Fig. 6: Interactions of residue 324 with the DNA are critical for Pif1 function in Okazaki fragment processing but not for mitochondrial function or suppression of gross chromosomal rearrangements.

a, b Assay for Okazaki fragment processing. Adapted from Gao J, Proffit DR, Marecki JC, Protacio RU, Wahls WP, Byrd AK, Raney KD⁶³. Translated and reproduced by permission of Oxford University Press. Translation Disclaimer: OUP is not responsible or in any way liable for the accuracy of the translation. The Licensee is solely responsible for the translation in this publication/reprint. a A plasmid encoding a wild type or mutant Pif1 allele was transformed into pif1Δ dna2Δ haploid cells. b Plates from the transformation of each Pif1 allele were imaged. Cells expressing wild type Pif1, R324W, R324Y, and R324K are unable to suppress the lethality of dna2Δ, thus do not grow on selective plates. ATPase deficient Pif1 K264A, and wedge-altering R324A, R324E, and R324N grow on selective plates indicating null-Pif1 function. c To test for mitochondrial function, serial dilutions of cells were plated onto SD-Trp agar plates containing 2% glucose, and in parallel onto SG-Trp agar plates containing 3% glycerol. All tested Pif1-DNA interaction variants maintain mitochondrial respiration. d Rates of gross chromosomal rearrangements (GCR) (median and 95% confidence interval) are based on fluctuation analyses of frequencies of 16 individual cultures. Source data are provided as a Source Data file.