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The TORC1-Sch9-Rim15 signaling pathway represses yeast-to-hypha transition in response to glycerol availability in the oleaginous yeast Yarrowia lipolytica.

Identifieur interne : 000716 ( Main/Exploration ); précédent : 000715; suivant : 000717

The TORC1-Sch9-Rim15 signaling pathway represses yeast-to-hypha transition in response to glycerol availability in the oleaginous yeast Yarrowia lipolytica.

Auteurs : Shu-Heng Liang [République populaire de Chine] ; Heng Wu [République populaire de Chine] ; Rui-Rui Wang [République populaire de Chine] ; Qiang Wang [République populaire de Chine] ; Tao Shu [République populaire de Chine] ; Xiang-Dong Gao [République populaire de Chine]

Source :

RBID : pubmed:28188651

Descripteurs français

English descriptors

Abstract

The yeast-to-hypha dimorphic transition is important for survival under nutrient starvation in fungi. The oleaginous yeast Yarrowia lipolytica grows in the oval-shaped yeast form in glycerol media whereas it adopts a filamentous form in glucose media. It is not clear why this yeast responds differently to glycerol and glucose. Here, we show that glycerol blocks dimorphic transition even in the presence of glucose whereas glycerol depletion induces filamentous growth, suggesting that dimorphic transition is repressed in response to glycerol availability. We show that the repression of dimorphic transition in glycerol media is mediated by the TORC1-Sch9 signaling pathway as both TORC1 inhibition and the loss of YlSch9 cause hyperfilamentation. TORC1-Sch9 signaling inhibits the nuclear translocation of YlRim15, a protein kinase that positively regulates filamentous growth, preventing it from entering the nucleus to activate the transcription of genes implicated in filamentous growth. Interestingly, TORC1-Sch9 signaling appears not to inhibit YlRim15 in glucose media, which could explain why Y. lipolytica responds differently to glycerol and glucose. We identified MHY1, a transcription factor-encoding gene known to be critical for filamentous growth, as one target regulated by the TORC1-Sch9-Rim15 signaling pathway. Our results provide new insights in the regulation of dimorphic transition in yeast.

DOI: 10.1111/mmi.13645
PubMed: 28188651


Affiliations:


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<term>Amino Acid Sequence (MeSH)</term>
<term>Fungal Proteins (metabolism)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>Glucose (metabolism)</term>
<term>Glycerol (metabolism)</term>
<term>Hyphae (growth & development)</term>
<term>Hyphae (metabolism)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Multiprotein Complexes (genetics)</term>
<term>Multiprotein Complexes (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Transcription Factors (metabolism)</term>
<term>Yarrowia (genetics)</term>
<term>Yarrowia (growth & development)</term>
<term>Yarrowia (metabolism)</term>
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<term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term>
<term>Complexes multiprotéiques (génétique)</term>
<term>Complexes multiprotéiques (métabolisme)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Glucose (métabolisme)</term>
<term>Glycérol (métabolisme)</term>
<term>Hyphae (croissance et développement)</term>
<term>Hyphae (métabolisme)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Protéines fongiques (métabolisme)</term>
<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Séquence d'acides aminés (MeSH)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
<term>Yarrowia (croissance et développement)</term>
<term>Yarrowia (génétique)</term>
<term>Yarrowia (métabolisme)</term>
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<term>TOR Serine-Threonine Kinases</term>
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<term>Glycerol</term>
<term>Multiprotein Complexes</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transcription Factors</term>
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<term>Hyphae</term>
<term>Yarrowia</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Yarrowia</term>
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<keywords scheme="MESH" qualifier="growth & development" xml:lang="en">
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<term>Yarrowia</term>
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<term>Hyphae</term>
<term>Protein-Serine-Threonine Kinases</term>
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<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Régulation de l'expression des gènes fongiques</term>
<term>Séquence d'acides aminés</term>
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<div type="abstract" xml:lang="en">The yeast-to-hypha dimorphic transition is important for survival under nutrient starvation in fungi. The oleaginous yeast Yarrowia lipolytica grows in the oval-shaped yeast form in glycerol media whereas it adopts a filamentous form in glucose media. It is not clear why this yeast responds differently to glycerol and glucose. Here, we show that glycerol blocks dimorphic transition even in the presence of glucose whereas glycerol depletion induces filamentous growth, suggesting that dimorphic transition is repressed in response to glycerol availability. We show that the repression of dimorphic transition in glycerol media is mediated by the TORC1-Sch9 signaling pathway as both TORC1 inhibition and the loss of YlSch9 cause hyperfilamentation. TORC1-Sch9 signaling inhibits the nuclear translocation of YlRim15, a protein kinase that positively regulates filamentous growth, preventing it from entering the nucleus to activate the transcription of genes implicated in filamentous growth. Interestingly, TORC1-Sch9 signaling appears not to inhibit YlRim15 in glucose media, which could explain why Y. lipolytica responds differently to glycerol and glucose. We identified MHY1, a transcription factor-encoding gene known to be critical for filamentous growth, as one target regulated by the TORC1-Sch9-Rim15 signaling pathway. Our results provide new insights in the regulation of dimorphic transition in yeast.</div>
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<DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName>
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<DescriptorName UI="D025301" MajorTopicYN="N">Hyphae</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading>
<DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
<DescriptorName UI="D025062" MajorTopicYN="N">Yarrowia</DescriptorName>
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<QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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</MedlineCitation>
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<Year>2017</Year>
<Month>02</Month>
<Day>07</Day>
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<Year>2017</Year>
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<li>République populaire de Chine</li>
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<region>
<li>Hubei</li>
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<settlement>
<li>Wuhan</li>
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<orgName>
<li>Université de Wuhan</li>
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<country name="République populaire de Chine">
<region name="Hubei">
<name sortKey="Liang, Shu Heng" sort="Liang, Shu Heng" uniqKey="Liang S" first="Shu-Heng" last="Liang">Shu-Heng Liang</name>
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<name sortKey="Gao, Xiang Dong" sort="Gao, Xiang Dong" uniqKey="Gao X" first="Xiang-Dong" last="Gao">Xiang-Dong Gao</name>
<name sortKey="Gao, Xiang Dong" sort="Gao, Xiang Dong" uniqKey="Gao X" first="Xiang-Dong" last="Gao">Xiang-Dong Gao</name>
<name sortKey="Shu, Tao" sort="Shu, Tao" uniqKey="Shu T" first="Tao" last="Shu">Tao Shu</name>
<name sortKey="Wang, Qiang" sort="Wang, Qiang" uniqKey="Wang Q" first="Qiang" last="Wang">Qiang Wang</name>
<name sortKey="Wang, Rui Rui" sort="Wang, Rui Rui" uniqKey="Wang R" first="Rui-Rui" last="Wang">Rui-Rui Wang</name>
<name sortKey="Wu, Heng" sort="Wu, Heng" uniqKey="Wu H" first="Heng" last="Wu">Heng Wu</name>
</country>
</tree>
</affiliations>
</record>

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