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. 2013 Mar;193(3):751–770. doi: 10.1534/genetics.112.146910

Table 3. Rates of spontaneous CAN1 mutations in pol2-4,eex msh6Δ strains.

pol2-4,eex msh6Δ
pol2-4msh6Δ G435C V522A T850M K966Q A1153D
Transitionsa
 G→A (C•dATP) 360 (1.0) 150 (0.4) 20 (0.06) 18 (0.05) 120 (0.3) 25 (0.07)
 C→T (G•dTTP) 90 (1.0) ∼32 (∼0.4) 16 (0.2) ∼3 (∼0.04) 27 (0.3) ∼5 (∼0.05)
Transversionsa
 G→T (C•dTTP) 380 (1.0) 180 (0.5) 58 (0.2) 5 (0.01) 55 (0.1) 22 (0.06)
 C→A (G•dATP) ∼18 (1.0) <8 (ND) <2 (ND) 7 (ND) ∼18 (ND) ∼1 (ND)
Frameshifts
 +1 160 (1.0) <8 (<0.05) ∼6 (∼0.04) ∼3 (∼0.02) ∼9 (∼0.06) ∼4 (∼0.02)
 −1 <18 (1.0) <8 (ND) ∼4 (ND) 4 (ND) <5 (ND) ∼1 (ND)
  Overall 1001 (1.0) 365 (0.36) 104 (0.10) 43 (0.04) 247 (0.25) 60 (0.06)

Expressed as the number of Canr mutants per cell division (×10−7). Rates for individual mutation types were calculated by multiplying the overall Canr mutation rate of a strain (last row of table) by the percentage of the corresponding mutation in the CAN1 mutation spectrum from that strain (Table 2). Rates relative to those in pol2-4 msh6Δ are in parentheses. Values were calculated to three decimal places and then rounded to one or two significant figures. < or ∼: incidence values (Table 2) were zero or not significantly different from zero, respectively (P > 0.05, Fisher’s exact test). ND: relative rates could not be reliably determined because mutations of this type were not detected at significant levels in the pol2-4 msh6Δ strain (Table 2).

a

Base changes in the CAN1 coding sequence are shown with presumed causal mispairs in parentheses (template base•incoming dNTP), if Pol ε catalyzes leading-strand DNA synthesis (Pursell et al. 2007; Kunkel and Burgers 2008; Pavlov and Shcherbakova 2010) initiated from the ARS507 origin of replication (Raghuraman et al. 2001; Yabuki et al. 2002; Kumar et al. 2011; Siow et al. 2012).