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Figure 4.6 Analysis of olfactory discrimination in CNS-ActbKO mice. Control and CNS-
Actb KO mice were exposed to novel and social odor cues in three consecutive trials to
assess the rate of olfactory habituation. Following the third trial, mice were exposed
to the next cue to measure dishabituation and recognition of a novel odor. CNS- Act-
b KO mice showed similar habituation and dishabituation to novel and social odor cues
compared to controls. However, CNS- Actb KO mice did not exhibit dishabituation to the
water control suggesting they were unable to smell this cue or had a heightened attrac-
tion to it. Data represent mean ± standard error of the mean. n  = 9 mice per genotype.
mislocalization of other ZBP1 targets. A ZBP1/IMP1 KO mouse gener-
ated by gene trap insertion has indeed been characterized, and interestingly,
exhibits significant perinatal lethality and stunted growth similar to CNS-
Actb KO mice ( Hansen et al., 2004 ). However, these phenotypes are rela-
tively nonspecific and commonly found in many diverse transgenic and KO
mouse lines. Aside from noting a proportionally reduced brain size in IMP1
KO mice, no brain pathology was reported although it is unclear to what
extent brain histology was actually analyzed ( Hansen et al., 2004 ). It was dis-
cussed, however, that the few surviving IMP1 KO mice exhibited restlessness
and circular movements, perhaps indicating neurobehavioral abnormalities.
The most prominent histological phenotypes noted included a reduction
in primary fibroblast proliferation, reduced size of intestinal microvilli, and
less prominent malformations of the small intestine, colon, kidney and liver.
It was concluded that the abnormalities in the latter organ systems likely
caused the significant perinatal lethality in the IMP1 KO mice.
Some insight into potential neuronal functions of ZBP1 in vivo was
recently acquired when a report characterized DRG development and sci-
atic nerve regeneration in heterozygous ZBP1 mice ( Donnelly et al., 2011 ).
This group demonstrated that overexpression of the β-actin 3′ UTR fused
to GFP can decrease the axonal localization of endogenous β-actin mRNA,
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