ChloroquineV1, Pmc, Checkpoint, bibRecord, 000A41

Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB

Identifieur interne : 000A41 ( Pmc/Checkpoint ); précédent : 000A40; suivant : 000A42

Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB

Auteurs : Yusha Wang ; Yewei Huang ; Jiaqi Liu ; Jinna Zhang ; Mingming Xu ; Zhiyuan You ; Chao Peng ; Zhefeng Gong ; Wei Liu

Source :

EMBO Reports [ 1469-221X ] ; 2019.

RBID : PMC:6945067

Abstract

Accumulating evidence highlights the role of histone acetyltransferase GCN5 in the regulation of cell metabolism in metazoans. Here, we report that GCN5 is a negative regulator of autophagy, a lysosome‐dependent catabolic mechanism. In animal cells and Drosophila, GCN5 inhibits the biogenesis of autophagosomes and lysosomes by targeting TFEB, the master transcription factor for autophagy‐ and lysosome‐related gene expression. We show that GCN5 is a specific TFEB acetyltransferase, and acetylation by GCN5 results in the decrease in TFEB transcriptional activity. Induction of autophagy inactivates GCN5, accompanied by reduced TFEB acetylation and increased lysosome formation. We further demonstrate that acetylation at K274 and K279 disrupts the dimerization of TFEB and the binding of TFEB to its target gene promoters. In a Tau‐based neurodegenerative Drosophila model, deletion of dGcn5 improves the clearance of Tau protein aggregates and ameliorates the neurodegenerative phenotypes. Together, our results reveal GCN5 as a novel conserved TFEB regulator, and the regulatory mechanisms may be involved in autophagy‐ and lysosome‐related physiological and pathological processes.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6945067

DOI: 10.15252/embr.201948335
PubMed: 31750630
PubMed Central: 6945067

Affiliations:

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<p>Accumulating evidence highlights the role of histone acetyltransferase GCN5 in the regulation of cell metabolism in metazoans. Here, we report that GCN5 is a negative regulator of autophagy, a lysosome‐dependent catabolic mechanism. In animal cells and <italic>Drosophila</italic>
, GCN5 inhibits the biogenesis of autophagosomes and lysosomes by targeting TFEB, the master transcription factor for autophagy‐ and lysosome‐related gene expression. We show that GCN5 is a specific TFEB acetyltransferase, and acetylation by GCN5 results in the decrease in TFEB transcriptional activity. Induction of autophagy inactivates GCN5, accompanied by reduced TFEB acetylation and increased lysosome formation. We further demonstrate that acetylation at K274 and K279 disrupts the dimerization of TFEB and the binding of TFEB to its target gene promoters. In a Tau‐based neurodegenerative <italic>Drosophila</italic>
 model, deletion of dGcn5 improves the clearance of Tau protein aggregates and ameliorates the neurodegenerative phenotypes. Together, our results reveal GCN5 as a novel conserved TFEB regulator, and the regulatory mechanisms may be involved in autophagy‐ and lysosome‐related physiological and pathological processes.</p>
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<title-group><article-title>Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB</article-title>
<alt-title alt-title-type="left-running-head">Yusha Wang <italic>et al</italic>
</alt-title>
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<contrib-group><contrib id="embr201948335-cr-0001" contrib-type="author"><name><surname>Wang</surname>
<given-names>Yusha</given-names>
</name>
<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
</xref>
</contrib>
<contrib id="embr201948335-cr-0002" contrib-type="author"><name><surname>Huang</surname>
<given-names>Yewei</given-names>
</name>
<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
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<contrib id="embr201948335-cr-0003" contrib-type="author"><name><surname>Liu</surname>
<given-names>Jiaqi</given-names>
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<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
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<contrib id="embr201948335-cr-0004" contrib-type="author"><name><surname>Zhang</surname>
<given-names>Jinna</given-names>
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<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
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<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
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<contrib id="embr201948335-cr-0006" contrib-type="author"><name><surname>You</surname>
<given-names>Zhiyuan</given-names>
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<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
</xref>
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<contrib id="embr201948335-cr-0007" contrib-type="author"><name><surname>Peng</surname>
<given-names>Chao</given-names>
</name>
<xref ref-type="aff" rid="embr201948335-aff-0002"><sup>2</sup>
</xref>
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<contrib id="embr201948335-cr-0008" contrib-type="author"><name><surname>Gong</surname>
<given-names>Zhefeng</given-names>
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<xref ref-type="aff" rid="embr201948335-aff-0003"><sup>3</sup>
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<contrib id="embr201948335-cr-0011" contrib-type="author" corresp="yes"><name><surname>Liu</surname>
<given-names>Wei</given-names>
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<xref ref-type="aff" rid="embr201948335-aff-0001"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="embr201948335-aff-0004"><sup>4</sup>
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<address><email>liuwei666@zju.edu.cn</email>
</address>
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<aff id="embr201948335-aff-0001"><label><sup>1</sup>
</label>
<named-content content-type="organisation-division">Department of Biochemistry and Department of Cardiology of the Second Affiliated Hospital</named-content>
<institution>Zhejiang University School of Medicine</institution>
<city>Hangzhou</city>
<country country="CN">China</country>
</aff>
<aff id="embr201948335-aff-0002"><label><sup>2</sup>
</label>
<named-content content-type="organisation-division">National Center for Protein Science Shanghai</named-content>
<named-content content-type="organisation-division">Institute of Biochemistry and Cell Biology</named-content>
<named-content content-type="organisation-division">Shanghai Institutes of Biological Sciences</named-content>
<institution>Chinese Academy of Sciences</institution>
<city>Shanghai</city>
<country country="CN">China</country>
</aff>
<aff id="embr201948335-aff-0003"><label><sup>3</sup>
</label>
<named-content content-type="organisation-division">Department of Neurobiology</named-content>
<named-content content-type="organisation-division">Key Laboratory of Medical Neurobiology of the Ministry of Health of China</named-content>
<institution>Zhejiang University School of Medicine</institution>
<city>Hangzhou</city>
<country country="CN">China</country>
</aff>
<aff id="embr201948335-aff-0004"><label><sup>4</sup>
</label>
<named-content content-type="organisation-division">Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease</named-content>
<named-content content-type="organisation-division">First Affiliated Hospital</named-content>
<institution>Zhejiang University School of Medicine</institution>
<city>Hangzhou</city>
<country country="CN">China</country>
</aff>
<author-notes><corresp id="correspondenceTo"><label>*</label>
Corresponding author. Tel: +86 5718 8208357; E‐mail: <email>liuwei666@zju.edu.cn</email>
</corresp>
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<abstract id="embr201948335-abs-0001"><title>Abstract</title>
<p>Accumulating evidence highlights the role of histone acetyltransferase GCN5 in the regulation of cell metabolism in metazoans. Here, we report that GCN5 is a negative regulator of autophagy, a lysosome‐dependent catabolic mechanism. In animal cells and <italic>Drosophila</italic>
, GCN5 inhibits the biogenesis of autophagosomes and lysosomes by targeting TFEB, the master transcription factor for autophagy‐ and lysosome‐related gene expression. We show that GCN5 is a specific TFEB acetyltransferase, and acetylation by GCN5 results in the decrease in TFEB transcriptional activity. Induction of autophagy inactivates GCN5, accompanied by reduced TFEB acetylation and increased lysosome formation. We further demonstrate that acetylation at K274 and K279 disrupts the dimerization of TFEB and the binding of TFEB to its target gene promoters. In a Tau‐based neurodegenerative <italic>Drosophila</italic>
 model, deletion of dGcn5 improves the clearance of Tau protein aggregates and ameliorates the neurodegenerative phenotypes. Together, our results reveal GCN5 as a novel conserved TFEB regulator, and the regulatory mechanisms may be involved in autophagy‐ and lysosome‐related physiological and pathological processes.</p>
</abstract>
<abstract abstract-type="graphical" id="embr201948335-abs-0003"><p>GCN5‐mediated TFEB acetylation inhibits autophagy and lysosome biogenesis by disrupting the dimerization and DNA binding of TFEB.<boxed-text position="anchor" content-type="graphic" id="embr201948335-blkfxd-0002" orientation="portrait"><graphic xlink:href="EMBR-21-e48335-g014.jpg" position="anchor" id="nlm-graphic-3" orientation="portrait"></graphic>
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<kwd>Post-translational Modifications, Proteolysis & Proteomics</kwd>
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<funding-group><award-group id="funding-0001"><funding-source>National Basic Research Program of China</funding-source>
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<affiliations><list></list>
<tree><noCountry><name sortKey="Gong, Zhefeng" sort="Gong, Zhefeng" uniqKey="Gong Z" first="Zhefeng" last="Gong">Zhefeng Gong</name>
<name sortKey="Huang, Yewei" sort="Huang, Yewei" uniqKey="Huang Y" first="Yewei" last="Huang">Yewei Huang</name>
<name sortKey="Liu, Jiaqi" sort="Liu, Jiaqi" uniqKey="Liu J" first="Jiaqi" last="Liu">Jiaqi Liu</name>
<name sortKey="Liu, Wei" sort="Liu, Wei" uniqKey="Liu W" first="Wei" last="Liu">Wei Liu</name>
<name sortKey="Peng, Chao" sort="Peng, Chao" uniqKey="Peng C" first="Chao" last="Peng">Chao Peng</name>
<name sortKey="Wang, Yusha" sort="Wang, Yusha" uniqKey="Wang Y" first="Yusha" last="Wang">Yusha Wang</name>
<name sortKey="Xu, Mingming" sort="Xu, Mingming" uniqKey="Xu M" first="Mingming" last="Xu">Mingming Xu</name>
<name sortKey="You, Zhiyuan" sort="You, Zhiyuan" uniqKey="You Z" first="Zhiyuan" last="You">Zhiyuan You</name>
<name sortKey="Zhang, Jinna" sort="Zhang, Jinna" uniqKey="Zhang J" first="Jinna" last="Zhang">Jinna Zhang</name>
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HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A41 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Pmc/Checkpoint/biblio.hfd -nk 000A41 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Pmc
   |étape=   Checkpoint
   |type=    RBID
   |clé=     PMC:6945067
   |texte=   Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Checkpoint/RBID.i   -Sk "pubmed:31750630" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB

Acetyltransferase GCN5 regulates autophagy and lysosome biogenesis by targeting TFEB

Source :

Abstract

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Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki