scholarly journals Superoxide is a mediator of an altruistic aging program in Saccharomyces cerevisiae

2004 ◽  
Vol 166 (7) ◽  
pp. 1055-1067 ◽  
Author(s):  
Paola Fabrizio ◽  
Luisa Battistella ◽  
Raffaello Vardavas ◽  
Cristina Gattazzo ◽  
Lee-Loung Liou ◽  
...  
Keyword(s):  
Mutation Frequency ◽  
Premature Aging ◽  
Natural Environments ◽  
Computational Simulations ◽  
Changing Environments ◽  
High Mutation Frequency ◽  
Aging Program ◽  
Programmed Aging ◽  
Age Dependent

Aging is believed to be a nonadaptive process that escapes the force of natural selection. Here, we challenge this dogma by showing that yeast laboratory strains and strains isolated from grapes undergo an age- and pH-dependent death with features of mammalian programmed cell death (apoptosis). After 90–99% of the population dies, a small mutant subpopulation uses the nutrients released by dead cells to grow. This adaptive regrowth is inversely correlated with protection against superoxide toxicity and life span and is associated with elevated age-dependent release of nutrients and increased mutation frequency. Computational simulations confirm that premature aging together with a relatively high mutation frequency can result in a major advantage in adaptation to changing environments. These results suggest that under conditions that model natural environments, yeast organisms undergo an altruistic and premature aging and death program, mediated in part by superoxide. The role of similar pathways in the regulation of longevity in organisms ranging from yeast to mice raises the possibility that mammals may also undergo programmed aging.

Mutation frequency of Escherichia coli isolated from river water: potential role in the development of antimicrobial resistance

2021 ◽  
Author(s):  
Tomohiro Yamazaki ◽  
Junji Matsuo
Keyword(s):  
Antimicrobial Resistance ◽  
River Water ◽  
Mutation Frequency ◽  
Potential Role ◽  
Relative Increase ◽  
Natural Environments ◽  
E Coli ◽  
Stressful Environment ◽  
Antimicrobial Sensitivity

Bacteria acquire genetic variations to adapt to stressful environmental conditions, which may be associated with the development of antimicrobial resistance. Here we investigated the mutation frequencies of 270 E. coli isolates from river water, representing a relatively less stressful environment. As we predicted, mutation frequencies of such E. coli isolates ranged from < 1 ×10<sup>-11 </sup>to 6.3 ×10<sup>-8</sup> (median, 1.7 × 10<sup>-9</sup>), and a strong mutator (4×10<sup>-7</sup> ≤) was not detected. To better understand the role of mutation frequency in the development of antimicrobial resistance, we assessed antimicrobial sensitivity after exposure of the E. coli isolates to subinhibitory concentrations of ciprofloxacin as a surrogate for stress. We found that antimicrobial resistance increased in bacteria with a low mutation frequency after exposure, and the relative increase in antimicrobial resistance generally increased depending on the mutation frequency. Thus, mutation frequency may contribute to the development of antimicrobial resistance of bacteria in natural environments.

scholarly journals The Evolutionary Processes of Canine Coronaviruses

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Annamaria Pratelli
Keyword(s):  
Mutation Frequency ◽  
Diagnostic Methods ◽  
Evolutionary Processes ◽  
Pathogenetic Role ◽  
High Mutation Frequency ◽  
Canine Coronavirus ◽  
Virus Strains

Since the first identification of the virus in 1971, the disease caused by canine coronavirus (CCoV) has not been adequately investigated, and the role that the virus plays in canine enteric illness has not been well established. Only after the emergence in 2002 of SARS in human has new attention been focused on coronaviruses. As a consequence of the relatively high mutation frequency of RNA-positive stranded viruses, CCoV has evolved and, with the biomolecular techniques developed over the last two decades, new virus strains, serotypes, and subtypes have been identified in infected dogs. Considering the widespread nature of CCoV infections among dog populations, several studies have been carried out, focusing upon the epidemiological relevance of these viruses and underlining the need for further investigation into the biology of CCoVs and into the pathogenetic role of the infections. This paper reports the evolutionary processes of CCoVs with a note onto recent diagnostic methods.

The Role of Cellular Senescence in Werner Syndrome: Toward Therapeutic Intervention in Human Premature Aging

2007 ◽  
Vol 1100 (1) ◽  
pp. 455-469 ◽  
Author(s):  
T. DAVIS ◽  
F. S. WYLLIE ◽  
M. J. ROKICKI ◽  
M. C. BAGLEY ◽  
D. KIPLING
Keyword(s):  
Cellular Senescence ◽  
Therapeutic Intervention ◽  
Werner Syndrome ◽  
Premature Aging

scholarly journals Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs

2021 ◽  
Author(s):  
Amit Ketkar ◽  
Lane Smith ◽  
Callie Johnson ◽  
Alyssa Richey ◽  
Makayla Berry ◽  
...  
Keyword(s):  
Amino Acids ◽  
Mutation Frequency ◽  
Control Sequence ◽  
Wild Type ◽  
Binding Properties ◽  
High Affinity ◽  
G4 Dna ◽  
G Quadruplex ◽  
Forward Mutagenesis

Abstract We previously reported that human Rev1 (hRev1) bound to a parallel-stranded G-quadruplex (G4) from the c-MYC promoter with high affinity. We have extended those results to include other G4 motifs, finding that hRev1 exhibited stronger affinity for parallel-stranded G4 than either anti-parallel or hybrid folds. Amino acids in the αE helix of insert-2 were identified as being important for G4 binding. Mutating E466 and Y470 to alanine selectively perturbed G4 binding affinity. The E466K mutant restored wild-type G4 binding properties. Using a forward mutagenesis assay, we discovered that loss of hRev1 increased G4 mutation frequency &gt;200-fold compared to the control sequence. Base substitutions and deletions occurred around and within the G4 motif. Pyridostatin (PDS) exacerbated this effect, as the mutation frequency increased &gt;700-fold over control and deletions upstream of the G4 site more than doubled. Mutagenic replication of G4 DNA (±PDS) was partially rescued by wild-type and E466K hRev1. The E466A or Y470A mutants failed to suppress the PDS-induced increase in G4 mutation frequency. These findings have implications for the role of insert-2, a motif conserved in vertebrates but not yeast or plants, in Rev1-mediated suppression of mutagenesis during G4 replication.

scholarly journals SPONTANEOUS UNSTABLE UNC-22 IV MUTATIONS IN C. ELEGANS VAR. BERGERAC

Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 859-877
Author(s):  
D G Moerman ◽  
R H Waterston
Keyword(s):  
Mutation Frequency ◽  
Spontaneous Mutation ◽  
Phenotypic Effect ◽  
C Elegans ◽  
High Mutation Frequency ◽  
Mutator Activity ◽  
Discrete Site ◽  
Unstable Mutations ◽  
Spontaneous Mutation Frequency ◽  
Forward Mutation

ABSTRACT This paper describes a mutator system in the nematode Caenorhabditis elegans var. Bergerac for the gene unc-22. Of nine C. elegans and two C. briggsae strains tested only the Bergerac BO strain yielded mutant animals at a high frequency and the unc-22 IV gene is a preferred mutational target. The forward spontaneous mutation frequency at the unc-22 locus in Bergerac BO is about 1 × 10-4, and most of these spontaneous unc-22 mutations revert at frequencies between 2 × 10-3 and 2 × 10-4. Both the forward mutation frequency and the reversion frequency are sensitive to genetic background. Spontaneous unc-22 mutations derived in a Bergerac background and placed in a primarily Bristol background revert at frequencies of &lt;10-6. When reintroduced into a Bergerac/Bristol hybrid background the mutations once again become unstable. The mutator activity could not be localized to a discrete site in the Bergerac genome. Nor did mutator activity require the Bergerac unc-22 gene as a target since the Bristol unc-22 homolog placed in a Bergerac background also showed high mutation frequency. Intragenic mapping of two spontaneous unc-22 alleles, st136 and st137, place both mutations in the central region of the known unc-22 map. However, these mutations probably recombine with one another, suggesting that the unstable mutations can occur in more than one site in unc-22. Examination of the phenotypic effect of these mutations on muscle structure indicates that they are less severe in their effect than a known amber allele. We suggest that this mutator system is polygenic and dispersed over the nematode genome and could represent activity of the transposable element Tc1.

scholarly journals Chloroplast Hsp70 Isoform Is Required for Age-Dependent Tissue Preference of Bamboo mosaic virus in Mature Nicotiana benthamiana Leaves

2017 ◽  
Vol 30 (8) ◽  
pp. 631-645 ◽  
Author(s):  
Ying Wen Huang ◽  
Chung Chi Hu ◽  
Ching Hsiu Tsai ◽  
Na Sheng Lin ◽  
Yau Heiu Hsu
Keyword(s):  
Mosaic Virus ◽  
Nicotiana Benthamiana ◽  
Transit Peptide ◽  
Plant Viruses ◽  
Age Dependent ◽  
Efficient Replication ◽  
Underlying Mechanisms ◽  
Lines Of Evidence ◽  
Suitable Environment

Plant viruses may exhibit age-dependent tissue preference in their hosts but the underlying mechanisms are not well understood. In this study, we provide several lines of evidence to reveal the determining role of a protein of the Nicotiana benthamiana chloroplast Hsp70 (NbcpHsp70) family, NbcpHsp70-2, involved in the preference of Bamboo mosaic virus (BaMV) to infect older tissues. NbcpHsp70 family proteins were identified in complexes pulled down with BaMV replicase as the bait. Among the isoforms of NbcpHsp70, only the specific silencing of NbcpHsp70-2 resulted in the significant decrease of BaMV RNA in N. benthamiana protopalsts, indicating that NbcpHsp70-2 is involved in the efficient replication of BaMV RNA. We further identified the age-dependent import regulation signal contained in the transit peptide of NbcpHsp70-2. Deletion, overexpression, and substitution experiments revealed that the signal in the transit peptide of NbcpHsp70-2 is crucial for both the import of NbcpHsp70-2 into older chloroplasts and the preference of BaMV for infecting older leaves of N. benthamiana. Together, these data demonstrated that BaMV may exploit a cellular age-dependent transportation mechanism to target a suitable environment for viral replication.

Stochastic models in cell kinetics

1988 ◽  
Vol 25 (A) ◽  
pp. 91-111
Author(s):  
Peter J. Brockwell
Keyword(s):  
Life Cycle ◽  
Stochastic Models ◽  
Death Rate ◽  
Cell Kinetics ◽  
Branching Processes ◽  
Experimental Studies ◽  
Renewal Theory ◽  
Biological Cell ◽  
Age Dependent

We discuss the role of stochastic processes in modelling the life-cycle of a biological cell and the growth of cell populations. Results for multiphase age-dependent branching processes have proved invaluable for the interpretation of many of the basic experimental studies of the life-cycle. Moreover problems from cell kinetics, in particular those related to diurnal rhythm in cell-growth, have stimulated research into ‘periodic' renewal theory, and the asymptotic behaviour of populations of cells with periodic death rate.

Time- and age-dependent effects of serotonin on gasping and autoresuscitation in neonatal mice

2013 ◽  
Vol 114 (12) ◽  
pp. 1668-1676 ◽  
Author(s):  
Jianping Chen ◽  
Jennifer Magnusson ◽  
Gerard Karsenty ◽  
Kevin J. Cummings
Keyword(s):  
Heart Rate ◽  
Tryptophan Hydroxylase ◽  
Single Injection ◽  
Heart Rate Recovery ◽  
Wild Type ◽  
Tryptophan Hydroxylase 2 ◽  
Age Dependent ◽  
Long Time ◽  
Time Required

The role of brain stem serotonin (5-hydroxytryptamine, 5-HT) in autoresuscitation in neonatal life is unclear. We hypothesized that a specific loss of 5-HT would compromise gasping and autoresuscitation mainly in the second postnatal week and that acute restoration of 5-HT would reverse the defects. We exposed postnatal day (P)4–5, P8–9, and P11–12 tryptophan-hydroxylase-2 knockout ( TPH2−/−) and wild-type littermates (WT) to 10 episodes of anoxia (97% N2, 3% CO2), measuring survival, gasp latency, gasp frequency ( fB), and the time required to restore eupnea and heart rate. We also tested P8–9 TPH2−/− mice after restoring 5-HT with a single injection of 5-hydroxytryptophan (5-HTP) 1–2 h before testing or with multiple injections beginning 24 h before testing. At P4–5 and P8–9, but not at P11–12, gasp latency and the recovery of eupnea were delayed ∼2- to 3-fold in TPH2−/− pups compared with WT ( P < 0.001). At all ages, TPH2−/− pups displayed reduced gasp fB (∼20–30%; P < 0.001) and delayed heart rate recovery (∼60%; P = 0.002) compared with WT littermates. TPH2−/− survival was reduced compared with WT ( P < 0.001), especially at P8–9 and P11–12 ( P = 0.004). Whereas 1–2 h of 5-HTP treatment improved the gasp latency and fB of P8–9 TPH2−/− pups, improved cardiorespiratory recovery and survival required 24 h of treatment. Our data suggest that 5-HT operates over a long time span (∼24 h) to improve survival during episodic severe hypoxia. Early in development (P4–9), 5-HT is critical for both respiratory and cardiovascular components of autoresuscitation; later (P11–12), it is critical mainly for cardiovascular components. Nevertheless, the effect of 5-HT deficiency on survival is most striking from P8 to P12.

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