Phenotypes associated with this allele

• Allele Symbol: Gna11^tm1Soff
• Allele Name: targeted mutation 1, Stefan Offermanns
• Allele ID: MGI:2151589
• Summary: 17 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Gna11^tm1Soff/Gna11^tm1Soff	involves: 129S7/SvEvBrd	MGI:2661793
hm2	Gna11^tm1Soff/Gna11^tm1Soff	involves: 129S7/SvEvBrd * C57BL/6	MGI:3796548
cn3	Cd19^tm1(cre)Cgn/Cd19^+ Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff	B6N.129-Cd19^tm1(cre)Cgn Gna11^tm1Soff Gnaq^tm2Soff	MGI:3699321
cn4	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(Tek-icre/ERT2)1Soff/0	B6N.Cg-Gna11^tm1Soff Gnaq^tm2Soff Tg(Tek-icre/ERT2)1Soff	MGI:5800455
cn5	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Myl2^tm1(cre)Krc/Myl2^+	involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * C57BL	MGI:3706996
cn6	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(PTH-cre)4167Slib/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6	MGI:3796551
cn7	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(Mpz-cre)94Imeg/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6	MGI:3796532
cn8	Gna11^tm1Soff/Gna11^+ Gnaq^tm2Soff/Gnaq^tm2Soff Tg(PTH-cre)4167Slib/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6	MGI:3796552
cn9	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^+ Tg(PTH-cre)4167Slib/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6	MGI:3796553
cn10	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(Tg-cre)1Soff/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6	MGI:3796562
cn11	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(Camk2a-cre)1Gsc/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N	MGI:3796547
cn12	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff Tg(Tek-icre/ERT2)1Soff/?	involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N	MGI:3837458
cn13	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff X/Tg(Myh11-icre/ERT2)1Soff	involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N	MGI:3819271
cx14	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm1Soff/Gnaq^tm1Soff	involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6	MGI:2661813
cx15	Gna11^tm1Soff/Gna11^+ Gnaq^tm1Soff/Gnaq^tm1Soff	involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6	MGI:3037556
cx16	Gna11^tm1Soff/Gna11^+ Gnaq^tm1Soff/Gnaq^+	involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6	MGI:3037554
cx17	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm1Soff/Gnaq^+	involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6	MGI:3037555

Genotype
MGI:2661793

hm1

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff
• Genetic Background: involves: 129S7/SvEvBrd

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

homeostasis/metabolism

increased circulating triglyceride level ( J:172091 )

• on a high-fat, high-sucrose diet

increased liver triglyceride level ( J:172091 )

• on a high-fat, high-sucrose diet

immune system

decreased susceptibility to type I hypersensitivity reaction ( J:146132 )

• mice have a 20% survival rate in an active systemic anaphylaxis model compared to no survival for wild-type controls

nervous system

nervous system phenotype ( J:70180 )

N • mice do not exhibit defects in brain architechture, synaptic transmission, LTP or LTD

liver/biliary system

increased liver triglyceride level ( J:172091 )

• on a high-fat, high-sucrose diet

hepatic steatosis ( J:172091 )

• on a high-fat, high-sucrose diet

Genotype
MGI:3796548

hm2

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

nervous system

nervous system phenotype ( J:126972 )

N • modulation of sI_AHP in hippocampus are not significantly different from wild-type responses to muscarinic and glutamate receptor agonists

Genotype
MGI:3699321

cn3

• Allelic Composition: Cd19^tm1(cre)Cgn/Cd19⁺; Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff
• Genetic Background: B6N.129-Cd19^tm1(cre)Cgn Gna11^tm1Soff Gnaq^tm2Soff

hematopoietic system

hematopoietic system phenotype ( J:117663 )

N • double deficient B cells do not show abnormalities is lysophospholipid-induced adhesion

Genotype
MGI:5800455

cn4

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(Tek-icre/ERT2)1Soff/0
• Genetic Background: B6N.Cg-Gna11^tm1Soff Gnaq^tm2Soff Tg(Tek-icre/ERT2)1Soff

cardiovascular system

increased susceptibility to hypertension ( J:224523 )

• in response to tamoxifen

decreased vasodilation ( J:224523 )

• 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

abnormal vascular wound healing ( J:224523 )

• 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

homeostasis/metabolism

abnormal vascular wound healing ( J:224523 )

• 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 nitrate level ( J:224523 )

• decreased in the plasma of tamoxifen-treated mice

muscle

decreased vasodilation ( J:224523 )

• 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

cn5

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Myl2^tm1(cre)Krc/Myl2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * C57BL

mortality/aging

perinatal lethality, incomplete penetrance ( J:77461 )

• about 75% die perinatally

cardiovascular system

heart hypoplasia ( J:77461 )

• pups that die perinatally exhibit varying degrees of myocardial hypoplasia

• however, mutants that survive to adulthood, appear normal and are fertile

decreased response of heart to induced stress ( J:77461 )

• 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

decreased response of heart to induced stress ( J:77461 )

• 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

cn6

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(PTH-cre)4167Slib/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6

mortality/aging

postnatal lethality ( J:116986 )

growth/size/body

short snout ( J:116986 )

• anterior-posterior shortening of craniofacial complex is most pronounced in the snout

decreased body weight ( J:116986 )

• drastically reduced P9 compared to controls

decreased body length ( J:116986 )

• drastically reduced P9 compared to controls

proportional dwarf ( J:116986 )

• severe dwarfism by P9

postnatal growth retardation ( J:116986 )

• internal organs are reduced in size according to general growth retardation of mutants

craniofacial

wide cranial sutures ( J:116986 )

• sutures are much wider than in controls

domed cranium ( J:116986 )

• doming of cranial vault is observed at P9

short snout ( J:116986 )

• anterior-posterior shortening of craniofacial complex is most pronounced in the snout

skeleton

wide cranial sutures ( J:116986 )

• sutures are much wider than in controls

domed cranium ( J:116986 )

• doming of cranial vault is observed at P9

rachitic rosary ( J:116986 )

• bulging of costochondral junction (rachitic rosary) is observed in ribs

decreased bone mineral density ( J:116986 )

• severe osteopenia is observed throughout the skeleton

abnormal epiphyseal plate morphology ( J:116986 )

• all growth plates display rachitic changes

abnormal bone mineralization ( J:116986 )

• barely detectable in bones of paws and caudal vertebrae at P9

• mineralization of ventral ribs is lacking

delayed endochondral bone ossification ( J:116986 )

• noted in cervical and caudal vertebrae, bones of paws, and all long bones

• epiphyseal ossification of femur and tibia is lacking at P9

increased bone resorption ( J:116986 )

• evidence of bone resorption is observed in mutants at P9

endocrine/exocrine glands

abnormal parathyroid gland morphology ( J:116986 )

• proliferation of cells is significantly enhance compared to controls

small thyroid gland ( J:116986 )

• massively growth-retarded

homeostasis/metabolism

increased circulating parathyroid hormone level ( J:116986 )

• significantly increased levels are observed at P9

increased urine calcium level ( J:116986 )

• urine calcium level is strongly increased

renal/urinary system

increased urine calcium level ( J:116986 )

• urine calcium level is strongly increased

respiratory system

abnormal larynx morphology ( J:116986 )

• massively growth-retarded

Genotype
MGI:3796532

cn7

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(Mpz-cre)94Imeg/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6

craniofacial

craniofacial phenotype ( J:131382 )

N • incisive alveolar bone in distal mandibular region is relatively well-developed

abnormal sphenoid bone morphology ( J:131382 )

abnormal alisphenoid bone morphology ( J:131382 )

• lamina obturans is duplicated

abnormal pterygoid process morphology ( J:131382 )

• duplicated in mutants

abnormal hyoid bone morphology ( J:131382 )

• 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

lower jaw to upper jaw transformation ( J:131382 )

• maxillary bones are duplicated in mandibular region

abnormal palatine bone morphology ( J:131382 )

• duplication of palatine bone is observed

abnormal zygomatic bone morphology ( J:131382 )

• duplication of jugal bone in mandibular region is observed

skeleton

abnormal sphenoid bone morphology ( J:131382 )

abnormal alisphenoid bone morphology ( J:131382 )

• lamina obturans is duplicated

abnormal pterygoid process morphology ( J:131382 )

• duplicated in mutants

abnormal hyoid bone morphology ( J:131382 )

• 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

lower jaw to upper jaw transformation ( J:131382 )

• maxillary bones are duplicated in mandibular region

abnormal palatine bone morphology ( J:131382 )

• duplication of palatine bone is observed

abnormal zygomatic bone morphology ( J:131382 )

• duplication of jugal bone in mandibular region is observed

growth/size/body

abnormal hyoid bone morphology ( J:131382 )

• 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

lower jaw to upper jaw transformation ( J:131382 )

• maxillary bones are duplicated in mandibular region

abnormal palatine bone morphology ( J:131382 )

• duplication of palatine bone is observed

abnormal zygomatic bone morphology ( J:131382 )

• duplication of jugal bone in mandibular region is observed

Genotype
MGI:3796552

cn8

• Allelic Composition: Gna11^tm1Soff/Gna11⁺; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(PTH-cre)4167Slib/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6

growth/size/body

decreased body weight ( J:116986 )

• reduced at P9 compared to controls

homeostasis/metabolism

increased circulating parathyroid hormone level ( J:116986 )

• levels are increased compared to controls at P9

abnormal circulating calcium level ( J:116986 )

• increased relative to controls

abnormal urine calcium level ( J:116986 )

• increased relative to controls at P9

renal/urinary system

abnormal urine calcium level ( J:116986 )

• increased relative to controls at P9

Genotype
MGI:3796553

cn9

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq⁺; Tg(PTH-cre)4167Slib/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6

growth/size/body

decreased body weight ( J:116986 )

• reduced at P9 compared to controls

homeostasis/metabolism

increased circulating parathyroid hormone level ( J:116986 )

• levels are increased compared to controls

abnormal circulating calcium level ( J:116986 )

• increased relative to controls at P9

abnormal urine calcium level ( J:116986 )

• increased relative to controls

renal/urinary system

abnormal urine calcium level ( J:116986 )

• increased relative to controls

Genotype
MGI:3796562

cn10

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(Tg-cre)1Soff/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:127484 )

N • as mutants age, no significant differences in thyroid size or weight is observed relative to wild-type

abnormal thyroid gland morphology ( J:127484 )

• 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

abnormal thyroid follicular cell morphology ( J:127484 )

• cells are often enlarged, columnar and have large nuclei at 6 months of age

abnormal thyroid gland physiology ( J:127484 )

• 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

decreased activity of thyroid gland ( J:127484 )

• after 6 months of age, about half of animals display overt hypothyroidism

homeostasis/metabolism

decreased circulating thyroxine level ( J:127484 )

• at 6 months, mice show low T4 levels compared to wild-type

increased circulating thyroid-stimulating hormone level ( J:127484 )

• 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

Genotype
MGI:3796547

cn11

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(Camk2a-cre)1Gsc/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N

mortality/aging

premature death ( J:111559 )

• age-dependent reduction in survival due to tonic-clonic seizures

nervous system

seizures ( J:111559 )

• 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

clonic seizures ( J:111559 )

• most seizures are myoclonic

tonic-clonic seizures ( J:111559 )

• some animals exhibit tonic-clonic seizures with age

gliosis ( J:111559 )

• older mice display reactive gliosis in CA1 region of hippocampus

hippocampal neuron degeneration ( J:111559 )

• older animals particularly those with symptomatic epilepsy show neuronal degeneration in CA1 region

abnormal nervous system electrophysiology ( J:123222 )

• no CCK4-induced (cholecystokinin receptor₂ agonist) current is detected in amygdala slices while inward current response in wild-type is unaffected

behavior/neurological

seizures ( J:111559 )

• 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

clonic seizures ( J:111559 )

• most seizures are myoclonic

tonic-clonic seizures ( J:111559 )

• some animals exhibit tonic-clonic seizures with age

cellular

gliosis ( J:111559 )

• older mice display reactive gliosis in CA1 region of hippocampus

Genotype
MGI:3837458

cn12

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; Tg(Tek-icre/ERT2)1Soff/?
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N

cardiovascular system

decreased vascular permeability ( J:146132 )

• 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

immune system phenotype ( J:146132 )

N • while resistant to shock induced by IgE or vasoactive substances, mice are not resistant to shock induced by LPS

decreased susceptibility to type I hypersensitivity reaction ( J:146132 )

• 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

Genotype
MGI:3819271

cn13

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm2Soff/Gnaq^tm2Soff; X/Tg(Myh11-icre/ERT2)1Soff
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N

cardiovascular system

decreased systemic arterial blood pressure ( J:141641 )

♂ • 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

decreased mean systemic arterial blood pressure ( J:141641 )

♂ • 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

decreased vasoconstriction ( J:141641 )

♂ • 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

muscle

decreased vasoconstriction ( J:141641 )

♂ • 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:2661813

cx14

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm1Soff/Gnaq^tm1Soff
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:49140 )

• mutant embryos appear normal ar E9.5, growth arrests prior to E10.5 and die by E11

cardiovascular system

trabecula carnea hypoplasia ( J:49140 )

• apparent by E9.5; underdeveloped trabecular ventricular myocardium

ventricular myocardium compact layer hypoplasia ( J:49140 )

• apparent by E9.5; underdeveloped subepicardial layer

hemopericardium ( J:49140 )

• enlarged heart due to bleeding into the space between the myocardial and pericardial layers

homeostasis/metabolism

hemopericardium ( J:49140 )

• enlarged heart due to bleeding into the space between the myocardial and pericardial layers

muscle

trabecula carnea hypoplasia ( J:49140 )

• apparent by E9.5; underdeveloped trabecular ventricular myocardium

ventricular myocardium compact layer hypoplasia ( J:49140 )

• apparent by E9.5; underdeveloped subepicardial layer

Genotype
MGI:3037556

cx15

• Allelic Composition: Gna11^tm1Soff/Gna11⁺; Gnaq^tm1Soff/Gnaq^tm1Soff
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6

mortality/aging

neonatal lethality, complete penetrance ( J:49140 )

• animals die within 1-2 hours after birth

behavior/neurological

hyporesponsive to tactile stimuli ( J:49140 )

• poorly responsive to tactile stimuli

cardiovascular system

common ventricle ( J:49140 )

• high incidence of univentricular hearts

craniofacial

short mandible ( J:49140 )

incus hypoplasia ( J:49140 )

• poorly developed incus

malleus hypoplasia ( J:49140 )

• poorly developed malleus

stapes hypoplasia ( J:49140 )

• poorly developed stapes

growth/size/body

short mandible ( J:49140 )

decreased body size ( J:49140 )

• animals appear runted at birth

hearing/vestibular/ear

incus hypoplasia ( J:49140 )

• poorly developed incus

malleus hypoplasia ( J:49140 )

• poorly developed malleus

stapes hypoplasia ( J:49140 )

• poorly developed stapes

abnormal tympanic ring morphology ( J:49140 )

• vestigial tympanic ring

respiratory system

abnormal breathing pattern ( J:49140 )

• arrhythmic breathing

decreased pulmonary respiratory rate ( J:49140 )

• animals breathed at approximately half the rate of controls

skeleton

short mandible ( J:49140 )

incus hypoplasia ( J:49140 )

• poorly developed incus

malleus hypoplasia ( J:49140 )

• poorly developed malleus

stapes hypoplasia ( J:49140 )

• poorly developed stapes

homeostasis/metabolism

hypoxia ( J:49140 )

• noted at birth

Genotype
MGI:3037554

cx16

• Allelic Composition: Gna11^tm1Soff/Gna11⁺; Gnaq^tm1Soff/Gnaq⁺
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6

normal phenotype

no abnormal phenotype detected ( J:49140 )

• mice are viable and fertile

Genotype
MGI:3037555

cx17

• Allelic Composition: Gna11^tm1Soff/Gna11^tm1Soff; Gnaq^tm1Soff/Gnaq⁺
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6

mortality/aging

neonatal lethality, complete penetrance ( J:49140 )

• animals die within 1-2 hours after birth

behavior/neurological

hyporesponsive to tactile stimuli ( J:49140 )

• poorly responsive to tactile stiluli

cardiovascular system

abnormal heart size ( J:49140 )

• hearts are described as malformed, either hypertrophic or hypotrophic

growth/size/body

decreased body size ( J:49140 )

• animals appear runted at birth

respiratory system

abnormal breathing pattern ( J:49140 )

• arrythmic breathing

decreased pulmonary respiratory rate ( J:49140 )

• animals breathed at approximately half the rate of controls

homeostasis/metabolism

hypoxia ( J:49140 )

• apparent at birth