Inhibition of Chlamydia trachomatis Growth and Uptake of Sphingolipids Is Independent of p38-Regulated/Activated Protein Kinase (PRAK)

We previously found that rottlerin, a plant-derived small molecule compound, profoundly inhibited Chlamydia trachomatis growth and blocked sphingolipid trafficking from host cell Golgi into chlamydial inclusions. Since the p38-regulated/activated protein kinase (PRAK) is a known target of rottlerin and is activated in Chlamydia trachomatis-infected cells, we investigated the potential role of this kinase in rottlerin-mediated anti-chlamydial activity. However, we found that a PRAK-specific inhibitor failed to inhibit chlamydial growth, suggesting that the kinase activity of PRAK may not be required for chlamydial intracellular replication. This conclusion was supported by the observation that chlamydial organisms replicated equally well in mouse embryonic fibroblast cells with or without PRAK. Moreover, neither the PRAK inhibitor nor PRAK deficiency altered host sphingolipid trafficking into chlamydial inclusions. Finally, rottlerin maintained its anti-chlamydial activity in PRAK-deficient cells. Together, these observations have demonstrated that PRAK is not required for either the rottlerin-mediated anti-chlamydial activity or rottlerin inhibition of sphingolipid trafficking, suggesting that rottlerin may achieve its inhibitory role by targeting other host factors.     

The quorum-sensing system in a plant bacterium Mesorhizobium huakuii affects growth rate and symbiotic nodulation

Mesorhizobium huakuii is a free-living bacterium which is capable of establishing a specific symbiotic relationship with Astragalus sinicus, an important winter green manure widely used in Eastern Asia, allowing for nitrogen fixing during this process. Previous studies demonstrate that M.␣huakuii produces quorum-sensing molecules at high cell density and quorum sensing plays a role in biofilm formations. In this study, we isolated and characterized two quorum-sensing deficient mutants in M. huakuii. Analysis of the flanking region of transposon insertions indicated that autoinducer synthase related genes are not homologous to acyl homoserine lactone (AHL) synthase genes that are shared among many Gram-negative bacteria, but related to peptide synthesis, indicating that M. huakuii quorum-sensing signals are distinct from AHLs. Compared with the wild-type strains, these quorum-sensing deficient mutants promoted their growth rate and were defective in nodule formation on host plants, indicative of a critical role of quorum sensing in M.␣huakuii during the host–bacterium symbiotic interaction.Yijing Gao and Zengtao Zhong contributed equally to this work.     

南瓜属4个栽培种种子蛋白质电泳分析

通过聚丙烯酰胺凝胶电泳(PAGE)对南瓜属4个栽培种中国南瓜、印度南瓜、美洲南瓜及黑籽南瓜的12个品种种子蛋白组分进行了分析。结果显示,黑籽南瓜种子以盐溶蛋白条带居多;其它3个栽培种以水溶蛋白条带居多,其次为盐溶蛋白;4个栽培种酸溶蛋白条带均较少;醇溶蛋白未分离得到蛋白谱带。水溶、盐溶、酸溶蛋白电泳图谱显示各栽培种间蛋白谱带差异明显,同一栽培种品种间蛋白谱带较为一致。     

Pharmacological and genetic evaluation of proposed roles of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK), extracellular signal-regulated kinase (ERK), and p90(RSK) in the control of mTORC1 protein signaling by phorbol esters

The mammalian target of rapamycin complex 1 (mTORC1) links the control of mRNA translation, cell growth, and metabolism to diverse stimuli. Inappropriate activation of mTORC1 can lead to cancer. Phorbol esters are naturally occurring products that act as potent tumor promoters. They activate isoforms of protein kinase C (PKCs) and stimulate the oncogenic MEK/ERK signaling cascade. They also activate mTORC1 signaling. Previous work indicated that mTORC1 activation by the phorbol ester PMA (phorbol 12-myristate 13-acetate) depends upon PKCs and may involve MEK. However, the precise mechanism(s) through which they activate mTORC1 remains unclear. Recent studies have implicated both the ERKs and the ERK-activated 90-kDa ribosomal S6 kinases (p90(RSK)) in activating mTORC1 signaling via phosphorylation of TSC2 (a regulator of mTORC1) and/or the mTORC1 component raptor. However, the relative importance of each of these kinases and phosphorylation events for the activation of mTORC1 signaling is unknown. The recent availability of MEK (PD184352) and p90(RSK) (BI-D1870) inhibitors of improved specificity allowed us to address the roles of these protein kinases in controlling mTORC1 in a variety of human and rodent cell types. In parallel, we used specific shRNAs against p90(RSK1) and p90(RSK2) to further test their roles in regulating mTORC1 signaling. Our data indicate that p90(RSKs) are dispensable for the activation of mTORC1 signaling by phorbol esters in all cell types tested. Our data also reveal striking diversity in the requirements for MEK/ERK in the control of mTORC1 between different cell types, pointing to additional signaling connections between phorbol esters and mTORC1, which do not involve MEK/ERK. This study provides important information for the design of efficient strategies to combat the hyperactivation of mTORC1 signaling by oncogenic pathways.