Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control
Tight coupling of cell growth and cell cycle progression enable cells to adjust their rate of division, and therefore size, to the demands of proliferation in varying nutritional environments. Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, re...
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| creator | Cobley, David Hálová, Lenka Schauries, Marie Kaczmarek, Adrian Franz-Wachtel, Mirita Du, Wei Krug, Karsten Maček, Boris Petersen, Janni |
| description | Tight coupling of cell growth and cell cycle progression enable cells to adjust their rate of division, and therefore size, to the demands of proliferation in varying nutritional environments. Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, reduced TORC1 activity advances mitotic onset and switches growth to a sustained proliferation at reduced cell size. A screen for mutants, that failed to advance mitosis upon nitrogen stress, identified a mutant in the PIKFYVE 1-phosphatidylinositol-3-phosphate 5-kinase fission yeast homolog Ste12. Ste12PIKFYVE deficient mutants were unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. While it is well established that PI(3,5)P2 signalling is required for autophagy and that Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles had any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE deficient mutants reduced cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. However, no major impact on TORC1 or TORC2 activity was observed in the ste12 deficient mutants. In summary, Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division. |
| doi_str_mv | 10.1371/journal.pone.0172740 |
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Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, reduced TORC1 activity advances mitotic onset and switches growth to a sustained proliferation at reduced cell size. A screen for mutants, that failed to advance mitosis upon nitrogen stress, identified a mutant in the PIKFYVE 1-phosphatidylinositol-3-phosphate 5-kinase fission yeast homolog Ste12. Ste12PIKFYVE deficient mutants were unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. While it is well established that PI(3,5)P2 signalling is required for autophagy and that Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles had any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE deficient mutants reduced cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. However, no major impact on TORC1 or TORC2 activity was observed in the ste12 deficient mutants. In summary, Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0172740</identifier><identifier>PMID: 28273166</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Amino acids ; Analysis ; Autophagy ; Biology and Life Sciences ; Cancer ; Cell cycle ; Cell death ; Cell division ; Cell growth ; Cell size ; Cells (Biology) ; Deficient mutant ; Fission ; Growth ; Growth conditions ; Homology ; Kinases ; Life sciences ; Lysosomes ; Mechanistic Target of Rapamycin Complex 1 ; Medical research ; Medicine ; Mitosis ; Multiprotein Complexes - genetics ; Multiprotein Complexes - metabolism ; Mutants ; Mutation ; Nitrogen ; Nitrogen - metabolism ; Nutrient deficiency ; Phagocytosis ; Phosphates ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol phosphates ; Phosphorylation ; Physical Sciences ; Proline ; Protein Binding ; Protein Transport ; Proteins ; Rapamycin ; Research and Analysis Methods ; Schizosaccharomyces - cytology ; Schizosaccharomyces - physiology ; Schizosaccharomyces pombe ; Schizosaccharomyces pombe Proteins - genetics ; Schizosaccharomyces pombe Proteins - metabolism ; Signal Transduction ; Signaling ; Stress ; Stress, Physiological - genetics ; Stresses ; Switches ; TOR protein ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism ; Vacuoles ; Vacuoles - metabolism ; Yeast ; Yeasts</subject><ispartof>PloS one, 2017-03, Vol.12 (3), p.e0172740-e0172740</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Cobley 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. 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Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, reduced TORC1 activity advances mitotic onset and switches growth to a sustained proliferation at reduced cell size. A screen for mutants, that failed to advance mitosis upon nitrogen stress, identified a mutant in the PIKFYVE 1-phosphatidylinositol-3-phosphate 5-kinase fission yeast homolog Ste12. Ste12PIKFYVE deficient mutants were unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. While it is well established that PI(3,5)P2 signalling is required for autophagy and that Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles had any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE deficient mutants reduced cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. However, no major impact on TORC1 or TORC2 activity was observed in the ste12 deficient mutants. 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metabolism</subject><subject>Nutrient deficiency</subject><subject>Phagocytosis</subject><subject>Phosphates</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphatidylinositol phosphates</subject><subject>Phosphorylation</subject><subject>Physical Sciences</subject><subject>Proline</subject><subject>Protein Binding</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Research and Analysis Methods</subject><subject>Schizosaccharomyces - cytology</subject><subject>Schizosaccharomyces - physiology</subject><subject>Schizosaccharomyces pombe</subject><subject>Schizosaccharomyces pombe Proteins - genetics</subject><subject>Schizosaccharomyces pombe Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stress</subject><subject>Stress, Physiological - genetics</subject><subject>Stresses</subject><subject>Switches</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cobley, David</au><au>Hálová, Lenka</au><au>Schauries, Marie</au><au>Kaczmarek, Adrian</au><au>Franz-Wachtel, Mirita</au><au>Du, Wei</au><au>Krug, Karsten</au><au>Maček, Boris</au><au>Petersen, Janni</au><au>Mata, Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-03-08</date><risdate>2017</risdate><volume>12</volume><issue>3</issue><spage>e0172740</spage><epage>e0172740</epage><pages>e0172740-e0172740</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Tight coupling of cell growth and cell cycle progression enable cells to adjust their rate of division, and therefore size, to the demands of proliferation in varying nutritional environments. Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, reduced TORC1 activity advances mitotic onset and switches growth to a sustained proliferation at reduced cell size. A screen for mutants, that failed to advance mitosis upon nitrogen stress, identified a mutant in the PIKFYVE 1-phosphatidylinositol-3-phosphate 5-kinase fission yeast homolog Ste12. Ste12PIKFYVE deficient mutants were unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. While it is well established that PI(3,5)P2 signalling is required for autophagy and that Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles had any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE deficient mutants reduced cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. However, no major impact on TORC1 or TORC2 activity was observed in the ste12 deficient mutants. In summary, Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28273166</pmid><doi>10.1371/journal.pone.0172740</doi><tpages>e0172740</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_1875378512 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Amino acids Analysis Autophagy Biology and Life Sciences Cancer Cell cycle Cell death Cell division Cell growth Cell size Cells (Biology) Deficient mutant Fission Growth Growth conditions Homology Kinases Life sciences Lysosomes Mechanistic Target of Rapamycin Complex 1 Medical research Medicine Mitosis Multiprotein Complexes - genetics Multiprotein Complexes - metabolism Mutants Mutation Nitrogen Nitrogen - metabolism Nutrient deficiency Phagocytosis Phosphates Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphatidylinositol phosphates Phosphorylation Physical Sciences Proline Protein Binding Protein Transport Proteins Rapamycin Research and Analysis Methods Schizosaccharomyces - cytology Schizosaccharomyces - physiology Schizosaccharomyces pombe Schizosaccharomyces pombe Proteins - genetics Schizosaccharomyces pombe Proteins - metabolism Signal Transduction Signaling Stress Stress, Physiological - genetics Stresses Switches TOR protein TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Vacuoles Vacuoles - metabolism Yeast Yeasts |
| title | Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T10%3A03%3A21IST&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=Ste12/Fab1%20phosphatidylinositol-3-phosphate%205-kinase%20is%20required%20for%20nitrogen-regulated%20mitotic%20commitment%20and%20cell%20size%20control&rft.jtitle=PloS%20one&rft.au=Cobley,%20David&rft.date=2017-03-08&rft.volume=12&rft.issue=3&rft.spage=e0172740&rft.epage=e0172740&rft.pages=e0172740-e0172740&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0172740&rft_dat=%3Cgale_plos_%3EA484557784%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=1875378512&rft_id=info:pmid/28273166&rft_galeid=A484557784&rft_doaj_id=oai_doaj_org_article_43e7c48d8a1441029d2049f2f39ece76&rfr_iscdi=true |