Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus
After mitosis, nuclear reorganization occurs together with decondensation of mitotic chromosomes and reformation of the nuclear envelope, thereby restoring the Ran-GTP gradient between the nucleus and cytoplasm. The Ran-GTP gradient is dependent on Pim1/RCC1. Interestingly, a defect in Pim1/RCC1 in...
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Format: | Article |
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The Company of Biologists
2017-11-01
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Series: | Biology Open |
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Online Access: | http://bio.biologists.org/content/6/11/1614 |
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author | Keita Aoki Hironori Niki |
author_facet | Keita Aoki Hironori Niki |
author_sort | Keita Aoki |
collection | DOAJ |
description | After mitosis, nuclear reorganization occurs together with decondensation of mitotic chromosomes and reformation of the nuclear envelope, thereby restoring the Ran-GTP gradient between the nucleus and cytoplasm. The Ran-GTP gradient is dependent on Pim1/RCC1. Interestingly, a defect in Pim1/RCC1 in Schizosaccharomyces pombe causes postmitotic condensation of chromatin, namely hypercondensation, suggesting a relationship between the Ran-GTP gradient and chromosome decondensation. However, how Ran-GTP interacts with chromosome decondensation is unresolved. To examine this interaction, we used Schizosaccharomyces japonicus, which is known to undergo partial breakdown of the nuclear membrane during mitosis. We found that Pim1/RCC1 was localized on nuclear pores, but this localization failed in a temperature-sensitive mutant of Pim1/RCC1. The mutant cells exhibited hypercondensed chromatin after mitosis due to prolonged association of condensin on the chromosomes. Conceivably, a condensin-dephosphorylation defect might cause hypercondensed chromatin, since chromosomal localization of condensin is dependent on phosphorylation by cyclin-dependent kinase (CDK). Indeed, CDK-phospho-mimic mutation of condensin alone caused untimely condensin localization, resulting in hypercondensed chromatin. Together, these results suggest that dephosphorylation of CDK sites of condensin might require the Ran-GTP gradient produced by nuclear pore-localized Pim1/RCC1. |
first_indexed | 2024-12-21T17:52:57Z |
format | Article |
id | doaj.art-5641103a59374f41827f6779003ec60d |
institution | Directory Open Access Journal |
issn | 2046-6390 |
language | English |
last_indexed | 2024-12-21T17:52:57Z |
publishDate | 2017-11-01 |
publisher | The Company of Biologists |
record_format | Article |
series | Biology Open |
spelling | doaj.art-5641103a59374f41827f6779003ec60d2022-12-21T18:55:18ZengThe Company of BiologistsBiology Open2046-63902017-11-016111614162810.1242/bio.027193027193Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleusKeita Aoki0Hironori Niki1 Microbial Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan Microbial Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan After mitosis, nuclear reorganization occurs together with decondensation of mitotic chromosomes and reformation of the nuclear envelope, thereby restoring the Ran-GTP gradient between the nucleus and cytoplasm. The Ran-GTP gradient is dependent on Pim1/RCC1. Interestingly, a defect in Pim1/RCC1 in Schizosaccharomyces pombe causes postmitotic condensation of chromatin, namely hypercondensation, suggesting a relationship between the Ran-GTP gradient and chromosome decondensation. However, how Ran-GTP interacts with chromosome decondensation is unresolved. To examine this interaction, we used Schizosaccharomyces japonicus, which is known to undergo partial breakdown of the nuclear membrane during mitosis. We found that Pim1/RCC1 was localized on nuclear pores, but this localization failed in a temperature-sensitive mutant of Pim1/RCC1. The mutant cells exhibited hypercondensed chromatin after mitosis due to prolonged association of condensin on the chromosomes. Conceivably, a condensin-dephosphorylation defect might cause hypercondensed chromatin, since chromosomal localization of condensin is dependent on phosphorylation by cyclin-dependent kinase (CDK). Indeed, CDK-phospho-mimic mutation of condensin alone caused untimely condensin localization, resulting in hypercondensed chromatin. Together, these results suggest that dephosphorylation of CDK sites of condensin might require the Ran-GTP gradient produced by nuclear pore-localized Pim1/RCC1.http://bio.biologists.org/content/6/11/1614Pim1/RCC1CondensinChromosome decondensation |
spellingShingle | Keita Aoki Hironori Niki Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus Biology Open Pim1/RCC1 Condensin Chromosome decondensation |
title | Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus |
title_full | Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus |
title_fullStr | Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus |
title_full_unstemmed | Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus |
title_short | Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus |
title_sort | release of condensin from mitotic chromosomes requires the ran gtp gradient in the reorganized nucleus |
topic | Pim1/RCC1 Condensin Chromosome decondensation |
url | http://bio.biologists.org/content/6/11/1614 |
work_keys_str_mv | AT keitaaoki releaseofcondensinfrommitoticchromosomesrequirestherangtpgradientinthereorganizednucleus AT hironoriniki releaseofcondensinfrommitoticchromosomesrequirestherangtpgradientinthereorganizednucleus |