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...

Full description

Bibliographic Details
Main Authors: Keita Aoki, Hironori Niki
Format: Article
Language:English
Published: The Company of Biologists 2017-11-01
Series:Biology Open
Subjects:
Online Access:http://bio.biologists.org/content/6/11/1614
_version_ 1819073396462321664
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