Gene duplication and deletion, not horizontal transfer, drove intra-species mosaicism of Bartonella henselae

Bartonella henselae is a facultative intracellular pathogen that occurs worldwide and is responsible primarily for cat-scratch disease in young people and bacillary angiomatosis in immunocompromised patients. The principal source of genome-level diversity that contributes to B. henselae\u27s host-adaptive features is thought to be horizontal gene transfer events. However, our analyses did not reveal the acquisition of horizontally-transferred islands in B. henselae after its divergence from other Bartonella. Rather, diversity in gene content and genome size was apparently acquired through two alternative mechanisms, including deletion and, more predominantly, duplication of genes. Interestingly, a majority of these events occurred in regions that were horizontally transferred long before B. henselae\u27s divergence from other Bartonella species. Our study indicates the possibility that gene duplication, in response to positive selection pressures in specific clones of B. henselae, might be linked to the pathogen\u27s adaptation to arthropod vectors, the cat reservoir, or humans as incidental host-species

HIV Progression Depends on Codon and Amino Acid Usage Profile of Envelope Protein and Associated Host-Genetic Influence

Acquired immune deficiency syndrome (AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV). Two types of HIV have been characterized: HIV-1 and HIV-2. The present study investigated whether evolutionary selection pressure differs between rapid progressor (RP), slow progressor (SP), and long-term non-progressor (LTNP) of HIV-I infected individuals. An unexpected association between the evolutionary rate of substitution in envelope (env) gene and disease progression is observed. Our present study suggests that env genes of LTNP are subject to unusually strong functional constraint with respect to RP. We also observed that the three categories of env genes i.e., RP, SP, and LTNP, had their own characteristic pattern of amino acid usage and SP and LTNP sequences shared similar patterns of amino acid usage different from RP sequences and evolutionary rate significantly influenced the amino acid usage pattern of the three different types of env gene sequences. It was also noted that the evolutionary rate for the glycosylation sites of LTNP and SP sequences were even significantly less than the RP sequences. Comparative analysis on the influence of human host on the three categories of env genes are well correlated with the rates of disease progression suggesting the adaptive strategies of the viruses for successful residence and infection. Host associated selective constraints appeared most relaxed on the RP sequences and strongest in LTNP sequences. The present study clearly portrays how evolutionary selection pressure differs between three categories of env genes i.e., RP, SP, and LTNP. The env genes, coding for the env glycoproteins, experience severe selection constraints from the host due to their constant exposure to the host immune system. In this perspective it might be suggested that env gene evolution occurs mainly by negative selection with the occurrence of mutation that might not reach fixation in the viral population. This work also confers a deeper insight into the crucial effects of host factors that govern the overall progression of HIV infection

Interactions between hematological derivatives and dipalmitoyl phosphatidyl choline: implications for adult respiratory distress syndrome

Blood and its components flood the alveoli in adult respiratory distress syndrome (ARDS) and may be responsible for the inhibition of lung surfactant in this syndrome. We have evaluated the surface properties of dipalmitoyl phosphatidylcholine (DPPC) monolayers - the main component of lung surfactant, in the presence of blood and its components. Experiments were performed using a Langmuir-Blodgett trough at physiological temperature (37°C), pH 7.0 and using 0.9% saline as the sub-phase. Whole blood (WB), membranes obtained from whole blood cells (Mem), lysed blood (LB), homogenized blood clot (CLOT), serum (SER), platelet rich plasma (PRP), platelet poor plasma (PPP) and individual plasma proteins (albumin, fibrinogen) were added to the sub-phase in the equivalent proportion of 10 parts of DPPC per million parts (w/v) of hematological inhibitor. Cell membranes were found to be the most inhibitory agent for DPPC surface activity as evidenced by an increase in the minimum surface tension (from 0.818±0.219 to 7.373±0.854mN/m) and percentage area change required to reduce the surface tension from 30 to 10mN/m (from 21.24±0.99 to 66.83±4.44). The inhibitory potential of pure plasma proteins differed from those of more complex blood derivatives like platelet rich plasma and serum. Whole blood and platelet poor plasma were non-inhibitory, but serum, platelet rich plasma and clot significantly increased the minimum surface tension of DPPC to 6.819±0.925, 6.625±2.261 and 6.060±0.640mN/m, respectively. These results were statistically significant with one-way analysis of variance and Newman-Keul's test (P<0.05). The present study suggests that, not only the presence of the individual blood component(s) in the lung alveoli but also their interactions decide their inhibitory capability. Pure plasma proteins are not representative of the inhibitory effects of blood derivatives like serum, platelet rich plasma and blood cell membranes which would be more relevant for inhibitory models of ARDS.© Elsevie

Effects of albumin and erythrocyte membranes on spread monolayers of lung surfactant lipids

Dipalmitoyl phosphatidylcholine (DPPC), one of the main constituents of lung surfactant is mainly responsible for reduction of surface tension to near 0 mN/m during expiration, resisting alveolar collapse. Other unsaturated phospholipids like palmitoyloleoyl phosphatidylglycerol (PG), palmitoyloleoyl phosphatidylcholine (POPC) and neutral lipids help in adsorption of lung surfactant to the air-aqueous interface. Lung surfactant lipids may interact with plasma proteins and hematological agents flooding the alveoli in diseased states. In this study, we evaluated the effects of albumin and erythrocyte membranes on spread films of DPPC alone and mixtures of DPPC with each of PG, POPC, palmitoyloleoyl phosphatidylethanolamine (PE), cholesterol (CHOL) and palmitic acid (PA) in 9:1 molar ratios. Surface tension-area isotherms were recorded using a Langmuir-Blodgett (LB) trough at 37 °C with 0.9% saline as the sub-phase. In the presence of erythrocyte membranes, DPPC and DPPC + PA monolayers reached minimum surface tensions of 7.3 ± 0.9 and 9.6 ± 1.4 mN/m, respectively. Other lipid combinations reached significantly higher minimum surface tensions >18 mN/m in presence of membranes (Newman Keul's test, p [(DPPC + PA) = (DPPC)]. The differential response was more pronounced in case of albumin with DPPC and DPPC + PA monolayers reaching minimum surface tensions less than 2.4 mN/m in presence of albumin, whereas DPPC + PG and DPPC + POPC reached minimum surface tensions of around 20 mN/m in presence of albumin. Descending order of susceptibility of the spread monolayers of lipid mixtures to albumin destabilization was as follows: [(DPPC + PG, 7:3) = (DPPC + PG, 9:1) = (DPPC + POPC)] > [(DPPC + PE) = (DPPC + CHOL)] > [(DPPC + PA) = (DPPC)] The increase in minimum surface tension in presence of albumin and erythrocyte membranes was accompanied by sudden increases in compressibility at surface tensions of 15-30 mN/m. This suggests a monolayer destabilization and could be indicative of phase transitions in the mixed lipid films due to the presence of the hydrophobic constituents of erythrocyte membranes.© Elsevie

Codon pair ratio

The pathway/system -wise codon pair ratio data for all the species generated using Anaconda

Data from: Deconstruction of archaeal genome depict strategic consensus in core pathways coding sequence assembly

A comprehensive in silico analysis of 71 species representing the different taxonomic classes and physiological genre of the domain Archaea was performed. These organisms differed in their physiological attributes, particularly oxygen tolerance and energy metabolism. We explored the diversity and similarity in the codon usage pattern in the genes and genomes of these organisms, emphasizing on their core cellular pathways. Our thrust was to figure out whether there is any underlying similarity in the design of core pathways within these organisms. Analyses of codon utilization pattern, construction of hierarchical linear models of codon usage, expression pattern and codon pair preference pointed to the fact that, in the archaea there is a trend towards biased use of synonymous codons in the core cellular pathways and the Nc-plots appeared to display the physiological variations present within the different species. Our analyses revealed that aerobic species of archaea possessed a larger degree of freedom in regulating expression levels than could be accounted for by codon usage bias alone. This feature might be a consequence of their enhanced metabolic activities as a result of their adaptation to the relatively O2-rich environment. Species of archaea, which are related from the taxonomical viewpoint, were found to have striking similarities in their ORF structuring pattern. In the anaerobic species of archaea, codon bias was found to be a major determinant of gene expression. We have also detected a significant difference in the codon pair usage pattern between the whole genome and the genes related to vital cellular pathways, and it was not only species-specific but pathway specific too. This hints towards the structuring of ORFs with better decoding accuracy during translation. Finally, a codon-pathway interaction in shaping the codon design of pathways was observed where the transcription pathway exhibited a significantly different coding frequency signature

Codon Count

The total codon counts for each of the 71 organsim per pathway

All 71 genomes 5 pathways

This archive contains the different codon usage indices value for all the 71 species calculated separately for each of the five pathway systems and curated individually

Distinct molecular features facilitating ice-binding mechanisms in hyperactive antifreeze proteins closely related to an Antarctic sea ice bacterium

<div><p>Antifreeze proteins or ice-binding proteins (IBPs) facilitate the survival of certain cellular organisms in freezing environment by inhibiting the growth of ice crystals in solution. Present study identifies orthologs of the IBP of <i>Colwellia</i> sp. <i>SLW05</i>, which were obtained from a wide range of taxa. Phylogenetic analysis on the basis of conserved regions (predicted as the ‘ice-binding domain’ [IBD]) present in all the orthologs, separates the bacterial and archaeal orthologs from that of the eukaryotes’. Correspondence analysis pointed out that the bacterial and archaeal IBDs have relatively higher average hydrophobicity than the eukaryotic members. IBDs belonging to bacterial as well as archaeal AFPs contain comparatively more strands, and therefore are revealed to be under higher evolutionary selection pressure. Molecular docking studies prove that the ice crystals form more stable complex with the bacterial as well as archaeal proteins than the eukaryotic orthologs. Analysis of the docked structures have traced out the ice-binding sites (IBSs) in all the orthologs which continue to facilitate ice-binding activity even after getting mutated with respect to the well-studied IBSs of <i>Typhula ishikariensis</i> and notably, all these mutations performing ice-binding using ‘anchored clathrate mechanism’ have been found to prefer polar and hydrophilic amino acids. Horizontal gene transfer studies point toward a strong selection pressure favoring independent evolution of the IBPs in some polar organisms including prokaryotes as well as eukaryotes because these proteins facilitate the polar organisms to acclimatize to the adversities in their niche, thus safeguarding their existence.</p></div