Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability
Aurora B kinase regulates the proper biorientation of sister chromatids during mitosis. Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems w...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2014-09, Vol.111 (38), p.13688-13689 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Muñoz-Barrera, Marta Monje-Casas, Fernando |
| description | Aurora B kinase regulates the proper biorientation of sister chromatids during mitosis. Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems with chromosome segregation, and overexpression of this kinase has been observed in various types of cancer. However, little is known about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression and cell viability. Here, using a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers defects in chromosome segregation by promoting the continuous disruption of chromosome-microtubule attachments even when sister chromatids are correctly bioriented. This disruption leads to a constitutive activation of the spindle-assembly checkpoint, which therefore causes a lack of cytokinesis even though spindle elongation and chromosome segregation take place. Finally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitotic spindle by promoting instability of the spindle midzone. |
| doi_str_mv | 10.1073/pnas.1408017111 |
| format | Article |
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Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems with chromosome segregation, and overexpression of this kinase has been observed in various types of cancer. However, little is known about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression and cell viability. Here, using a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers defects in chromosome segregation by promoting the continuous disruption of chromosome-microtubule attachments even when sister chromatids are correctly bioriented. This disruption leads to a constitutive activation of the spindle-assembly checkpoint, which therefore causes a lack of cytokinesis even though spindle elongation and chromosome segregation take place. Finally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitotic spindle by promoting instability of the spindle midzone.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1408017111</identifier><identifier>PMID: 25201961</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Aurora Kinase B - genetics ; Aurora Kinase B - metabolism ; Biological Sciences ; Cells ; Chromatids - enzymology ; Chromatids - genetics ; Chromosomes ; Chromosomes, Fungal - genetics ; Chromosomes, Fungal - metabolism ; Gene expression ; Kinases ; Kinetochores - enzymology ; Microtubules - enzymology ; Microtubules - genetics ; PNAS Plus ; PNAS Plus Significance Statements ; Saccharomyces cerevisiae - enzymology ; Saccharomyces cerevisiae - genetics ; Saccharomyces cerevisiae Proteins - genetics ; Saccharomyces cerevisiae Proteins - metabolism ; Spindle Apparatus - enzymology ; Spindle Apparatus - genetics ; Yeast</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2014-09, Vol.111 (38), p.13688-13689</ispartof><rights>copyright © 1993–2008 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Sep 23, 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c534t-a0ada5e966563148153db94544d1893196b31e7f62180d2ad8974daefa8af8b73</citedby><cites>FETCH-LOGICAL-c534t-a0ada5e966563148153db94544d1893196b31e7f62180d2ad8974daefa8af8b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/111/38.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/43043186$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/43043186$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25201961$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Muñoz-Barrera, Marta</creatorcontrib><creatorcontrib>Monje-Casas, Fernando</creatorcontrib><title>Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Aurora B kinase regulates the proper biorientation of sister chromatids during mitosis. 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This disruption leads to a constitutive activation of the spindle-assembly checkpoint, which therefore causes a lack of cytokinesis even though spindle elongation and chromosome segregation take place. Finally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitotic spindle by promoting instability of the spindle midzone.</description><subject>Aurora Kinase B - genetics</subject><subject>Aurora Kinase B - metabolism</subject><subject>Biological Sciences</subject><subject>Cells</subject><subject>Chromatids - enzymology</subject><subject>Chromatids - genetics</subject><subject>Chromosomes</subject><subject>Chromosomes, Fungal - genetics</subject><subject>Chromosomes, Fungal - metabolism</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Kinetochores - enzymology</subject><subject>Microtubules - enzymology</subject><subject>Microtubules - genetics</subject><subject>PNAS Plus</subject><subject>PNAS Plus Significance Statements</subject><subject>Saccharomyces cerevisiae - enzymology</subject><subject>Saccharomyces cerevisiae - genetics</subject><subject>Saccharomyces cerevisiae Proteins - genetics</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><subject>Spindle Apparatus - enzymology</subject><subject>Spindle Apparatus - genetics</subject><subject>Yeast</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1u1DAUhSMEokNhzQpkiQ2btPfGdmJvkNqqlEqV2MDacmKH8ZCxB9upNDvegTfkSfB0huFnZen6u0f3nFNVLxHOEDp6vvE6nSEDAdgh4qNqgSCxbpmEx9UCoOlqwRp2Uj1LaQUAkgt4Wp00vAGULS6q7a0fotXJGnIxxxA1uSR6yO7e5S0Z9JxsIkPw2fk5zIkYl-K8yS54Ekby1Xmbw7AM0f78_mPthhjy3M-TJTpnPSzX1udEtDckbZw3Ze58yrp3U1F_Xj0Z9ZTsi8N7Wn1-f_3p6kN99_Hm9urirh44ZbnWoI3mVrYtbykygZyaXjLOmEEhaXHRU7Td2DYowDTaCNkxo-2ohR5F39HT6t1edzP3a2uGclPUk9pEt9Zxq4J26t8f75bqS7hXDAVtJBSBtweBGL7NNmW1dmmw06S9LZko5C3n0ADwgr75D12FOfpi74ESJf9WFup8T5W8Uop2PB6DoHa1ql2t6k-tZeP13x6O_O8eC0AOwG7zKIeoqFDXVMq2IK_2yCrlEI8Mo8Aoipb-AjXwtq8</recordid><startdate>20140923</startdate><enddate>20140923</enddate><creator>Muñoz-Barrera, Marta</creator><creator>Monje-Casas, Fernando</creator><general>National Academy of Sciences</general><general>National Acad Sciences</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140923</creationdate><title>Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability</title><author>Muñoz-Barrera, Marta ; Monje-Casas, Fernando</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c534t-a0ada5e966563148153db94544d1893196b31e7f62180d2ad8974daefa8af8b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aurora Kinase B - genetics</topic><topic>Aurora Kinase B - metabolism</topic><topic>Biological Sciences</topic><topic>Cells</topic><topic>Chromatids - enzymology</topic><topic>Chromatids - genetics</topic><topic>Chromosomes</topic><topic>Chromosomes, Fungal - genetics</topic><topic>Chromosomes, Fungal - metabolism</topic><topic>Gene expression</topic><topic>Kinases</topic><topic>Kinetochores - enzymology</topic><topic>Microtubules - enzymology</topic><topic>Microtubules - genetics</topic><topic>PNAS Plus</topic><topic>PNAS Plus Significance Statements</topic><topic>Saccharomyces cerevisiae - enzymology</topic><topic>Saccharomyces cerevisiae - genetics</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><topic>Spindle Apparatus - enzymology</topic><topic>Spindle Apparatus - genetics</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Muñoz-Barrera, Marta</creatorcontrib><creatorcontrib>Monje-Casas, Fernando</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Muñoz-Barrera, Marta</au><au>Monje-Casas, Fernando</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2014-09-23</date><risdate>2014</risdate><volume>111</volume><issue>38</issue><spage>13688</spage><epage>13689</epage><pages>13688-13689</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Aurora B kinase regulates the proper biorientation of sister chromatids during mitosis. Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems with chromosome segregation, and overexpression of this kinase has been observed in various types of cancer. However, little is known about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression and cell viability. Here, using a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers defects in chromosome segregation by promoting the continuous disruption of chromosome-microtubule attachments even when sister chromatids are correctly bioriented. 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| subjects | Aurora Kinase B - genetics Aurora Kinase B - metabolism Biological Sciences Cells Chromatids - enzymology Chromatids - genetics Chromosomes Chromosomes, Fungal - genetics Chromosomes, Fungal - metabolism Gene expression Kinases Kinetochores - enzymology Microtubules - enzymology Microtubules - genetics PNAS Plus PNAS Plus Significance Statements Saccharomyces cerevisiae - enzymology Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Spindle Apparatus - enzymology Spindle Apparatus - genetics Yeast |
| title | Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability |
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