This targeted deletion of the transient receptor potential cation channel is valuable for characterizing development and signal transduction in the vomeronasal and olfactory systems, particularly type B olfactory sensory neuron chemodetection of oxygen levels.
Peter Mombaerts, Max Planck Research Unit for Neurogenetics
Transient receptor potential cation channel (Trpc2), initially thought to be essential in vomeronasal sensory neuron signal transduction, has also been identified in two populations of olfactory sensory neurons that also express Cnga2. Population A, which is found scattered across both the dorsal and ventral main olfactory epithelium, also expresses adenylate cyclase 3 (Adcy3) and alpha stimulating olfactory type guanine nucleotide binding protein (Gnal), while population B, which is found in the lateralmost region of the main olfactory epithelium, does not express Adcy3 and has weak or no expression of Gnal. This targeted mutation of Trpc2, deletes the pore region of the cation channel and the transmembrane domain 6. Type B olfactory sensory neurons in mice homozygous for this deletion fail to flux calcium in response to reduced oxygen. However, homozygotes were found to have a normal hyperventilation response to low environmental oxygen, consistent with normal carotid body function.
The targeted knockout, Trpc2tm1Mom, was generated in 129P2-derived E14 ES cells and this allele was backcrossed onto 129S6/SvEvTac for seven generations. Sperm was cryopreserved from heterozygous males at generation N7.
|Allele Name||targeted mutation 2, Peter Mombaerts|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Trpc2, transient receptor potential cation channel, subfamily C, member 2|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||Exons 9 to 13 are replaced with pgk-neo in the opposite orientation. The non-coding sequence of exon 13 remains intact.|