Greatwall kinase

Author:

Yu Jiangtao1,Fleming Shawna L.2,Williams Byron1,Williams Erika V.1,Li ZeXiao1,Somma Patrizia3,Rieder Conly L.24,Goldberg Michael L.1

Affiliation:

1. Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853

2. Division of Molecular Medicine, Wadsworth Center, New York State Department of Health, Albany, NY 12201

3. Dipartimento di Genetica e Biologia Molecolare, Universitá di Roma La Sapienza, 00185 Roma, Italy

4. Department of Biomedical Sciences, University at Albany, State University of New York, Albany, NY 12222

Abstract

Mutations in the Drosophila gene greatwall cause improper chromosome condensation and delay cell cycle progression in larval neuroblasts. Chromosomes are highly undercondensed, particularly in the euchromatin, but nevertheless contain phosphorylated histone H3, condensin, and topoisomerase II. Cells take much longer to transit the period of chromosome condensation from late G2 through nuclear envelope breakdown. Mutant cells are also subsequently delayed at metaphase, due to spindle checkpoint activity. These mutant phenotypes are not caused by spindle aberrations, by global defects in chromosome replication, or by activation of a caffeine-sensitive checkpoint. The Greatwall proteins in insects and vertebrates are located in the nucleus and belong to the AGC family of serine/threonine protein kinases; the kinase domain of Greatwall is interrupted by a long stretch of unrelated amino acids.

Publisher

Rockefeller University Press

Subject

Cell Biology

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