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DOI: 10.1369/jhc.4A6545.2005
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Journal of Histochemistry and Cytochemistry
Volume 53 (6): 725-733, 2005
Copyright ©The Histochemical Society, Inc.

Polyploid Formation via Chromosome Duplication Induced by CTP:Phosphocholine Cytidylyltransferase Deficiency and Bcl-2 Overexpression : Identification of Two Novel Endogenous Factors

You-Jun Shen1, Cynthia J. DeLong2, Francois Tercé, Timothy Kute, Mark C. Willingham, Mark J. Pettenati and Zheng Cui

Departments of Biochemistry (Y-JS,CJD,ZC), Pathology (TK,MCW,ZC), and Pediatrics/Medical Genetics (MJP), Wake Forest University School of Medicine, Winston-Salem, North Carolina, and INSERM Unité 563, CPTP, Hôpital Purpan BP, Toulouse, France (FT)

Correspondence to: Zheng Cui, Departments of Biochemistry and Pathology/Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27599-7525. E-mail: zhengcui{at}wfubmc.edu

Polyploidy is a profound phenotype found in tumors and its mechanism is unknown. We report here that when B-cell lymphoma gene-2 (Bcl-2) was overexpressed in a Chinese hamster ovary cell line that was deficient in CTP:phosphocholine cytidylyltransferase (CT), cellular DNA content doubled. The higher DNA content was due to a permanent conversion from diploid cells to tetraploid cells. The mechanism of polyploid formation could be attributed to the duplication of 18 parental chromosomes. The rate of conversion from diploid to tetraploid was Bcl-2 dose dependent. The diploid genome was not affected by Bcl-2 expression or by CT deficiency alone. Endogenous CT or expression of recombinant rat liver CT{alpha} prior to Bcl-2 expression prevented the formation of polyploid cells. This conversion was irreversible even when both initiating factors were removed. In this study, we have identified Bcl-2 as a positive regulator and CT{alpha} as a negative regulator of polyploid formation. (J Histochem Cytochem 53:725–733, 2005)

Key Words: Bcl-2 • CTP:phosphocholine • cytidylyltransferase • polyploidy


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