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Both entrainment and masking are abnormal in Bmal1 brain knockout mice.
10.7554/eLife.04617.014 Figure 7. Intact FAA in Bmal1 brain knockout mice.
10.7554/eLife.04617.006 Figure 2. Complete loss of circadian rhythmicity of Bmal1 brain knockout mice in constant darkness and constant light.
DOI: http://dx.doi.org/10.7554/eLife.04617.014 10.7554/eLiFigure17 figuregure 7—figure supplement 1. Lack of Bmal1 expression in the DMH of Bmal1 brain knockout mice.
Therefore, we conclude that entrainment in Bmal1 brain knockout mice is abnormal under skeleton photoperiods, consistent with the idea that the coherence of phase during entrainment may be compromised.
DOI: http://dx.doi.org/10.7554/eLife.04617.003 10.7554/eLiFigure1 figureigure 1—figure supplement 1. Weights of Bmal1 brain knockout mice are similar to controls at 2 months and 4 6 months of age.
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In order to test whether Bmal1 brain knockouts entrain to light, we used a skeleton photoperiod (LDLD 1 10 1 12, Figure 3A E).
In contrast to controls, Bmal1 brain knockouts exhibited no circadian rhythm of activity in DD or in LL.
Yet it was unclear whether the pre-dark activity of Bmal1 brain knockouts around the light/dark transition was due to poor entrainment of a residual circadian pacemaker or to a defect in masking.
DOI: http://dx.doi.org/10.7554/eLife.04617.008 Since the skeleton photoperiod and LD photoperiod results both indicated some impairment of masking in BKOs, we next tested whether negative masking (the ability of light to acutely suppress locomotor activity) in Bmal1 brain knockouts was defective.
However, reduction of mTOR activity by rapamycin was not consistently found within the brain of knockout mice.
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