scholarly journals Life and Death of Selfish Genes: Comparative Genomics Reveals the Dynamic Evolution of Cytoplasmic Incompatibility

2020 ◽  
Vol 38 (1) ◽  
pp. 2-15 ◽  
Author(s):  
Julien Martinez ◽  
Lisa Klasson ◽  
John J Welch ◽  
Francis M Jiggins
Keyword(s):  
Cytoplasmic Incompatibility ◽  
Gene Gain ◽  
Evolutionary Models ◽  
Loss Of Function ◽  
Genome Sequences ◽  
Life And Death ◽  
Selfish Genes ◽  
Wolbachia Genome ◽  
The Cross ◽  
Gain Loss

Abstract Cytoplasmic incompatibility is a selfish reproductive manipulation induced by the endosymbiont Wolbachia in arthropods. In males Wolbachia modifies sperm, leading to embryonic mortality in crosses with Wolbachia-free females. In females, Wolbachia rescues the cross and allows development to proceed normally. This provides a reproductive advantage to infected females, allowing the maternally transmitted symbiont to spread rapidly through host populations. We identified homologs of the genes underlying this phenotype, cifA and cifB, in 52 of 71 new and published Wolbachia genome sequences. They are strongly associated with cytoplasmic incompatibility. There are up to seven copies of the genes in each genome, and phylogenetic analysis shows that Wolbachia frequently acquires new copies due to pervasive horizontal transfer between strains. In many cases, the genes have subsequently acquired loss-of-function mutations to become pseudogenes. As predicted by theory, this tends to occur first in cifB, whose sole function is to modify sperm, and then in cifA, which is required to rescue the cross in females. Although cif genes recombine, recombination is largely restricted to closely related homologs. This is predicted under a model of coevolution between sperm modification and embryonic rescue, where recombination between distantly related pairs of genes would create a self-incompatible strain. Together, these patterns of gene gain, loss, and recombination support evolutionary models of cytoplasmic incompatibility.

scholarly journals A Genomic Survey of Signalling in the Myxococcaceae

2020 ◽  
Vol 8 (11) ◽  
pp. 1739
Author(s):  
David E. Whitworth ◽  
Allison Zwarycz
Keyword(s):  
Core Genome ◽  
Gene Gain ◽  
Fruiting Body Formation ◽  
Two Component System ◽  
Genome Sequences ◽  
The Core ◽  
Accessory Genes ◽  
Two Component ◽  
Gain Loss ◽  
Core Genes

As prokaryotes diverge by evolution, essential ‘core’ genes required for conserved phenotypes are preferentially retained, while inessential ‘accessory’ genes are lost or diversify. We used the recently expanded number of myxobacterial genome sequences to investigate the conservation of their signalling proteins, focusing on two sister genera (Myxococcus and Corallococcus), and on a species within each genus (Myxococcus xanthus and Corallococcus exiguus). Four new C. exiguus genome sequences are also described here. Despite accessory genes accounting for substantial proportions of each myxobacterial genome, signalling proteins were found to be enriched in the core genome, with two-component system genes almost exclusively so. We also investigated the conservation of signalling proteins in three myxobacterial behaviours. The linear carotenogenesis pathway was entirely conserved, with no gene gain/loss observed. However, the modular fruiting body formation network was found to be evolutionarily plastic, with dispensable components in all modules (including components required for fruiting in the model myxobacterium M. xanthus DK1622). Quorum signalling (QS) is thought to be absent from most myxobacteria, however, they generally appear to be able to produce CAI-I (cholerae autoinducer-1), to sense other QS molecules, and to disrupt the QS of other organisms, potentially important abilities during predation of other prokaryotes.

scholarly journals Feedback regulation of Notch signaling and myogenesis connected by MyoD–Dll1 axis

PLoS Genetics ◽  
2021 ◽  
Vol 17 (8) ◽  
pp. e1009729
Author(s):  
Haifeng Zhang ◽  
Renjie Shang ◽  
Pengpeng Bi
Keyword(s):  
Notch Signaling ◽  
Muscle Development ◽  
Notch Pathway ◽  
Feedback Regulation ◽  
Gene Gain ◽  
Loss Of Function ◽  
Gain Loss ◽  
Regulatory Dna ◽  
Myogenic Program

Muscle precursor cells known as myoblasts are essential for muscle development and regeneration. Notch signaling is an ancient intercellular communication mechanism that plays prominent roles in controlling the myogenic program of myoblasts. Currently whether and how the myogenic cues feedback to refine Notch activities in these cells are largely unknown. Here, by mouse and human gene gain/loss-of-function studies, we report that MyoD directly turns on the expression of Notch-ligand gene Dll1 which activates Notch pathway to prevent precautious differentiation in neighboring myoblasts, while autonomously inhibits Notch to facilitate a myogenic program in Dll1 expressing cells. Mechanistically, we studied cis-regulatory DNA motifs underlying the MyoD–Dll1–Notch axis in vivo by characterizing myogenesis of a novel E-box deficient mouse model, as well as in human cells through CRISPR-mediated interference. These results uncovered the crucial transcriptional mechanism that mediates the reciprocal controls of Notch and myogenesis.

scholarly journals lnc-SAMD14-4 can regulate expression of the COL1A1 and COL1A2 in human chondrocytes

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7491 ◽  
Author(s):  
Haibin Zhang ◽  
Cheng Chen ◽  
Yinghong Cui ◽  
Yuqing Li ◽  
Zhaojun Wang ◽  
...  
Keyword(s):  
Biological Function ◽  
Expression Profiles ◽  
Differentially Expressed ◽  
Human Chondrocytes ◽  
Loss Of Function ◽  
Knee Oa ◽  
System Disease ◽  
Chondrocyte Death ◽  
Differentially Expressed Mrna ◽  
Gain Loss

Osteoarthritis (OA) is the most common motor system disease in aging people, characterized by matrix degradation, chondrocyte death, and osteophyte formation. OA etiology is unclear, but long noncoding RNAs (lncRNAs) that participate in numerous pathological and physiological processes may be key regulators in the onset and development of OA. Because profiling of lncRNAs and their biological function in OA is not understood, we measured lncRNA and mRNA expression profiles using high-throughput microarray to study human knee OA. We identified 2,042 lncRNAs and 2,011 mRNAs that were significantly differentially expressed in OA compared to non-OA tissue (>2.0- or < − 2.0-fold change; p < 0.5), including 1,137 lncRNAs that were upregulated and 905 lncRNAs that were downregulated. Also, 1,386 mRNA were upregulated and 625 mRNAs were downregulated. QPCR was used to validate chip results. Gene Ontology analysis and the Kyoto Encyclopedia of Genes and Genomes was used to study the biological function enrichment of differentially expressed mRNA. Additionally, coding-non-coding gene co-expression (CNC) network construction was performed to explore the relevance of dysregulated lncRNAs and mRNAs. Finally, the gain/loss of function experiments of lnc-SAMD14-4 was implemented in IL-1β-treated human chondrocytes. In general, this study provides a preliminary database for further exploring lncRNA-related mechnisms in OA.

scholarly journals progressiveMauve: Multiple Genome Alignment with Gene Gain, Loss and Rearrangement

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e11147 ◽  
Author(s):  
Aaron E. Darling ◽  
Bob Mau ◽  
Nicole T. Perna
Keyword(s):  
Gene Gain ◽  
Genome Alignment ◽  
Multiple Genome ◽  
Gain Loss ◽  
Multiple Genome Alignment

scholarly journals Life and death partners: apoptosis, autophagy and the cross-talk between them

2009 ◽  
Vol 16 (7) ◽  
pp. 966-975 ◽  
Author(s):  
A Eisenberg-Lerner ◽  
S Bialik ◽  
H-U Simon ◽  
A Kimchi
Keyword(s):  
Cross Talk ◽  
Life And Death ◽  
The Cross

scholarly journals Binding of EBP50 to Nox organizing subunit p47phox is pivotal to cellular reactive species generation and altered vascular phenotype

2016 ◽  
Vol 113 (36) ◽  
pp. E5308-E5317 ◽  
Author(s):  
Imad Al Ghouleh ◽  
Daniel N. Meijles ◽  
Stephanie Mutchler ◽  
Qiangmin Zhang ◽  
Sanghamitra Sahoo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Ex Vivo ◽  
Proximity Ligation Assay ◽  
Loss Of Function ◽  
Pdz Domains ◽  
Resistance Arteries ◽  
Functional Studies ◽  
Proximity Ligation ◽  
Critical Requirement ◽  
Gain Loss

Despite numerous reports implicating NADPH oxidases (Nox) in the pathogenesis of many diseases, precise regulation of this family of professional reactive oxygen species (ROS) producers remains unclear. A unique member of this family, Nox1 oxidase, functions as either a canonical or hybrid system using Nox organizing subunit 1 (NoxO1) or p47phox, respectively, the latter of which is functional in vascular smooth muscle cells (VSMC). In this manuscript, we identify critical requirement of ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50; aka NHERF1) for Nox1 activation and downstream responses. Superoxide (O2•−) production induced by angiotensin II (AngII) was absent in mouse EBP50 KO VSMC vs. WT. Moreover, ex vivo incubation of aortas with AngII showed a significant increase in O2•− in WT but not EBP50 or Nox1 nulls. Similarly, lipopolysaccharide (LPS)-induced oxidative stress was attenuated in femoral arteries from EBP50 KO vs. WT. In silico analyses confirmed by confocal microscopy, immunoprecipitation, proximity ligation assay, FRET, and gain-/loss-of-function mutagenesis revealed binding of EBP50, via its PDZ domains, to a specific motif in p47phox. Functional studies revealed AngII-induced hypertrophy was absent in EBP50 KOs, and in VSMC overexpressing EBP50, Nox1 gene silencing abolished VSMC hypertrophy. Finally, ex vivo measurement of lumen diameter in mouse resistance arteries exhibited attenuated AngII-induced vasoconstriction in EBP50 KO vs. WT. Taken together, our data identify EBP50 as a previously unidentified regulator of Nox1 and support that it promotes Nox1 activity by binding p47phox. This interaction is pivotal for agonist-induced smooth muscle ROS, hypertrophy, and vasoconstriction and has implications for ROS-mediated physiological and pathophysiological processes.

scholarly journals Interplay of Various Evolutionary Modes in Genome Diversification and Adaptive Evolution of the Family Sulfolobaceae

2021 ◽  
Vol 12 ◽  
Author(s):  
Rachana Banerjee ◽  
Narendrakumar M. Chaudhari ◽  
Abhishake Lahiri ◽  
Anupam Gautam ◽  
Debaleena Bhowmik ◽  
...  
Keyword(s):  
Evolutionary Dynamics ◽  
Sulfur Metabolism ◽  
Purifying Selection ◽  
Gene Gain ◽  
Sulfolobus Islandicus ◽  
Gene Acquisition ◽  
Genomic Adaptation ◽  
Differential Gene ◽  
Gain Loss ◽  
Geographical Locations

Sulfolobaceae family, comprising diverse thermoacidophilic and aerobic sulfur-metabolizing Archaea from various geographical locations, offers an ideal opportunity to infer the evolutionary dynamics across the members of this family. Comparative pan-genomics coupled with evolutionary analyses has revealed asymmetric genome evolution within the Sulfolobaceae family. The trend of genome streamlining followed by periods of differential gene gains resulted in an overall genome expansion in some species of this family, whereas there was reduction in others. Among the core genes, both Sulfolobus islandicus and Saccharolobus solfataricus showed a considerable fraction of positively selected genes and also higher frequencies of gene acquisition. In contrast, Sulfolobus acidocaldarius genomes experienced substantial amount of gene loss and strong purifying selection as manifested by relatively lower genome size and higher genome conservation. Central carbohydrate metabolism and sulfur metabolism coevolved with the genome diversification pattern of this archaeal family. The autotrophic CO2 fixation with three significant positively selected enzymes from S. islandicus and S. solfataricus was found to be more imperative than heterotrophic CO2 fixation for Sulfolobaceae. Overall, our analysis provides an insight into the interplay of various genomic adaptation strategies including gene gain–loss, mutation, and selection influencing genome diversification of Sulfolobaceae at various taxonomic levels and geographical locations.

scholarly journals Reconstruction of ancestral genomes in presence of gene gain and loss.

2016 ◽  
Author(s):  
Pavel Avdeyev ◽  
Shuai Jiang ◽  
Sergey Aganezov ◽  
Fei Hu ◽  
Max A. Alekseyev
Keyword(s):  
Software Tool ◽  
Single Copy ◽  
Genome Rearrangements ◽  
Superior Performance ◽  
Gene Gain ◽  
Gene Duplications ◽  
Genomic Changes ◽  
Breakpoint Reuse ◽  
Gain Loss ◽  
The Given

Since most dramatic genomic changes are caused by genome rearrangements as well as gene duplications and gain/loss events, it becomes crucial to understand their mechanisms and reconstruct ancestral genomes of the given genomes. This problem was shown to be NP-complete even in the "simplest" case of three genomes, thus calling for heuristic rather than exact algorithmic solutions. At the same time, a larger number of input genomes may actually simplify the problem in practice as it was earlier illustrated with MGRA, a state-of-the-art software tool for reconstruction of ancestral genomes of multiple genomes. One of the key obstacles for MGRA and other similar tools is presence of breakpoint reuses when the same breakpoint region is broken by several different genome rearrangements in the course of evolution. Furthermore, such tools are often limited to genomes composed of the same genes with each gene present in a single copy in every genome. This limitation makes these tools inapplicable for many biological datasets and degrades the resolution of ancestral reconstructions in diverse datasets. We address these deficiencies by extending the MGRA algorithm to genomes with unequal gene contents. The developed next-generation tool MGRA2 can handle gene gain/loss events and shares the ability of MGRA to reconstruct ancestral genomes uniquely in the case of limited breakpoint reuse. Furthermore, MGRA2 employs a number of novel heuristics to cope with higher breakpoint reuse and process datasets inaccessible for MGRA. In practical experiments, MGRA2 shows superior performance for simulated and real genomes as compared to other ancestral genomes reconstruction tools. The MGRA2 tool is distributed as an open-source software and can be downloaded from GitHub repository http://github.com/ablab/mgra/. It is also available in the form of a web-server at http://mgra.cblab.org, which makes it readily accessible for inexperienced users.

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