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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gnaqtm2Soff
targeted mutation 2, Stefan Offermanns
MGI:2446355
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cd19tm1(cre)Cgn/Cd19+
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
B6N.129-Cd19tm1(cre)Cgn Gna11tm1Soff Gnaqtm2Soff MGI:3699321
cn2
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tek-cre/ERT2)1Soff/0
B6N.Cg-Gna11tm1Soff Gnaqtm2Soff Tg(Tek-cre/ERT2)1Soff MGI:5800455
cn3
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Myl2tm1(cre)Krc/Myl2+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * C57BL MGI:3706996
cn4
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(PTH-cre)4167Slib/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3796551
cn5
Gna11tm1Soff/Gna11+
Gnaqtm2Soff/Gnaqtm2Soff
Tg(PTH-cre)4167Slib/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3796552
cn6
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaq+
Tg(PTH-cre)4167Slib/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3796553
cn7
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Mpz-cre)94Imeg/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3796532
cn8
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tg-cre)1Soff/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3796562
cn9
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Camk2a-cre)1Gsc/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3796547
cn10
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
X/Tg(Myh11-cre/ERT2)1Soff
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3819271
cn11
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tek-cre/ERT2)1Soff/?
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3837458


Genotype
MGI:3699321
cn1
Allelic
Composition
Cd19tm1(cre)Cgn/Cd19+
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Genetic
Background
B6N.129-Cd19tm1(cre)Cgn Gna11tm1Soff Gnaqtm2Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd19tm1(cre)Cgn mutation (8 available); any Cd19 mutation (15 available)
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• double deficient B cells do not show abnormalities is lysophospholipid-induced adhesion




Genotype
MGI:5800455
cn2
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tek-cre/ERT2)1Soff/0
Genetic
Background
B6N.Cg-Gna11tm1Soff Gnaqtm2Soff Tg(Tek-cre/ERT2)1Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Tek-cre/ERT2)1Soff mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• almost complete lost of dilation in response to flow
• inhibited acethylcholine-induced vasodilation
• however, vasodilation in response to sodium nitroprusside and vasoconstriction in response to phenylephrine are normal
• in response to ligation of the external carotid artery, mice exhibit a strong reduction in neointima formation compared with control mice
• however, there is no change in the diameter of the common carotid artery
• in response to tamoxifen

homeostasis/metabolism
• in response to ligation of the external carotid artery, mice exhibit a strong reduction in neointima formation compared with control mice
• however, there is no change in the diameter of the common carotid artery
• decreased in the plasma of tamoxifen-treated mice

muscle
• almost complete lost of dilation in response to flow
• inhibited acethylcholine-induced vasodilation
• however, vasodilation in response to sodium nitroprusside and vasoconstriction in response to phenylephrine are normal




Genotype
MGI:3706996
cn3
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Myl2tm1(cre)Krc/Myl2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Myl2tm1(cre)Krc mutation (2 available); any Myl2 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 75% die perinatally

cardiovascular system
• pups that die perinatally exhibit varying degrees of myocardial hypoplasia
• however, mutants that survive to adulthood, appear normal and are fertile
• homozygotes surviving to adulthood exhibit no ventricular hypertrophy in response to pressure-overload induced by aortic constriction, indicating a complete lack of a hypertrophic response

homeostasis/metabolism
• homozygotes surviving to adulthood exhibit no ventricular hypertrophy in response to pressure-overload induced by aortic constriction, indicating a complete lack of a hypertrophic response




Genotype
MGI:3796551
cn4
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(PTH-cre)4167Slib/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(PTH-cre)4167Slib mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

growth/size/body
• anterior-posterior shortening of craniofacial complex is most pronounced in the snout
• drastically reduced P9 compared to controls
• drastically reduced P9 compared to controls
• severe dwarfism by P9
• internal organs are reduced in size according to general growth retardation of mutants

craniofacial
• sutures are much wider than in controls
• doming of cranial vault is observed at P9
• anterior-posterior shortening of craniofacial complex is most pronounced in the snout

skeleton
• sutures are much wider than in controls
• doming of cranial vault is observed at P9
• bulging of costochondral junction (rachitic rosary) is observed in ribs
• severe osteopenia is observed throughout the skeleton
• all growth plates display rachitic changes
• barely detectable in bones of paws and caudal vertebrae at P9
• mineralization of ventral ribs is lacking
• noted in cervical and caudal vertebrae, bones of paws, and all long bones
• epiphyseal ossification of femur and tibia is lacking at P9
• evidence of bone resorption is observed in mutants at P9

endocrine/exocrine glands
• proliferation of cells is significantly enhance compared to controls
• massively growth-retarded

homeostasis/metabolism
• significantly increased levels are observed at P9
• urine calcium level is strongly increased

renal/urinary system
• urine calcium level is strongly increased

respiratory system
• massively growth-retarded




Genotype
MGI:3796552
cn5
Allelic
Composition
Gna11tm1Soff/Gna11+
Gnaqtm2Soff/Gnaqtm2Soff
Tg(PTH-cre)4167Slib/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(PTH-cre)4167Slib mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• reduced at P9 compared to controls

homeostasis/metabolism
• levels are increased compared to controls at P9
• increased relative to controls
• increased relative to controls at P9

renal/urinary system
• increased relative to controls at P9




Genotype
MGI:3796553
cn6
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaq+
Tg(PTH-cre)4167Slib/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(PTH-cre)4167Slib mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• reduced at P9 compared to controls

homeostasis/metabolism
• levels are increased compared to controls
• increased relative to controls at P9
• increased relative to controls

renal/urinary system
• increased relative to controls




Genotype
MGI:3796532
cn7
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Mpz-cre)94Imeg/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Mpz-cre)94Imeg mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
N
• incisive alveolar bone in distal mandibular region is relatively well-developed
• lamina obturans is duplicated
• duplicated in mutants
• hyoid is not fused to basisphenoid in all cases; body of hyoid has extended ossification center and is fused to lesser hyoid horn and often with superior horn of thyroid similar to Ednrb-knock-in homozygotes
• maxillary bones are duplicated in mandibular region
• duplication of palatine bone is observed
• duplication of jugal bone in mandibular region is observed

skeleton
• lamina obturans is duplicated
• duplicated in mutants
• hyoid is not fused to basisphenoid in all cases; body of hyoid has extended ossification center and is fused to lesser hyoid horn and often with superior horn of thyroid similar to Ednrb-knock-in homozygotes
• maxillary bones are duplicated in mandibular region
• duplication of palatine bone is observed
• duplication of jugal bone in mandibular region is observed




Genotype
MGI:3796562
cn8
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tg-cre)1Soff/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Tg-cre)1Soff mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• as mutants age, no significant differences in thyroid size or weight is observed relative to wild-type
• at 6 months of age, histology is altered; follicular structure is disturbed with few normal follicles remaining
• no increase in thyroid gland weight is observed in 6-8 week-old mice treated with TSH (thyroid stimulating hormone) for 1 week, whereas wild-type mice show a 100% increase in thyroid weight; glands in mutants actually decrease in weight due to slight decrease in follicular lumen size
• no increase in thyrocyte number is observed after TSH treatment in contrast to increase seen in wild-type; thryocytes show hypertrophic response to TSH treatment
• after TSH treatment, colloid area is reduced unlike wild-type thyroids
• mutant thyroids show no response to goitrogenic diet, whereas wild-type mice readily develop hyperplastic goiters
• cells are often enlarged, columnar and have large nuclei at 6 months of age
• TSH-induced thyroid hormone release is almost entirely abrogated in mutants
• impaired pinocytic uptake of colloid and reduction in pinocytic vesicle formation in thyroid follicular epithelium upon TSH stimulation is observed in mutants versus wild-type
• after 6 months of age, about half of animals display overt hypothyroidism

homeostasis/metabolism
• beginning at 2 months of age, TSH (thyroid stimulating hormone) plasma levels start to rise and are significantly higher than wild-type at 6 months of age
• at 6 months, mice show low T4 levels compared to wild-type




Genotype
MGI:3796547
cn9
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Camk2a-cre)1Gsc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Camk2a-cre)1Gsc mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• age-dependent reduction in survival due to tonic-clonic seizures

nervous system
• around 3 months of age, mice show spontaneous epileptic seizures; animals affected and seizure number per animal increase with age
• mutants show reduced latency to seizure onset and tendency to have stronger seizures when treated with kainic acid or PTZ than wild-type; seizure-induced lethality is greatly increased
• blockade of cannabinoid receptors does not result in aggravation of kainic acid-induced seizures in mutants but does in wild-type controls
• treatment of mutants with endocannabinoid reuptake inhibitor causes a significant amelioration of kainic acid induced seizures
• most seizures are myoclonic
• some animals exhibit tonic-clonic seizures with age
• older animals particularly those with symptomatic epilepsy show neuronal degeneration in CA1 region
• older mice display reactive gliosis in CA1 region of hippocampus
• no CCK4-induced (cholecystokinin receptor2 agonist) current is detected in amygdala slices while inward current response in wild-type is unaffected

behavior/neurological
• around 3 months of age, mice show spontaneous epileptic seizures; animals affected and seizure number per animal increase with age
• mutants show reduced latency to seizure onset and tendency to have stronger seizures when treated with kainic acid or PTZ than wild-type; seizure-induced lethality is greatly increased
• blockade of cannabinoid receptors does not result in aggravation of kainic acid-induced seizures in mutants but does in wild-type controls
• treatment of mutants with endocannabinoid reuptake inhibitor causes a significant amelioration of kainic acid induced seizures
• most seizures are myoclonic
• some animals exhibit tonic-clonic seizures with age




Genotype
MGI:3819271
cn10
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
X/Tg(Myh11-cre/ERT2)1Soff
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Myh11-cre/ERT2)1Soff mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice
• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice
• tamoxifen-treated mice exhibit decreased blood pressure following treatment with angiotensin II, vasopressin and endothelin compared to in wild-type mice
• tamoxifen-treated mice exposed to DOCA-salt do not develop hypertension and DOCA-salt treated mice exposed to tamoxifen following the onset of hypertension exhibit a drop in blood pressure compared to in similarly treated wild-type mice
• following a normal transient increase in mean arterial blood pressure upon treatment with tamoxifen, mice exhibit a drop in mean arterial blood pressure below normal levels
• slight in the absence of tamoxifen induction

muscle
• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice
• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice




Genotype
MGI:3837458
cn11
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
Tg(Tek-cre/ERT2)1Soff/?
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (4 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (8 available)
Tg(Tek-cre/ERT2)1Soff mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in mice with induction of cre recombinase, basal permeability is lower than controls
• vascular permeability does not increase above basal levels in response to histamine, IgE, platelet-activating factor (PAF), lysophosphatidic acid (LPA), or F2r-activating peptide
• mice are resistant to death resulting from PAF-induced shock

immune system
N
• while resistant to shock induced by IgE or vasoactive substances, mice are not resistant to shock induced by LPS
• tamoxifen treated mice are resistant to IgE-induced anaphylactic shock
• in an anti-DNP model, mice only have transient drops in systolic blood pressure compared to the sustained (>90 min) drops that occur in controls
• in an anti-BSA model, all mice survive anaphylactic challenge with only moderate decreases in body temperature compared to controls that suffer from severe hypothermia and death within 20 min of challenge





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last database update
03/24/2020
MGI 6.15
The Jackson Laboratory