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To study the mouse lineage, we compared mouse and rat and used human as an outgroup.
To investigate the cause and effect relationship between GC-content and meiotic recombination in the mouse lineage, we calculated correlation coefficients between GC* and CO rates.
Moreover, in the mouse lineage, we observe an association between male CO rates and CpG odds ratio (partial correlation =0.14, P value < 10−7 when controlling for GC-content).
Furthermore, in the mouse lineage, we can see that male-specific CO rates correlate more strongly with current GC-content or GC* than sex-averaged or female CO rates do (supplementary tables 1– 3, Supplementary Material online).
To test if the excessive duplicates are really created in the mouse lineage, we grouped the age of the duplicates (inferred from dS) according to the divergence time between the two species.
Because meiotic recombination only predicts a small fraction of substitution rates in the mouse lineage, we investigated how other genomic factors, such as GC-content, replication timing, and transposable elements density, predict substitution rates in the mouse lineage and compared it with the human lineage.
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Because substitution patterns appear to be different in both human and mouse lineages, we analyzed the influence of meiotic recombination and of other factors on substitution patterns in both lineages.
No clear difference in the parasite distribution was detected in the recta of the same animals, as in both mice lineages, we could find recta infected with either only the JG strain or the Col1.7G2 clone, or a mixture of both parasite populations.
On the contrary, we assign a mouse lineage origin to Bh if i) it does not overlap any human-dog breakpoint and ii) Bm1 and Bm2 overlap each a mouse-dog breakpoint.
We found that in the mouse lineage, gBGC is active but weaker than in the human lineage and that male-specific recombination better predicts GC-content evolution than female-specific recombination.
Because the mouse retrogenes are most similar to the mouse ortholog, as supported by the well-resolved parts of the gene tree [Additional file 3: Supplemental Figure S3], we assume the retrogenes split off the mouse lineage.
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