Disruption of the Regulatory β Subunit of Protein Kinase CK2 in Mice Leads to a Cell-Autonomous Defect and Early Embryonic Lethality
| Autor: | Thierry Buchou, Hervé Pointu, Hans H. Jensen, Birgitte Brinkmann Olsen, Muriel Vernet, Claude Cochet, Brigitte Boldyreff, Olaf-Georg Issinger, Olivier Blond |
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| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Cell Survival
Gestational Age Biology In Vitro Techniques Protein Serine-Threonine Kinases Embryonic and Fetal Development Mice Pregnancy Conditional gene knockout medicine Mammalian Genetic Models with Minimal or Complex Phenotypes Animals Blastocyst Protein kinase A MAPK1 Casein Kinase II Molecular Biology Fetal Death Mice Knockout Kinase Gene targeting Cell Biology Protein-Serine-Threonine Kinases Molecular biology Embryonic stem cell Mice Inbred C57BL Protein Subunits medicine.anatomical_structure Gene Targeting Female Casein kinase 2 Cell Division |
| Zdroj: | Buchou, T, Vernet, M, Blond, O, Jensen, H H, Pointu, H, Olsen, B B, Cochet, C, Issinger, O-G & Boldyreff, B 2003, ' Disruption of the regulatory beta subunit of protein kinase CK2 in mice leads to a cell-autonomous defect and early embryonic lethality ', Molecular and Cellular Biology, vol. 23, no. 3, pp. 908-915 . https://doi.org/10.1128/MCB.23.3.908-915.2003 |
| DOI: | 10.1128/MCB.23.3.908-915.2003 |
| Popis: | Udgivelsesdato: 2003-Feb Protein kinase CK2 is a ubiquitous protein kinase implicated in proliferation and cell survival. Its regulatory beta subunit, CK2beta, which is encoded by a single gene in mammals, has been suspected of regulating other protein kinases. In this work, we show that knockout of the CK2beta gene in mice leads to postimplantation lethality. Mutant embryos were reduced in size at embryonic day 6.5 (E6.5). They did not exhibit signs of apoptosis but did show reduced cell proliferation. Mutant embryos were resorbed at E7.5. In vitro, CK2beta(-/-) morula development stopped after the blastocyst stage. Attempts to generate homozygous embryonic stem (ES) cells failed. By using a conditional knockout approach, we show that lack of CK2beta is deleterious for mouse ES cells and primary embryonic fibroblasts. This is in contrast to what occurs with yeast cells, which can survive without functional CK2beta. Thus, our study demonstrates that in mammals, CK2beta is essential for viability at the cellular level, possibly because it acquired new functions during evolution. |
| Databáze: | OpenAIRE |
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