Next, compare blood glucose concentrations of wild type mice fed NCD to Cmah mice fed NCD. Do these data support, contradict or say nothing about the hypothesis that the \textit{Cmah} gene does not affect blood glucose? Explain your answer thoroughly.

please answer question number 5  asap.

Link: Lack of RAC1 in macrophages protects against atherosclerosis - PMC (nih.gov) Could somone explain exactly what this means below? NOT HW just trying to get a better understanding on what this experiment is about.  To produce mice that are deficient for RAC1 in macrophages, female C57BL/6 mice homozygously expressing the floxed Rac1 gene (Rac1fl/fl) [6] were crossbred with male mice homozygously expressing Cre under the monocyte-specific lysozyme M promoter (LC) [12]. Mice were genotyped for Rac1 deficiency as previously described

Following a mutagenesis experiment to identify novel genes affecting the circadian clock in Drosophila melanogaster you discover several mutants. You start considering two of those mutants that you call C and d. The two homozygous C/C and d/d are arrhythmic (arrhythmic is the definition of their phenotype), whereas the two heterozygous C/C and D/d are rhythmic (rhythmic is the definition of their phenotype) with a 24h period. You make two true-breeding stocks: stock 3 homozygous for C and stock 4 homozygous for d. You cross them in both directions and in both cases you observe complementation with no difference between males and females. Then you take the progeny of one cross, for instance the F1 of Females 3 x Males 4, and you perform a Testcross. Out of 1000 flies resulting from the Testcross only 125 are rhythmic. Using the number of flies expected for the Parental and the Recombinant genotypes and the formula that defines recombination frequency, what is the distance between loci C…