This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Carroll, S M Articles by Wahl, G M Search for Related Content PubMed PubMed Citation Articles by Carroll, S M Articles by Wahl, G M

 Previous Article  |  Next Article 

Mol Cell Biol. 1991 September; 11(9): 4779-4785

Replication timing control can be maintained in extrachromosomally amplified genes.

S M Carroll, J Trotter and G M Wahl

Salk Institute for Biological Studies, La Jolla, California 92037.

ABSTRACT

Extrachromosomal elements are common early intermediates of gene amplification in vivo and in cell culture. The time at which several extrachromosomal elements replicate was compared with that of the corresponding amplified or unamplified chromosomal sequences. The replication timing analysis employed a retroactive synchrony method in which fluorescence-activated cell sorting was used to obtain cells at different stages of the cell cycle. Extrachromosomally amplified Syrian hamster CAD genes (CAD is an acronym for the single gene which encodes the trifunctional protein which catalyzes the first three steps of uridine biosynthesis) replicated in a narrow window of early S-phase which was approximately the same as that of chromosomally amplified CAD genes. Similarly, extrachromosomally amplified mouse adenosine deaminase genes replicated at a discrete time in early S-phase which approximated the replication time of the unamplified adenosine deaminase gene. In contrast, the multicopy extrachromosomal Epstein-Barr virus genome replicated within a narrow window in late S-phase in latently infected human Rajii cells. The data indicate that localization within a chromosome is not required for the maintenance of replication timing control.

---

Mol Cell Biol. 1991 September; 11(9): 4779-4785

This article has been cited by other articles:

• Zhou, J., Snyder, A. R., Lieberman, P. M. (2009). Epstein-Barr Virus Episome Stability Is Coupled to a Delay in Replication Timing. J. Virol. 83: 2154-2162 [Abstract] [Full Text]  
• Wiedmer, A., Wang, P., Zhou, J., Rennekamp, A. J., Tiranti, V., Zeviani, M., Lieberman, P. M. (2008). Epstein-Barr Virus Immediate-Early Protein Zta Co-Opts Mitochondrial Single-Stranded DNA Binding Protein To Promote Viral and Inhibit Mitochondrial DNA Replication. J. Virol. 82: 4647-4655 [Abstract] [Full Text]  
• Valent, A., Benard, J., Clausse, B., Barrois, M., Valteau-Couanet, D., Terrier-Lacombe, M.-J., Spengler, B., Bernheim, A. (2001). In Vivo Elimination of Acentric Double Minutes Containing Amplified MYCN from Neuroblastoma Tumor Cells Through the Formation of Micronuclei. Am. J. Pathol. 158: 1579-1584 [Abstract] [Full Text]  
• Kanda, T, Otter, M, Wahl, G. (2001). Mitotic segregation of viral and cellular acentric extrachromosomal molecules by chromosome tethering. J. Cell Sci. 114: 49-58 [Abstract]  
• Kirchmaier, A. L., Sugden, B. (1998). Rep*: a Viral Element That Can Partially Replace the Origin of Plasmid DNA Synthesis of Epstein-Barr Virus. J. Virol. 72: 4657-4666 [Abstract] [Full Text]  
• Shimizu, N., Itoh, N., Utiyama, H., Wahl, G. M. (1998). Selective Entrapment of Extrachromosomally Amplified DNA by Nuclear Budding and Micronucleation during S Phase. JCB 140: 1307-1320 [Abstract] [Full Text]  
• Itoh, N, Shimizu, N (1998). DNA replication-dependent intranuclear relocation of double minute chromatin. J. Cell Sci. 111: 3275-3285 [Abstract]  
• Di Leonardo, A., Linke, S.P., Yin, Y., Wahl, G.M. (1993). Cell Cycle Regulation of Gene Amplification. Cold Spring Harb Symp Quant Biol 58: 655-667 [Abstract]