Evidence of potential hybridization in the Thaumetopoea pityocampa‐wilkinsoni complex

相似文献   

Conjugation in Tetrahymena thermophila: A temporal analysis of cytological stages

The time course and synchrony of the stages of conjugation in Tetrahymena thermophila as defined by cytologically observable changes in the morphology and position of the nuclei were established. The time required for 50% of the pairs to enter or pass a particular stage, as well as the duration of each stage were determined. The relative synchrony of the pairs as they went through conjugation was followed by correlating the maximum percentage of the population found in a stage with the duration of that stage. The degree of synchrony between the pairs was found to be high under the conditions of this study, with very little decrease in synchrony seen during the initial 9 h of conjugation. Although some variability in the degree of synchrony was seen between different matings, there was little change detected in the duration of each cytological stage. Prolonged starvation of the cells prior to their mating resulted in a gradual loss of synchrony.     

Microassay of inorganic sulfate in biological fluids by controlled flow anion chromatography

The application of controlled flow anion chromatography to the assay of inorganic sulfate in biological fluids is described. The sulfate anion is separated from other anions by ion-exchange chromatography and quantitated conductimetrically. Coefficient of variance is 3.4%, about half that for the barium precipitation assay. Interference from heparin in plasma samples and unknown sources in tissue extract analysis is avoided. Sulfate levels in plasma are not different from those measured in serum after protein precipitation. Normal levels for sulfate concentration in human plasma, cerebrospinal fluid and hepatic tissue extract are reported.     

Theoretical foundations for quantitative paleogenetics

Summary REH theory is extended by deriving the theoretical equations that permit one to analyze the nonrandom molecular divergence of homologous genes and proteins. The nonrandomicities considered are amino acid and base composition, the frequencies with which each of the four nucleotides is replaced by one of the other three, unequal usage of degenerate codons, distribution of fixed base replacements at the three nucleotide positions within codons, and distributions of fixed base replacements among codons. The latter two distributions turn out to dominate the accuracy of genetic distance estimates. The negative binomial density is used to allow for the unequal mutability of different codon sites, and the implications of its two limiting forms, the Poisson and geometric distributions, are considered. It is shown that the fixation intensity — the average number of base replacements per variable codon - is expressible as the simple product of two factors, the first describing the asymmetry of the distribution of base replacements over the gene and the second defining the ratio of the average probability that a codon will fix a mutation to the probability that it will not. Tables are given relating these features to experimentally observable quantities in hemoglobin, hemoglobin, myoglobin, cytochromec, and the parvalbumin group of proteins and to the structure of their corre-sponding genes or mRNAs. The principal results are (1) more accurate methods of estimating parameters of evolutionary interest from experimental gene and protein sequence data, and (2) the fact that change in gene and protein structure has been a much less efficient process than previously believed in the sense of requiring many more base replacements to effect a given structural change than earlier estimation procedures had indicated. This inefficiency is directly traceable to Darwinian selection for the nonrandom gene or protein structures necessary for biological function. The application of these methods is illustrated by detailed consideration of the rabbit -and hemoglobin mRNAs and the proteins for which they code. It is found that these two genes are separated by about 425 fixed base replacements, which is a factor of two greater than earlier estimates. The replacements are distributed over approximately 114 codon sites that were free to accept base mutations during the divergence of these two genes.     

Shaping the genome--restriction-modification systems as mobile genetic elements

A restriction enzyme gene is often linked to a modification methylase gene the role of which is to protect a recognition site on DNA from breakage by the former. Loss of some restriction-modification gene complexes leads to cell death through restriction breakage in the genome. Their behavior as genomic parasites/symbionts may explain the distribution of restriction sites and clarify certain aspects of bacterial recombination repair and mutagenesis. A comparison of bacterial genomes supports the hypothesis that restriction-modification gene complexes are mobile elements involved in various genome rearrangements and evolution.     

Genetically-encoded Molecular Probes to Study G Protein-coupled Receptors

To facilitate structural and dynamic studies of G protein-coupled receptor (GPCR) signaling complexes, new approaches are required to introduce informative probes or labels into expressed receptors that do not perturb receptor function. We used amber codon suppression technology to genetically-encode the unnatural amino acid, p-azido-L-phenylalanine (azF) at various targeted positions in GPCRs heterologously expressed in mammalian cells. The versatility of the azido group is illustrated here in different applications to study GPCRs in their native cellular environment or under detergent solubilized conditions. First, we demonstrate a cell-based targeted photocrosslinking technology to identify the residues in the ligand-binding pocket of GPCR where a tritium-labeled small-molecule ligand is crosslinked to a genetically-encoded azido amino acid. We then demonstrate site-specific modification of GPCRs by the bioorthogonal Staudinger-Bertozzi ligation reaction that targets the azido group using phosphine derivatives. We discuss a general strategy for targeted peptide-epitope tagging of expressed membrane proteins in-culture and its detection using a whole-cell-based ELISA approach. Finally, we show that azF-GPCRs can be selectively tagged with fluorescent probes. The methodologies discussed are general, in that they can in principle be applied to any amino acid position in any expressed GPCR to interrogate active signaling complexes.     

Studying Interactions of Staphylococcus aureus with Neutrophils by Flow Cytometry and Time Lapse Microscopy

We present methods to study the effect of phenol soluble modulins (PSMs) and other toxins produced and secreted by Staphylococcus aureus on neutrophils. To study the effects of the PSMs on neutrophils we isolate fresh neutrophils using density gradient centrifugation. These neutrophils are loaded with a dye that fluoresces upon calcium mobilization. The activation of neutrophils by PSMs initiates a rapid and transient increase in the free intracellular calcium concentration. In a flow cytometry experiment this rapid mobilization can be measured by monitoring the fluorescence of a pre-loaded dye that reacts to the increased concentration of free Ca²⁺. Using this method we can determine the PSM concentration necessary to activate the neutrophil, and measure the effects of specific and general inhibitors of the neutrophil activation.To investigate the expression of the PSMs in the intracellular space, we have constructed reporter fusions of the promoter of the PSMα operon to GFP. When these reporter strains of S. aureus are phagocytosed by neutrophils, the induction of expression can be observed using fluorescence microscopy.     

人类混血群体连锁不平衡的遗传学模型与基因定位

人类混血群体可以说是混合群体的一种特例．在无选择、无突变、无限随机交配群体的假定前提下,研究了亲本群体的基因频率对混血群体及其衍生后代群体连锁不平衡结构的影响,导出了各群体连锁不平衡值的表达式,建立了一个估计基因间重组率的简便方法;同时, 采用估算分子标记与QTL之间连锁不平衡系数的统计分析方法,分析了人类混血群体及其衍生后代群体QTL检测与估计的关系,建立了该关系的系列理论公式．研究结果表明,本方法不仅适用于人类疾病(包括复杂遗传疾病)基因定位,而且适合于人类正常基因的定位,同时也适用于人类普通多基因性状的QTL分析．     

Immunity Genes and Susceptibility to Otitis Media: A Comprehensive Review

Otitis media (OM) is a middle ear infection associated with inflammation and pain. This disease frequently afflicts humans and is the major cause of hearing loss worldwide. OM continues to be one of the most challenging diseases in the medical field due to its diverse host targets and wide range of clinical manifestations. Substantial morbidity associated with OM is further exacerbated by high frequency of recurrent infections leading to chronic suppurative otitis media (CSOM). Children have greater susceptibility to, and thus, suffer most frequently from OM, which can cause significant deterioration in quality of life. Genetic factors have been demonstrated, in large part by twin and family studies, to be key determinants of OM susceptibility. In this review, we summarize the current knowledge on immunity genes and selected variants that have been associated with predisposition to OM. In particular, polymorphisms in innate immunity and cytokine genes have been strongly linked with the risk of developing OM. Future studies employing state-of-the-art technologies, including next-generation sequencing (NGS), will aid in the identification of novel genes associated with susceptibility to OM. This, in turn, will open up avenues for identifying high-risk individuals and designing novel therapeutic strategies based on precise targeting of these genes.