Figure 6.

Ablation of Dicer Function in Mature Olfactory Sensory Neurons Does Not Cause Any Apparent Molecular or Behavioral Defects

(A) OMP-Cre; Dicer^loxP/loxP adult MOE (P60) showed normal expression of molecular markers that identifies olfactory progenitor proliferation (Ki67), olfactory neuron differentiation (NCAM), and mature olfactory neurons (OMP and olfactory receptors).

(B) Time required to discover a hidden cookie (latency) by OMP-Cre; Dicer^loxP/loxP mutant mice and control animals (mean ± SEM, WT 66.14 ± 27.91 s; mutant 88.63 ± 19.83 s; p = 0.53, Students t test) was statistically indistinguishable. Similarly, quantification of resident average attack frequency in a resident-intruder assay designed to test VNO function in OMP-Cre; Dicer^loxP/loxP mutants and control animals (mean ± SEM, WT 35.6 ± 13.65 s; mutant 35.75 ± 15.93 s; p = 0.99, Student's t test) showed no significant difference.

(C) OMP-Cre; Dicer^loxP/loxP adult MOE (P60) showed normal expression of molecular markers for vomeronasal neuronal differentiation (NCAM), zonal patterning (G protein subunits) and mature function (V1 receptors).

(D) Quantification of phospho-histone H3 immunoreactive cells (mean ± SEM, WT 5.79 ± 0.50, n = 3; mutant 5.05 ± 0.37, n = 3, p = 0.24, Student's t test) and active caspase-3 immunoreactive cells (mean ± SEM, WT 12.19 ± 0.77, n = 3; mutant 11.76 ± 0.74, n = 3, p = 0.69, Student's t test) in adult MOE of OMP-Cre; Dicer^loxP/loxP mutants and controls reveals no statistically significant differences in proliferation or apoptosis rates.

(E) OMP-Cre; Dicer^loxP/loxP; P2-IRES-TauLacZ triple-transgenic mice (P45) showed normal expression and axon targeting of LacZ in P2-expressing olfactory neurons.