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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(ACTB-MAP2K1*K97M)1Stl
transgene insertion 1, Susumu Tonegawa
MGI:3707556
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Tg(ACTB-MAP2K1*K97M)1Stl/0
Tg(Camk2a-cre)T29-1Stl/0
involves: BALB/c * C57BL/6 MGI:3707564


Genotype
MGI:3707564
cn1
Allelic
Composition
Tg(ACTB-MAP2K1*K97M)1Stl/0
Tg(Camk2a-cre)T29-1Stl/0
Genetic
Background
involves: BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-MAP2K1*K97M)1Stl mutation (1 available)
Tg(Camk2a-cre)T29-1Stl mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• when tested for retention 24 hours after contextual fear conditioning, mutants show reduced levels of freezing relative to wild-type (mutant - 36.6% vs wild-type - 57.5%)
• 48 hours after a cued fear conditioning test, where a tone was the conditioned stimulus, mutants show a low level of freezing prior to tone presentation, indicating impairment of contextual memory
• in the Morris water maze test, mutants showed a tendency toward longer escape latencies compared to wild-type
• in probe trials with the platform hidden, mutant mice spend less time searching the target quadrant, and show less accurate identification of the precise platform location by having a reduced number of platform crossings

nervous system
• field EPSPs in mutant hippocampal slice preparations return to levels near unstimulated levels by 3 hours posttetaniziation, while in control slices the fEPSPs (ie. late LTP remains elevated
• application of 4 trains of tetanic stimulation at 5 minute intervals, elicits long-lasting (>3 hours) potentiation in control hippocampal slices, but in mutants potentiation is unstable and decays progressively
• mutants display selective impairment in translational component of late-LTP (L-LTP); the defect is transcription-independent, translation-dependent, as shown by difference in inhibition kinetics of actinomycin-D (transcriptional inhibitor) and anisomycin (translational inhibitor)

homeostasis/metabolism
• ERK activation in the forebrain is inhibited, causing selective deficits in hippocampal memory retention and translation-dependent phase of late-LTP





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory