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Updated: Aug 5, 2026

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome
Published on: March 22, 2018
c-Myc initiates illegitimate replication of the ribonucleotide reductase R2 gene
T I Kuschak1, B C Kuschak, C L Taylor
1Department of Microbiology, Manitoba Institute of Cell Biology, The University of Manitoba, 675 McDermot Ave., Winnipeg, MB, R3E 0V9, Canada.
Abstract:
The mechanisms through which the oncoprotein c-Myc initiates locus-specific gene amplification are not understood. When analysing the initiation mechanism of c-Myc-dependent amplification of the mouse ribonucleotide reductase R2 (R2) gene, we observe c-Myc-dependent initiation of illegitimate DNA replication of the R2 gene. We demonstrate multiple simultaneous c-Myc-induced R2 replication forks, whereas R2 normally replicates with a single fork. In contrast, cyclin C replicates with only a single replication fork irrespective of c-Myc deregulation. In addition to de novo replication forks, c-Myc also initiates bi-allelic replication of R2, abrogating its normal mono-allelic replication pattern. Moreover, several chromosomal regions also display c-Myc-induced illegitimate replication profiles. Thus, c-Myc can act as an illegitimate replication-licensing factor that promotes de novo replication initiation and illegitimate replication timing that adversely impacts upon genomic stability.
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