Journal
CELL CYCLE
Volume 7, Issue 19, Pages 3037-3047Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cc.7.19.6736
Keywords
cyclin-dependent kinase; speedy/ringo C; cell cycle; cyclin; S-G(2) phase
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Funding
- National Institutes of Health [GM47830]
- American Heart Association [0455851T]
- Robert Leet and Clara Guthrie Patterson Trust
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM047830] Funding Source: NIH RePORTER
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Cyclin-dependent kinases (CDKs) control cell cycle transitions and progression. In addition to their activation via binding to cyclins, CDKs can be activated via binding to an unrelated class of cell cycle regulators termed Speedy/Ringo (S/R) proteins. Although mammals contain at least five distinct Speedy/Ringo homologues, the specific functions of members of this growing family of CDK activators remain largely unknown. We investigated the cell cycle roles of human Speedy/Ringo C in HEK293 cells. Down-regulation of Speedy/Ringo C by RNA interference delayed S and G(2) progression whereas ectopic expression had the opposite effect, reducing S and G(2)/M populations. Double thymidine arrest and release experiments showed that overexpression of Speedy/Ringo C promoted late S phase progression. Using a novel three-color FACS protocol to determine the length of G(2) phase, we found that the suppression of Speedy/Ringo C by RNAi prolonged G(2) phase by similar to 30 min whereas ectopic expression of Speedy/Ringo C shortened G(2) phase by similar to 25 min. In addition, overexpression of Speedy/Ringo C disrupted the G(2) DNA damage checkpoint, increased cell death and caused a cell cycle delay at the G(1)-to-S transition. These observations indicate that CDK-Speedy/Ringo C complexes positively regulate cell cycle progression during the late S and G(2) phases of the cell cycle.
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