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"McDonald, Michael"
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Sex speeds adaptation by altering the dynamics of molecular evolution
In a comparison between replicate sexual and asexual populations of
Saccharomyces cerevisiae
, sexual reproduction increases fitness by reducing clonal interference and alters the type of mutations that get fixed by natural selection.
Sex makes natural selection more efficient
Explaining the prevalence of sexual reproduction despite its costly nature is a famously long-standing question in evolutionary biology. Theory and some experimental studies suggest various mechanisms responsible, such as a reduction in clonal interference or the ability to reduce hitchhiking of deleterious mutations. Using the experimental evolution of
Saccharomyces cerevisiae
as a model system, Michael Desai and colleagues compared the sequence-level dynamics of adaptation in sexual and asexual populations. They find that sexual reproduction increases fitness by reducing clonal interference between beneficial mutations and alters the type of mutations that are fixed by natural selection. The net effect is that that sex speeds adaptation and allows natural selection to more efficiently sort beneficial from deleterious mutations.
Sex and recombination are pervasive throughout nature despite their substantial costs
1
. Understanding the evolutionary forces that maintain these phenomena is a central challenge in biology
2
,
3
. One longstanding hypothesis argues that sex is beneficial because recombination speeds adaptation
4
. Theory has proposed several distinct population genetic mechanisms that could underlie this advantage. For example, sex can promote the fixation of beneficial mutations either by alleviating interference competition (the Fisher–Muller effect)
5
,
6
or by separating them from deleterious load (the ruby in the rubbish effect)
7
,
8
. Previous experiments confirm that sex can increase the rate of adaptation
9
,
10
,
11
,
12
,
13
,
14
,
15
,
16
,
17
, but these studies did not observe the evolutionary dynamics that drive this effect at the genomic level. Here we present the first, to our knowledge, comparison between the sequence-level dynamics of adaptation in experimental sexual and asexual
Saccharomyces cerevisiae
populations, which allows us to identify the specific mechanisms by which sex speeds adaptation. We find that sex alters the molecular signatures of evolution by changing the spectrum of mutations that fix, and confirm theoretical predictions that it does so by alleviating clonal interference. We also show that substantially deleterious mutations hitchhike to fixation in adapting asexual populations. In contrast, recombination prevents such mutations from fixing. Our results demonstrate that sex both speeds adaptation and alters its molecular signature by allowing natural selection to more efficiently sort beneficial from deleterious mutations.
Journal Article
Food culture in Central America
This entry in the Food Culture around the World series helps those in the United States understand the new immigrants from Central America who have brought their food cultures with them.
Book
The dynamics of molecular evolution over 60,000 generations
The outcomes of evolution are determined by a stochastic dynamical process that governs how mutations arise and spread through a population. However, it is difficult to observe these dynamics directly over long periods and across entire genomes. Here we analyse the dynamics of molecular evolution in twelve experimental populations of
Escherichia coli
, using whole-genome metagenomic sequencing at five hundred-generation intervals through sixty thousand generations. Although the rate of fitness gain declines over time, molecular evolution is characterized by signatures of rapid adaptation throughout the duration of the experiment, with multiple beneficial variants simultaneously competing for dominance in each population. Interactions between ecological and evolutionary processes play an important role, as long-term quasi-stable coexistence arises spontaneously in most populations, and evolution continues within each clade. We also present evidence that the targets of natural selection change over time, as epistasis and historical contingency alter the strength of selection on different genes. Together, these results show that long-term adaptation to a constant environment can be a more complex and dynamic process than is often assumed.
Using data from sixty thousand generations of the
E. coli
long-term evolution experiment, the authors shed new light on the processes that govern molecular evolution.
60,000 generations of bacterial evolution
The
Escherichia coli
long-term evolution experiment (LTEE) is the longest running bacterial evolution experiment, including 12 replicate populations of
E. coli
serially propagated for more than 60,000 generations. Michael Desai, Richard Lenski and colleagues now report whole-genome sequencing at 500-generation intervals over the course of the 60,000 generations from the LTEE. Their analyses reveal a complex and dynamic evolutionary process of long-term bacterial adaptation in this controlled environment, and include findings on clonal inference, genetic drift and shifting targets of selection.
Journal Article
Randomized Trial of a Third Dose of mRNA-1273 Vaccine in Transplant Recipients
It is known that people receiving immune suppressive therapy, such as recipients of solid-organ transplants, have a suboptimal response to SARS-CoV-2 vaccination. In a randomized, double-blind trial, a third dose of the mRNA-1273 vaccine was compared with placebo. The third dose of vaccine produced a significant boost in neutralizing antibodies.
Journal Article
Diverse hydrogen production and consumption pathways influence methane production in ruminants
Farmed ruminants are the largest source of anthropogenic methane emissions globally. The methanogenic archaea responsible for these emissions use molecular hydrogen (H
2
), produced during bacterial and eukaryotic carbohydrate fermentation, as their primary energy source. In this work, we used comparative genomic, metatranscriptomic and co-culture-based approaches to gain a system-wide understanding of the organisms and pathways responsible for ruminal H
2
metabolism. Two-thirds of sequenced rumen bacterial and archaeal genomes encode enzymes that catalyse H
2
production or consumption, including 26 distinct hydrogenase subgroups. Metatranscriptomic analysis confirmed that these hydrogenases are differentially expressed in sheep rumen. Electron-bifurcating [FeFe]-hydrogenases from carbohydrate-fermenting Clostridia (e.g.,
Ruminococcus
) accounted for half of all hydrogenase transcripts. Various H
2
uptake pathways were also expressed, including methanogenesis (
Methanobrevibacter
), fumarate and nitrite reduction (
Selenomonas
), and acetogenesis (
Blautia
). Whereas methanogenesis-related transcripts predominated in high methane yield sheep, alternative uptake pathways were significantly upregulated in low methane yield sheep. Complementing these findings, we observed significant differential expression and activity of the hydrogenases of the hydrogenogenic cellulose fermenter
Ruminococcus albus
and the hydrogenotrophic fumarate reducer
Wolinella succinogenes
in co-culture compared with pure culture. We conclude that H
2
metabolism is a more complex and widespread trait among rumen microorganisms than previously recognised. There is evidence that alternative hydrogenotrophs, including acetogenic and respiratory bacteria, can prosper in the rumen and effectively compete with methanogens for H
2
. These findings may help to inform ongoing strategies to mitigate methane emissions by increasing flux through alternative H
2
uptake pathways, including through animal selection, dietary supplementation and methanogenesis inhibitors.
Journal Article
DNA Double-Strand Break Accumulation in Alzheimer’s Disease: Evidence from Experimental Models and Postmortem Human Brains
Alzheimer’s disease (AD) is a progressive neurodegenerative disease that accounts for a majority of dementia cases. AD is characterized by progressive neuronal death associated with neuropathological lesions consisting of neurofibrillary tangles and senile plaques. While the pathogenesis of AD has been widely investigated, significant gaps in our knowledge remain about the cellular and molecular mechanisms promoting AD. Recent studies have highlighted the role of DNA damage, particularly DNA double-strand breaks (DSBs), in the progression of neuronal loss in a broad spectrum of neurodegenerative diseases. In the present study, we tested the hypothesis that accumulation of DNA DSB plays an important role in AD pathogenesis. To test our hypothesis, we examined DNA DSB expression and DNA repair function in the hippocampus of human AD and non-AD brains by immunohistochemistry, ELISA, and RT-qPCR. We observed increased DNA DSB accumulation and reduced DNA repair function in the hippocampus of AD brains compared to the non-AD control brains. Next, we found significantly increased levels of DNA DSB and altered levels of DNA repair proteins in the hippocampus of 5xFAD mice compared to non-transgenic mice. Interestingly, increased accumulation of DNA DSBs and altered DNA repair proteins were also observed in cellular models of AD. These findings provided compelling evidence that AD is associated with accumulation of DNA DSB and/or alteration in DSB repair proteins which may influence an important early part of the pathway toward neural damage and memory loss in AD.
Journal Article