MOF maintains transcriptional programs regulating cellular stress response
MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in Drosophila and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differe...
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| Veröffentlicht in: | Oncogene 2016-05, Vol.35 (21), p.2698-2710 |
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| creator | Sheikh, B N Bechtel-Walz, W Lucci, J Karpiuk, O Hild, I Hartleben, B Vornweg, J Helmstädter, M Sahyoun, A H Bhardwaj, V Stehle, T Diehl, S Kretz, O Voss, A K Thomas, T Manke, T Huber, T B Akhtar, A |
| description | MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in
Drosophila
and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is dispensable for terminally differentiated, postmitotic glomerular podocytes under physiological conditions. However, in response to injury, MOF is absolutely critical for podocyte maintenance
in vivo
. Consistently, we detect defective nuclear, endoplasmic reticulum and Golgi structures, as well as presence of multivesicular bodies
in vivo
in podocytes lacking
Mof
following injury. Undertaking genome-wide expression analysis of podocytes, we uncover several MOF-regulated pathways required for stress response. We find that MOF, along with the members of the non-specific lethal but not the male-specific lethal complex, directly binds to genes encoding the lysosome, endocytosis and vacuole pathways, which are known regulators of podocyte maintenance. Thus, our work identifies MOF as a key regulator of cellular stress response in glomerular podocytes. |
| doi_str_mv | 10.1038/onc.2015.335 |
| format | Article |
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Drosophila
and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is dispensable for terminally differentiated, postmitotic glomerular podocytes under physiological conditions. However, in response to injury, MOF is absolutely critical for podocyte maintenance
in vivo
. Consistently, we detect defective nuclear, endoplasmic reticulum and Golgi structures, as well as presence of multivesicular bodies
in vivo
in podocytes lacking
Mof
following injury. Undertaking genome-wide expression analysis of podocytes, we uncover several MOF-regulated pathways required for stress response. We find that MOF, along with the members of the non-specific lethal but not the male-specific lethal complex, directly binds to genes encoding the lysosome, endocytosis and vacuole pathways, which are known regulators of podocyte maintenance. Thus, our work identifies MOF as a key regulator of cellular stress response in glomerular podocytes.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2015.335</identifier><identifier>PMID: 26387537</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>101/28 ; 13/1 ; 45/41 ; 631/208/176/1433 ; 64/60 ; Animals ; Apoptosis ; Cell Biology ; Cell Cycle Checkpoints - genetics ; Cellular biology ; Cellular control mechanisms ; Drosophila ; Embryos ; Genetic aspects ; Heat-Shock Proteins - genetics ; Heat-Shock Proteins - metabolism ; Histone Acetyltransferases - genetics ; Histone Acetyltransferases - metabolism ; Human Genetics ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncology ; Original ; original-article ; Podocytes - cytology ; Podocytes - metabolism ; Podocytes - physiology ; Properties ; Scavenger Receptors, Class A - genetics ; Scavenger Receptors, Class A - metabolism ; Stress ; Stress (Physiology) ; Stress, Physiological - genetics ; Tissues ; Transcription factors ; Transcription, Genetic</subject><ispartof>Oncogene, 2016-05, Vol.35 (21), p.2698-2710</ispartof><rights>The Author(s) 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 26, 2016</rights><rights>Copyright © 2016 Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-8c8ad1eef546ad025bc5e40909e5948b0e9f6e09e65b56d5608a73812e87ff2a3</citedby><cites>FETCH-LOGICAL-c550t-8c8ad1eef546ad025bc5e40909e5948b0e9f6e09e65b56d5608a73812e87ff2a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2015.335$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2015.335$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26387537$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sheikh, B N</creatorcontrib><creatorcontrib>Bechtel-Walz, W</creatorcontrib><creatorcontrib>Lucci, J</creatorcontrib><creatorcontrib>Karpiuk, O</creatorcontrib><creatorcontrib>Hild, I</creatorcontrib><creatorcontrib>Hartleben, B</creatorcontrib><creatorcontrib>Vornweg, J</creatorcontrib><creatorcontrib>Helmstädter, M</creatorcontrib><creatorcontrib>Sahyoun, A H</creatorcontrib><creatorcontrib>Bhardwaj, V</creatorcontrib><creatorcontrib>Stehle, T</creatorcontrib><creatorcontrib>Diehl, S</creatorcontrib><creatorcontrib>Kretz, O</creatorcontrib><creatorcontrib>Voss, A K</creatorcontrib><creatorcontrib>Thomas, T</creatorcontrib><creatorcontrib>Manke, T</creatorcontrib><creatorcontrib>Huber, T B</creatorcontrib><creatorcontrib>Akhtar, A</creatorcontrib><title>MOF maintains transcriptional programs regulating cellular stress response</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in
Drosophila
and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is dispensable for terminally differentiated, postmitotic glomerular podocytes under physiological conditions. However, in response to injury, MOF is absolutely critical for podocyte maintenance
in vivo
. Consistently, we detect defective nuclear, endoplasmic reticulum and Golgi structures, as well as presence of multivesicular bodies
in vivo
in podocytes lacking
Mof
following injury. Undertaking genome-wide expression analysis of podocytes, we uncover several MOF-regulated pathways required for stress response. We find that MOF, along with the members of the non-specific lethal but not the male-specific lethal complex, directly binds to genes encoding the lysosome, endocytosis and vacuole pathways, which are known regulators of podocyte maintenance. Thus, our work identifies MOF as a key regulator of cellular stress response in glomerular podocytes.</description><subject>101/28</subject><subject>13/1</subject><subject>45/41</subject><subject>631/208/176/1433</subject><subject>64/60</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Biology</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cellular biology</subject><subject>Cellular control mechanisms</subject><subject>Drosophila</subject><subject>Embryos</subject><subject>Genetic aspects</subject><subject>Heat-Shock Proteins - genetics</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Histone Acetyltransferases - genetics</subject><subject>Histone Acetyltransferases - metabolism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>Original</subject><subject>original-article</subject><subject>Podocytes - cytology</subject><subject>Podocytes - metabolism</subject><subject>Podocytes - physiology</subject><subject>Properties</subject><subject>Scavenger Receptors, Class A - genetics</subject><subject>Scavenger Receptors, Class A - metabolism</subject><subject>Stress</subject><subject>Stress (Physiology)</subject><subject>Stress, Physiological - genetics</subject><subject>Tissues</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkktr3TAQhUVpaG7S7rouhm66iG_H1tObQghJH6Rk066Frjx2FWzJlexA_31kbpomJRCE0GO-ORoNh5C3FWwroOpj8HZbQ8W3lPIXZFMxKUrOG_aSbKDhUDY1rQ_JUUrXACAbqF-Rw1pQJTmVG_Lt-9VFMRrn5zxTMUfjk41uml3wZiimGPpoxlRE7JfBzM73hcVhyPtYpDliWkNpCj7ha3LQmSHhm7v1mPy8OP9x9qW8vPr89ez0srScw1wqq0xbIXacCdNCzXeWI4MGGsxVqx1g0wnMJ8F3XLRcgDKSqqpGJbuuNvSYfNrrTstuxNaiz1UPeopuNPGPDsbpxxHvfuk-3GimGiooywIf7gRi-L1gmvXo0vor4zEsSVcKlGTAhHoelbm9klEQGX3_H3odlpibuKekooyzf1RvBtTOdyGXaFdRfcq44rJScn12-wSVR4ujs8Fj5_L9o4STfYKNIaWI3X07KtCrTXS2iV5torNNMv7uYQvv4b--yEC5B1IO-R7jg888JXgLkr7G6w</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Sheikh, B N</creator><creator>Bechtel-Walz, W</creator><creator>Lucci, J</creator><creator>Karpiuk, O</creator><creator>Hild, I</creator><creator>Hartleben, B</creator><creator>Vornweg, J</creator><creator>Helmstädter, M</creator><creator>Sahyoun, A H</creator><creator>Bhardwaj, V</creator><creator>Stehle, T</creator><creator>Diehl, S</creator><creator>Kretz, O</creator><creator>Voss, A K</creator><creator>Thomas, T</creator><creator>Manke, T</creator><creator>Huber, T B</creator><creator>Akhtar, A</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160501</creationdate><title>MOF maintains transcriptional programs regulating cellular stress response</title><author>Sheikh, B N ; Bechtel-Walz, W ; Lucci, J ; Karpiuk, O ; Hild, I ; Hartleben, B ; Vornweg, J ; Helmstädter, M ; Sahyoun, A H ; Bhardwaj, V ; Stehle, T ; Diehl, S ; Kretz, O ; Voss, A K ; Thomas, T ; Manke, T ; Huber, T B ; Akhtar, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c550t-8c8ad1eef546ad025bc5e40909e5948b0e9f6e09e65b56d5608a73812e87ff2a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>101/28</topic><topic>13/1</topic><topic>45/41</topic><topic>631/208/176/1433</topic><topic>64/60</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Biology</topic><topic>Cell Cycle Checkpoints - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sheikh, B N</au><au>Bechtel-Walz, W</au><au>Lucci, J</au><au>Karpiuk, O</au><au>Hild, I</au><au>Hartleben, B</au><au>Vornweg, J</au><au>Helmstädter, M</au><au>Sahyoun, A H</au><au>Bhardwaj, V</au><au>Stehle, T</au><au>Diehl, S</au><au>Kretz, O</au><au>Voss, A K</au><au>Thomas, T</au><au>Manke, T</au><au>Huber, T B</au><au>Akhtar, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MOF maintains transcriptional programs regulating cellular stress response</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>35</volume><issue>21</issue><spage>2698</spage><epage>2710</epage><pages>2698-2710</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in
Drosophila
and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is dispensable for terminally differentiated, postmitotic glomerular podocytes under physiological conditions. However, in response to injury, MOF is absolutely critical for podocyte maintenance
in vivo
. Consistently, we detect defective nuclear, endoplasmic reticulum and Golgi structures, as well as presence of multivesicular bodies
in vivo
in podocytes lacking
Mof
following injury. Undertaking genome-wide expression analysis of podocytes, we uncover several MOF-regulated pathways required for stress response. We find that MOF, along with the members of the non-specific lethal but not the male-specific lethal complex, directly binds to genes encoding the lysosome, endocytosis and vacuole pathways, which are known regulators of podocyte maintenance. Thus, our work identifies MOF as a key regulator of cellular stress response in glomerular podocytes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26387537</pmid><doi>10.1038/onc.2015.335</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2016-05, Vol.35 (21), p.2698-2710 |
| issn | 0950-9232 1476-5594 |
| language | eng |
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| source | MEDLINE; Springer Journals; Nature Journals Online |
| subjects | 101/28 13/1 45/41 631/208/176/1433 64/60 Animals Apoptosis Cell Biology Cell Cycle Checkpoints - genetics Cellular biology Cellular control mechanisms Drosophila Embryos Genetic aspects Heat-Shock Proteins - genetics Heat-Shock Proteins - metabolism Histone Acetyltransferases - genetics Histone Acetyltransferases - metabolism Human Genetics Humans Internal Medicine Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Transgenic Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology Original original-article Podocytes - cytology Podocytes - metabolism Podocytes - physiology Properties Scavenger Receptors, Class A - genetics Scavenger Receptors, Class A - metabolism Stress Stress (Physiology) Stress, Physiological - genetics Tissues Transcription factors Transcription, Genetic |
| title | MOF maintains transcriptional programs regulating cellular stress response |
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