Search tips
Search criteria 


Logo of mbcLink to Publisher's site
Mol Biol Cell. Jun 1995; 6(6): 741–756.
PMCID: PMC301233
The origin recognition complex in silencing, cell cycle progression, and DNA replication.
S Loo, C A Fox, J Rine, R Kobayashi, B Stillman, and S Bell
Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.
This report describes the isolation of ORC5, the gene encoding the fifth largest subunit of the origin recognition complex, and the properties of mutants with a defective allele of ORC5. The orc5-1 mutation caused temperature-sensitive growth and, at the restrictive temperature, caused cell cycle arrest. At the permissive temperature, the orc5-1 mutation caused an elevated plasmid loss rate that could be suppressed by additional tandem origins of DNA replication. The sequence of ORC5 revealed a potential ATP binding site, making Orc5p a candidate for a subunit that mediates the ATP-dependent binding of ORC to origins. Genetic interactions among orc2-1 and orc5-1 and other cell cycle genes provided further evidence for a role for the origin recognition complex (ORC) in DNA replication. The silencing defect caused by orc5-1 strengthened previous connections between ORC and silencing, and combined with the phenotypes caused by orc2 mutations, suggested that the complex itself functions in both processes.
Full text
Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (3.7M), or click on a page image below to browse page by page.
Images in this article
Articles from Molecular Biology of the Cell are provided here courtesy of
American Society for Cell Biology