A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila

Myofiber atrophy occurs with aging and in many diseases but the underlying mechanisms are incompletely understood. Here, we have used >1,100 muscle-targeted RNAi interventions to comprehensively assess the function of 447 transcription factors in the developmental growth of body wall skeletal mus...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:PLoS genetics 2021-11, Vol.17 (11), p.e1009926-e1009926
Hauptverfasser: Graca, Flavia A, Sheffield, Natalie, Puppa, Melissa, Finkelstein, David, Hunt, Liam C, Demontis, Fabio
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page e1009926
container_issue 11
container_start_page e1009926
container_title PLoS genetics
container_volume 17
creator Graca, Flavia A
Sheffield, Natalie
Puppa, Melissa
Finkelstein, David
Hunt, Liam C
Demontis, Fabio
description Myofiber atrophy occurs with aging and in many diseases but the underlying mechanisms are incompletely understood. Here, we have used >1,100 muscle-targeted RNAi interventions to comprehensively assess the function of 447 transcription factors in the developmental growth of body wall skeletal muscles in Drosophila. This screen identifies new regulators of myofiber atrophy and hypertrophy, including the transcription factor Deaf1. Deaf1 RNAi increases myofiber size whereas Deaf1 overexpression induces atrophy. Consistent with its annotation as a Gsk3 phosphorylation substrate, Deaf1 and Gsk3 induce largely overlapping transcriptional changes that are opposed by Deaf1 RNAi. The top category of Deaf1-regulated genes consists of glycolytic enzymes, which are suppressed by Deaf1 and Gsk3 but are upregulated by Deaf1 RNAi. Similar to Deaf1 and Gsk3 overexpression, RNAi for glycolytic enzymes reduces myofiber growth. Altogether, this study defines the repertoire of transcription factors that regulate developmental myofiber growth and the role of Gsk3/Deaf1/glycolysis in this process.
doi_str_mv 10.1371/journal.pgen.1009926
format Article
fullrecord <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_2610943808</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A684564177</galeid><doaj_id>oai_doaj_org_article_5d5191f57c5148c0abfe03ddee05aa91</doaj_id><sourcerecordid>A684564177</sourcerecordid><originalsourceid>FETCH-LOGICAL-c726t-3a1ced1420ed52cc1cbc9e0281761b9c7dd16b3f9535ff6583b5cf7857d79b7f3</originalsourceid><addsrcrecordid>eNqVk9-L1DAQx4so3rn6H4gWBNGHXZOmadoXYTl_LRx3cP54DWky6WbJNmuSiudfb9btHVu5ByUPCZPPfCczk8mypxgtMGH4zcYNvhd2seugX2CEmqao7mWnmFIyZyUq7x-dT7JHIWwQIrRu2MPshJSsRmVFTjO3zK3wHcyDFBby6EUfkqCR-dXF0uRBeoA-Nwr6aLSBcCCkN7toXJ9rIaPzyboWMd86NVgRId9eO21a8HkwvyA3ff7Ou-B2a2PF4-yBFjbAk3GfZV8_vP9y9ml-fvlxdbY8n0tWVHFOBJagcFkgULSQEstWNoCKGrMKt41kSuGqJbqhhGpd0Zq0VGpWU6ZY0zJNZtnzg-7OusDHWgVeVBg1JalRnYjVgVBObPjOm63w19wJw_8YnO-48NFIC5wqihusKZMUl7VEotWAiFIAiArR4KT1dow2tFtQMlXLCzsRnd70Zs0794PXVdGQlMQsezUKePd9gBD51gQJ1ooe3JDeTZsaMcoKlNAXf6F3ZzdSXWorN712Ka7ci_JlVZe0KjFjiVrcQaWlYGuk60GbZJ84vJ44JCbCz9iJIQS--nz1H-zFv7OX36bsyyN2DcLGdXB22H_IMAXLAyjT9wse9G1DMOL7GbqpHN_PEB9nKLk9O27mrdPN0JDfaRYXpg</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2610943808</pqid></control><display><type>article</type><title>A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Graca, Flavia A ; Sheffield, Natalie ; Puppa, Melissa ; Finkelstein, David ; Hunt, Liam C ; Demontis, Fabio</creator><contributor>Wang, Hongyan</contributor><creatorcontrib>Graca, Flavia A ; Sheffield, Natalie ; Puppa, Melissa ; Finkelstein, David ; Hunt, Liam C ; Demontis, Fabio ; Wang, Hongyan</creatorcontrib><description>Myofiber atrophy occurs with aging and in many diseases but the underlying mechanisms are incompletely understood. Here, we have used &gt;1,100 muscle-targeted RNAi interventions to comprehensively assess the function of 447 transcription factors in the developmental growth of body wall skeletal muscles in Drosophila. This screen identifies new regulators of myofiber atrophy and hypertrophy, including the transcription factor Deaf1. Deaf1 RNAi increases myofiber size whereas Deaf1 overexpression induces atrophy. Consistent with its annotation as a Gsk3 phosphorylation substrate, Deaf1 and Gsk3 induce largely overlapping transcriptional changes that are opposed by Deaf1 RNAi. The top category of Deaf1-regulated genes consists of glycolytic enzymes, which are suppressed by Deaf1 and Gsk3 but are upregulated by Deaf1 RNAi. Similar to Deaf1 and Gsk3 overexpression, RNAi for glycolytic enzymes reduces myofiber growth. Altogether, this study defines the repertoire of transcription factors that regulate developmental myofiber growth and the role of Gsk3/Deaf1/glycolysis in this process.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1009926</identifier><identifier>PMID: 34780463</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adults ; Aging ; Animals ; Animals, Genetically Modified - genetics ; Atrophy ; Biology and life sciences ; Body wall ; Chemical properties ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; Drosophila ; Drosophila melanogaster - genetics ; Drosophila Proteins - genetics ; Embryonic Development - genetics ; Enzymes ; Gene expression ; Genetic aspects ; Genomes ; Glycogen Synthase Kinase 3 - genetics ; Glycolysis ; Glycolysis - genetics ; Humans ; Hypertrophy ; Identification and classification ; Insects ; Kinases ; Medicine and Health Sciences ; Muscle, Skeletal - growth &amp; development ; Muscle, Skeletal - metabolism ; Muscular Atrophy - genetics ; Muscular Atrophy - pathology ; Musculoskeletal system ; Myofibrils - genetics ; Myofibrils - metabolism ; Phosphorylation ; Physiological aspects ; Protein synthesis ; Proteins ; Research and Analysis Methods ; RNA Interference ; RNA-mediated interference ; Skeletal muscle ; Transcription factors ; Transcription Factors - genetics</subject><ispartof>PLoS genetics, 2021-11, Vol.17 (11), p.e1009926-e1009926</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Graca et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Graca et al 2021 Graca et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c726t-3a1ced1420ed52cc1cbc9e0281761b9c7dd16b3f9535ff6583b5cf7857d79b7f3</citedby><cites>FETCH-LOGICAL-c726t-3a1ced1420ed52cc1cbc9e0281761b9c7dd16b3f9535ff6583b5cf7857d79b7f3</cites><orcidid>0000-0003-3826-0003 ; 0000-0001-5192-1473 ; 0000-0001-8947-113X ; 0000-0002-7342-6534 ; 0000-0002-8698-9555</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8629395/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8629395/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34780463$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wang, Hongyan</contributor><creatorcontrib>Graca, Flavia A</creatorcontrib><creatorcontrib>Sheffield, Natalie</creatorcontrib><creatorcontrib>Puppa, Melissa</creatorcontrib><creatorcontrib>Finkelstein, David</creatorcontrib><creatorcontrib>Hunt, Liam C</creatorcontrib><creatorcontrib>Demontis, Fabio</creatorcontrib><title>A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila</title><title>PLoS genetics</title><addtitle>PLoS Genet</addtitle><description>Myofiber atrophy occurs with aging and in many diseases but the underlying mechanisms are incompletely understood. Here, we have used &gt;1,100 muscle-targeted RNAi interventions to comprehensively assess the function of 447 transcription factors in the developmental growth of body wall skeletal muscles in Drosophila. This screen identifies new regulators of myofiber atrophy and hypertrophy, including the transcription factor Deaf1. Deaf1 RNAi increases myofiber size whereas Deaf1 overexpression induces atrophy. Consistent with its annotation as a Gsk3 phosphorylation substrate, Deaf1 and Gsk3 induce largely overlapping transcriptional changes that are opposed by Deaf1 RNAi. The top category of Deaf1-regulated genes consists of glycolytic enzymes, which are suppressed by Deaf1 and Gsk3 but are upregulated by Deaf1 RNAi. Similar to Deaf1 and Gsk3 overexpression, RNAi for glycolytic enzymes reduces myofiber growth. Altogether, this study defines the repertoire of transcription factors that regulate developmental myofiber growth and the role of Gsk3/Deaf1/glycolysis in this process.</description><subject>Adults</subject><subject>Aging</subject><subject>Animals</subject><subject>Animals, Genetically Modified - genetics</subject><subject>Atrophy</subject><subject>Biology and life sciences</subject><subject>Body wall</subject><subject>Chemical properties</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Drosophila</subject><subject>Drosophila melanogaster - genetics</subject><subject>Drosophila Proteins - genetics</subject><subject>Embryonic Development - genetics</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glycogen Synthase Kinase 3 - genetics</subject><subject>Glycolysis</subject><subject>Glycolysis - genetics</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Identification and classification</subject><subject>Insects</subject><subject>Kinases</subject><subject>Medicine and Health Sciences</subject><subject>Muscle, Skeletal - growth &amp; development</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscular Atrophy - genetics</subject><subject>Muscular Atrophy - pathology</subject><subject>Musculoskeletal system</subject><subject>Myofibrils - genetics</subject><subject>Myofibrils - metabolism</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>RNA Interference</subject><subject>RNA-mediated interference</subject><subject>Skeletal muscle</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><issn>1553-7404</issn><issn>1553-7390</issn><issn>1553-7404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVk9-L1DAQx4so3rn6H4gWBNGHXZOmadoXYTl_LRx3cP54DWky6WbJNmuSiudfb9btHVu5ByUPCZPPfCczk8mypxgtMGH4zcYNvhd2seugX2CEmqao7mWnmFIyZyUq7x-dT7JHIWwQIrRu2MPshJSsRmVFTjO3zK3wHcyDFBby6EUfkqCR-dXF0uRBeoA-Nwr6aLSBcCCkN7toXJ9rIaPzyboWMd86NVgRId9eO21a8HkwvyA3ff7Ou-B2a2PF4-yBFjbAk3GfZV8_vP9y9ml-fvlxdbY8n0tWVHFOBJagcFkgULSQEstWNoCKGrMKt41kSuGqJbqhhGpd0Zq0VGpWU6ZY0zJNZtnzg-7OusDHWgVeVBg1JalRnYjVgVBObPjOm63w19wJw_8YnO-48NFIC5wqihusKZMUl7VEotWAiFIAiArR4KT1dow2tFtQMlXLCzsRnd70Zs0794PXVdGQlMQsezUKePd9gBD51gQJ1ooe3JDeTZsaMcoKlNAXf6F3ZzdSXWorN712Ka7ci_JlVZe0KjFjiVrcQaWlYGuk60GbZJ84vJ44JCbCz9iJIQS--nz1H-zFv7OX36bsyyN2DcLGdXB22H_IMAXLAyjT9wse9G1DMOL7GbqpHN_PEB9nKLk9O27mrdPN0JDfaRYXpg</recordid><startdate>20211115</startdate><enddate>20211115</enddate><creator>Graca, Flavia A</creator><creator>Sheffield, Natalie</creator><creator>Puppa, Melissa</creator><creator>Finkelstein, David</creator><creator>Hunt, Liam C</creator><creator>Demontis, Fabio</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3826-0003</orcidid><orcidid>https://orcid.org/0000-0001-5192-1473</orcidid><orcidid>https://orcid.org/0000-0001-8947-113X</orcidid><orcidid>https://orcid.org/0000-0002-7342-6534</orcidid><orcidid>https://orcid.org/0000-0002-8698-9555</orcidid></search><sort><creationdate>20211115</creationdate><title>A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila</title><author>Graca, Flavia A ; Sheffield, Natalie ; Puppa, Melissa ; Finkelstein, David ; Hunt, Liam C ; Demontis, Fabio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c726t-3a1ced1420ed52cc1cbc9e0281761b9c7dd16b3f9535ff6583b5cf7857d79b7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adults</topic><topic>Aging</topic><topic>Animals</topic><topic>Animals, Genetically Modified - genetics</topic><topic>Atrophy</topic><topic>Biology and life sciences</topic><topic>Body wall</topic><topic>Chemical properties</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Drosophila</topic><topic>Drosophila melanogaster - genetics</topic><topic>Drosophila Proteins - genetics</topic><topic>Embryonic Development - genetics</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Glycogen Synthase Kinase 3 - genetics</topic><topic>Glycolysis</topic><topic>Glycolysis - genetics</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Identification and classification</topic><topic>Insects</topic><topic>Kinases</topic><topic>Medicine and Health Sciences</topic><topic>Muscle, Skeletal - growth &amp; development</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscular Atrophy - genetics</topic><topic>Muscular Atrophy - pathology</topic><topic>Musculoskeletal system</topic><topic>Myofibrils - genetics</topic><topic>Myofibrils - metabolism</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>RNA Interference</topic><topic>RNA-mediated interference</topic><topic>Skeletal muscle</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Graca, Flavia A</creatorcontrib><creatorcontrib>Sheffield, Natalie</creatorcontrib><creatorcontrib>Puppa, Melissa</creatorcontrib><creatorcontrib>Finkelstein, David</creatorcontrib><creatorcontrib>Hunt, Liam C</creatorcontrib><creatorcontrib>Demontis, Fabio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Graca, Flavia A</au><au>Sheffield, Natalie</au><au>Puppa, Melissa</au><au>Finkelstein, David</au><au>Hunt, Liam C</au><au>Demontis, Fabio</au><au>Wang, Hongyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2021-11-15</date><risdate>2021</risdate><volume>17</volume><issue>11</issue><spage>e1009926</spage><epage>e1009926</epage><pages>e1009926-e1009926</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>Myofiber atrophy occurs with aging and in many diseases but the underlying mechanisms are incompletely understood. Here, we have used &gt;1,100 muscle-targeted RNAi interventions to comprehensively assess the function of 447 transcription factors in the developmental growth of body wall skeletal muscles in Drosophila. This screen identifies new regulators of myofiber atrophy and hypertrophy, including the transcription factor Deaf1. Deaf1 RNAi increases myofiber size whereas Deaf1 overexpression induces atrophy. Consistent with its annotation as a Gsk3 phosphorylation substrate, Deaf1 and Gsk3 induce largely overlapping transcriptional changes that are opposed by Deaf1 RNAi. The top category of Deaf1-regulated genes consists of glycolytic enzymes, which are suppressed by Deaf1 and Gsk3 but are upregulated by Deaf1 RNAi. Similar to Deaf1 and Gsk3 overexpression, RNAi for glycolytic enzymes reduces myofiber growth. Altogether, this study defines the repertoire of transcription factors that regulate developmental myofiber growth and the role of Gsk3/Deaf1/glycolysis in this process.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>34780463</pmid><doi>10.1371/journal.pgen.1009926</doi><orcidid>https://orcid.org/0000-0003-3826-0003</orcidid><orcidid>https://orcid.org/0000-0001-5192-1473</orcidid><orcidid>https://orcid.org/0000-0001-8947-113X</orcidid><orcidid>https://orcid.org/0000-0002-7342-6534</orcidid><orcidid>https://orcid.org/0000-0002-8698-9555</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1553-7404
ispartof PLoS genetics, 2021-11, Vol.17 (11), p.e1009926-e1009926
issn 1553-7404
1553-7390
1553-7404
language eng
recordid cdi_plos_journals_2610943808
source MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Adults
Aging
Animals
Animals, Genetically Modified - genetics
Atrophy
Biology and life sciences
Body wall
Chemical properties
Disease Models, Animal
DNA-Binding Proteins - genetics
Drosophila
Drosophila melanogaster - genetics
Drosophila Proteins - genetics
Embryonic Development - genetics
Enzymes
Gene expression
Genetic aspects
Genomes
Glycogen Synthase Kinase 3 - genetics
Glycolysis
Glycolysis - genetics
Humans
Hypertrophy
Identification and classification
Insects
Kinases
Medicine and Health Sciences
Muscle, Skeletal - growth & development
Muscle, Skeletal - metabolism
Muscular Atrophy - genetics
Muscular Atrophy - pathology
Musculoskeletal system
Myofibrils - genetics
Myofibrils - metabolism
Phosphorylation
Physiological aspects
Protein synthesis
Proteins
Research and Analysis Methods
RNA Interference
RNA-mediated interference
Skeletal muscle
Transcription factors
Transcription Factors - genetics
title A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T19%3A20%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20large-scale%20transgenic%20RNAi%20screen%20identifies%20transcription%20factors%20that%20modulate%20myofiber%20size%20in%20Drosophila&rft.jtitle=PLoS%20genetics&rft.au=Graca,%20Flavia%20A&rft.date=2021-11-15&rft.volume=17&rft.issue=11&rft.spage=e1009926&rft.epage=e1009926&rft.pages=e1009926-e1009926&rft.issn=1553-7404&rft.eissn=1553-7404&rft_id=info:doi/10.1371/journal.pgen.1009926&rft_dat=%3Cgale_plos_%3EA684564177%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2610943808&rft_id=info:pmid/34780463&rft_galeid=A684564177&rft_doaj_id=oai_doaj_org_article_5d5191f57c5148c0abfe03ddee05aa91&rfr_iscdi=true