The roles of Cdc2, cyclin B1,wee1, andcdc25C in G2 cell cycle arrest following ionizing radiation

Kenneth Albert Schafer, Purdue University

Abstract

Cdc2, cyclin B1, cdc25C, and wee1 are cell cycle regulators of the G$\sb2$-M transition. Following ionizing radiation, cdc2, cyclin B1, and cdc25C are thought to regulate the DNA damage-induced G$\sb2$ cell cycle arrest, but the role of wee1 is uncertain. Because X-rays and $\alpha$-particles have markedly different physical properties and produce markedly different types of DNA damage, this thesis investigates whether the G$\sb2$ arrests induced by X-rays and $\alpha$-particles are regulated differently. The roles of these cell cycle regulations in G$\sb2$-synchronized A549 cells, a type II pneumocyte cell line, following 2 and 6 Gy of X-rays or 0.5 and 1.5 Gy of $\alpha$-particles, were investigated. For both X-rays and $\alpha$-particles, results were similar. Cdc2 and cdc25C were phosphorylated and hypophosphorylated, respectively, at time points associated with G$\sb2$ cell cycle arrest. Levels of cyclin B1 did not correlate with cell cycle arrest induced by either the higher or the lower doses, contrary to previous results. No alterations were observed in wee1 expression. These results indicate that cdc2 and cdc25C, but not cyclin B1, are involved in the regulation of cell cycle arrest of A549 cells irradiated in G$\sb2$. Additionally, no differences were observed when sparsely and densely ionizing radiations were compared.

Degree

Ph.D.

Advisors

Rebar, Purdue University.

Subject Area

Molecular biology|Cellular biology

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