Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4
For a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast, a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic ex...
| Main Authors: | , , |
|---|---|
| Other Authors: | |
| Format: | Article |
| Language: | en_US |
| Published: |
National Academy of Sciences (U.S.)
2012
|
| Online Access: | http://hdl.handle.net/1721.1/70141 https://orcid.org/0000-0003-2910-9803 https://orcid.org/0000-0001-9837-0314 |
| _version_ | 1826200822878306304 |
|---|---|
| author | Chan, Leon Y. Falk, Jill Amon, Angelika B |
| author2 | Massachusetts Institute of Technology. Department of Biological Engineering |
| author_facet | Massachusetts Institute of Technology. Department of Biological Engineering Chan, Leon Y. Falk, Jill Amon, Angelika B |
| author_sort | Chan, Leon Y. |
| collection | MIT |
| description | For a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast, a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from mitosis. The protein kinase Kin4 is a central component of the spindle position checkpoint. Kin4 primarily localizes to the mother cell and associates with spindle pole bodies (SPBs) located in the mother cell to inhibit MEN signaling. In contrast, the kinase does not associate with the SPB in the bud. Thus, only when a MEN bearing SPB leaves the mother cell and the spindle is accurately positioned along the mother–bud axis can MEN signaling occur and cell division proceed. Here, we describe a mechanism ensuring that Kin4 only associates with mother cell-located SPBs. The bud-localized MEN regulator Lte1, whose molecular function has long been unclear, prevents Kin4 that escapes into the bud from associating with SPBs in the daughter cell. |
| first_indexed | 2024-09-23T11:42:21Z |
| format | Article |
| id | mit-1721.1/70141 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T11:42:21Z |
| publishDate | 2012 |
| publisher | National Academy of Sciences (U.S.) |
| record_format | dspace |
| spelling | mit-1721.1/701412022-09-27T21:19:30Z Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 Chan, Leon Y. Falk, Jill Amon, Angelika B Massachusetts Institute of Technology. Department of Biological Engineering Koch Institute for Integrative Cancer Research at MIT Amon, Angelika B. Amon, Angelika B. Falk, Jill E. Chan, Leon Y. For a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast, a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from mitosis. The protein kinase Kin4 is a central component of the spindle position checkpoint. Kin4 primarily localizes to the mother cell and associates with spindle pole bodies (SPBs) located in the mother cell to inhibit MEN signaling. In contrast, the kinase does not associate with the SPB in the bud. Thus, only when a MEN bearing SPB leaves the mother cell and the spindle is accurately positioned along the mother–bud axis can MEN signaling occur and cell division proceed. Here, we describe a mechanism ensuring that Kin4 only associates with mother cell-located SPBs. The bud-localized MEN regulator Lte1, whose molecular function has long been unclear, prevents Kin4 that escapes into the bud from associating with SPBs in the daughter cell. Howard Hughes Medical Institute National Science Foundation (U.S.) (Predoctoral Fellowship) National Institutes of Health (U.S.) (Grant GM056800) 2012-04-25T21:06:02Z 2012-04-25T21:06:02Z 2011-08 2011-04 Article http://purl.org/eprint/type/JournalArticle 0027-8424 1091-6490 http://hdl.handle.net/1721.1/70141 Falk, J. E., L. Y. Chan, and A. Amon. “Lte1 Promotes Mitotic Exit by Controlling the Localization of the Spindle Position Checkpoint Kinase Kin4.” Proceedings of the National Academy of Sciences 108.31 (2011): 12584–12590. Web. https://orcid.org/0000-0003-2910-9803 https://orcid.org/0000-0001-9837-0314 en_US http://dx.doi.org/10.1073/pnas.1107784108 Proceedings of the National Academy of Sciences of the United States of America Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. application/pdf National Academy of Sciences (U.S.) PNAS |
| spellingShingle | Chan, Leon Y. Falk, Jill Amon, Angelika B Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title | Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title_full | Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title_fullStr | Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title_full_unstemmed | Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title_short | Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4 |
| title_sort | lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase kin4 |
| url | http://hdl.handle.net/1721.1/70141 https://orcid.org/0000-0003-2910-9803 https://orcid.org/0000-0001-9837-0314 |
| work_keys_str_mv | AT chanleony lte1promotesmitoticexitbycontrollingthelocalizationofthespindlepositioncheckpointkinasekin4 AT falkjill lte1promotesmitoticexitbycontrollingthelocalizationofthespindlepositioncheckpointkinasekin4 AT amonangelikab lte1promotesmitoticexitbycontrollingthelocalizationofthespindlepositioncheckpointkinasekin4 |