Type III Adenylyl Cyclase Gene Knockout Mice
Introduction The olfactory sensory system has the remarkable capacity to detect and discriminate among a wide array of odorants and translate them into cognitive representations. Cyclic nucleotide–gated ion channels in olfactory sensory neurons (OSNs) are hypothesized to play a critical role in olfaction. Type III adenylyl cyclase (AC3) is obligatory for olfactory signaling and this enzyme is likely the primary source of cAMP required for olfactory signaling. Technology description Dr Daniel Storm’s laboratory has generated type III adenylyl cyclase null (AC3-M) mice. AC3 mutant mice were made by targeted gene disruption of embryonic stem (ES) cells derived from 129Sv/J mice. Chimeric mice were mated to C57/BL6 mice to establish germline transmission of the mutant AC3 allele, and F1 hybrid heterozygous mice originating from different chimeras were mated to generate mice homozygous for the AC3 mutation. Electrophysiological studies of AC3-M mice demonstrated anosmia toward both IP3- and cAMP-generating odorants, despite the presence of other adenylyl cyclases in olfactory cilia. Furthermore, AC3-M mice also failed olfactory-dependent behavioral assays. This mouse is a useful animal model to screen drugs for modulation of olfaction. Related Publication(s)
Neuron 27(3):487-497, 2000.
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