利用重组自交系群体对黄瓜侧枝相关性状进行QTL定位分析

侧枝与黄瓜(Cucumis sativus)产量有密切关系. 本实验利用侧枝长势较弱、萌发较早的华北类型品系S94和侧枝长势较强、萌发较晚的欧洲类型品系S06构建的224个F6:7家系进行黄瓜侧枝相关性状的研究. 利用已构建的重组自交系群体遗传图谱, 使用软件WinQTLCart 2.5进行复合区间定位. 在2006年秋和2007年春两季, 共检测到4个侧枝相关性状(侧枝均长LBAL、侧枝总长LBTL、侧枝数目LBN和第一侧枝节位FLBN)的36个QTL, 单个QTL的贡献率在3.1%(lbtl2.1, 春季)~32.3%(lbn2.3, 春季)之间. 结果显示, 4个不同性状的11个QTL (lbal1.1, lbtl1.1, lbn1.2, flbn1.2等)在两季中都聚集在第1连锁群e23m18d~ME23EM6c之间(7.4 cM), 并且在第2连锁群的S94A1~ME4SA4a之间(13.9 cM)也检测到了4个不同性状的15个QTL (lbal2.1, lbtl2.1, lbn2.1和flbn2.1等). 两季共有21个QTL贡献率超过10%, 其中lbn2.3的贡献率(春季32.3%, LOD=18.4)为最大, lbtl1.3(秋季26.2%, LOD=17.4; 春季26.9%, LOD=17.9)在两季的位置和贡献率都稳定. 这些基因座为将来进行QTL精细定位提供了参考, 同时利用其紧密连锁(<10 cM)的特异标记(CMBR40, F, CS30, S94A1, CSWTA11B)可进行黄瓜侧枝性状的分子标记辅助育种.     

Inbreeding and extinction: Effects of purging

Deleterious alleles may be removed (purged) bynatural selection in populations undergoinginbreeding. However, there is controversyregarding the effectiveness of purging inreducing the extinction risk due to inbreeding,particularly in conservation contexts. Weevaluated the effects of purging on theextinction risk due to inbreeding in Drosophila melanogaster using two basepopulations, an outbred population (non-purged)and four-way crosses between highly inbredlines derived from the same population(purged). The inbred lines used in the four-waycrosses were previously subjected to 20generations of full-sib mating. The impact offull-sib inbreeding over a further 12generations was compared in 200 populationsfrom each of the two base populations. Therewas a small and non-significant differencebetween the extinction rates at an inbreedingcoefficient of 0.93 in the non-purged (0.74± 0.03) and purged (0.69 ± 0.03)treatments. This is consistent with otherevidence indicating that the effects of purgingare often small. Purging using rapid inbreedingin very small populations cannot be relied uponto eliminate the deleterious effects ofinbreeding.     

Candida albicans hyphal invasion: thigmotropism or chemotropism?

Hyphae of the human pathogenic fungus Candida albicans exhibit thigmotropic behaviour in vitro, in common with phytopathogenic and saprotrophic fungi. An examination of the literature on C. albicans hyphal penetration of epithelial and endothelial membranes does not support the premise that hyphal thigmotropism plays a major role in tissue invasion. Further experimentation is now required to assess thigmotropic behaviour on host membranes and vaginal epithelial cells are suggested as a test model. It is proposed that while thigmotropism may and invasion of tissue invaginations, chemotropism can explain C. albicans hyphal invasion patterns of both endothelium and epithelium.     

Sustainable agriculture and plant diseases: an epidemiological perspective

The potential for modern biology to identify new sources for genetical, chemical and biological control of plant disease is remarkably high. Successful implementation of these methods within globally and locally changing agricultural environments demands new approaches to durable control. This, in turn, requires fusion of population genetics and epidemiology at a range of scales from the field to the landscape and even to continental deployment of control measures. It also requires an understanding of economic and social constraints that influence the deployment of control. Here I propose an epidemiological framework to model invasion, persistence and variability of epidemics that encompasses a wide range of scales and topologies through which disease spreads. By considering how to map control methods onto epidemiological parameters and variables, some new approaches towards optimizing the efficiency of control at the landscape scale are introduced. Epidemiological strategies to minimize the risks of failure of chemical and genetical control are presented and some consequences of heterogeneous selection pressures in time and space on the persistence and evolutionary changes of the pathogen population are discussed. Finally, some approaches towards embedding epidemiological models for the deployment of control in an economically plausible framework are presented.     

DNA methyltransferase homologue TRDMT1 in Plasmodium falciparum specifically methylates endogenous aspartic acid tRNA

In eukaryotes, cytosine methylation regulates diverse biological processes such as gene expression, development and maintenance of genomic integrity. However, cytosine methylation and its functions in pathogenic apicomplexan protozoans remain enigmatic. To address this, here we investigated the presence of cytosine methylation in the nucleic acids of the protozoan Plasmodium falciparum. Interestingly, P. falciparum has TRDMT1, a conserved homologue of DNA methyltransferase DNMT2. However, we found that TRDMT1 did not methylate DNA, in vitro. We demonstrate that TRDMT1 methylates cytosine in the endogenous aspartic acid tRNA of P. falciparum. Through RNA bisulfite sequencing, we mapped the position of 5-methyl cytosine in aspartic acid tRNA and found methylation only at C38 position. P. falciparum proteome has significantly higher aspartic acid content and a higher proportion of proteins with poly aspartic acid repeats than other apicomplexan pathogenic protozoans. Proteins with such repeats are functionally important, with significant roles in host-pathogen interactions. Therefore, TRDMT1 mediated C38 methylation of aspartic acid tRNA might play a critical role by translational regulation of important proteins and modulate the pathogenicity of the malarial parasite.     

SDS-stable complex formation between native apolipoprotein E3 and beta-amyloid peptides

Extracellular senile plaques composed predominantly of fibrillar amyloid-beta (Abeta) are a major neuropathological feature of Alzheimer's disease (AD). Genetic evidence and in vivo studies suggest that apolipoprotein E (apoE) may contribute to amyloid clearance and/or deposition. In vitro studies demonstrate that native apoE2 and E3 form an SDS-stable complex with Abeta(1-40), while apoE4 forms little such complex. Our current work extends these observations by presenting evidence that apoE3 also binds to Abeta(1-42) and with less avidity to modified species of the peptide found in senile plaque cores. These modified peptides include a form that originates at residue 3-Glu as pyroglutamyl and another with isomerization at the 1-Asp and 7-Asp positions. In addition, we used binding reactions between apoE3 and various Abeta fragments, as well as binding reactions with apoE3 and Abeta(1-40) plus Abeta fragments as competitors, to identify the domain(s) of Abeta involved in the formation of an SDS-stable complex with apoE3. Residues 13-28 of Abeta appear to be necessary, while complex formation is further enhanced by the presence of residues at the C-terminus of the peptide. These results contribute to our understanding of the biochemical basis for the SDS-stable apoE3/Abeta complex and support the hypothesis that Abeta can be transported in vivo complexed with apoE. This complex may then be cleared from the interstitial space by apoE receptors in the brain or become part of an extracellular amyloid deposit.