Rad53 is essential for a mitochondrial DNA inheritance checkpoint regulating G1 to S progression

• DOI: 10.1083/jcb.201205193
• Publication Date: 2012-08-28T02:53:18Z
• Authors: David G. Crider; Luis J. García-Ro...; Pallavi Srivastava; Leonardo Peraza-R...; Krishna Upadhyaya; Istvan R. Boldogh; Liza A. Pon
• Keywords: Inheritance; Checkpoint Kinase 2; CHEK1

The Chk2-mediated deoxyribonucleic acid (DNA) damage checkpoint pathway is important for mitochondrial DNA (mtDNA) maintenance. We show in this paper that mtDNA itself affects cell cycle progression. Saccharomyces cerevisiae rho0 cells, which lack mtDNA, were defective G1- to S-phase Deletion of subunit Va cytochrome c oxidase, inhibition F1F0 adenosine triphosphatase, or replacement all mtDNA-encoded genes with noncoding did not affect Thus, the progression defect cells caused by loss within mitochondria and respiratory activity genes. Rad53p, yeast Chk2 homologue, was required cells. Pif1p, a helicase Rad53p target, underwent Rad53p-dependent phosphorylation activated an established kinase inhibited These findings support existence Rad53p-regulated regulates response mtDNA.