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1. p53 and cell cycle dependent transcription of kinesin family member 23 (KIF23) is controlled via a CHR promoter element bound by DREAM and MMB complexes.

Author

Martin Fischer, Inga Grundke, Sindy Sohr, Marianne Quaas, Saskia Hoffmann, Arne Knörck, Catalina Gumhold, and Karen Rother

Subjects
Medicine, Science
Abstract

The microtubule-dependent molecular motor KIF23 (Kinesin family member 23) is one of two components of the centralspindlin complex assembled during late stages of mitosis. Formation of this complex is known as an essential step for cytokinesis. Here, we identified KIF23 as a new transcriptional target gene of the tumor suppressor protein p53. We showed that p53 reduces expression of KIF23 on the mRNA as well as the protein level in different cell types. Promoter reporter assays revealed that this repression results from downregulation of KIF23 promoter activity. CDK inhibitor p21(WAF1/CIP1) was shown to be necessary to mediate p53-dependent repression. Furthermore, we identified the highly conserved cell cycle genes homology region (CHR) in the KIF23 promoter to be strictly required for p53-dependent repression as well as for cell cycle-dependent expression of KIF23. Cell cycle- and p53-dependent regulation of KIF23 appeared to be controlled by differential binding of DREAM and MMB complexes to the CHR element. With this study, we describe a new mechanism for transcriptional regulation of KIF23. Considering the strongly supporting function of KIF23 in cytokinesis, its p53-dependent repression may contribute to the prevention of uncontrolled cell growth.

Published
2013
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2. p53 and Cell Cycle Dependent Transcription of kinesin family member 23 (KIF23) Is Controlled Via a CHR Promoter Element Bound by DREAM and MMB Complexes

Author

Karen Rother, Sindy Sohr, Marianne Quaas, Arne Knörck, Saskia Hoffmann, Catalina Gumhold, Inga Grundke, and Martin Fischer

Subjects
Transcription, Genetic, KIF23, Mice, Molecular cell biology, Basic Cancer Research, Protein Isoforms, Promoter Regions, Genetic, Multidisciplinary, Protein Stability, Cell Cycle, Kv Channel-Interacting Proteins, Cell cycle, Cell Cycle Gene, Oncology, Kinesin, Medicine, Microtubule-Associated Proteins, Cell Division, Research Article, Protein Binding, Cyclin-Dependent Kinase Inhibitor p21, Science, DNA transcription, Biology, Response Elements, Molecular Genetics, Genetics, Human Cloning, Animals, Humans, Gene Regulation, Gene Silencing, RNA, Messenger, Psychological repression, Mitosis, Cytokinesis, Centralspindlin complex, HCT116 Cells, Molecular biology, Oncogene Proteins v-myb, Repressor Proteins, Gene Expression Regulation, NIH 3T3 Cells, Gene expression, Tumor Suppressor Protein p53, Cloning
Abstract

The microtubule-dependent molecular motor KIF23 (Kinesin family member 23) is one of two components of the centralspindlin complex assembled during late stages of mitosis. Formation of this complex is known as an essential step for cytokinesis. Here, we identified KIF23 as a new transcriptional target gene of the tumor suppressor protein p53. We showed that p53 reduces expression of KIF23 on the mRNA as well as the protein level in different cell types. Promoter reporter assays revealed that this repression results from downregulation of KIF23 promoter activity. CDK inhibitor p21(WAF1/CIP1) was shown to be necessary to mediate p53-dependent repression. Furthermore, we identified the highly conserved cell cycle genes homology region (CHR) in the KIF23 promoter to be strictly required for p53-dependent repression as well as for cell cycle-dependent expression of KIF23. Cell cycle- and p53-dependent regulation of KIF23 appeared to be controlled by differential binding of DREAM and MMB complexes to the CHR element. With this study, we describe a new mechanism for transcriptional regulation of KIF23. Considering the strongly supporting function of KIF23 in cytokinesis, its p53-dependent repression may contribute to the prevention of uncontrolled cell growth.

Published
2013

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