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"Genetic Fitness"
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Genetic Diversity and the Efficacy of Purifying Selection across Plant and Animal Species
A central question in evolutionary biology is why some species have more genetic diversity than others and a no less important question is why selection efficacy varies among species. Although these questions have started to be tackled in animals, they have not been addressed to the same extent in plants. Here, we estimated nucleotide diversity at synonymous, πS, and nonsynonymous sites, πN, and a measure of the efficacy of selection, the ratio πN/πS, in 34 animal and 28 plant species using full genome data. We then evaluated the relationship of nucleotide diversity and selection efficacy with effective population size, the distribution of fitness effect and life history traits. In animals, our data confirm that longevity and propagule size are the variables that best explain the variation in πS among species. In plants longevity also plays a major role as well as mating system. As predicted by the nearly neutral theory of molecular evolution, the log of πN/πS decreased linearly with the log of πS but the slope was weaker in plants than in animals. This appears to be due to a higher mutation rate in long lived plants, and the difference disappears when πS is rescaled by the mutation rate. Differences in the distribution of fitness effect of new mutations also contributed to variation in πN/πS among species.
Journal Article
Surviving and thriving with an invisible chronic illness : how to stay sane and live one step ahead of your symptoms
\"Popular blogger Ilana Jacqueline writes poignantly about living with two debilitating autoimmune diseases and presents advice and practical tips for living with an invisible chronic illness. Do you live with a chronic, debilitating, yet invisible condition? You may feel isolated, out of step, judged, lonely, or misunderstood--and that's on top of dealing with the symptoms of your actual illness. Take heart. You are not alone, although sometimes it can feel that way. Written by a blogger who suffers from two autoimmune diseases, Surviving and Thriving with an Invisible Chronic Illness offers peer-to-peer support to help you stay sane, be your own advocate, and get back to living your life. This smart, compelling guide is written for anyone suffering with an illness no one can see--such as postural orthostatic tachycardia syndrome (POTS), chronic fatigue syndrome (CFS), fibromyalgia, multiple chemical sensitivity (MCS), Lyme disease, lupus, dysautonomia, or even multiple sclerosis (MP). This book will tell you everything you need to know about living with a complicated, invisible condition--from how to balance sex, dating, and relationships to handling work and school with unavoidable absences. You'll also learn to navigate judg-y or skeptical relatives and strangers and--most importantly--manage your medical care. Suffering from a chronic illness doesn't mean you can't live an active, engaged life. This book will show you how\"-- Provided by publisher.
Book
Characterization of SARS-CoV-2 Omicron BA.4 and BA.5 isolates in rodents
The BA.2 sublineage of the SARS-CoV-2 Omicron variant has become dominant in most countries around the world; however, the prevalence of BA.4 and BA.5 is increasing rapidly in several regions. BA.2 is less pathogenic in animal models than previously circulating variants of concern
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. Compared with BA.2, however, BA.4 and BA.5 possess additional substitutions in the spike protein, which play a key role in viral entry, raising concerns that the replication capacity and pathogenicity of BA.4 and BA.5 are higher than those of BA.2. Here we have evaluated the replicative ability and pathogenicity of BA.4 and BA.5 isolates in wild-type Syrian hamsters, human ACE2 (hACE2) transgenic hamsters and hACE2 transgenic mice. We have observed no obvious differences among BA.2, BA.4 and BA.5 isolates in growth ability or pathogenicity in rodent models, and less pathogenicity compared to a previously circulating Delta (B.1.617.2 lineage) isolate. In addition, in vivo competition experiments revealed that BA.5 outcompeted BA.2 in hamsters, whereas BA.4 and BA.2 exhibited similar fitness. These findings suggest that BA.4 and BA.5 clinical isolates have similar pathogenicity to BA.2 in rodents and that BA.5 possesses viral fitness superior to that of BA.2.
Results indicate that the sublineages BA.4 and BA.5 of SARS-CoV-2 Omicron variants have similar pathogenicity to that of the BA.2 sublineage in rodents, highlighting the importance of evaluating viral replication and pathogenesis using clinical isolates.
Journal Article
Jellyfish age backwards : nature's secrets to longevity
Blending together the most cutting-edge research and stories from habitats all over the world, a molecular biologist explores what nature has to teach us about aging, revealing life spans we cannot imagine and physiological gifts that feel closer to magic than reality.
Book
A randomised trial examining inflammatory signaling in acutely induced hyperinsulinemia and hyperlipidemia in normal weight women-the reprometabolic syndrome
Obesity, is a state of chronic inflammation, characterized by elevated lipids, insulin resistance and relative hypogonadotropic hypogonadism. We have defined the accompanying decreased Luteinizing Hormone (LH), Follicle-Stimulating Hormone (FSH), ovarian steroids and reduced pituitary response to Gonadotropin-releasing Hormone (GnRH) as Reprometabolic syndrome, a phenotype that can be induced in healthy normal weight women (NWW) by acute infusion of free fatty acids and insulin.
To identify potential mediators of insulin and lipid-related reproductive endocrine dysfunction.
Secondary analysis of crossover study of eumenorrheic reproductive aged women of normal Body Mass Index (BMI) (<25 kg/m2) at an academic medical center.
Participants underwent 6-hour infusions of either saline/heparin or insulin plus fatty acids (Intralipid plus heparin), in the early follicular phase of sequential menstrual cycles, in random order. Euglycemia was maintained by glucose infusion. Frequent blood samples were obtained.
Pooled serum from each woman was analyzed for cytokines, interleukins, chemokines, adipokines, Fibroblast Growth Factor-21 (FGF-21) and markers of endoplasmic reticulum (ER) stress (CHOP and GRP78). Wilcoxon signed-rank tests were used to compare results across experimental conditions.
Except for Macrophage Inflammatory Protein-1β (MIP-1β), no significant differences were observed in serum levels of any of the inflammatory signaling or ER stress markers tested.
Acute infusion of lipid and insulin, to mimic the metabolic syndrome of obesity, was not associated with an increase in inflammatory markers. These results imply that the endocrine disruption and adverse reproductive outcomes of obesity are not a consequence of the ambient inflammatory environment but may be mediated by direct lipotoxic effects on the hypothalamic-pituitary-ovarian (HPO) axis.
Journal Article
Salt in my soul : an unfinished life
\"Diagnosed with cystic fibrosis at the age of three, Mallory Smith grew into a determined, talented young woman who inspired others even as she raged against her illness. Despite the daily challenges of endless medical treatments and a deep understanding that she'd never lead a normal life, Mallory was determined to 'live happy,' a mantra she followed until her death\"-- Provided by publisher.
Book
The crucial role of genome-wide genetic variation in conservation
The unprecedented rate of extinction calls for efficient use of genetics to help conserve biodiversity. Several recent genomic and simulation-based studies have argued that the field of conservation biology has placed too much focus on conserving genome-wide genetic variation, and that the field should instead focus on managing the subset of functional genetic variation that is thought to affect fitness. Here, we critically evaluate the feasibility and likely benefits of this approach in conservation. We find that population genetics theory and empirical results show that conserving genome-wide genetic variation is generally the best approach to prevent inbreeding depression and loss of adaptive potential from driving populations toward extinction. Focusing conservation efforts on presumably functional genetic variation will only be feasible occasionally, often misleading, and counterproductive when prioritized over genome-wide genetic variation. Given the increasing rate of habitat loss and other environmental changes, failure to recognize the detrimental effects of lost genome-wide genetic variation on long-term population viability will only worsen the biodiversity crisis.
Journal Article
A predictive fitness model for influenza
The seasonal human influenza A/H3N2 virus undergoes rapid evolution, which produces significant year-to-year sequence turnover in the population of circulating strains. Adaptive mutations respond to human immune challenge and occur primarily in antigenic epitopes, the antibody-binding domains of the viral surface protein haemagglutinin. Here we develop a fitness model for haemagglutinin that predicts the evolution of the viral population from one year to the next. Two factors are shown to determine the fitness of a strain: adaptive epitope changes and deleterious mutations outside the epitopes. We infer both fitness components for the strains circulating in a given year, using population-genetic data of all previous strains. From fitness and frequency of each strain, we predict the frequency of its descendent strains in the following year. This fitness model maps the adaptive history of influenza A and suggests a principled method for vaccine selection. Our results call for a more comprehensive epidemiology of influenza and other fast-evolving pathogens that integrates antigenic phenotypes with other viral functions coupled by genetic linkage.
A computational approach for predicting the future evolution of the human influenza virus, based on population-genetic data of previous strains, is presented; this model holds promise for improving vaccine strain selection for seasonal influenza.
Keeping tabs on influenza virus evolution
Marta Łuksza and Michael Lässig present a computational approach for predicting the future evolution of influenza virus. The authors develop a fitness model for the influenza haemagglutinin protein, based on population-genetic data from all previous strains, that allows them to predict the future evolution of currently existing clades. This computational model holds promise for improving vaccine strain selection.
Journal Article
Synonymous mutations in representative yeast genes are mostly strongly non-neutral
Synonymous mutations in protein-coding genes do not alter protein sequences and are thus generally presumed to be neutral or nearly neutral
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. Here, to experimentally verify this presumption, we constructed 8,341 yeast mutants each carrying a synonymous, nonsynonymous or nonsense mutation in one of 21 endogenous genes with diverse functions and expression levels and measured their fitness relative to the wild type in a rich medium. Three-quarters of synonymous mutations resulted in a significant reduction in fitness, and the distribution of fitness effects was overall similar—albeit nonidentical—between synonymous and nonsynonymous mutations. Both synonymous and nonsynonymous mutations frequently disturbed the level of mRNA expression of the mutated gene, and the extent of the disturbance partially predicted the fitness effect. Investigations in additional environments revealed greater across-environment fitness variations for nonsynonymous mutants than for synonymous mutants despite their similar fitness distributions in each environment, suggesting that a smaller proportion of nonsynonymous mutants than synonymous mutants are always non-deleterious in a changing environment to permit fixation, potentially explaining the common observation of substantially lower nonsynonymous than synonymous substitution rates. The strong non-neutrality of most synonymous mutations, if it holds true for other genes and in other organisms, would require re-examination of numerous biological conclusions about mutation, selection, effective population size, divergence time and disease mechanisms that rely on the assumption that synoymous mutations are neutral.
A survey of 8,341 mutations in 21 yeast genes shows that synonymous mutations are nearly as harmful as nonsynonymous mutations, in part because they both affect the mRNA level of the gene mutated.
Journal Article