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TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes

Chromosomal instability can arise from defects in chromosome–microtubule attachment. Using a variety of drug treatments, we show that TAO1 kinase is required for ensuring the normal congression of chromosomes. Depletion of TAO1 reduces the density of growing interphase and mitotic microtubules in hu...

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Autores principales: Shrestha, Roshan L., Tamura, Naoka, Fries, Anna, Levin, Nicolas, Clark, Joanna, Draviam, Viji M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Royal Society 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077056/
https://www.ncbi.nlm.nih.gov/pubmed/24898139
http://dx.doi.org/10.1098/rsob.130108
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author Shrestha, Roshan L.
Tamura, Naoka
Fries, Anna
Levin, Nicolas
Clark, Joanna
Draviam, Viji M.
author_facet Shrestha, Roshan L.
Tamura, Naoka
Fries, Anna
Levin, Nicolas
Clark, Joanna
Draviam, Viji M.
author_sort Shrestha, Roshan L.
collection PubMed
description Chromosomal instability can arise from defects in chromosome–microtubule attachment. Using a variety of drug treatments, we show that TAO1 kinase is required for ensuring the normal congression of chromosomes. Depletion of TAO1 reduces the density of growing interphase and mitotic microtubules in human cells, showing TAO1's role in controlling microtubule dynamics. We demonstrate the aneugenic nature of chromosome–microtubule attachment defects in TAO1-depleted cells using an error-correction assay. Our model further strengthens the emerging paradigm that microtubule regulatory pathways are important for resolving erroneous kinetochore–microtubule attachments and maintaining the integrity of the genome, regardless of the spindle checkpoint status.
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spelling pubmed-40770562014-07-14 TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes Shrestha, Roshan L. Tamura, Naoka Fries, Anna Levin, Nicolas Clark, Joanna Draviam, Viji M. Open Biol Research Chromosomal instability can arise from defects in chromosome–microtubule attachment. Using a variety of drug treatments, we show that TAO1 kinase is required for ensuring the normal congression of chromosomes. Depletion of TAO1 reduces the density of growing interphase and mitotic microtubules in human cells, showing TAO1's role in controlling microtubule dynamics. We demonstrate the aneugenic nature of chromosome–microtubule attachment defects in TAO1-depleted cells using an error-correction assay. Our model further strengthens the emerging paradigm that microtubule regulatory pathways are important for resolving erroneous kinetochore–microtubule attachments and maintaining the integrity of the genome, regardless of the spindle checkpoint status. The Royal Society 2014-06-04 /pmc/articles/PMC4077056/ /pubmed/24898139 http://dx.doi.org/10.1098/rsob.130108 Text en http://creativecommons.org/licenses/by/3.0/ © 2014 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/, which permits unrestricted use, provided the original author and source are credited.
spellingShingle Research
Shrestha, Roshan L.
Tamura, Naoka
Fries, Anna
Levin, Nicolas
Clark, Joanna
Draviam, Viji M.
TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title_full TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title_fullStr TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title_full_unstemmed TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title_short TAO1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
title_sort tao1 kinase maintains chromosomal stability by facilitating proper congression of chromosomes
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077056/
https://www.ncbi.nlm.nih.gov/pubmed/24898139
http://dx.doi.org/10.1098/rsob.130108
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