褐飞虱不同地理种群生物学特性的比较

在实验条件下比较了四个(龙州、九宫山、监利、新会)褐飞虱Nilaparvata lugens(Stal)地理种群的发育、繁殖、内禀增长能力等参数的异同。结果表明：1.北迁的迁入当代九宫山种群雌虫降落取食3.6d开始产卵,产卵量平均为522粒,低于其第二代居留型种群的714粒;2.四个种群在若虫l龄、5龄历期上有显著差异(a＝0.05).但决定翅型分化的2、3、4龄历期上无显著差异;成虫寿命、产卵历期无显著差异;新会种群产卵量高于其它三个种群;同龄期若虫的世代存活率,九宫山种群低于其它三个种群;综合反映发育、存活、繁殖等生命信息的内禀增长能力rm差异较小,在0.1874～0.1982间变化。本文还分析了产生上述异同的原因。     

慢性缺氧对大鼠左右心室功能、心肌肌原纤维Ca~（2＋），Mg~（2＋）－ATP

模拟５０００ｍ中度缺氧时,大鼠右室功能显著加强,而左室功能加强不显著;左右心室肌原纤维Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶活性下降,肌球蛋白同功酶Ｖ２和Ｖ３百分含量增加,Ｖ１百分含量减少。８０００ｍ重度缺氧时,右室功能减弱,但无统计学意义,左室功能减弱有显著性;ＡＴＰ酶活性和同功酶的变化超过５０００ｍ组。此外,右室ＡＴＰ酶活性与ＰＡＰ呈反比且有显著性,左室ＡＴＰ酶活性与ＣＡＳＰ虽也呈反比但无显著性;右室同功酶Ｖ３百分含量与ＰＡＰ呈正比,左室同功酶Ｖ３百分含量与ＣＡＳＰ不呈比例。上述结果表明,因短期突发严重缺氧引起的心肌供氧不足对左心室心肌的直接损伤作用大于右心室心肌。     

Synthesis,Stability and Direct Antiproliferative Effect of New Cysteine Modified GnRH Analogs

International Journal of Peptide Research and Therapeutics - It is demonstrated that gonadotropin-releasing hormone (GnRH) analogs can directly inhibit the proliferation of reproductive tissue...     

Role of the sonchus yellow net virus N protein in formation of nuclear viroplasms

Sonchus yellow net virus is a plant nucleorhabdovirus whose nucleocapsid (N), phosphoprotein (P), and polymerase (L) proteins form large viroplasms in the nuclei of infected plants (C. R. F. Martins, J. A. Johnson, D. M. Lawrence, T. J. Choi, A. Pisi, S. L. Tobin, D. Lapidus, J. D. O. Wagner, S. Ruzin, K. McDonald, and A. O. Jackson, J. Virol. 72:5669-5679, 1998). When expressed alone, the N protein localizes to the nuclei of plant and yeast (Saccharomyces cerevisiae) cells and the P protein is distributed throughout the cells, but coexpression of N and P results in formation of subnuclear viroplasm-like foci (M. M. Goodin, J. Austin, R. Tobias, M. Fujita, C. Morales, and A. O. Jackson, J. Virol. 75:9393-9406, 2001; M. M. Goodin, R. G. Dietzgen, D. Schichnes, S. Ruzin, and A. O. Jackson, Plant J. 31:375-383, 2002). We now show that the N protein and various fluorescent derivatives form similar subnuclear foci in plant cells and that homologous interactions mediated by a helix-loop-helix region near the amino terminus are required for formation of the foci. Mutations within the helix-loop-helix region also interfere with N- and P-protein interactions that are required for N and P colocalization in the subnuclear foci. Affinity purification of N proteins harboring single mutations within the motif revealed that Tyr40 is critical for N-N and N-P interactions. Additional in vitro binding assays also indicated that the N protein binds to yeast and plant importin alpha homologues, whereas mutations in the carboxy-terminal nuclear localization signal abrogate importin alpha binding. The P protein did not bind to the importin alpha homologues, suggesting that the N and P proteins use different pathways for nuclear entry. Our results in toto support a model suggesting that during infection, the N and P proteins enter the nucleus independently, that viroplasm formation requires homologous N-protein interactions, and that P protein targeting to the viroplasm requires N-P protein interactions that occur after N and P protein import into the nucleus.     

Two-component sensor RhpS promotes induction of Pseudomonas syringae type III secretion system by repressing negative regulator RhpR

The Pseudomonas syringae type III secretion system (T3SS) is induced during interaction with the plant or culture in minimal medium (MM). How the bacterium senses these environments to activate the T3SS is poorly understood. Here, we report the identification of a novel two-component system (TCS), RhpRS, that regulates the induction of P. syringae T3SS genes. The rhpR and rhpS genes are organized in an operon with rhpR encoding a putative TCS response regulator and rhpS encoding a putative biphasic sensor kinase. Transposon insertion in rhpS severely reduced the induction of P. syringae T3SS genes in the plant as well as in MM and significantly compromised the pathogenicity on host plants and hypersensitive response-inducing activity on nonhost plants. However, deletion of the rhpRS locus allowed the induction of T3SS genes to the same level as in the wild-type strain and the recovery of pathogenicity upon infiltration into plants. Overexpression of RhpR in the deltarhpRS deletion strain abolished the induction of T3SS genes. However, overexpression of RhpR in the wild-type strain or overexpression of RhpR(D70A), a mutant of the predicted phosphorylation site of RhpR, in the deltarhpRS deletion strain only slightly reduced the induction of T3SS genes. Based on these results, we propose that the phosphorylated RhpR represses the induction of T3SS genes and that RhpS reverses phosphorylation of RhpR under the T3SS-inducing conditions. Epistasis analysis indicated that rhpS and rhpR act upstream of hrpR to regulate T3SS genes.     

Binding of the Heterogeneous Ribonucleoprotein K (hnRNP K) to the Epstein-Barr Virus Nuclear Antigen 2 (EBNA2) Enhances Viral LMP2A Expression

The Epstein-Barr Virus (EBV) -encoded EBNA2 protein, which is essential for the in vitro transformation of B-lymphocytes, interferes with cellular processes by binding to proteins via conserved sequence motifs. Its Arginine-Glycine (RG) repeat element contains either symmetrically or asymmetrically di-methylated arginine residues (SDMA and ADMA, respectively). EBNA2 binds via its SDMA-modified RG-repeat to the survival motor neurons protein (SMN) and via the ADMA-RG-repeat to the NP9 protein of the human endogenous retrovirus K (HERV-K (HML-2) Type 1). The hypothesis of this work was that the methylated RG-repeat mimics an epitope shared with cellular proteins that is used for interaction with target structures. With monoclonal antibodies against the modified RG-repeat, we indeed identified cellular homologues that apparently have the same surface structure as methylated EBNA2. With the SDMA-specific antibodies, we precipitated the Sm protein D3 (SmD3) which, like EBNA2, binds via its SDMA-modified RG-repeat to SMN. With the ADMA-specific antibodies, we precipitated the heterogeneous ribonucleoprotein K (hnRNP K). Specific binding of the ADMA- antibody to hnRNP K was demonstrated using E. coli expressed/ADMA-methylated hnRNP K. In addition, we show that EBNA2 and hnRNP K form a complex in EBV- infected B-cells. Finally, hnRNP K, when co-expressed with EBNA2, strongly enhances viral latent membrane protein 2A (LMP2A) expression by an unknown mechanism as we did not detect a direct association of hnRNP K with DNA-bound EBNA2 in gel shift experiments. Our data support the notion that the methylated surface of EBNA2 mimics the surface structure of cellular proteins to interfere with or co-opt their functional properties.     

A Bayesian Analysis for Identifying DNA Copy Number Variations Using a Compound Poisson Process

To study chromosomal aberrations that may lead to cancer formation or genetic diseases, the array-based Comparative Genomic Hybridization (aCGH) technique is often used for detecting DNA copy number variants (CNVs). Various methods have been developed for gaining CNVs information based on aCGH data. However, most of these methods make use of the log-intensity ratios in aCGH data without taking advantage of other information such as the DNA probe (e.g., biomarker) positions/distances contained in the data. Motivated by the specific features of aCGH data, we developed a novel method that takes into account the estimation of a change point or locus of the CNV in aCGH data with its associated biomarker position on the chromosome using a compound Poisson process. We used a Bayesian approach to derive the posterior probability for the estimation of the CNV locus. To detect loci of multiple CNVs in the data, a sliding window process combined with our derived Bayesian posterior probability was proposed. To evaluate the performance of the method in the estimation of the CNV locus, we first performed simulation studies. Finally, we applied our approach to real data from aCGH experiments, demonstrating its applicability.     

Identification of quantitative trait loci for shank length and growth at different development stages in chicken

Shank length affects chicken leg health and longer shanks are a source of leg problems in heavy-bodied chickens. Identification of quantitative trait loci (QTL) affecting shank length traits may be of value to genetic improvement of these traits in chickens. A genome scan was conducted on 238 F₂ chickens from a reciprocal cross between the Silky Fowl and the White Plymouth Rock breeds using 125 microsatellite markers to detect static and developmental QTL affecting weekly shank length and growth (from 1 to 12 weeks) in chickens. Static QTL affected shank length from birth to time t , while developmental QTL affected shank growth from time t− 1 to time t . Seven static QTL on six chromosomes (GGA2, GGA3, GGA4, GGA7, GGA9 and GGA23) were detected at ages of 2, 3, 4, 5, 6, 7, 9 and 12 weeks, and six developmental QTL on five chromosomes (GGA1, GGA2, GGA4, GGA5 and GGA23) were detected for five shank growth periods, weeks 2–3, 4–5, 5–6, 10–11 and 11–12. A static QTL and a developmental QTL ( SQSL1 and DQSL2 ) were identified at GGA2 (between ADL0190 and ADL0152 ). SQSL1 explained 2.87–5.30% of the phenotypic variation in shank length from 3 to 7 weeks. DQSL2 explained 2.70% of the phenotypic variance of shank growth between 2 and 3 weeks. Two static and two developmental QTL were involved chromosome 4 and chromosome 23. Two chromosomes (GGA7 and GGA9) had static QTL but no developmental QTL and another two chromosomes (GGA1 and GGA5) had developmental QTL but no static QTL. The results of this study show that shank length and shank growth at different developmental stages involve different QTL.