Overlapping functions of microRNAs in control of apoptosis during Drosophila embryogenesis
Regulation of apoptosis is crucial for tissue homeostasis under normal development and environmental stress. In Drosophila , cell death occurs in different developmental processes including embryogenesis. Here, we report that two members of the miR-2 seed family of microRNAs, miR-6 and miR-11 , func...
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| Veröffentlicht in: | Cell death and differentiation 2012-05, Vol.19 (5), p.839-846 |
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| creator | Ge, W Chen, Y-W Weng, R Lim, S F Buescher, M Zhang, R Cohen, S M |
| description | Regulation of apoptosis is crucial for tissue homeostasis under normal development and environmental stress. In
Drosophila
, cell death occurs in different developmental processes including embryogenesis. Here, we report that two members of the miR-2 seed family of microRNAs,
miR-6
and
miR-11
, function together to limit the level of apoptosis during
Drosophila
embryonic development. Mutants lacking both
miR-6
and
miR-11
show embryonic lethality and defects in the central nervous system (CNS). We provide evidence that
miR-6/11
functions through regulation of the proapoptotic genes,
reaper
(
rpr
),
head involution defective
(
hid
),
grim
and
sickle
(
skl
). Upregulation of these proapoptotic genes is responsible for the elevated apoptosis and the CNS defects in the mutants. These findings demonstrate that the activity of the proapoptotic genes is kept in check by
miR-6/11
to ensure normal development. |
| doi_str_mv | 10.1038/cdd.2011.161 |
| format | Article |
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Drosophila
, cell death occurs in different developmental processes including embryogenesis. Here, we report that two members of the miR-2 seed family of microRNAs,
miR-6
and
miR-11
, function together to limit the level of apoptosis during
Drosophila
embryonic development. Mutants lacking both
miR-6
and
miR-11
show embryonic lethality and defects in the central nervous system (CNS). We provide evidence that
miR-6/11
functions through regulation of the proapoptotic genes,
reaper
(
rpr
),
head involution defective
(
hid
),
grim
and
sickle
(
skl
). Upregulation of these proapoptotic genes is responsible for the elevated apoptosis and the CNS defects in the mutants. These findings demonstrate that the activity of the proapoptotic genes is kept in check by
miR-6/11
to ensure normal development.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2011.161</identifier><identifier>PMID: 22095284</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Animals, Genetically Modified ; Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell cycle ; Cell Cycle Analysis ; Cell death ; Cell growth ; Central Nervous System - embryology ; Central Nervous System - metabolism ; Drosophila - embryology ; Drosophila - genetics ; Drosophila - metabolism ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Embryonic Development - genetics ; Embryonic Development - physiology ; Genes ; Genomics ; Insects ; Life Sciences ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Nervous system ; Neuropeptides - genetics ; Neuropeptides - metabolism ; Original Paper ; Stem Cells</subject><ispartof>Cell death and differentiation, 2012-05, Vol.19 (5), p.839-846</ispartof><rights>The Author(s) 2012</rights><rights>Copyright Nature Publishing Group May 2012</rights><rights>Copyright © 2012 Macmillan Publishers Limited 2012 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-998a7348004df9f70b3367ce0f3dcbde9acb6b5666f71644ebec8f5bc07039473</citedby><cites>FETCH-LOGICAL-c448t-998a7348004df9f70b3367ce0f3dcbde9acb6b5666f71644ebec8f5bc07039473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321623/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321623/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,41486,42555,51317,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22095284$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ge, W</creatorcontrib><creatorcontrib>Chen, Y-W</creatorcontrib><creatorcontrib>Weng, R</creatorcontrib><creatorcontrib>Lim, S F</creatorcontrib><creatorcontrib>Buescher, M</creatorcontrib><creatorcontrib>Zhang, R</creatorcontrib><creatorcontrib>Cohen, S M</creatorcontrib><title>Overlapping functions of microRNAs in control of apoptosis during Drosophila embryogenesis</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Regulation of apoptosis is crucial for tissue homeostasis under normal development and environmental stress. In
Drosophila
, cell death occurs in different developmental processes including embryogenesis. Here, we report that two members of the miR-2 seed family of microRNAs,
miR-6
and
miR-11
, function together to limit the level of apoptosis during
Drosophila
embryonic development. Mutants lacking both
miR-6
and
miR-11
show embryonic lethality and defects in the central nervous system (CNS). We provide evidence that
miR-6/11
functions through regulation of the proapoptotic genes,
reaper
(
rpr
),
head involution defective
(
hid
),
grim
and
sickle
(
skl
). Upregulation of these proapoptotic genes is responsible for the elevated apoptosis and the CNS defects in the mutants. These findings demonstrate that the activity of the proapoptotic genes is kept in check by
miR-6/11
to ensure normal development.</description><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle Analysis</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Central Nervous System - embryology</subject><subject>Central Nervous System - metabolism</subject><subject>Drosophila - embryology</subject><subject>Drosophila - genetics</subject><subject>Drosophila - metabolism</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Embryonic Development - genetics</subject><subject>Embryonic Development - physiology</subject><subject>Genes</subject><subject>Genomics</subject><subject>Insects</subject><subject>Life Sciences</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Nervous system</subject><subject>Neuropeptides - genetics</subject><subject>Neuropeptides - metabolism</subject><subject>Original Paper</subject><subject>Stem Cells</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkUFPHSEUhUljU62669pM3LjpPC8DA8OmibFVmxhNTLtxQxgGnpgZGGHGxH8vk6fWNl1BuB_nnnsPQl8wrDCQ5lh33aoCjFeY4Q9oB1POypoC2cp3UkMpgPJt9DmlewBgXLBPaLuqQNRVQ3fQ7fWjib0aR-fXhZ29nlzwqQi2GJyO4ebqJBXOFzr4KYZ-eVdjGKeQXCq6OS6_vseQwnjnelWYoY1PYW28yfU99NGqPpn9l3MX_T778ev0ory8Pv95enJZakqbqRSiUZzQBoB2VlgOLSGMawOWdLrtjFC6ZW3NGLMcM0pNa3Rj61YDByIoJ7vo20Z3nNvBdNpkq6qXY3SDik8yKCf_rnh3J9fhURJSYVaRLHD0IhDDw2zSJAeXtOl75U2YkxSCYKgYW1od_kPehzn6PF2G8j5rjhfo6wbK-0spGvtmBYNcIpM5MrlEJnNkGT94b_8Nfs0oA-UGSOOybxP_NP2v4DME4aLl</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Ge, W</creator><creator>Chen, Y-W</creator><creator>Weng, R</creator><creator>Lim, S F</creator><creator>Buescher, M</creator><creator>Zhang, R</creator><creator>Cohen, S M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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></search><sort><creationdate>20120501</creationdate><title>Overlapping functions of microRNAs in control of apoptosis during Drosophila embryogenesis</title><author>Ge, W ; Chen, Y-W ; Weng, R ; Lim, S F ; Buescher, M ; Zhang, R ; Cohen, S M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-998a7348004df9f70b3367ce0f3dcbde9acb6b5666f71644ebec8f5bc07039473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Cycle Analysis</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Central Nervous System - embryology</topic><topic>Central Nervous System - metabolism</topic><topic>Drosophila - embryology</topic><topic>Drosophila - genetics</topic><topic>Drosophila - metabolism</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Embryonic Development - genetics</topic><topic>Embryonic Development - physiology</topic><topic>Genes</topic><topic>Genomics</topic><topic>Insects</topic><topic>Life Sciences</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Nervous system</topic><topic>Neuropeptides - genetics</topic><topic>Neuropeptides - metabolism</topic><topic>Original Paper</topic><topic>Stem Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ge, W</creatorcontrib><creatorcontrib>Chen, Y-W</creatorcontrib><creatorcontrib>Weng, R</creatorcontrib><creatorcontrib>Lim, S F</creatorcontrib><creatorcontrib>Buescher, M</creatorcontrib><creatorcontrib>Zhang, R</creatorcontrib><creatorcontrib>Cohen, S M</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Ge, W</au><au>Chen, Y-W</au><au>Weng, R</au><au>Lim, S F</au><au>Buescher, M</au><au>Zhang, R</au><au>Cohen, S M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overlapping functions of microRNAs in control of apoptosis during Drosophila embryogenesis</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>19</volume><issue>5</issue><spage>839</spage><epage>846</epage><pages>839-846</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Regulation of apoptosis is crucial for tissue homeostasis under normal development and environmental stress. In
Drosophila
, cell death occurs in different developmental processes including embryogenesis. Here, we report that two members of the miR-2 seed family of microRNAs,
miR-6
and
miR-11
, function together to limit the level of apoptosis during
Drosophila
embryonic development. Mutants lacking both
miR-6
and
miR-11
show embryonic lethality and defects in the central nervous system (CNS). We provide evidence that
miR-6/11
functions through regulation of the proapoptotic genes,
reaper
(
rpr
),
head involution defective
(
hid
),
grim
and
sickle
(
skl
). Upregulation of these proapoptotic genes is responsible for the elevated apoptosis and the CNS defects in the mutants. These findings demonstrate that the activity of the proapoptotic genes is kept in check by
miR-6/11
to ensure normal development.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22095284</pmid><doi>10.1038/cdd.2011.161</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death and differentiation, 2012-05, Vol.19 (5), p.839-846 |
| issn | 1350-9047 1476-5403 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | Animals Animals, Genetically Modified Apoptosis Apoptosis - genetics Apoptosis - physiology Biochemistry Biomedical and Life Sciences Cell Biology Cell cycle Cell Cycle Analysis Cell death Cell growth Central Nervous System - embryology Central Nervous System - metabolism Drosophila - embryology Drosophila - genetics Drosophila - metabolism Drosophila Proteins - genetics Drosophila Proteins - metabolism Embryonic Development - genetics Embryonic Development - physiology Genes Genomics Insects Life Sciences MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Nervous system Neuropeptides - genetics Neuropeptides - metabolism Original Paper Stem Cells |
| title | Overlapping functions of microRNAs in control of apoptosis during Drosophila embryogenesis |
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