vldlr −/− and lrp8 −/− single mutant mice display no defects, while double mutant mice show more severe phenotype than reln −/− null mutant (See above), providing evidence for compensatory functions between the two receptors.
MGE explants were collected from 4 different genotypes: control, Rac1 mutant, Rac3 mutant, and double mutant (see Materials and Methods section describing mice).
This level of impact on branch formation is consistent with that seen in mouse mutants of other genes required for branching morphogenesis (46– 50).
Stimulation of the BCR on peripheral blood B cells from SLE patients has been reported to cause exaggerated calcium increases, recapitulating functional cellular phenotypes seen in mouse mutants with SLE (for example, Lyn-/-, FcγRIIb-/-, and CD22-/) [ 37].
Although post hoc analysis showed the time exploring the novel object was significantly greater in both the wild type and the Δ8b mutants compared with Δ9b mutant mice, the wild type mice showed significantly greater exploration of the novel object compared with the Δ8b mutant mice (see Figure 5B).
Such a phenotype is also seen in other mouse mutants, such as the pirouette/GRXCR1 mutant.
In this second test however, there was no difference between the time spent exploring the novel object between wild type and Δ8b mutant mice (see Figure 5C).
To determine whether Per2 may play a role in regulating synaptic physiology, we examined LTP in Per2-mutant mice (see Supplementary Figure S3 at http://www.asnneuro.org/an/001/an001e012add.htm).htm
We next prepared Matr3Gt-ex13-mutant mice (see Materials and Methods, and Fig. 4A) to assess whether the MATR3 disruption could be causal for the DGAP105 BAV, CoA and PDA phenotypes.
Fortunately, and as would be expected based on the high penetrance of MECP2 mutations in humans, at least some phenotypes that mimic symptoms of human RTT are common to multiple Mecp2-mutant mouse models (see below).
