This strain has a targeted null allele of the C1-type vomeronasal receptor Vmn2r1. Homozygotes are viable and fertile with normal general appearance. The number of vomeronasal sensory neurons that express VMN2R26, a receptor often co-expressed with VMN2R1 on a subset of vomeronasal sensory neurons, in the absence of VMN2R1 is normal at birth, but decreased to 21.5% of normal at 4 weeks of age and 9.5% of normal at 10 weeks of age. This is a more severe change in expression than that found in the tm2Mom null mutant, which has an additional IRES-GFP reporter (see Stock Number <a href="https://www.jax.org/strain/026765"">026765</a>). Despite being diminished in number, these neurons still form a few glomeruli in the correct position of the accessory olfactory bulb, although these glomeruli are smaller than normal, proving that VMN2R1 is not required for axon migration and correct glomeruli formation. Absence of VMN2R1 was not found to result in a compensatory increase in C2-expresssing vomeronasal sensory neurons, which are present in normal numbers in these mice.

This strain has a targeted null allele of the C1-type vomeronasal receptor Vmn2r1. It is valuable in tracing vomeronasal sensory neuron development, vomeronasal receptor selection, glomeruli formation, and studies of chemosensation.

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