scholarly journals Evolutionary Study of the Crassphage Virus at Gene Level

Viruses ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 1035
Author(s):  
Alessandro Rossi ◽  
Laura Treu ◽  
Stefano Toppo ◽  
Henrike Zschach ◽  
Stefano Campanaro ◽  
...  
Keyword(s):  
Human Population ◽  
Evolutionary Dynamics ◽  
Genetic Interaction ◽  
Protein Sequences ◽  
Capsid Proteins ◽  
Evolutionary Trees ◽  
Gene Duplications ◽  
Functional Categories ◽  
Gene Level ◽  
Genes Encoding

crAss-like viruses are a putative family of bacteriophages recently discovered. The eponym of the clade, crAssphage, is an enteric bacteriophage estimated to be present in at least half of the human population and it constitutes up to 90% of the sequences in some human fecal viral metagenomic datasets. We focused on the evolutionary dynamics of the genes encoded on the crAssphage genome. By investigating the conservation of the genes, a consistent variation in the evolutionary rates across the different functional groups was found. Gene duplications in crAss-like genomes were detected. By exploring the differences among the functional categories of the genes, we confirmed that the genes encoding capsid proteins were the most ubiquitous, despite their overall low sequence conservation. It was possible to identify a core of proteins whose evolutionary trees strongly correlate with each other, suggesting their genetic interaction. This group includes the capsid proteins, which are thus established as extremely suitable for rebuilding the phylogenetic tree of this viral clade. A negative correlation between the ubiquity and the conservation of viral protein sequences was shown. Together, this study provides an in-depth picture of the evolution of different genes in crAss-like viruses.

scholarly journals Divergence in Coding Sequence and Expression of Different Functional Categories of Immune Genes between Two Wild Rodent Species

2021 ◽  
Vol 13 (3) ◽  
Author(s):  
Xiuqin Zhong ◽  
Max Lundberg ◽  
Lars Råberg
Keyword(s):  
Signal Transduction ◽  
Transcription Factors ◽  
Immune Function ◽  
Sequence Divergence ◽  
Expression Divergence ◽  
Functional Categories ◽  
Coding Sequence ◽  
Immune Genes ◽  
Genes Encoding ◽  
Signal Transduction Proteins

Abstract Differences in immune function between species could be a result of interspecific divergence in coding sequence and/or expression of immune genes. Here, we investigate how the degree of divergence in coding sequence and expression differs between functional categories of immune genes, and if differences between categories occur independently of other factors (expression level, pleiotropy). To this end, we compared spleen transcriptomes of wild-caught yellow-necked mice and bank voles. Immune genes expressed in the spleen were divided into four categories depending on the function of the encoded protein: pattern recognition receptors (PRR); signal transduction proteins; transcription factors; and cyto- and chemokines and their receptors. Genes encoding PRR and cyto-/chemokines had higher sequence divergence than genes encoding signal transduction proteins and transcription factors, even when controlling for potentially confounding factors. Genes encoding PRR also had higher expression divergence than genes encoding signal transduction proteins and transcription factors. There was a positive correlation between expression divergence and coding sequence divergence, in particular for PRR genes. We propose that this is a result of that divergence in PRR coding sequence leads to divergence in PRR expression through positive feedback of PRR ligand binding on PRR expression. When controlling for sequence divergence, expression divergence of PRR genes did not differ from other categories. Taken together, the results indicate that coding sequence divergence of PRR genes is a major cause of differences in immune function between species.

scholarly journals Expression of the apoptosis-releated genes in patients with newly diagnosed chronic lymphocytic leukemia in clinical data context

2018 ◽  
Vol 17 (2) ◽  
pp. 41-46 ◽  
Author(s):  
S. G. Zakharov ◽  
A. K. Golenkov ◽  
A. V. Misyurin ◽  
E. V. Kataeva ◽  
A. A. Rudakova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clinical Manifestations ◽  
Multivariate Regression Analysis ◽  
Lymphocytic Leukemia ◽  
Newly Diagnosed ◽  
Expression Of Genes ◽  
Gene Level ◽  
Genes Encoding ◽  
Group Ii ◽  
High Level

Introduction.The given data of fundamental studies of apoptosis processes in B-cell lymphocytic leukemia (B-CLL) testifies about the complexity and variety of mechanisms affecting the kinetics of normal cells and tumor lymphocytes in this disease. It is important to study the severity of clinical manifestations of the disease depending on the expression of the genes that modulate apoptosis.The purposeof the study is to compare the activity of genes encoding apoptosis modulators, the cell cycle and cancer-testicular PRAME protein with clinical manifestations of the disease in primary patients with B-CLL.Materials and methods.The level of expression of the proapoptotic genes FAS, TRAIL, TNFR2, DR4/5 and DR3, as well as the HSP27, XIAP genes, blocking apoptosis was determined in 23 patients with newly diagnosed chronic B-CLL. In addition, expression of genes TP53 and P21 and cancer-testis gene PRAME are tested.Results.According to the multivariate regression analysis, the FAS gene expression in the onset of the disease had the greatest impact on the clinical characteristics of the disease. In this connection, the patients were divided into groups with normal (group) and low gene level (group II). A low level of FAS expression (Me 387 %) was associated with stage II disease (p = 0.03), a large number of lympho cytes (p = 0.001), fewer erythrocytes (p = 0.08), and a lower level of TNFR2 gene expression (p = 0.08), high level of expression of XIAP, HSP27, P21. Overall, the anti-apoptotic potential in Group II patients was higher, which was accompanied by more pronounced clinical manifestations of the disease.Conclusions.The increased anti-apoptotic potential of tumor lymphocytes in newly diagnosed B-CLL is accompanied by a larger tumor mass and greater clinical and hematological manifestation of the disease.

scholarly journals Recent gene duplications dominate evolutionary dynamics of adaptor protein complex subunits in embryophytes

Traffic ◽  
2019 ◽  
Vol 20 (12) ◽  
pp. 961-973 ◽  
Author(s):  
Raegan T. Larson ◽  
Joel B. Dacks ◽  
Lael D. Barlow
Keyword(s):  
Protein Complex ◽  
Evolutionary Dynamics ◽  
Adaptor Protein ◽  
Gene Duplications

scholarly journals Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Haipeng Guo ◽  
Yao Wei Lu ◽  
Zhiqiang Lin ◽  
Zhan-Peng Huang ◽  
Jianming Liu ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiac Function ◽  
Heart Development ◽  
Genetic Interaction ◽  
Specific Cell ◽  
Cardiomyocyte Proliferation ◽  
Intercalated Disc ◽  
Knock Out ◽  
Genes Encoding ◽  
Knock Out Mice

Abstract Intercalated discs (ICD), specific cell-to-cell contacts that connect adjacent cardiomyocytes, ensure mechanical and electrochemical coupling during contraction of the heart. Mutations in genes encoding ICD components are linked to cardiovascular diseases. Here, we show that loss of Xinβ, a newly-identified component of ICDs, results in cardiomyocyte proliferation defects and cardiomyopathy. We uncovered a role for Xinβ in signaling via the Hippo-YAP pathway by recruiting NF2 to the ICD to modulate cardiac function. In Xinβ mutant hearts levels of phosphorylated NF2 are substantially reduced, suggesting an impairment of Hippo-YAP signaling. Cardiac-specific overexpression of YAP rescues cardiac defects in Xinβ knock-out mice—indicating a functional and genetic interaction between Xinβ and YAP. Our study reveals a molecular mechanism by which cardiac-expressed intercalated disc protein Xinβ modulates Hippo-YAP signaling to control heart development and cardiac function in a tissue specific manner. Consequently, this pathway may represent a therapeutic target for the treatment of cardiovascular diseases.

scholarly journals Transcriptional Mutagenesis Prevents Ribosomal DNA Deterioration: The Role of Duplications and Deletions

2019 ◽  
Vol 11 (11) ◽  
pp. 3207-3217
Author(s):  
Enrico Sandro Colizzi ◽  
Paulien Hogeweg
Keyword(s):  
Genome Stability ◽  
Evolutionary Dynamics ◽  
Point Mutations ◽  
Gene Duplications ◽  
Genetic Operators ◽  
Theory Of Evolution ◽  
Long Term Stability ◽  
Number Variation

Abstract Clashes between transcription and replication complexes can cause point mutations and chromosome rearrangements on heavily transcribed genes. In eukaryotic ribosomal RNA genes, the system that prevents transcription–replication conflicts also causes frequent copy number variation. Such fast mutational dynamics do not alter growth rates in yeast and are thus selectively near neutral. It was recently found that yeast regulates these mutations by means of a signaling cascade that depends on the availability of nutrients. Here, we investigate the long-term evolutionary effect of the mutational dynamics observed in yeast. We developed an in silico model of single-cell organisms whose genomes mutate more frequently when transcriptional load is larger. We show that mutations induced by high transcriptional load are beneficial when biased toward gene duplications and deletions: they decrease mutational load even though they increase the overall mutation rates. In contrast, genome stability is compromised when mutations are not biased toward gene duplications and deletions, even when mutations occur much less frequently. Taken together, our results show that the mutational dynamics observed in yeast are beneficial for the long-term stability of the genome and pave the way for a theory of evolution where genetic operators are themselves cause and outcome of the evolutionary dynamics.

scholarly journals Protective immunization of horses with a recombinant canarypox virus vectored vaccine co-expressing genes encoding the outer capsid proteins of African horse sickness virus

Vaccine ◽  
2009 ◽  
Vol 27 (33) ◽  
pp. 4434-4438 ◽  
Author(s):  
Alan J. Guthrie ◽  
Melvyn Quan ◽  
Carina W. Lourens ◽  
Jean-Christophe Audonnet ◽  
Jules M. Minke ◽  
...  
Keyword(s):  
Capsid Proteins ◽  
African Horse Sickness ◽  
African Horse Sickness Virus ◽  
Genes Encoding ◽  
Vectored Vaccine ◽  
Outer Capsid ◽  
Canarypox Virus

scholarly journals Mapping DNA damage-dependent genetic interactions in yeast via party mating and barcode fusion genetics

2017 ◽  
Author(s):  
J. Javier Díaz-Mejía ◽  
Albi Celaj ◽  
Joseph C. Mellor ◽  
Atina Coté ◽  
Attila Balint ◽  
...  
Keyword(s):  
Double Mutant ◽  
Genetic Interaction ◽  
Culture Conditions ◽  
Genetic Interactions ◽  
Specific Gene ◽  
Functional Relationships ◽  
Mutant Strains ◽  
Genes Encoding ◽  
Standard Culture ◽  
Yeast Genetic

AbstractCondition-dependent genetic interactions can reveal functional relationships between genes that are not evident under standard culture conditions. State-of-the-art yeast genetic interaction mapping, which relies on robotic manipulation of arrays of double mutant strains, does not scale readily to multi-condition studies. Here we describe Barcode Fusion Genetics to map Genetic Interactions (BFG-GI), by which double mutant strains generated via en masse ‘party’ mating can also be monitored en masse for growth and genetic interactions. By using site-specific recombination to fuse two DNA barcodes, each representing a specific gene deletion, BFG-GI enables multiplexed quantitative tracking of double mutants via next-generation sequencing. We applied BFG-GI to a matrix of DNA repair genes under nine different conditions, including methyl methanesulfonate (MMS), 4-nitroquinoline 1-oxide (4NQO), bleomycin, zeocin, and three other DNA-damaging environments. BFG-GI recapitulated known genetic interactions and yielded new condition-dependent genetic interactions. We validated and further explored a subnetwork of condition-dependent genetic interactions involving MAG1, SLX4, and genes encoding the Shu complex, and inferred that loss of the Shu complex leads to a decrease in the activation or activity of the checkpoint protein kinase Rad53.

scholarly journals Rampant prophage movement among transient competitors drives rapid adaptation during infection

2021 ◽  
Author(s):  
Christopher W. Marshall ◽  
Erin S. Gloag ◽  
Christina Lim ◽  
Daniel J. Wozniak ◽  
Vaughn S. Cooper
Keyword(s):  
Microbial Communities ◽  
Chronic Infection ◽  
Evolutionary Dynamics ◽  
Functional Genes ◽  
Rapid Adaptation ◽  
Chronic Infections ◽  
Global Regulators ◽  
New Genes ◽  
Biofilm Production ◽  
Genes Encoding

AbstractInteractions between bacteria, their close competitors, and viral parasites are common in infections but understanding of these eco-evolutionary dynamics is limited. Most examples of adaptations caused by phage lysogeny are through the acquisition of new genes. However, integrated prophages can also insert into functional genes and impart a fitness benefit by disrupting their expression, a process called active lysogeny. Here, we show that active lysogeny can fuel rapid, parallel adaptations in establishing a chronic infection. These recombination events repeatedly disrupted genes encoding global regulators, leading to increased cyclic-di-GMP levels and elevated biofilm production. The implications of prophage-mediated adaptation are broad, as even transient members of microbial communities can alter the course of evolution and generate persistent phenotypes associated with poor clinical outcomes.One Sentence SummaryBacteriophage act as genetic regulators that are key to establishing chronic infections and are rapidly shared among co-infecting strains.

scholarly journals Rules of Nonallelic Noncomplementation at the Synapse in Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 158 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Karen J Yook ◽  
Stephen R Proulx ◽  
Erik M Jorgensen
Keyword(s):  
Caenorhabditis Elegans ◽  
Gene Product ◽  
Genetic Interaction ◽  
Synaptic Proteins ◽  
Null Alleles ◽  
Nematode Caenorhabditis Elegans ◽  
Recessive Mutations ◽  
Genes Encoding ◽  
Physical Interactions ◽  
Encoding Gene

Abstract Nonallelic noncomplementation occurs when recessive mutations in two different loci fail to complement one another, in other words, the double heterozygote exhibits a phenotype. We observed that mutations in the genes encoding the physically interacting synaptic proteins UNC-13 and syntaxin/UNC-64 failed to complement one another in the nematode Caenorhabditis elegans. Noncomplementation was not observed between null alleles of these genes and thus this genetic interaction does not occur with a simple decrease in dosage at the two loci. However, noncomplementation was observed if at least one gene encoded a partially functional gene product. Thus, this genetic interaction requires a poisonous gene product to sensitize the genetic background. Nonallelic noncomplementation was not limited to interacting proteins: Although the strongest effects were observed between loci encoding gene products that bind to one another, interactions were also observed between proteins that do not directly interact but are members of the same complex. We also observed noncomplementation between genes that function at distant points in the same pathway, implying that physical interactions are not required for nonallelic noncomplementation. Finally, we observed that mutations in genes that function in different processes such as neurotransmitter synthesis or synaptic development complement one another. Thus, this genetic interaction is specific for genes acting in the same pathway, that is, for genes acting in synaptic vesicle trafficking.

Sign in / Sign up

Export Citation Format

Share Document