Faculty Opinions recommendation of Rapid evolution of enormous, multichromosomal genomes in flowering plant mitochondria with exceptionally high mutation rates.

2012 ◽  
Author(s):  
Nicolas Galtier ◽  
Benoit Nabholz
Keyword(s):  
Plant Mitochondria ◽  
Rapid Evolution ◽  
Flowering Plant ◽  
Mutation Rates

scholarly journals Rapid Evolution of Enormous, Multichromosomal Genomes in Flowering Plant Mitochondria with Exceptionally High Mutation Rates

PLoS Biology ◽  
2012 ◽  
Vol 10 (1) ◽  
pp. e1001241 ◽  
Author(s):  
Daniel B. Sloan ◽  
Andrew J. Alverson ◽  
John P. Chuckalovcak ◽  
Martin Wu ◽  
David E. McCauley ◽  
...  
Keyword(s):  
Plant Mitochondria ◽  
Rapid Evolution ◽  
Flowering Plant ◽  
Mutation Rates

scholarly journals Frequent, Phylogenetically Local Horizontal Transfer of the cox1 Group I Intron in Flowering Plant Mitochondria

2008 ◽  
Vol 25 (8) ◽  
pp. 1762-1777 ◽  
Author(s):  
M. V. Sanchez-Puerta ◽  
Y. Cho ◽  
J. P. Mower ◽  
A. J. Alverson ◽  
J. D. Palmer
Keyword(s):  
Horizontal Transfer ◽  
Plant Mitochondria ◽  
Group I Intron ◽  
Flowering Plant ◽  
Group I

scholarly journals CARD8 inflammasome mediates pyroptosis of HIV-1-infected cells by sensing viral protease activity

2020 ◽  
Author(s):  
Qiankun Wang ◽  
Hongbo Gao ◽  
Kolin M. Clark ◽  
Pengfei Tang ◽  
Gray H. Harlan ◽  
...  
Keyword(s):  
Rapid Evolution ◽  
Mutation Rates ◽  
Host Immune System ◽  
Virus Reactivation ◽  
Viral Protease ◽  
Viral Budding ◽  
Infected Cells ◽  
Latent Hiv ◽  
Hiv 1 ◽  
Recognition Receptor

AbstractHIV-1 has high mutation rates and exists as mutant swarms in the host. Rapid evolution of HIV-1 allows the virus to outpace host immune system, leading to viral persistence. Novel approaches to target immutable components are needed to clear HIV-1 infection. Here we report a pattern-recognition receptor CARD8 that senses enzymatic activity of the HIV-1 protease, which is indispensable for the virus. All subtypes of HIV-1 can be sensed by CARD8 despite substantial viral diversity. HIV-1 evades CARD8 sensing because the viral protease remains inactive in infected cells prior to viral budding. Induction of premature intracellular activation of the viral protease triggers CARD8 inflammasome-mediated pyroptosis of HIV-1-infected cells. This strategy leads to clearance of latent HIV-1 in patient CD4+ T cells after virus reactivation. Taken together, our study identifies CARD8 as an inflammasome sensor of HIV-1 that holds promise as a strategy for clearance of persistent HIV-1 infection.

scholarly journals Rapid evolution of the human mutation spectrum

2016 ◽  
Author(s):  
Kelley Harris ◽  
Jonathan K. Pritchard
Keyword(s):  
Mutation Rate ◽  
Genetic Modifier ◽  
Rapid Evolution ◽  
Biological Information ◽  
Mutation Rates ◽  
Specific Sequence ◽  
Mutational Spectra ◽  
Damage Repair ◽  
Human Mutation ◽  
System Selection

AbstractDNA is a remarkably precise medium for copying and storing biological information. This high fidelity results from the action of hundreds of genes involved in replication, proofreading, and damage repair. Evolutionary theory suggests that in such a system, selection has limited ability to remove genetic variants that change mutation rates by small amounts or in specific sequence contexts. Consistent with this, using SNV variation as a proxy for mutational input, we report here that mutational spectra differ substantially among species, human continental groups and even some closely-related populations. Close examination of one signal, an increased TCC→TTC mutation rate in Europeans, indicates a burst of mutations from about 15,000 to 2,000 years ago, perhaps due to the appearance, drift, and ultimate elimination of a genetic modifier of mutation rate. Our results suggest that mutation rates can evolve markedly over short evolutionary timescales and suggest the possibility of mapping mutational modifiers.

scholarly journals Selection constrains high rates of satellite DNA mutation in Daphnia pulex

2017 ◽  
Author(s):  
Jullien M. Flynn ◽  
Ian Caldas ◽  
Melania E. Cristescu ◽  
Andrew G. Clark
Keyword(s):  
Satellite Dna ◽  
Related Species ◽  
Rapid Evolution ◽  
Daphnia Pulex ◽  
Selective Constraint ◽  
Mutation Rates ◽  
Stabilizing Selection ◽  
Closely Related Species ◽  
Dna Mutation ◽  
Evolutionary Forces

AbstractA long-standing evolutionary puzzle is that all eukaryotic genomes contain large amounts of tandemly-repeated satellite DNA whose composition varies greatly among even closely related species. To elucidate the evolutionary forces governing satellite dynamics, quantification of the rates and patterns of mutations in satellite DNA copy number and tests of its selective neutrality are necessary. Here we used whole-genome sequences of 28 mutation accumulation (MA) lines of Daphnia pulex in addition to six isolates from a non-MA population originating from the same progenitor to both estimate mutation rates of abundances of satellite sequences and evaluate the selective regime acting upon them. We found that mutation rates of individual satellite sequence “kmers” were both high and highly variable, ranging from additions/deletions of 0.29 – 105 copies per generation (reflecting changes of 0.12 - 0.80 percent per generation). Our results also provide evidence that new kmer sequences are often formed from existing ones. The non-MA population isolates showed a signal of either purifying or stabilizing selection, with 33 % lower variation in kmer abundance on average than the MA lines, although the level of selective constraint was not evenly distributed across all kmers. The changes between many pairs of kmers were correlated, and the pattern of correlations was significantly different between the MA lines and the non-MA population. Our study demonstrates that kmer sequences can experience extremely rapid evolution in abundance, which can lead to high levels of divergence in genome-wide satellite DNA composition between closely related species.

scholarly journals CARD8 is an inflammasome sensor for HIV-1 protease activity

Science ◽  
2021 ◽  
Vol 371 (6535) ◽  
pp. eabe1707 ◽  
Author(s):  
Qiankun Wang ◽  
Hongbo Gao ◽  
Kolin M. Clark ◽  
Christian Shema Mugisha ◽  
Keanu Davis ◽  
...  
Keyword(s):  
Protease Activity ◽  
Rapid Evolution ◽  
Viral Persistence ◽  
Viral Reactivation ◽  
Mutation Rates ◽  
Host Immune System ◽  
Viral Budding ◽  
Infected Cells ◽  
Latent Hiv ◽  
Hiv 1

HIV-1 has high mutation rates and exists as mutant swarms within the host. Rapid evolution of HIV-1 allows the virus to outpace the host immune system, leading to viral persistence. Approaches to targeting immutable components are needed to clear HIV-1 infection. Here, we report that the caspase recruitment domain–containing protein 8 (CARD8) inflammasome senses HIV-1 protease activity. HIV-1 can evade CARD8 sensing because its protease remains inactive in infected cells before viral budding. Premature intracellular activation of the viral protease triggered CARD8 inflammasome–mediated pyroptosis of HIV-1–infected cells. This strategy led to the clearance of latent HIV-1 in patient CD4+ T cells after viral reactivation. Thus, our study identifies CARD8 as an inflammasome sensor of HIV-1, which holds promise as a strategy for the clearance of persistent HIV-1 infection.

scholarly journals Phylogenetic Evidence for the Rapid Evolution of Human B19 Erythrovirus

2006 ◽  
Vol 80 (7) ◽  
pp. 3666-3669 ◽  
Author(s):  
Laura A. Shackelton ◽  
Edward C. Holmes
Keyword(s):  
Host Cell ◽  
Evolutionary Dynamics ◽  
Rna Viruses ◽  
Rapid Evolution ◽  
Evolutionary Change ◽  
High Rate ◽  
Mutation Rates ◽  
Genome Replication ◽  
Nucleotide Substitutions ◽  
Viral Pathogen

ABSTRACT Human B19 erythrovirus is a ubiquitous viral pathogen, commonly infecting individuals before adulthood. As with all autonomous parvoviruses, its small single-stranded DNA genome is replicated with host cell machinery. While the mechanism of parvovirus genome replication has been studied in detail, the rate at which B19 virus evolves is unknown. By inferring the phylogenetic history and evolutionary dynamics of temporally sampled B19 sequences, we observed a surprisingly high rate of evolutionary change, at approximately 10−4 nucleotide substitutions per site per year. This rate is more typical of RNA viruses and suggests that high mutation rates are characteristic of the Parvoviridae.

scholarly journals The mutation rates and mutational bias of influenza A virus

2017 ◽  
Author(s):  
Matthew D. Pauly ◽  
Megan Procario ◽  
Adam S. Lauring
Keyword(s):  
Influenza Virus ◽  
Influenza A Virus ◽  
Mutation Rate ◽  
Influenza A ◽  
Rapid Evolution ◽  
Viral Fitness ◽  
High Mutation Rate ◽  
Mutation Rates ◽  
Mutational Bias ◽  
Neutral Mutations

AbstractInfluenza virus has a high mutation rate, and this low replicative fidelity contributes to its capacity for rapid evolution. Clonal sequencing and fluctuation tests have suggested that the mutation rate of influenza A virus is 7.1 × 10−6− 4.5 × 10−5substitutions per nucleotide per cell infection cycle and 2.7 × 10−6− 3.0 × 10−5substitutions per nucleotide per strand copied (s/n/r). However, sequencing assays are biased toward mutations with minimal impacts on viral fitness and fluctuation tests typically investigate only a subset of the twelve mutational classes. We developed a fluctuation test based on reversion to fluorescence in a set of virally encoded mutant green fluorescent proteins. This method allowed us to measure the rates of selectively neutral mutations representative of all 12 mutational classes in the context of an unstructured RNA. We measured an overall mutation rate of 1.8 × 10−4s/n/r for PR8 (H1N1) and 2.5 × 10−4s/n/r for Hong Kong 2014 (H3N2). The replication mode was linear. The mutation rates of these divergent strains are significantly higher than previous estimates and suggest that each replicated genome will have an average of 2-3 mutations. The viral mutational spectrum is heavily biased toward A to G and U to C transitions, resulting in a transition to transversion bias of 2.7 and 3.6 for the two strains. These mutation rates were relatively constant over a range of physiological temperatures. Our high-resolution analysis of influenza virus mutation rates will enable more refined models of its molecular evolution.SignificanceThe rapid evolution of influenza virus is a major problem in public health. A key factor driving this rapid evolution is the virus’ very high mutation rate. We developed a new method for measuring the rates of all 12 mutational classes in influenza virus, which eliminates some of the biases of existing assays. We find that the influenza virus mutation rate is much higher than previously reported and is consistent across two distinct strains and a range of temperatures. Our data suggest that influenza viruses replicate at their maximally tolerable mutation rates, highlighting both the virus’ evolutionary potential and its significant constraints.

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