scholarly journals Role of BgaA as a Pneumococcal Virulence Factor Elucidated by Molecular Evolutionary Analysis

2020 ◽  
Vol 11 ◽  
Author(s):  
Masaya Yamaguchi ◽  
Moe Takemura ◽  
Kotaro Higashi ◽  
Kana Goto ◽  
Yujiro Hirose ◽  
...  
Keyword(s):  
Virulence Factor ◽  
Evolutionary Analysis ◽  
Molecular Evolutionary Analysis

scholarly journals The Location of Substitutions and Bacterial Genome Arrangements

2020 ◽  
Author(s):  
Daniella F Lato ◽  
G Brian Golding
Keyword(s):  
Sinorhizobium Meliloti ◽  
Bacterial Genome ◽  
Evolutionary Analysis ◽  
Origin Of Replication ◽  
Ancestral Reconstruction ◽  
Molecular Change ◽  
E Coli ◽  
A Genome ◽  
The Impact ◽  
Molecular Evolutionary Analysis

Abstract Increasing evidence supports the notion that different regions of a genome have unique rates of molecular change. This variation is particularly evident in bacterial genomes where previous studies have reported gene expression and essentiality tend to decrease, while substitution rates usually increases with increasing distance from the origin of replication. Genomic reorganization such as rearrangements occur frequently in bacteria and allow for the introduction and restructuring of genetic content, creating gradients of molecular traits along genomes. Here, we explore the interplay of these phenomena by mapping substitutions to the genomes of Escherichia coli, Bacillus subtilis, Streptomyces, and Sinorhizobium meliloti, quantifying how many substitutions have occurred at each position in the genome. Preceding work indicates that substitution rate significantly increases with distance from the origin. Using a larger sample size and accounting for genome rearrangements through ancestral reconstruction, our analysis demonstrates that the correlation between the number of substitutions and distance from the origin of replication is often significant but small and inconsistent in direction. Some replicons had a significantly decreasing trend (E. coli and the chromosome of S. meliloti), while others showed the opposite significant trend (B. subtilis, Streptomyces, pSymA and pSymB in S. meliloti). dN, dS and ω were examined across all genes and there was no significant correlation between those values and distance from the origin. This study highlights the impact that genomic rearrangements and location have on molecular trends in some bacteria, illustrating the importance of considering spatial trends in molecular evolutionary analysis. Assuming that molecular trends are exclusively in one direction can be problematic.

scholarly journals Potential Role of Phospholipases in Virulence and Fungal Pathogenesis

2000 ◽  
Vol 13 (1) ◽  
pp. 122-143 ◽  
Author(s):  
Mahmoud A. Ghannoum
Keyword(s):  
Virulence Factor ◽  
Cell Damage ◽  
Pathogenic Fungi ◽  
Microbial Pathogens ◽  
Immunogold Electron Microscopy ◽  
Lytic Enzymes ◽  
Fungal Virulence ◽  
Phospholipase B ◽  
Genes Encoding

SUMMARY Microbial pathogens use a number of genetic strategies to invade the host and cause infection. These common themes are found throughout microbial systems. Secretion of enzymes, such as phospholipase, has been proposed as one of these themes that are used by bacteria, parasites, and pathogenic fungi. The role of extracellular phospholipase as a potential virulence factor in pathogenic fungi, including Candida albicans, Cryptococcus neoformans, and Aspergillus, has gained credence recently. In this review, data implicating phospholipase as a virulence factor in C. albicans, Candida glabrata, C. neoformans, and A. fumigatus are presented. A detailed description of the molecular and biochemical approaches used to more definitively delineate the role of phospholipase in the virulence of C. albicans is also covered. These approaches resulted in cloning of three genes encoding candidal phospholipases (caPLP1, caPLB2, and PLD). By using targeted gene disruption, C. albicans null mutants that failed to secrete phospholipase B, encoded by caPLB1, were constructed. When these isogenic strain pairs were tested in two clinically relevant murine models of candidiasis, deletion of caPLB1 was shown to lead to attenuation of candidal virulence. Importantly, immunogold electron microscopy studies showed that C. albicans secretes this enzyme during the infectious process. These data indicate that phospholipase B is essential for candidal virulence. Although the mechanism(s) through which phospholipase modulates fungal virulence is still under investigations, early data suggest that direct host cell damage and lysis are the main mechanisms contributing to fungal virulence. Since the importance of phospholipases in fungal virulence is already known, the next challenge will be to utilize these lytic enzymes as therapeutic and diagnostic targets.

scholarly journals Molecular and Functional Characterization of a ToxR-Regulated Lipoprotein from a Clinical Isolate of Aeromonas hydrophila

2006 ◽  
Vol 74 (7) ◽  
pp. 3742-3755 ◽  
Author(s):  
Lakshmi Pillai ◽  
Jian Sha ◽  
Tatiana E. Erova ◽  
Amin A. Fadl ◽  
Bijay K. Khajanchi ◽  
...  
Keyword(s):  
Virulence Factor ◽  
Aeromonas Hydrophila ◽  
Functional Characterization ◽  
Affinity Column ◽  
Serum Resistance ◽  
Classical Pathway ◽  
Dependent Manner ◽  
T7 Promoter

ABSTRACT Human diseases caused by species of Aeromonas have been classified into two major groups: septicemia and gastroenteritis. In this study, we reported the molecular and functional characterization of a new virulence factor, ToxR-regulated lipoprotein, or TagA, from a diarrheal isolate, SSU, of Aeromonas hydrophila. The tagA gene of A. hydrophila exhibited 60% identity with that of a recently identified stcE gene from Escherichia coli O157:H7, which encoded a protein (StcE) that provided serum resistance to the bacterium and prevented erythrocyte lysis by controlling classical pathway of complement activation by cleaving the complement C1-esterase inhibitor (C1-INH). We purified A. hydrophila TagA as a histidine-tagged fusion protein (rTagA) from E. coli DE3 strain using a T7 promoter-based pET30 expression vector and nickel affinity column chromatography. rTagA cleaved C1-INH in a time-dependent manner. The tagA isogenic mutant of A. hydrophila, unlike its corresponding wild-type (WT) or the complemented strain, was unable to cleave C1-INH, which is required to potentiate the C1-INH-mediated lysis of host and bacterial cells. We indeed demonstrated colocalization of C1-INH and TagA on the bacterial surface by confocal fluorescence microscopy, which ultimately resulted in increased serum resistance of the WT bacterium. Likewise, we delineated the role of TagA in contributing to the enhanced ability of C1-INH to inhibit the classical complement-mediated lysis of erythrocytes. Importantly, we provided evidence that the tagA mutant was significantly less virulent in a mouse model of infection (60%) than the WT bacterium at two 50% lethal doses, which resulted in 100% mortality within 48 h. Taken together, our data provided new information on the role of TagA as a virulence factor in bacterial pathogenesis. This is the first report of TagA characterization from any species of Aeromonas.

Classification of hepatitis C virus into major types and subtypes based on molecular evolutionary analysis

1995 ◽  
Vol 36 (2-3) ◽  
pp. 201-214 ◽  
Author(s):  
Ken-ichi Ohba ◽  
Masashi Mizokami ◽  
Tomoyoshi Ohno ◽  
Kaoru Suzuki ◽  
Etsuro Orito ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Evolutionary Analysis ◽  
Molecular Evolutionary Analysis

Molecular evolutionary analysis of decapentaplegic (dpp) gene in Drosophilidae

The Nucleus ◽  
2014 ◽  
Vol 57 (1) ◽  
pp. 61-65
Author(s):  
Arpita Rakshit ◽  
Rabindra Nath Chatterjee
Keyword(s):  
Evolutionary Analysis ◽  
Molecular Evolutionary Analysis

scholarly journals Discovery of genes encoding a Streptolysin S-like toxin biosynthetic cluster in a select highly pathogenic methicillin resistant Staphylococcus aureus JKD6159 strain

2019 ◽  
Author(s):  
Trevor Kane ◽  
Katelyn E. Carothers ◽  
Yunjuan Bao ◽  
Won-Sik Yeo ◽  
Taeok Bae ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Gene Cluster ◽  
Virulence Factor ◽  
Gene Organization ◽  
Biosynthetic Gene ◽  
Bacterial Gene ◽  
Methicillin Resistant ◽  
Streptolysin S

AbstractBackgroundStaphylococcus aureus (S. aureus) is a major human pathogen owing to its arsenal of virulence factors, as well as its acquisition of multi-antibiotic resistance. Here we report the identification of a Streptolysin S (SLS) like biosynthetic gene cluster in a highly virulent community-acquired methicillin resistant S. aureus (MRSA) isolate, JKD6159. Examination of the SLS-like gene cluster in JKD6159 shows significant homology and gene organization to the SLS-associated biosynthetic gene (sag) cluster responsible for the production of the major hemolysin SLS in Group A Streptococcus.ResultsWe took a comprehensive approach to elucidating the putative role of the sag gene cluster in JKD6159 by constructing a mutant in which one of the biosynthesis genes (sagB homologue) was deleted in the parent JKD6159 strain. Assays to evaluate bacterial gene regulation, biofilm formation, antimicrobial activity, as well as complete host cell response profile and comparative in vivo infections in Balb/Cj mice were conducted.ConclusionsAlthough no significant phenotypic changes were observed in our assays, we postulate that the SLS-like toxin produced by this strain of S. aureus may be a highly specialized virulence factor utilized in specific environments for selective advantage; studies to better understand the role of this newly discovered virulence factor in S. aureus warrant further investigation.

scholarly journals Ancestry of the AUTS2 family–A novel group of polycomb-complex proteins involved in human neurological disease

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0232101
Author(s):  
Robert A. Sellers ◽  
David L. Robertson ◽  
May Tassabehji
Keyword(s):  
Autosomal Dominant ◽  
Large Population ◽  
Evolutionary Analysis ◽  
Genome Data ◽  
High Prevalence ◽  
And Function ◽  
Polycomb Complex ◽  
Putative Domain ◽  
Human Specific

Autism susceptibility candidate 2 (AUTS2) is a neurodevelopmental regulator associated with an autosomal dominant intellectual disability syndrome, AUTS2 syndrome, and is implicated as an important gene in human-specific evolution. AUTS2 exists as part of a tripartite gene family, the AUTS2 family, which includes two relatively undefined proteins, Fibrosin (FBRS) and Fibrosin-like protein 1 (FBRSL1). Evolutionary ancestors of AUTS2 have not been formally identified outside of the Animalia clade. A Drosophila melanogaster protein, Tay bridge, with a role in neurodevelopment, has been shown to display limited similarity to the C-terminal of AUTS2, suggesting that evolutionary ancestors of the AUTS2 family may exist within other Protostome lineages. Here we present an evolutionary analysis of the AUTS2 family, which highlights ancestral homologs of AUTS2 in multiple Protostome species, implicates AUTS2 as the closest human relative to the progenitor of the AUTS2 family, and demonstrates that Tay bridge is a divergent ortholog of the ancestral AUTS2 progenitor gene. We also define regions of high relative sequence identity, with potential functional significance, shared by the extended AUTS2 protein family. Using structural predictions coupled with sequence conservation and human variant data from 15,708 individuals, a putative domain structure for AUTS2 was produced that can be used to aid interpretation of the consequences of nucleotide variation on protein structure and function in human disease. To assess the role of AUTS2 in human-specific evolution, we recalculated allele frequencies at previously identified human derived sites using large population genome data, and show a high prevalence of ancestral alleles, suggesting that AUTS2 may not be a rapidly evolving gene, as previously thought.

scholarly journals Phylogenetic and molecular evolutionary analysis of SENV DNA isolated from Iraqi Hepatitis Patients

Bionatura ◽  
2021 ◽  
Vol 6 (4) ◽  
pp. 2251-2255
Author(s):  
Arwa Mujahid Al-Shuwaikh ◽  
Ealaf Abbas khudair ◽  
Dalya Basil Hanna
Keyword(s):  
Dna Sequences ◽  
Genetic Alterations ◽  
Torque Teno Virus ◽  
Nucleotide Sequencing ◽  
Evolutionary Analysis ◽  
Dna Viruses ◽  
Post Transfusion Hepatitis ◽  
Substitution Mutations ◽  
Sen Virus ◽  
Molecular Evolutionary Analysis

SEN Virus (SENV) is a newly discovered group of transmissible, hepatotropic, single-stranded, circular, non-enveloped DNA viruses that are distantly linked to the widely distributed Torque Teno Virus (TTV) family. This research aimed to use nucleotide sequencing to identify the genetic alterations of SEN-V and to investigate the similarities between isolates. Seven DNA samples of SENV, which were previously extracted from blood of post transfusion hepatitis, were used to identify the genetic variation of SEN-V by nucleotide sequencing. According to the current analysis results, specific primer pairs were used to detect SENV DNA sequences isolated from Iraqi patients with hepatitis; however, those specific primers can also detect two new variants of SENV that are closely related to the Torque Teno Virus. In addition, four SENV isolates showed several substitution mutations, and one of them revealed the replacement of Proline (P) at position 11 with Serine (S). Only one local isolate of SENV was 100% identical to the Iranian isolate (GenBank acc. no. GQ452051.1) from thalassemia.

scholarly journals The inlA Gene of Listeria monocytogenesLO28 Harbors a Nonsense Mutation Resulting in Release of Internalin

1998 ◽  
Vol 66 (7) ◽  
pp. 3420-3422 ◽  
Author(s):  
Renaud Jonquières ◽  
Hélène Bierne ◽  
Jérôme Mengaud ◽  
Pascale Cossart
Keyword(s):  
Cell Adhesion ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Adhesion Molecule ◽  
Nonsense Mutation ◽  
Cell Adhesion Molecule ◽  
Culture Medium ◽  
Surface Protein ◽  
Truncated Protein

ABSTRACT Internalin is a surface protein that mediates entry ofListeria monocytogenes EGD into epithelial cells expressing the cell adhesion molecule human E-cadherin or its chicken homolog, L-CAM, which act as receptors for internalin. After observing that entry of L. monocytogenes LO28 into S180 fibroblasts, in contrast to that of EGD, did not increase after transfection with L-CAM, we examined both the expression and the structure of internalin in strain LO28. We discovered a nonsense mutation in inlA which results in a truncated protein released in the culture medium. Mutations leading to release of internalin were also detected in clinical and food isolates. These results question the role of internalin as a virulence factor in murine listeriosis.

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