Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis

Hideo Nishitani, Motoaki Ohtsubo, Katsumi Yamashita, Hiroshi Iida, Jonathon Pines, Hideyo Yasudo, Yosaburo Shibata, Tony Hunter, Takeharu Nishimoto

研究成果: ジャーナルへの寄稿記事

146 引用 (Scopus)

抄録

The temperature-sensitive mutant cell line tsBN2, was derived from the BHK21 cell line and has a point mutation in the RCC1 gene. In tsBN2 cells, the RCC1 protein disappeared after a shift to the non-permissive temperature at any time in the cell cycle. From S phase onwards, once RCC1 function was lost at the non-permissive temperature, p34cdc2 was dephosphorylated and M-phase specific histone H1 kinase was activated. However, in G1 phase, shifting to the non-permissive temperature did not activate p34cdc2 histone H1 kinase. The activation of p34cdc2 histone H1 kinase required protein synthesis in addition to the presence of a complex between p34cdc2 and cyclin B. Upon the loss of RCC1 in S phase of tsBN2 cells and the consequent p34cdc2 histone H1 kinase activation, a normal mitotic cycle is induced, including the formation of a mitotic spindle and subsequent reformation of the interphase-microtubule network. Exit from mitosis was accompanied by the disappearance of cyclin B, and a decrease in p34cdc2 histone H1 kinase activity. The kinetics of p34cdc2 histone H1 kinase activation correlated well with the appearance of premature mitotic cells and was not affected by the presence of a DNA synthesis inhibitor. Thus the normal inhibition of p34cdc2 activation by incompletely replicated DNA is abrogated by the loss of RCC1.

元の言語英語
ページ(範囲)1555-1564
ページ数10
ジャーナルEMBO Journal
10
発行部数6
出版物ステータス出版済み - 1991

Fingerprint

CDC2 Protein Kinase
DNA-Binding Proteins
Nuclear Proteins
DNA Replication
Mitosis
Protein Kinases
Chemical activation
DNA
Cyclin B
Temperature
Cells
S Phase
Maturation-Promoting Factor
Nucleic Acid Synthesis Inhibitors
Cell Line
Spindle Apparatus
Interphase
G1 Phase
Point Mutation
Microtubules

All Science Journal Classification (ASJC) codes

  • Cell Biology
  • Genetics

これを引用

Nishitani, H., Ohtsubo, M., Yamashita, K., Iida, H., Pines, J., Yasudo, H., ... Nishimoto, T. (1991). Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis. EMBO Journal, 10(6), 1555-1564.

Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis. / Nishitani, Hideo; Ohtsubo, Motoaki; Yamashita, Katsumi; Iida, Hiroshi; Pines, Jonathon; Yasudo, Hideyo; Shibata, Yosaburo; Hunter, Tony; Nishimoto, Takeharu.

:: EMBO Journal, 巻 10, 番号 6, 1991, p. 1555-1564.

研究成果: ジャーナルへの寄稿記事

Nishitani, H, Ohtsubo, M, Yamashita, K, Iida, H, Pines, J, Yasudo, H, Shibata, Y, Hunter, T & Nishimoto, T 1991, 'Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis', EMBO Journal, 巻. 10, 番号 6, pp. 1555-1564.
Nishitani, Hideo ; Ohtsubo, Motoaki ; Yamashita, Katsumi ; Iida, Hiroshi ; Pines, Jonathon ; Yasudo, Hideyo ; Shibata, Yosaburo ; Hunter, Tony ; Nishimoto, Takeharu. / Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis. :: EMBO Journal. 1991 ; 巻 10, 番号 6. pp. 1555-1564.
@article{ee3386e1f3e44146a443eb85066b83b4,
title = "Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis",
abstract = "The temperature-sensitive mutant cell line tsBN2, was derived from the BHK21 cell line and has a point mutation in the RCC1 gene. In tsBN2 cells, the RCC1 protein disappeared after a shift to the non-permissive temperature at any time in the cell cycle. From S phase onwards, once RCC1 function was lost at the non-permissive temperature, p34cdc2 was dephosphorylated and M-phase specific histone H1 kinase was activated. However, in G1 phase, shifting to the non-permissive temperature did not activate p34cdc2 histone H1 kinase. The activation of p34cdc2 histone H1 kinase required protein synthesis in addition to the presence of a complex between p34cdc2 and cyclin B. Upon the loss of RCC1 in S phase of tsBN2 cells and the consequent p34cdc2 histone H1 kinase activation, a normal mitotic cycle is induced, including the formation of a mitotic spindle and subsequent reformation of the interphase-microtubule network. Exit from mitosis was accompanied by the disappearance of cyclin B, and a decrease in p34cdc2 histone H1 kinase activity. The kinetics of p34cdc2 histone H1 kinase activation correlated well with the appearance of premature mitotic cells and was not affected by the presence of a DNA synthesis inhibitor. Thus the normal inhibition of p34cdc2 activation by incompletely replicated DNA is abrogated by the loss of RCC1.",
author = "Hideo Nishitani and Motoaki Ohtsubo and Katsumi Yamashita and Hiroshi Iida and Jonathon Pines and Hideyo Yasudo and Yosaburo Shibata and Tony Hunter and Takeharu Nishimoto",
year = "1991",
language = "English",
volume = "10",
pages = "1555--1564",
journal = "EMBO Journal",
issn = "0261-4189",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Loss of RCC1, a nuclear DNA-binding protein, uncouples the completion of DNA replication from the activation of cdc2 protein kinase and mitosis

AU - Nishitani, Hideo

AU - Ohtsubo, Motoaki

AU - Yamashita, Katsumi

AU - Iida, Hiroshi

AU - Pines, Jonathon

AU - Yasudo, Hideyo

AU - Shibata, Yosaburo

AU - Hunter, Tony

AU - Nishimoto, Takeharu

PY - 1991

Y1 - 1991

N2 - The temperature-sensitive mutant cell line tsBN2, was derived from the BHK21 cell line and has a point mutation in the RCC1 gene. In tsBN2 cells, the RCC1 protein disappeared after a shift to the non-permissive temperature at any time in the cell cycle. From S phase onwards, once RCC1 function was lost at the non-permissive temperature, p34cdc2 was dephosphorylated and M-phase specific histone H1 kinase was activated. However, in G1 phase, shifting to the non-permissive temperature did not activate p34cdc2 histone H1 kinase. The activation of p34cdc2 histone H1 kinase required protein synthesis in addition to the presence of a complex between p34cdc2 and cyclin B. Upon the loss of RCC1 in S phase of tsBN2 cells and the consequent p34cdc2 histone H1 kinase activation, a normal mitotic cycle is induced, including the formation of a mitotic spindle and subsequent reformation of the interphase-microtubule network. Exit from mitosis was accompanied by the disappearance of cyclin B, and a decrease in p34cdc2 histone H1 kinase activity. The kinetics of p34cdc2 histone H1 kinase activation correlated well with the appearance of premature mitotic cells and was not affected by the presence of a DNA synthesis inhibitor. Thus the normal inhibition of p34cdc2 activation by incompletely replicated DNA is abrogated by the loss of RCC1.

AB - The temperature-sensitive mutant cell line tsBN2, was derived from the BHK21 cell line and has a point mutation in the RCC1 gene. In tsBN2 cells, the RCC1 protein disappeared after a shift to the non-permissive temperature at any time in the cell cycle. From S phase onwards, once RCC1 function was lost at the non-permissive temperature, p34cdc2 was dephosphorylated and M-phase specific histone H1 kinase was activated. However, in G1 phase, shifting to the non-permissive temperature did not activate p34cdc2 histone H1 kinase. The activation of p34cdc2 histone H1 kinase required protein synthesis in addition to the presence of a complex between p34cdc2 and cyclin B. Upon the loss of RCC1 in S phase of tsBN2 cells and the consequent p34cdc2 histone H1 kinase activation, a normal mitotic cycle is induced, including the formation of a mitotic spindle and subsequent reformation of the interphase-microtubule network. Exit from mitosis was accompanied by the disappearance of cyclin B, and a decrease in p34cdc2 histone H1 kinase activity. The kinetics of p34cdc2 histone H1 kinase activation correlated well with the appearance of premature mitotic cells and was not affected by the presence of a DNA synthesis inhibitor. Thus the normal inhibition of p34cdc2 activation by incompletely replicated DNA is abrogated by the loss of RCC1.

UR - http://www.scopus.com/inward/record.url?scp=0025734777&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025734777&partnerID=8YFLogxK

M3 - Article

C2 - 1851087

AN - SCOPUS:0025734777

VL - 10

SP - 1555

EP - 1564

JO - EMBO Journal

JF - EMBO Journal

SN - 0261-4189

IS - 6

ER -