In particular, the alteration of Per2 in hypothalamus, pre-frontal cortex and striatum during the dark phase of Afh mutants could explain the deficits that mutants showed in FAA, NREM sleep and interval timing, as all these phenotypes are associated with Per2 functioning and occurred mainly during the dark phase.
The decreased resistance of these coi1-1 mutants could explain the increased oviposition rate on these plants.
Such altered interactions in our mutants could explain the dramatic tropism for the plasmalemma and the concomitant increase of phosphorylation.
Furthermore, we have suggested that the cell death phenotype caused by expression of the EKV-associated mutants could explain the in vivo skin disease phenotype by leading to the hyperproliferation that is characteristic of this disease.
Differences in binding affinity between IDH WT WT, mutant:WT, and mutant:mutant dimers could explain this phenomenon.
Alternatively, secondary mutations in the mutant strains could explain phenotypes observed in mutants but not with RNAi.
The aggregation of such fibers in the autosomal dominant mutant, D226N, could explain the onset of the retinopathy adRP10.
The presence of another mutant allele could explain the lower homozygosity signals since each allele may be associated with different SNPs and therefore appear heterozygous.
Desensitization of NMDARs in spinal cord of mutant mice could explain also behavioural data showing that neuropathic pain in Ddo−/− was almost unaltered compared to wild type mice except at day 3 and day 21.
To determine whether ongoing DNA synthesis in the recombination mutant strains could explain our results, we tested whether these strains incorporate EdU, a thymidine analog, into their DNA during stationary phase.
