Effect of the early social environment on behavioural and genomic responses to a social challenge in a cooperatively breeding vertebrate

The early social environment can have substantial, lifelong effects on vertebrate social behaviour, which can be mediated by developmental plasticity of brain gene expression. Early‐life effects can influence immediate behavioural responses towards later‐life social challenges and can activate different gene expression responses. However, while genomic responses to social challenges have been reported frequently, how developmental experience influences the shape of these genomic reaction norms remains largely unexplored. We tested how manipulating the early social environment of juvenile cooperatively breeding cichlids, Neolamprologus pulcher, affects their behavioural and brain genomic responses when competing over a resource. Juveniles were reared either with or without a breeder pair and a helper. Fish reared with family members behaved more appropriately in the competition than when reared without. We investigated whether the different social rearing environments also affected the genomic responses to the social challenge. A set of candidate genes, coding for hormones and receptors influencing social behaviour, were measured in the telencephalon and hypothalamus. Social environment and social challenge both influenced gene expression of egr‐1 (early growth response 1) and gr1 (glucocorticoid receptor 1) in the telencephalon and of bdnf (brain‐derived neurotrophic factor) in the hypothalamus. A global analysis of the 11 expression patterns in the two brain areas showed that neurogenomic states diverged more strongly between intruder fish and control fish when they had been reared in a natural social setting. Our results show that same molecular pathways may be used differently in response to a social challenge depending on early‐life experiences.     

Mapping of homoeologous chromosome exchanges influencing quantitative trait variation in Brassica napus

Genomic rearrangements arising during polyploidization are an important source of genetic and phenotypic variation in the recent allopolyploid crop Brassica napus. Exchanges among homoeologous chromosomes, due to interhomoeologue pairing, and deletions without compensating homoeologous duplications are observed in both natural B. napus and synthetic B. napus. Rearrangements of large or small chromosome segments induce gene copy number variation (CNV) and can potentially cause phenotypic changes. Unfortunately, complex genome restructuring is difficult to deal with in linkage mapping studies. Here, we demonstrate how high‐density genetic mapping with codominant, physically anchored SNP markers can detect segmental homoeologous exchanges (HE) as well as deletions and accurately link these to QTL. We validated rearrangements detected in genetic mapping data by whole‐genome resequencing of parental lines along with cytogenetic analysis using fluorescence in situ hybridization with bacterial artificial chromosome probes (BAC‐FISH) coupled with PCR using primers specific to the rearranged region. Using a well‐known QTL region influencing seed quality traits as an example, we confirmed that HE underlies the trait variation in a DH population involving a synthetic B. napus trait donor, and succeeded in narrowing the QTL to a small defined interval that enables delineation of key candidate genes.     

鸡贫血病毒哈尔滨分离株全基因克隆和序列分析

通过PCR方法克隆了从哈尔滨分离的一株鸡贫血病毒(CAV)的全基因,并对其进行了测序,该病毒基因组为环状,全长2298bp,含有三个互相重叠的开放读码框和一个调控区。将克隆的基因与GenBank收录的CAV基因比较,同源性至少为97%,未发现与本次克隆的CAV基因完全一致的分离株。与德国分离株Cuxla、26p4和马来西亚分离株分别有42、42和72个核苷酸不同,同源性分别为98.2%、98.2%和96.9%。与德国分离株Cux1b相比,除在调控区内少一个类似增强子的重复序列外,尚有39处核苷酸不同。它与分离于欧洲的几株CAV的亲源性要比来自亚洲的马来西亚株近。对CAV哈尔滨分离株、26p4、Cux1b、Cux1a和马来西亚株的VP1、VP2和VP3蛋白比较,VP2的保守性最高。     

Automated docking to multiple target structures: incorporation of protein mobility and structural water heterogeneity in AutoDock.

Protein motion and heterogeneity of structural waters are approximated in ligand-docking simulations, using an ensemble of protein structures. Four methods of combining multiple target structures within a single grid-based lookup table of interaction energies are tested. The method is evaluated using complexes of 21 peptidomimetic inhibitors with human immunodeficiency virus type 1 (HIV-1) protease. Several of these structures show motion of an arginine residue, which is essential for binding of large inhibitors. A structural water is also present in 20 of the structures, but it must be absent in the remaining one for proper binding. Mean and minimum methods perform poorly, but two weighted average methods permit consistent and accurate ligand docking, using a single grid representation of the target protein structures.     

Correlation of Local Changes in the Temperature-Dependent Conformational Flexibility of Thioredoxins with Their Thermostability

For the development of a method capable of predicting single point mutations substantially affecting protein thermostability, we studied the effect of the E85R and R82E mutations on the thermostability of thioredoxins from Escherichia coli (Trx) andBacillus acidocaldarius (BacTrx), respectively. The basic method of investigation was the molecular dynamics simulation of 3D protein models in an explicit solvent at different temperatures (300 and 373 K). Some thermolabile regions in Trx, BacTrx, and their mutants were revealed by analyzing the temperature effect on the molecular dynamics of the protein molecule. The effect of single point mutations on the temperature changes of the protein conformation flexibility in several thermolabile regions was found. The results of the simulations are in accord with experimental data indicating that the mutation E85R increases Trx thermostability, whereas the mutation R82E decreases BacTrx thermostability. The thermostability of these proteins was revealed to depend on ionic interactions between the thermolabile regions. The single point mutations change the parameters of these interactions and make them more favorable in the E85R-Trx mutant and less favorable in the R82E-BacTrx mutant.     

32株SARS冠状病毒基因组比对在PCR检测中的应用

进行了32株SARS冠状病毒基因组的多序列比对分析.所得无根进化树揭示SARS冠状病毒之间的同源性.同时,验证了所设计的PCR检测引物对全部32株SARS冠状病毒检测的适用性.     

Deciphering apicoplast targeting signals – feature extraction from nuclear-encoded precursors of Plasmodium falciparum apicoplast proteins

The malaria causing protozoan Plasmodium falciparum contains a vestigal, non-photosynthetic plastid, the apicoplast. Numerous proteins encoded by nuclear genes are targeted to the apicoplast courtesy of N-terminal extensions. With the impending sequence completion of an entire genome of the malaria parasite, it is important to have software tools in place for prediction of subcellular locations for all proteins. Apicoplast targeting signals are bipartite; containing a signal peptide and a transit peptide. Nuclear-encoded apicoplast protein precursors were analyzed for characteristic features by statistical methods, principal component analysis, self-organizing maps, and supervised neural networks. The transit peptide contains a net positive charge and is rich in asparagine, lysine, and isoleucine residues. A novel prediction system (PATS, predict apicoplast-targeted sequences) was developed based on various sequence features, yielding a Matthews correlation coefficient of 0.91 (97% correct predictions) in a 40-fold cross-validation study. This system predicted 22% apicoplast proteins of the 205 potential proteins on P. falciparum chromosome 2, and 21% of 243 chromosome 3 proteins. A combination of the PATS results with a signal peptide prediction yields 15% potentially nuclear-encoded apicoplast proteins on chromosomes 2 and 3. The prediction tool will advance P. falciparum genome analysis, and it might help to identify apicoplast proteins as drug targets for the development of novel anti-malaria agents.     

The Comparative Genomics of Polyglutamine Repeats: Extreme Difference in the Codon Organization of Repeat-Encoding Regions Between Mammals and Drosophila

Polyglutamine repeats within proteins are common in eukaryotes and are associated with neurological diseases in humans. Many are encoded by tandem repeats of the codon CAG that are likely to mutate primarily by replication slippage. However, a recent study in the yeast Saccharomyces cerevisiae has indicated that many others are encoded by mixtures of CAG and CAA which are less likely to undergo slippage. Here we attempt to estimate the proportions of polyglutamine repeats encoded by slippage-prone structures in species currently the subject of genome sequencing projects. We find a general excess over random expectation of polyglutamine repeats encoded by tandem repeats of codons. We nevertheless find many repeats encoded by nontandem codon structures. Mammals and Drosophila display extreme opposite patterns. Drosophila contains many proteins with polyglutamine tracts but these are generally encoded by interrupted structures. These structures may have been selected to be resistant to slippage. In contrast, mammals (humans and mice) have a high proportion of proteins in which repeats are encoded by tandem codon structures. In humans, these include most of the triplet expansion disease genes. Received: 17 August 2000 / Accepted: 20 November 2000