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We therefore used a codon by codon maximum likelihood test, to ask if we could detect any codons that have been under repeated, strong positive selection.
For each gene we used a likelihood ratio test to ask if the two-branch model fit significantly better than the one-branch model.
We then used a Wilcoxon rank sum test to ask whether hybrids lay fewer eggs than conspecific females after mating with each male species.
We additionally used Wilcoxon's test to ask whether the regulatory domains of PSGs contain a higher average proportion of recently evolved enhancers, compared to those of non-PSGs.
Combining these ideas, we devised a test to ask whether all pairwise crosses between any two of the 86 species in our data set would produce F2 hybrids transgressive for KT.
A more sophisticated analysis would be to again proceed in two stages: (1) normalise the data for fat mass, and then perform the JOHNSON-NEYMAN TEST to ask at what lean masses the effect of treatment is significant and (2) go back to the original data and normalise for lean mass and then perform the JOHNSON-NEYMAN TEST to ask at what fat masses the effect of treatment is significant.
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For each focal pair, we performed a t-test to ask whether the average epistatic deviation was significantly different from zero.
Finally, in some countries, it is common practice for presymptomatic tests to ask for a second independent blood sample to confirm the result.
For interpretation, we aim at combining the results of these tests to ask whether there is evidence from the collection of tests that we might reject the null hypothesis of no differential expression.
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