Mapping Viral Susceptibility Loci in Mice

Kane, Melissa; Golovkina, Tatyana V.

doi:10.1146/annurev-virology-092818-015544

Cited by 7 publications

(10 citation statements)

References 141 publications

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“…Sample sizes are small, and results sometimes conflicting, hence no firm conclusions can be drawn. There are several studies identifying genes of interest from mouse models (Kane and Golovkina, 2019) and some information from interspecies comparisons (Hou et al, 2010;Sironi et al, 2015). To date, candidate genes for published human studies have included pathogen receptor genes and loci controlling innate and adaptive immunity.…”

Section: Genetic Control Of Susceptibility and Approaches To Studymentioning

confidence: 99%

SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

Sironi

Hasnain

Rosenthal

et al. 2020

Infection, Genetics and Evolution

133

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In less than five months, COVID-19 has spread from a small focus in Wuhan, China, to more than 5 million people in almost every country in the world, dominating the concern of most governments and public health systems. The social and political distresses caused by this epidemic will certainly impact our world for a long time to come. Here, we synthesize lessons from a range of scientific perspectives rooted in epidemiology, virology, genetics, ecology and evolutionary biology so as to provide perspective on how this pandemic started, how it is developing, and how best we can stop it. The origin of SARS-CoV-2 and COVID-19The novel human coronavirus (SARS-CoV-2), responsible for the current COVID-19 pandemic, was first identified in December 2019, in the Hubei province of China (Zhu et al., 2020). After SARS-CoV (severe acute respiratory syndrome coronavirus) and MERS-CoV (Middle East

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Section: Genetic Control Of Susceptibility and Approaches To Studymentioning

confidence: 99%

SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

Sironi

Hasnain

Rosenthal

et al. 2020

Infection, Genetics and Evolution

133

View full text Add to dashboard Cite

show abstract

“…If resistance has no fitness cost, such variants will rapidly fix within host species. Even if these variants are slightly deleterious, such variants could be maintained in quasi-equilibrium in host species 4-7 . Studies in diverse biological taxa have leveraged genetic mapping strategies to identify quantitative trait loci (QTL) for host resistance to parasites [8][9][10][11] . Such studies have revealed that host populations are more likely to harbor variation in resistance to coevolved, rather than to recently introduced, parasites 12 .…”

Section: Introductionmentioning

confidence: 99%

“…Studies in diverse biological taxa have leveraged genetic mapping strategies to identify quantitative trait loci (QTL) for host resistance to parasites ( Kane and Golovkina, 2019 ; Cogni et al, 2016 ; Kelleher et al, 2018 ; Duffy and Sivars-Becker, 2007 ). Such studies have revealed that host populations are more likely to harbor variation in resistance to coevolved, rather than to recently introduced, parasites ( Duxbury et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

A natural variant of the essential host gene MMS21 restricts the parasitic 2-micron plasmid in Saccharomyces cerevisiae

Hays

Young

Levan

et al. 2020

eLife

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Antagonistic coevolution with selfish genetic elements (SGEs) can drive evolution of host resistance. Here, we investigated host suppression of 2-micron (2m) plasmids, multicopy nuclear parasites that have co-evolved with budding yeasts. We developed SCAMPR (Single-Cell Assay for Measuring Plasmid Retention) to measure copy number heterogeneity and 2m plasmid loss in live cells. We identified three S. cerevisiae strains that lack endogenous 2m plasmids and reproducibly inhibit mitotic plasmid stability. Focusing on the Y9 ragi strain, we determined that plasmid restriction is heritable and dominant. Using bulk segregant analysis, we identified a high-confidence Quantitative Trait Locus (QTL) with a single variant of MMS21 associated with increased 2m instability. MMS21 encodes a SUMO E3 ligase and an essential component of the Smc5/6 complex, involved in sister chromatid cohesion, chromosome segregation, and DNA repair. Our analyses leverage natural variation to uncover a novel means by which budding yeasts can overcome highly successful genetic parasites.

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“…Studies in diverse biological taxa have leveraged genetic mapping strategies to identify quantitative trait loci (QTL) for host resistance to parasites [8][9][10][11] . Such studies have revealed that host populations are more likely to harbor variation in resistance to coevolved, rather than to recently introduced, parasites 12 .…”

Section: Introductionmentioning

confidence: 99%

“…Even if there were fitness consequences, such variants could be maintained in quasi-equilibrium in host metapopulations [4][5][6][7] . Studies in diverse biological taxa have leveraged genetic mapping strategies to identify quantitative trait loci (QTL) for host resistance to parasites [8][9][10][11] . Host populations are more likely to harbor variation in resistance to coevolved, rather than to recently introduced, parasites 12 .…”

Section: Introductionmentioning

confidence: 99%

A natural variant of the essential host geneMMS21restricts the parasitic 2-micron plasmid inSaccharomyces cerevisiae

Hays

Young

Levan

et al. 2020

Preprint

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Ongoing antagonistic coevolution with selfish genetic elements (SGEs) can drive the evolution of host genomes. Here, we investigated whether natural variation allows some Saccharomyces cerevisiae strains to suppress their endogenous SGEs, 2-micron plasmids. 2-micron plasmids are multicopy nuclear parasites that have co-evolved with budding yeasts. To quantitatively measure plasmid stability, we developed a new Single-Cell Assay for Measuring Plasmid Retention (SCAMPR) that measures copy number heterogeneity and 2-micron plasmid loss dynamics in live cells. Next, using a survey of 52 natural S. cerevisiae isolates, we identified three strains that lack endogenous 2micron plasmids, and find that plasmid resistance is heritable. Focusing on one isolate (Y9 ragi strain), we determined that plasmid restriction is dominant and is a multigenic trait. Through Quantitative Trait Locus (QTL) mapping by bulk segregant analysis, we identified a high-confidence QTL for plasmid instability on Y9 chromosome V. We show that a single amino acid change in MMS21 is associated with increased 2-micron resistance. MMS21 encodes a SUMO E3 ligase and is an essential member of the Smc5/6 complex involved in sister chromatid cohesion, chromosome segregation, and DNA repair. Our analyses leverage standing variation in natural yeast isolates to identify a novel host determinant of plasmid stability and reveal variants in essential genes that may help hosts mitigate the fitness costs of genetic conflicts with SGEs.

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Mapping Viral Susceptibility Loci in Mice

Cited by 7 publications

References 141 publications

SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

A natural variant of the essential host gene MMS21 restricts the parasitic 2-micron plasmid in Saccharomyces cerevisiae

A natural variant of the essential host geneMMS21restricts the parasitic 2-micron plasmid inSaccharomyces cerevisiae

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