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Mol. Cells 2011; 31(6): 515-521

Published online April 20, 2011

https://doi.org/10.1007/s10059-011-2292-8

© The Korean Society for Molecular and Cellular Biology

Neural Wiskott-Aldrich Syndrome Protein Is Required for Accurate Chromosome Congression and Segregation

Sun Joo Park*, and Tadaomi Takenawa1

Department of Chemistry, Pukyong National University, Busan 608-737, Korea, 1Division of Lipid Biochemistry, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan

Correspondence to : *Correspondence: parksj@pknu.ac.kr

Received: November 26, 2011; Revised: March 3, 2011; Accepted: March 14, 2011

Abstract

The accurate distribution and segregation of replicated chromosomes through mitosis is crucial for cellular viability and development of organisms. Kinetochores are responsible for the proper congression and segregation of chromosomes. Here, we show that neural Wiskott-Aldrich syndrome protein (N-WASP) localizes to and forms a complex with kinetochores in mitotic cells. Depletion of N-WASP by RNA interference causes chromosome misalignment, prolonged mitosis, and abnormal chromosomal segregation, which is associated with decreased proliferation of N-WASP-deficient cells. N-WASP-deficient cells display defects in the kinetochores recruitment of inner and outer kinetochore components, CENP-A, CENP-E, and Mad2. Live-cell imaging analysis of GFP-?-tubulin revealed that depletion of N-WASP impairs microtubule attachment to chromosomes in mitotic cells. All these results indicate that N-WASP plays a role in efficient assembly of kinetochores and attachment of microtubules to chromosomes, which is essential for accurate chromosome congression and segregation.

Keywords chromosome, congression, mitosis, N-WASP, segregation

Article

Research Article

Mol. Cells 2011; 31(6): 515-521

Published online June 30, 2011 https://doi.org/10.1007/s10059-011-2292-8

Copyright © The Korean Society for Molecular and Cellular Biology.

Neural Wiskott-Aldrich Syndrome Protein Is Required for Accurate Chromosome Congression and Segregation

Sun Joo Park*, and Tadaomi Takenawa1

Department of Chemistry, Pukyong National University, Busan 608-737, Korea, 1Division of Lipid Biochemistry, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan

Correspondence to:*Correspondence: parksj@pknu.ac.kr

Received: November 26, 2011; Revised: March 3, 2011; Accepted: March 14, 2011

Abstract

The accurate distribution and segregation of replicated chromosomes through mitosis is crucial for cellular viability and development of organisms. Kinetochores are responsible for the proper congression and segregation of chromosomes. Here, we show that neural Wiskott-Aldrich syndrome protein (N-WASP) localizes to and forms a complex with kinetochores in mitotic cells. Depletion of N-WASP by RNA interference causes chromosome misalignment, prolonged mitosis, and abnormal chromosomal segregation, which is associated with decreased proliferation of N-WASP-deficient cells. N-WASP-deficient cells display defects in the kinetochores recruitment of inner and outer kinetochore components, CENP-A, CENP-E, and Mad2. Live-cell imaging analysis of GFP-?-tubulin revealed that depletion of N-WASP impairs microtubule attachment to chromosomes in mitotic cells. All these results indicate that N-WASP plays a role in efficient assembly of kinetochores and attachment of microtubules to chromosomes, which is essential for accurate chromosome congression and segregation.

Keywords: chromosome, congression, mitosis, N-WASP, segregation

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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