Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis

Asha Recino, Victoria Sherwood, A Flaxman, Wendy N Cooper, Farida Latif, Andrew Ward, Andrew D Chalmers

Research output: Contribution to journalArticle

  • 18 Citations

Abstract

RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.
LanguageEnglish
Pages207-213
Number of pages7
JournalBiochemical Journal
Volume430
Issue number2
Early online date13 Jul 2010
DOIs
StatusPublished - 1 Sep 2010

Fingerprint

Cytoskeleton
Mitosis
Microtubules
Chemical activation
Cells
Defects
Cell growth
Assays
Proteins
Association reactions
Centrosome
Xenopus
Embryonic Structures
Cell Line
Growth
Neoplasms

Cite this

Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis. / Recino, Asha; Sherwood, Victoria; Flaxman, A; Cooper, Wendy N; Latif, Farida; Ward, Andrew; Chalmers, Andrew D.

In: Biochemical Journal, Vol. 430, No. 2, 01.09.2010, p. 207-213.

Research output: Contribution to journalArticle

@article{f9e38abf5cb547c7984e00f7e69c90a1,
title = "Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis",
abstract = "RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.",
author = "Asha Recino and Victoria Sherwood and A Flaxman and Wendy N Cooper and Farida Latif and Andrew Ward and Chalmers, {Andrew D}",
year = "2010",
month = "9",
day = "1",
doi = "10.1042/BJ20100883",
language = "English",
volume = "430",
pages = "207--213",
journal = "Biochemical journal",
issn = "0264-6021",
publisher = "Portland Press Ltd.",
number = "2",

}

TY - JOUR

T1 - Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis

AU - Recino,Asha

AU - Sherwood,Victoria

AU - Flaxman,A

AU - Cooper,Wendy N

AU - Latif,Farida

AU - Ward,Andrew

AU - Chalmers,Andrew D

PY - 2010/9/1

Y1 - 2010/9/1

N2 - RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.

AB - RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.

UR - http://www.scopus.com/inward/record.url?scp=77956713463&partnerID=8YFLogxK

UR - http://dx.doi.org/10.1042/BJ20100883

U2 - 10.1042/BJ20100883

DO - 10.1042/BJ20100883

M3 - Article

VL - 430

SP - 207

EP - 213

JO - Biochemical journal

T2 - Biochemical journal

JF - Biochemical journal

SN - 0264-6021

IS - 2

ER -