Homozygotes are viable and fertile with complete absence of the wildtype allele mRNA in forebrain tissues. Mice homozygous for this M1 muscarinic acetylcholine receptor deficiency have elevated dopaminergic transmission in the striatum, significantly increased locomotor activity, increased response to the stimulatory effects of amphetamine. These mutant mice may be useful in neurological studies, including the regulation of dopaminergic transmission by the M1 receptor and M1 dysfunction in psychiatric disorders.
A targeting vector was designed to replace a 3kb genomic fragment containing the entire coding sequence of the targeted gene with the neomycin resistance gene. The construct was electroporated into C57BL/6-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into BALB/c blastocysts. The resulting chimeric mice were bred to C57BL/6 mice and then intercrossed to generate mutant mice on a pure C57BL/6 genetic background prior to arrival at The Jackson Laboratory.
|Allele Name||targeted mutation 1, Susumu Tonegawa|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||M1 -|
|Gene Symbol and Name||Chrm1, cholinergic receptor, muscarinic 1, CNS|
|Strain of Origin||C57BL/6|
|Molecular Note||A 3 kb genomic fragment containing the entire coding region of the gene was replaced with a neomycin selection cassette. Northern blot analysis on RNA derived from forebrain of homozygous mice demonstrated that no detectable transcript was produced from this allele. In situ hybridization analysis on sagittal brain sections of homozygous mice further confirmed that the transcript was not expressed.|
|Mutations Made By|| |
Dr. Susumu Tonegawa, Massachusetts Institute of Technology
When maintaining a live colony, homozygous mice are bred.
When using the M1- mouse strain in a publication, please cite the originating article(s) and include JAX stock #006468 in your Materials and Methods section.