Autophagy in animal development
Macroautophagy (autophagy) delivers intracellular constituents to the lysosome to promote catabolism. During development in multiple organisms, autophagy mediates various cellular processes, including survival during starvation, programmed cell death, phagocytosis, organelle elimination, and miRNA r...
Gespeichert in:
Veröffentlicht in: | Cell death and differentiation 2020-03, Vol.27 (3), p.903-918 |
---|---|
Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 918 |
---|---|
container_issue | 3 |
container_start_page | 903 |
container_title | Cell death and differentiation |
container_volume | 27 |
creator | Allen, Elizabeth A. Baehrecke, Eric H. |
description | Macroautophagy (autophagy) delivers intracellular constituents to the lysosome to promote catabolism. During development in multiple organisms, autophagy mediates various cellular processes, including survival during starvation, programmed cell death, phagocytosis, organelle elimination, and miRNA regulation. Our current understanding of autophagy has been enhanced by developmental biology research during the last quarter of a century. Through experiments that focus on animal development, fundamental mechanisms that control autophagy and that contribute to disease were elucidated. Studies in embryos revealed specific autophagy molecules that mediate the removal of paternally derived mitochondria, and identified autophagy components that clear protein aggregates during development. Importantly, defects in mtDNA inheritance, or removal of paternal mtDNA via mitochondrial autophagy, can contribute to mitochondrial-associated disease. In addition, impairment of the clearance of protein aggregates by autophagy underlies neurodegenerative diseases. Experiments in multiple organisms also reveal conserved mechanisms of tissue remodeling that rely on the cooperation between autophagy and apoptosis to clear cell corpses, and defects in autophagy and apoptotic cell clearance can contribute to inflammation and autoimmunity. Here we provide an overview of key developmental processes that are mediated by autophagy in multiple animals. |
doi_str_mv | 10.1038/s41418-020-0497-0 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7206001</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2474990354</sourcerecordid><originalsourceid>FETCH-LOGICAL-c498t-446703c861be70b2faf0c12d2280b48507e8432eb9859b6f0af49c72f0f4af0b3</originalsourceid><addsrcrecordid>eNp9kU1Lw0AQhhdRbK3-AC9a8OIlOrs7ye5ehFL8goIXPS-bdNOm5MtsUui_d0tq_QA9zcA8874zvIScU7ihwOWtQ4pUBsAgAFQigAMypCiiIETgh77nIQQKUAzIiXMrAIiEio7JgFMlJSockstJ11b10iw246wcmzIrTD6e27XNq7qwZXtKjlKTO3u2qyPy9nD_On0KZi-Pz9PJLEhQyTZAjATwREY0tgJilpoUEsrmjEmIUYYgrETObKxkqOIoBZOiSgRLIUWPxnxE7nrduosLO0-8dWNyXTf-oGajK5Ppn5MyW-pFtdaCQQRAvcD1TqCp3jvrWl1kLrF5bkpbdU4zjiKkDJTy6NUvdFV1Tenf0wwFKgU8xH8p7i1DETLhKdpTSVM519h0fzIFvQ1J9yFpH5LehqTB71x8_3W_8ZmKB1gPOD8qF7b5sv5b9QOJIZpF</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2360057527</pqid></control><display><type>article</type><title>Autophagy in animal development</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Allen, Elizabeth A. ; Baehrecke, Eric H.</creator><creatorcontrib>Allen, Elizabeth A. ; Baehrecke, Eric H.</creatorcontrib><description>Macroautophagy (autophagy) delivers intracellular constituents to the lysosome to promote catabolism. During development in multiple organisms, autophagy mediates various cellular processes, including survival during starvation, programmed cell death, phagocytosis, organelle elimination, and miRNA regulation. Our current understanding of autophagy has been enhanced by developmental biology research during the last quarter of a century. Through experiments that focus on animal development, fundamental mechanisms that control autophagy and that contribute to disease were elucidated. Studies in embryos revealed specific autophagy molecules that mediate the removal of paternally derived mitochondria, and identified autophagy components that clear protein aggregates during development. Importantly, defects in mtDNA inheritance, or removal of paternal mtDNA via mitochondrial autophagy, can contribute to mitochondrial-associated disease. In addition, impairment of the clearance of protein aggregates by autophagy underlies neurodegenerative diseases. Experiments in multiple organisms also reveal conserved mechanisms of tissue remodeling that rely on the cooperation between autophagy and apoptosis to clear cell corpses, and defects in autophagy and apoptotic cell clearance can contribute to inflammation and autoimmunity. Here we provide an overview of key developmental processes that are mediated by autophagy in multiple animals.</description><identifier>ISSN: 1350-9047</identifier><identifier>ISSN: 1476-5403</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/s41418-020-0497-0</identifier><identifier>PMID: 31988494</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Autoimmunity ; Autophagy ; Autophagy - genetics ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Cycle Analysis ; Cell death ; Cell survival ; Developmental biology ; Embryonic Development - genetics ; Embryos ; Inflammation ; Life Sciences ; Metamorphosis, Biological - genetics ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Mitochondria ; Mitochondrial DNA ; Neurodegenerative diseases ; Phagocytosis ; Regeneration - genetics ; Review ; Review Article ; Starvation ; Stem Cells</subject><ispartof>Cell death and differentiation, 2020-03, Vol.27 (3), p.903-918</ispartof><rights>The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2020</rights><rights>2020© The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2020</rights><rights>The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-446703c861be70b2faf0c12d2280b48507e8432eb9859b6f0af49c72f0f4af0b3</citedby><cites>FETCH-LOGICAL-c498t-446703c861be70b2faf0c12d2280b48507e8432eb9859b6f0af49c72f0f4af0b3</cites><orcidid>0000-0001-6324-1758</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/PMC7206001/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7206001/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31988494$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Allen, Elizabeth A.</creatorcontrib><creatorcontrib>Baehrecke, Eric H.</creatorcontrib><title>Autophagy in animal development</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Macroautophagy (autophagy) delivers intracellular constituents to the lysosome to promote catabolism. During development in multiple organisms, autophagy mediates various cellular processes, including survival during starvation, programmed cell death, phagocytosis, organelle elimination, and miRNA regulation. Our current understanding of autophagy has been enhanced by developmental biology research during the last quarter of a century. Through experiments that focus on animal development, fundamental mechanisms that control autophagy and that contribute to disease were elucidated. Studies in embryos revealed specific autophagy molecules that mediate the removal of paternally derived mitochondria, and identified autophagy components that clear protein aggregates during development. Importantly, defects in mtDNA inheritance, or removal of paternal mtDNA via mitochondrial autophagy, can contribute to mitochondrial-associated disease. In addition, impairment of the clearance of protein aggregates by autophagy underlies neurodegenerative diseases. Experiments in multiple organisms also reveal conserved mechanisms of tissue remodeling that rely on the cooperation between autophagy and apoptosis to clear cell corpses, and defects in autophagy and apoptotic cell clearance can contribute to inflammation and autoimmunity. Here we provide an overview of key developmental processes that are mediated by autophagy in multiple animals.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Autoimmunity</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell death</subject><subject>Cell survival</subject><subject>Developmental biology</subject><subject>Embryonic Development - genetics</subject><subject>Embryos</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Metamorphosis, Biological - genetics</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Neurodegenerative diseases</subject><subject>Phagocytosis</subject><subject>Regeneration - genetics</subject><subject>Review</subject><subject>Review Article</subject><subject>Starvation</subject><subject>Stem Cells</subject><issn>1350-9047</issn><issn>1476-5403</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU1Lw0AQhhdRbK3-AC9a8OIlOrs7ye5ehFL8goIXPS-bdNOm5MtsUui_d0tq_QA9zcA8874zvIScU7ihwOWtQ4pUBsAgAFQigAMypCiiIETgh77nIQQKUAzIiXMrAIiEio7JgFMlJSockstJ11b10iw246wcmzIrTD6e27XNq7qwZXtKjlKTO3u2qyPy9nD_On0KZi-Pz9PJLEhQyTZAjATwREY0tgJilpoUEsrmjEmIUYYgrETObKxkqOIoBZOiSgRLIUWPxnxE7nrduosLO0-8dWNyXTf-oGajK5Ppn5MyW-pFtdaCQQRAvcD1TqCp3jvrWl1kLrF5bkpbdU4zjiKkDJTy6NUvdFV1Tenf0wwFKgU8xH8p7i1DETLhKdpTSVM519h0fzIFvQ1J9yFpH5LehqTB71x8_3W_8ZmKB1gPOD8qF7b5sv5b9QOJIZpF</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Allen, Elizabeth A.</creator><creator>Baehrecke, Eric H.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6324-1758</orcidid></search><sort><creationdate>20200301</creationdate><title>Autophagy in animal development</title><author>Allen, Elizabeth A. ; Baehrecke, Eric H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-446703c861be70b2faf0c12d2280b48507e8432eb9859b6f0af49c72f0f4af0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Autoimmunity</topic><topic>Autophagy</topic><topic>Autophagy - genetics</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell death</topic><topic>Cell survival</topic><topic>Developmental biology</topic><topic>Embryonic Development - genetics</topic><topic>Embryos</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Metamorphosis, Biological - genetics</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Mitochondria</topic><topic>Mitochondrial DNA</topic><topic>Neurodegenerative diseases</topic><topic>Phagocytosis</topic><topic>Regeneration - genetics</topic><topic>Review</topic><topic>Review Article</topic><topic>Starvation</topic><topic>Stem Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allen, Elizabeth A.</creatorcontrib><creatorcontrib>Baehrecke, Eric H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Allen, Elizabeth A.</au><au>Baehrecke, Eric H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagy in animal development</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>27</volume><issue>3</issue><spage>903</spage><epage>918</epage><pages>903-918</pages><issn>1350-9047</issn><issn>1476-5403</issn><eissn>1476-5403</eissn><abstract>Macroautophagy (autophagy) delivers intracellular constituents to the lysosome to promote catabolism. During development in multiple organisms, autophagy mediates various cellular processes, including survival during starvation, programmed cell death, phagocytosis, organelle elimination, and miRNA regulation. Our current understanding of autophagy has been enhanced by developmental biology research during the last quarter of a century. Through experiments that focus on animal development, fundamental mechanisms that control autophagy and that contribute to disease were elucidated. Studies in embryos revealed specific autophagy molecules that mediate the removal of paternally derived mitochondria, and identified autophagy components that clear protein aggregates during development. Importantly, defects in mtDNA inheritance, or removal of paternal mtDNA via mitochondrial autophagy, can contribute to mitochondrial-associated disease. In addition, impairment of the clearance of protein aggregates by autophagy underlies neurodegenerative diseases. Experiments in multiple organisms also reveal conserved mechanisms of tissue remodeling that rely on the cooperation between autophagy and apoptosis to clear cell corpses, and defects in autophagy and apoptotic cell clearance can contribute to inflammation and autoimmunity. Here we provide an overview of key developmental processes that are mediated by autophagy in multiple animals.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31988494</pmid><doi>10.1038/s41418-020-0497-0</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-6324-1758</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1350-9047 |
ispartof | Cell death and differentiation, 2020-03, Vol.27 (3), p.903-918 |
issn | 1350-9047 1476-5403 1476-5403 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7206001 |
source | MEDLINE; Springer Nature - Complete Springer Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Animals Apoptosis Apoptosis - genetics Autoimmunity Autophagy Autophagy - genetics Biochemistry Biomedical and Life Sciences Cell Biology Cell Cycle Analysis Cell death Cell survival Developmental biology Embryonic Development - genetics Embryos Inflammation Life Sciences Metamorphosis, Biological - genetics MicroRNAs - genetics MicroRNAs - metabolism miRNA Mitochondria Mitochondrial DNA Neurodegenerative diseases Phagocytosis Regeneration - genetics Review Review Article Starvation Stem Cells |
title | Autophagy in animal development |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T20%3A10%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Autophagy%20in%20animal%20development&rft.jtitle=Cell%20death%20and%20differentiation&rft.au=Allen,%20Elizabeth%20A.&rft.date=2020-03-01&rft.volume=27&rft.issue=3&rft.spage=903&rft.epage=918&rft.pages=903-918&rft.issn=1350-9047&rft.eissn=1476-5403&rft_id=info:doi/10.1038/s41418-020-0497-0&rft_dat=%3Cproquest_pubme%3E2474990354%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2360057527&rft_id=info:pmid/31988494&rfr_iscdi=true |