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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Srrm3Gt(IST12726F8)Tigm
gene trap IST12726F8, Texas A&M Institute for Genomic Medicine
MGI:4088169
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Srrm3Gt(IST12726F8)Tigm/Srrm3Gt(IST12726F8)Tigm involves: C57BL/6N MGI:6378725
cx2
Srrm3Gt(IST12726F8)Tigm/Srrm3Gt(IST12726F8)Tigm
Srrm4bv/Srrm4bv
involves: C57BL/6N MGI:6378726


Genotype
MGI:6378725
hm1
Allelic
Composition
Srrm3Gt(IST12726F8)Tigm/Srrm3Gt(IST12726F8)Tigm
Genetic
Background
involves: C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Srrm3Gt(IST12726F8)Tigm mutation (0 available); any Srrm3 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show decreased survival after P21, with most dying before P200

growth/size/body

behavior/neurological
• mice spend less time on the rotarod than wild-type mice at 1, 2, and 3 months of age

nervous system
• the external germinal layer of the cerebellum, which forms from granule cell precursors, persists longer than normal and is thus thicker at P16
• most Purkinje cells degenerate between P40 and P90
• however, neurodegeneration in the cortex is not seen




Genotype
MGI:6378726
cx2
Allelic
Composition
Srrm3Gt(IST12726F8)Tigm/Srrm3Gt(IST12726F8)Tigm
Srrm4bv/Srrm4bv
Genetic
Background
involves: C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Srrm3Gt(IST12726F8)Tigm mutation (0 available); any Srrm3 mutation (28 available)
Srrm4bv mutation (2 available); any Srrm4 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die neonatally due to an inability to start breathing

respiratory system
• none of the newborn mice start to breathe and alveoli of newborns are not expanded with air

nervous system
• cortical neurons form functional synapses in vitro, but their spontaneous activity is abnormal, with calcium oscillations being of an abnormally high amplitude and low frequency and they are highly synchronized
• however, no anatomical defects are seen in the brain at E19
• cortical neurons are defective for the developmental switch in GABAergic neurotransmission
• cortical neuron cultures treated with the GABA(A)R inhibitor gabazine show a reduction in the amplitude and an increase in the frequency of calcium oscillations, the opposite of wild-type cultures which show increased amplitude and decreased frequency of calcium oscillations
• cortical neuron cultures and brain slice cultures treated with the GABA(A)R agonist muscimol show increased intracellular calcium compared to wild-type cultures in which few neurons respond to muscimol
• more neurons from spinal cord slices respond to a mix of GABA and glycine with elevated intracellular calcium than in wild-type slices





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory