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Natural Variation in SER1 and ENA6 Underlie Condition-Specific Growth Defects in Saccharomyces cerevisiae.

Identifieur interne : 000540 ( Main/Exploration ); précédent : 000539; suivant : 000541

Natural Variation in SER1 and ENA6 Underlie Condition-Specific Growth Defects in Saccharomyces cerevisiae.

Auteurs : Amy Sirr [États-Unis] ; Adrian C. Scott [États-Unis] ; Gareth A. Cromie [États-Unis] ; Catherine L. Ludlow [États-Unis] ; Vida Ahyong [États-Unis] ; Trey S. Morgan [États-Unis] ; Teresa Gilbert ; Aimée M. Dudley [Oman]

Source :

RBID : pubmed:29138237

Descripteurs français

English descriptors

Abstract

Despite their ubiquitous use in laboratory strains, naturally occurring loss-of-function mutations in genes encoding core metabolic enzymes are relatively rare in wild isolates of Saccharomyces cerevisiae Here, we identify a naturally occurring serine auxotrophy in a sake brewing strain from Japan. Through a cross with a honey wine (white tecc) brewing strain from Ethiopia, we map the minimal medium growth defect to SER1, which encodes 3-phosphoserine aminotransferase and is orthologous to the human disease gene, PSAT1 To investigate the impact of this polymorphism under conditions of abundant external nutrients, we examine growth in rich medium alone or with additional stresses, including the drugs caffeine and rapamycin and relatively high concentrations of copper, salt, and ethanol. Consistent with studies that found widespread effects of different auxotrophies on RNA expression patterns in rich media, we find that the SER1 loss-of-function allele dominates the quantitative trait locus (QTL) landscape under many of these conditions, with a notable exacerbation of the effect in the presence of rapamycin and caffeine. We also identify a major-effect QTL associated with growth on salt that maps to the gene encoding the sodium exporter, ENA6 We demonstrate that the salt phenotype is largely driven by variation in the ENA6 promoter, which harbors a deletion that removes binding sites for the Mig1 and Nrg1 transcriptional repressors. Thus, our results identify natural variation associated with both coding and regulatory regions of the genome that underlie strong growth phenotypes.

DOI: 10.1534/g3.117.300392
PubMed: 29138237
PubMed Central: PMC5765352


Affiliations:


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Le document en format XML

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<term>Culture Media (pharmacology)</term>
<term>Ethanol (pharmacology)</term>
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<term>Humans (MeSH)</term>
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<term>Repressor Proteins (metabolism)</term>
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<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (growth & development)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
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<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Salts (pharmacology)</term>
<term>Sirolimus (pharmacology)</term>
<term>Sodium-Potassium-Exchanging ATPase (deficiency)</term>
<term>Sodium-Potassium-Exchanging ATPase (genetics)</term>
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<term>Transaminases (genetics)</term>
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<term>Caféine (pharmacologie)</term>
<term>Cuivre (pharmacologie)</term>
<term>Fermentation (MeSH)</term>
<term>Génome fongique (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Locus de caractère quantitatif (MeSH)</term>
<term>Milieux de culture (pharmacologie)</term>
<term>Polymorphisme génétique (MeSH)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines de répression (métabolisme)</term>
<term>Régions promotrices (génétique) (MeSH)</term>
<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Saccharomyces cerevisiae (croissance et développement)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Sels (pharmacologie)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Sodium-Potassium-Exchanging ATPase (déficit)</term>
<term>Sodium-Potassium-Exchanging ATPase (génétique)</term>
<term>Transaminases (déficit)</term>
<term>Transaminases (génétique)</term>
<term>Éthanol (pharmacologie)</term>
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<term>Transaminases</term>
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<term>Sodium-Potassium-Exchanging ATPase</term>
<term>Transaminases</term>
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<term>Culture Media</term>
<term>Ethanol</term>
<term>Salts</term>
<term>Sirolimus</term>
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<term>Saccharomyces cerevisiae</term>
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<term>Sodium-Potassium-Exchanging ATPase</term>
<term>Transaminases</term>
</keywords>
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<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Saccharomyces cerevisiae</term>
</keywords>
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<term>Saccharomyces cerevisiae</term>
</keywords>
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<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines de répression</term>
<term>Saccharomyces cerevisiae</term>
<term>Sodium-Potassium-Exchanging ATPase</term>
<term>Transaminases</term>
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<term>Saccharomyces cerevisiae</term>
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<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines de répression</term>
<term>Saccharomyces cerevisiae</term>
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<term>Cuivre</term>
<term>Milieux de culture</term>
<term>Sels</term>
<term>Sirolimus</term>
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<term>Humains</term>
<term>Locus de caractère quantitatif</term>
<term>Polymorphisme génétique</term>
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<front>
<div type="abstract" xml:lang="en">Despite their ubiquitous use in laboratory strains, naturally occurring loss-of-function mutations in genes encoding core metabolic enzymes are relatively rare in wild isolates of
<i>Saccharomyces cerevisiae</i>
Here, we identify a naturally occurring serine auxotrophy in a sake brewing strain from Japan. Through a cross with a honey wine (white tecc) brewing strain from Ethiopia, we map the minimal medium growth defect to
<i>SER1</i>
, which encodes 3-phosphoserine aminotransferase and is orthologous to the human disease gene,
<i>PSAT1</i>
To investigate the impact of this polymorphism under conditions of abundant external nutrients, we examine growth in rich medium alone or with additional stresses, including the drugs caffeine and rapamycin and relatively high concentrations of copper, salt, and ethanol. Consistent with studies that found widespread effects of different auxotrophies on RNA expression patterns in rich media, we find that the
<i>SER1</i>
loss-of-function allele dominates the quantitative trait locus (QTL) landscape under many of these conditions, with a notable exacerbation of the effect in the presence of rapamycin and caffeine. We also identify a major-effect QTL associated with growth on salt that maps to the gene encoding the sodium exporter,
<i>ENA6</i>
We demonstrate that the salt phenotype is largely driven by variation in the
<i>ENA6</i>
promoter, which harbors a deletion that removes binding sites for the Mig1 and Nrg1 transcriptional repressors. Thus, our results identify natural variation associated with both coding and regulatory regions of the genome that underlie strong growth phenotypes.</div>
</front>
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Underlie Condition-Specific Growth Defects in
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<Abstract>
<AbstractText>Despite their ubiquitous use in laboratory strains, naturally occurring loss-of-function mutations in genes encoding core metabolic enzymes are relatively rare in wild isolates of
<i>Saccharomyces cerevisiae</i>
Here, we identify a naturally occurring serine auxotrophy in a sake brewing strain from Japan. Through a cross with a honey wine (white tecc) brewing strain from Ethiopia, we map the minimal medium growth defect to
<i>SER1</i>
, which encodes 3-phosphoserine aminotransferase and is orthologous to the human disease gene,
<i>PSAT1</i>
To investigate the impact of this polymorphism under conditions of abundant external nutrients, we examine growth in rich medium alone or with additional stresses, including the drugs caffeine and rapamycin and relatively high concentrations of copper, salt, and ethanol. Consistent with studies that found widespread effects of different auxotrophies on RNA expression patterns in rich media, we find that the
<i>SER1</i>
loss-of-function allele dominates the quantitative trait locus (QTL) landscape under many of these conditions, with a notable exacerbation of the effect in the presence of rapamycin and caffeine. We also identify a major-effect QTL associated with growth on salt that maps to the gene encoding the sodium exporter,
<i>ENA6</i>
We demonstrate that the salt phenotype is largely driven by variation in the
<i>ENA6</i>
promoter, which harbors a deletion that removes binding sites for the Mig1 and Nrg1 transcriptional repressors. Thus, our results identify natural variation associated with both coding and regulatory regions of the genome that underlie strong growth phenotypes.</AbstractText>
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<Grant>
<GrantID>R01 GM089978</GrantID>
<Acronym>GM</Acronym>
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<name sortKey="Ludlow, Catherine L" sort="Ludlow, Catherine L" uniqKey="Ludlow C" first="Catherine L" last="Ludlow">Catherine L. Ludlow</name>
<name sortKey="Morgan, Trey S" sort="Morgan, Trey S" uniqKey="Morgan T" first="Trey S" last="Morgan">Trey S. Morgan</name>
<name sortKey="Scott, Adrian C" sort="Scott, Adrian C" uniqKey="Scott A" first="Adrian C" last="Scott">Adrian C. Scott</name>
</country>
<country name="Oman">
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<name sortKey="Dudley, Aimee M" sort="Dudley, Aimee M" uniqKey="Dudley A" first="Aimée M" last="Dudley">Aimée M. Dudley</name>
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EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000540 | SxmlIndent | more

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{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:29138237
   |texte=   Natural Variation in SER1 and ENA6 Underlie Condition-Specific Growth Defects in Saccharomyces cerevisiae.
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This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020