喀斯特山地煤矿废弃地几种优势植物的重金属耐性特征

对贵阳花溪区麦坪乡煤矿废弃地进行了野外调查, 对该地优势植物和土壤进行了采样, 测定样品As、Cd、Cu、Hg、Pb和Zn的含量, 发现当地优势植物雀稗(Paspalum thunbergii Kunth ex Steud.)地上部分Cu含量达到1058.12 mg•kg-1, 转移系数2.89, 富集系数16.07。研究了雀稗在铜离子胁迫实验中的根系活力变化和叶绿素浓度变化, 雀稗根系活力随实验进行而逐渐降低, 铜离子浓度为500 µg•mL-1的实验进行到第四周时TTC还原量达到最低值; 叶绿素浓度随着铜离子浓度的增加而缓慢降低, 进一步确认当地土著植物雀稗对铜离子有一定的耐受性。     

棉田绿盲蝽微生物多样性研究

昆虫在长期的进化过程中与其体内微生物形成了互利共生的关系,共生微生物参与调节寄主的多种生命活动,例如生殖、代谢等。在黄河流域棉区绿盲蝽Apolygus lucorum是棉花的主要害虫之一。为明确绿盲蝽体内共生菌的种类与群落结构,通过HiSeq平台对棉田绿盲蝽体内共生菌的16S rRNA基因V3～V4区进行高通量测序,分析绿盲蝽体内共生菌的种类与多样性。结果显示,变形菌门Proteobacteria(89.18%)、放线菌门Actinobacteria(2.99%)、厚壁菌门Firmicutes(2.48%)为绿盲蝽的3个优势菌门。在属水平上立克次氏体Rickettsia(32.86%)、欧文氏菌属Erwinia(20.21%)为优势菌群。本文初步明确了绿盲蝽体内微生物群落的组成和动态变化,为进一步研究绿盲蝽与共生菌的相互作用提供了基础,为今后从共生菌出发防治绿盲蝽提供新思路。     

Use of expression constructs to dissect the functional domains of the CHS/beige protein: identification of multiple phenotypes

The Chediak-Higashi Syndrome (CHS) and the orthologous murine disorder beige are characterized at the cellular level by the presence of giant lysosomes. The CHS1/Beige protein is a 3787 amino acid protein of unknown function. To determine functional domains of the CHS1/Beige protein, we generated truncated constructs of the gene/protein. These truncated proteins were transiently expressed in Cos-7 or HeLa cells and their effect on membrane trafficking was examined. Beige is apparently a cytosolic protein, as are most transiently expressed truncated Beige constructs. Expression of the Beige construct FM (amino acids 1-2037) in wild-type cells led to enlarged lysosomes. Similarly, expression of a 5.5-kb region (amino acids 2035-3787) of the carboxyl terminal of Beige (22B) also resulted in enlarged lysosomes. Expression of FM solely affected lysosome size, whereas expression of 22B led to alterations in lysosome size, changes in the Golgi and eventually cell death. The two constructs could be used to further dissect phenotypes resulting from loss of the Beige protein. CHS or beigej fibroblasts show an absence of nuclear staining using a monoclonal antibody directed against phosphatidylinositol 4,5 bisphosphate [PtdIns(4,5) P2]. Transformation of beige j fibroblasts with a YAC containing the full-length Beige gene resulted in the normalization of lysosome size and nuclear PtdIns(4,5)P2 staining. Expression of the carboxyl dominant negative construct 22B led to loss of nuclear PtdIns(4,5)P2 staining. Expression of the FM dominant negative clone did not alter nuclear PtdIns(4,5) P2 localization. These results suggest that the Beige protein interacts with at least two different partners and that the Beige protein affects cellular events, such as nuclear PtdIns(4,5)P2 localization, in addition to lysosome size.     

Characterization of the OFD1/Ofd1 genes on the human and mouse sex chromosomes and exclusion of Ofd1 for the Xpl mouse mutant

Oral-facial-digital type 1 (OFD1) syndrome is an X-linked dominant condition characterized by malformations of the face, oral cavity, and digits. The responsible gene, OFD1, maps to human Xp22 and has an unknown function. We isolated and characterized the mouse Ofd1 gene and showed that it is subject to X-inactivation, in contrast to the human gene. Furthermore, we excluded a role for Ofd1 in the pathogenesis of the spontaneous mouse mutant Xpl, which had been proposed as a mouse model for this condition. Comparative sequence analysis demonstrated that OFD1 is conserved among vertebrates and absent in invertebrates. This analysis allowed the identification of evolutionarily conserved domains in the protein. Finally, we report the identification of 18 apparently nonfunctional OFD1 copies, organized in repeat units on the human Y chromosome. These degenerate OFD1-Y genes probably derived from the ancestral Y homologue of the X-linked gene. The high level of sequence identity among the different units suggests that duplication events have recently occurred during evolution.     

Arf1 GTPase plays roles in the protein traffic between the endoplasmic reticulum and the Golgi apparatus in tobacco and Arabidopsis cultured cells

Arf GTPases are known to be key regulators of vesicle budding in various steps of membrane traffic in yeast and animal cells. We cloned the Arabidopsis Arf1 homologue, AtArf1, and examined its function. AtArf1 complements yeast arf1 arf2 mutants and its GFP-fusion is localized to the Golgi apparatus in plant cells like its animal counterpart. The expression of dominant negative mutants of AtArf1 in tobacco and Arabidopsis cultured cells affected the localization of co-expressed GFP-tagged proteins in a variety of ways. AtArf1 Q71L and AtArf1 T31N, GTP- and GDP-fixed mutants, respectively, changed the localization of a cis-Golgi marker, AtErd2-GFP, from the Golgi apparatus to the endoplasmic reticulum but not that of GFP-AtRer1B or GFP-AtSed5. GFP-AtRer1B and GFP-AtSed5 were accumulated in aberrant structures of the Golgi by AtArf1 Q71L. A soluble vacuolar protein, sporamin-GFP, was also located to the ER by AtArf1 Q71L. These results indicate that AtArf1 play roles in the vesicular transport between the ER and the Golgi and in the maintenance of the normal Golgi organization in plant cells.     

汀棠湖轮虫主要食性功能群及其优势种群的周年动态对水环境变化的响应

为探讨轻度富营养湖泊中轮虫主要食性功能群及其优势种群的动态对水环境响应的生态机理,于2011年7月至2012年6月每月4次采集了芜湖市汀棠湖水体中的浮游动物样品,同步测定了水温、水体透明度、p H值、水体叶绿素a含量和氮磷含量,利用相关分析和多元线性回归分析方法分析了轮虫主要食性功能群及其优势种群的密度与非生物因子(如水温等)、食物资源(以粒径大小不同的藻类中的叶绿素a含量作为指标)及生物因子(枝角类、桡足类和晶囊轮虫等轮虫潜在竞争者和捕食者的密度)间的关系。结果显示:(1)汀棠湖中,掠食性轮虫的优势轮虫为针簇多肢轮虫(Polyarthra trigla);滤食性轮虫的优势种包括裂足臂尾轮虫(Brachionus diversicornis)、长三肢轮虫(Filinia longiseta)和裂痕龟纹轮虫(Anuraeopsis fissa);(2)主成分分析表明,水温、叶绿素a含量、枝角类、桡足类及其无节幼体和晶囊轮虫的密度是影响与汀塘湖轮虫群落结构有关的变动最大的水环境因子。水温和藻类叶绿素a总含量分别对滤食性轮虫和掠食性轮虫总密度的周年变动的影响最大,而轮虫的潜在竞争者和捕食者对它们的负面影响均不大;(3)轮虫的潜在竞争者和捕食者对于轮虫优势种群密度动态的负面影响也不大。水温、藻类叶绿素a总含量及小型藻类叶绿素a含量(经孔径为25μm的筛绢过滤后水样中的叶绿素a含量(Chl-a25μm))均与滤食性裂足臂尾轮虫和长三肢轮虫的密度间呈现显著或极显著的正相关关系。仅小型藻类的叶绿素a含量对裂足臂尾轮虫和长三肢轮虫密度的周年变动的影响最大。水温是影响滤食性裂痕龟纹轮虫密度动态的主要因子;(4)两食性功能群中的优势轮虫种群的卵率均未与其潜在竞争者和捕食者密度间呈现显著的负相关性。裂足臂尾轮虫、长三肢轮虫和针簇多肢轮虫种群卵率的变动受水温的影响最大,且它们之间均分别呈现显著的负相关性。研究结果表明,水温和食物资源可能是影响汀塘湖中滤食性轮虫和掠食性轮虫密度变动的重要的生态因子。     

Notch signaling and Notch signaling modifiers

Originally discovered nearly a century ago, the Notch signaling pathway is critical for virtually all developmental programs and modulates an astounding variety of pathogenic processes. The DSL (Delta, Serrate, LAG-2 family) proteins have long been considered canonical activators of the core Notch pathway. More recently, a wide and expanding network of non-canonical extracellular factors has also been shown to modulate Notch signaling, conferring newly appreciated complexity to this evolutionarily conserved signal transduction system. Here, I review current concepts in Notch signaling, with a focus on work from the last decade elucidating novel extracellular proteins that up- or down-regulate signal potency.     

Systemic amyloidosis in transgenic mice carrying the human mutant transthyretin (Met 30) gene

To analyze the pathologic processes of amyloid deposition in type I familial amyloidotic polyneuropathy (FAP), mice were made transgenic by introducing the human mutant transthyretin (TTR) gene(MT-hMet 30). An inbred strain of mouse, C57 BL/6, was chosen. Transgenic mice were killed using ether anesthesia at 3-mo intervals up to 24 mo after birth. In these transgenic mice, amyloid deposition started in the gastrointestinal tract, cardiovascular system, and kidneys and extended to various other organs and tissues with advancing age. The pattern of amyloid deposition was similar to that observed in human autopsy cases of FAP, except for its absence in the choroid plexus and in the peripheral and autonomic nervous systems. We extracted the amyloid fibrils from kidneys of these mice with a human mutant TTR gene and analyzed them immunochemically and electronmicroscopically. Deposited amyloid was shown to be composed of human mutant TTR and mouse serum amyloid P component. Amyloid fibril from transgenic mice was morphologically and immunohistochemically similar to that of human FAP. The most striking pathologic feature of the transgenic mice was the absence of amyloid deposition in the peripheral and autonomic nervous tissues. Thus, other intrinsic factors may be involved in amyloid deposition in the nervous tissues of human FAP.     

A novel variant in DMXL2 gene is associated with autosomal dominant non-syndromic hearing impairment (DFNA71) in a Cameroonian family

Approximately half of congenital hearing impairment cases are inherited, with non-syndromic hearing impairment (NSHI) being the most frequent clinical entity of genetic hearing impairment cases. A family from Cameroon with NSHI was investigated by performing exome sequencing using DNA samples obtained from three family members, followed by direct Sanger sequencing in additional family members and controls participants. We identified an autosomal dominantly inherited novel missense variant [NM_001174116.2:c.918G>T; p.(Q306H)] in DMXL2 gene (MIM:612186) that co-segregates with mild to profound non-syndromic sensorineural hearing impairment . The p.(Q306H) variant which substitutes a highly conserved glutamine residue is predicted deleterious by various bioinformatics tools and is absent from several genome databases. This variant was also neither found in 121 apparently healthy controls without a family history of hearing impairment , nor 112 sporadic NSHI cases from Cameroon. There is one previous report of a large Han Chinese NSHI family that segregates a missense variant in DMXL2. The present study provides additional evidence that DMXL2 is involved in hearing impairment etiology, and we suggest DMXL2 should be considered in diagnostic hearing impairment panels.     

伏牛山森林生态系统灌木植物功能群分类

伏牛山国家级自然保护区位于中国东部亚热带和暖温带的过渡区,植被优势种明显,以灌木优势种为主体进行植物功能群分类,可以对森林生态系统的功能、框架结构及类群分布有一个明确的认识.采用群落生态学的调查方法,在伏牛山南北坡设置66个典型样方.根据调查结果,通过计算重要值,选取优势度相对较大的灌木树种进行种间联结及相关性分析,以X2(卡方)检验为基础,结合联结系数AC和共同出现百分率PC来测定灌木优势种间的联结性,根据优势种间的联结性及其在海拔梯度上的变化异同来划分植物功能群,把灌木优势种划分为7组植物功能群.植物功能群间物种表现出显著正联结,一起在同一生境中出现的几率较大,在长期的生长演化过程中,能适应相似的资源环境和对干扰有相似的响应,所以将其划分同一组植物功能群.植物功能群内有一些重要的形态特征有相似之处,功能群间的形态特征有明显的区别,如叶片的大小、形状等,功能群的这些相似及区别还需要生理生态学的进一步研究.