In the article by M. Shinohara, D. K. Bishop, and A. Shinohara (Genetics, 213: 1255–1269) entitled “Distinct Functions in Regulation of Meiotic Crossovers for DNA Damage Response Clamp Loader Rad24 (Rad17) and Mec1(ATR) Kinase,” errors were made in preparing Table 1, Table 3, and Table 4. These errors had no impact on any of the conclusions of the paper. The errors involved data entry and statistical analysis. P-values that were significantly altered, with respect to the conventional threshold of 0.05, are underlined in the corrected versions of Table 1, Table 3, and Table 4 presented here.

Genetic analysis of meiotic recombination on chromosome V in rad24 and mec1 mutants

Genetic analysis of meiotic recombination on chromosome III in rad24 and mec1 mutants

Genetic analysis of meiotic recombination on chromosome VII in rad24 and mec1 mutants

First, the original version of Table 3 contained minor typographical errors (Table 3, footnote “f”) and also a significant data entry error for the number of nonparental ditypes (NPDs) expected from the value obtained from the Papazian equation (NPDe) for the HIS4-MAT interval data in wild-type. The corrected NPDe value and the corresponding P-value are indicated by footnote “g” (Table 3). Correcting this data entry error strengthens the original conclusion that the mutants display significant defects in crossover interference compared with wild-type.

Second, the chi square test function of Microsoft Excel software was applied incorrectly in the original analysis. The resulting errors included, but were not limited to, failure to adhere to the conventional restriction for chi square tests that no more than 25% of cells may have expected values of <5. In the corrected tables shown here, multinomial exact tests are used to determine whether data for mutant strains differ significantly from that for wild-type (footnote “c”). The only important impact of these errors is that the defects detected for the two mec1 alleles are not as extensive as previously indicated; the conclusion that both mec1-1 and mec1-kd mutants display significant defects, and the conclusion that the defects displayed by mec1-kd are less extensive than those displayed by mec1-1, remain valid.

Finally, we inadvertently used the outdated method of Papazian (1952) to obtain evidence for crossover interference from NPD ratios and also used an invalid method to determine P-values from the Papazian NPDe values. We have now replaced Papazian analysis with the more statistically accurate method referred to as “a better way” (BW; Stahl 2008; see rightmost column in each table; footnote “e”). We also show the results of properly applied Papazian analysis (columns titled “Papazian P-value for NPD ratio <1”; footnote “d”). Note that there are four cases (indicated with asterisks) where, had we properly analyzed NPDe from Papazian, we would have concluded there was significant interference, but BW analysis leads us to conclude that the data do not provide evidence for interference. However, there are no cases in which the P-values that were published, and those calculated here for the BW, differ with respect to meeting or failing to meet the conventional threshold for significance of 0.05. Thus, correcting the errors made in assessing interference from NPD ratios has no impact on any of the conclusions of the paper. We apologize for any confusion caused by these errors.