The mice also display a selective facilitation of long-term potentiation (LTP) in the medial perforant path and a selective enhancement in rapid-acquisition spatial memory, phenotypes that are reversed by direct application of a cell-permeant peptide (DNIP) designed to interfere with NCS-1 binding to the dopamine type-2 receptor (D2R).
Lmna-/ mice also display smaller spleens and thymuses.
Interestingly, 5-HTT−/− mice also display less sociability and perseverance-like behaviors [37] [39].
R1441C LRRK2 mice also display a smaller yet significant increase in the density of autophagic vacuoles (Figure 7G).
In addition to the semi-lethality, coilin knockout mice also display reduced litter size and litter number, compared to wild-type controls.
Similarly, primary myoblasts isolated from Pax7 null mice also display perturbation of the cell cycle and consequently, decreased colony size [15], [17].
AID−/− mice also display abnormal expansion of anaerobic commensal bacteria in the small intestine, which induces hypertrophic enlargement of Peyer's patches and protrusion of isolated lymphoid follicles (ILFs).
Even though obese mice also display increased SAA levels in serum, absence of SAA3 in the serum was recently reported [25], indicating that in obese mice, SAA in the circulation has a hepatic origin.
Most importantly however, Krm2-deficient mice also display a high trabecular bone mass phenotype at 24 weeks of age, which is especially relevant given the absence of obvious abnormalities outside the skeleton.
