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Explant of Brn3c containing retina in Brn3b −/− mutant mice has remarkable recovery in the neurite outgrowth, demonstrating its growth promoting function.
Generation of Dyrk1A mutant mice has been described previously [19].
The generation and genotyping of RIIβ−/− mutant mice has been described previously [7].
The onset of puberty in other circadian mutant mice has not been described, though an isolated report suggests a slight delay in puberty in Bmal1 knockout mice [21].
Autopsy of both RS patients and Mecp2 mutant mice has revealed that the brain size is reduced without reduction of the number of neurons [36].
Analysis of SHIP mutant mice has demonstrated a pivotal role for SHIP in vivo in regulating the homeostasis of various cell types including tissue macrophages, osteoclasts, myeloid, natural killer (NK) and hematopoietic stem cells (HSC) [4] [7].
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Combined EEG/calcium imaging experiments confirmed that neurons in mutant mice have abnormally high firing and synchrony during sleep/rest.
Compared to wild-type and heterozygous mice, the mutant mice had an unstable periodicity, fragmented activity, and a sixfold reduction in wheel running activity.
However, both SM22alpha TRE-Cre R26R Bmpr1a(flox/+) and flox/flox mutant mice had fewer muscularized distal pulmonary arteries and attenuated loss of peripheral pulmonary arteries compared with age-matched control littermates in hypoxia.
Serial microCT from 4-20 week-olds revealed that Zdhhc13 mutant mice had reduced bone mineral density.
GAP-43 −/− mutant mice have a comparable number of ipsilaterally and contralaterally projecting neurons growing in semicircular trajectories.
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