Phenotypes associated with this allele

• Allele Symbol: Gna13^tm2.1Soff
• Allele Name: targeted mutation 2.1, Stefan Offermanns
• Allele ID: MGI:3697690
• Summary: 6 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff Tg(Tek-icre/ERT2)1Soff/?	involves: 129P2/OlaHsd * 129S1/Sv * FVB/N	MGI:3837460
cn2	Cd19^tm1(cre)Cgn/Cd19^+ Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6N	MGI:3699320
cn3	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff Tg(Lck-cre)548Jxm/0	involves: 129S1/Sv * C57BL/6 * CBA	MGI:3849203
cn4	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff Tg(Mx1-cre)1Cgn/0	involves: 129S1/Sv * C57BL/6 * CBA * FVB/N	MGI:3699352
cn5	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff X/Tg(Myh11-icre/ERT2)1Soff	involves: 129S1/Sv * FVB/N	MGI:3819345
cn6	Gna13^tm2.1Soff/Gna13^tm2.1Soff Tg(Mx1-cre)1Cgn/0	involves: C57BL/6 * CBA * FVB/N	MGI:3699351

Genotype
MGI:3837460

cn1

• Allelic Composition: Gna12^tm1Citb/Gna12^tm1Citb; Gna13^tm2.1Soff/Gna13^tm2.1Soff; Tg(Tek-icre/ERT2)1Soff/?
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * FVB/N

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

cardiovascular system

cardiovascular system phenotype ( J:146132 )

N • tamoxifen-treated mice respond similar to wild-type controls in experiments testing response to anaphylactic shock

Genotype
MGI:3699320

cn2

• Allelic Composition: Cd19^tm1(cre)Cgn/Cd19⁺; Gna12^tm1Citb/Gna12^tm1Citb; Gna13^tm2.1Soff/Gna13^tm2.1Soff
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6N

hematopoietic system

decreased marginal zone B cell number ( J:117663 )

• marginal zone B cell numbers are strongly reduced compared to controls

abnormal B cell physiology ( J:117663 )

• lysophospholipid-induced induced adhesion is completely abrogated in marginal zone mutant B cells and is reduced in follicular B cells

• lysophospholipid-induced induced LFA-1 (integrin) clustering is abolished in mutant B cells

immune system

decreased marginal zone B cell number ( J:117663 )

• marginal zone B cell numbers are strongly reduced compared to controls

abnormal B cell physiology ( J:117663 )

• lysophospholipid-induced induced adhesion is completely abrogated in marginal zone mutant B cells and is reduced in follicular B cells

• lysophospholipid-induced induced LFA-1 (integrin) clustering is abolished in mutant B cells

Genotype
MGI:3849203

cn3

• Allelic Composition: Gna12^tm1Citb/Gna12^tm1Citb; Gna13^tm2.1Soff/Gna13^tm2.1Soff; Tg(Lck-cre)548Jxm/0
• Genetic Background: involves: 129S1/Sv * C57BL/6 * CBA

immune system

increased T cell proliferation ( J:149560 )

• homeostatic CD4⁺ T cell proliferation is increased within the lymph nodes

• allogenic stimulation of CD4⁺ T cells is also increased

thymus hyperplasia ( J:149560 )

• thymus weight and cellularity is increased by about a third

increased CD4-positive, alpha-beta T cell number ( J:149560 )

• CD4⁺ T cell numbers in the lymph nodes and blood are increased by about a third

increased CD8-positive, alpha-beta T cell number ( J:149560 )

• CD8⁺ T cell numbers in the lymph nodes are slightly increased

abnormal CD4-positive, alpha-beta T cell physiology ( J:149560 )

• CD4⁺ T cells have longer interactions between themselves and with allogenic dendritic cells

• CD4⁺ T cells have a higher affinity for ICAM-coated surfaces

• CD4⁺ T cells have decreased motility through transwell filters

• CD4⁺ T cells transferred into wild-type mice have enhanced enhanced transendothelial migration into lymph nodes

lymph node hyperplasia ( J:149560 )

• axillary, cervical, inguinal and mesenteric lymph nodes are increased in weight and cell number by about a third

increased susceptibility to type IV hypersensitivity reaction ( J:149560 )

• an increase in ear thickness is observed after sensitization and challenge with DNFB

• CD4⁺ T cells in cervical lymph nodes have a higher proliferation rate than those of control mice after DNFB challenge

increased interleukin-2 secretion ( J:149560 )

• IL-2 secretion is enhanced by CD4⁺ T cells in response to allogenic stimulation

increased susceptibility to autoimmune diabetes ( J:149560 )

• diabetes development is accelerated and aggravated after streptozotocin induction with high glucose levels detected

• peripancreatic lymph nodes are enlarged 5-6 days after disease induction

• increased numbers of CD4⁺ T cells are noted in the pancreas 14 days after disease induction compared to controls

hematopoietic system

increased T cell proliferation ( J:149560 )

• homeostatic CD4⁺ T cell proliferation is increased within the lymph nodes

• allogenic stimulation of CD4⁺ T cells is also increased

thymus hyperplasia ( J:149560 )

• thymus weight and cellularity is increased by about a third

increased CD4-positive, alpha-beta T cell number ( J:149560 )

• CD4⁺ T cell numbers in the lymph nodes and blood are increased by about a third

increased CD8-positive, alpha-beta T cell number ( J:149560 )

• CD8⁺ T cell numbers in the lymph nodes are slightly increased

abnormal CD4-positive, alpha-beta T cell physiology ( J:149560 )

• CD4⁺ T cells have longer interactions between themselves and with allogenic dendritic cells

• CD4⁺ T cells have a higher affinity for ICAM-coated surfaces

• CD4⁺ T cells have decreased motility through transwell filters

• CD4⁺ T cells transferred into wild-type mice have enhanced enhanced transendothelial migration into lymph nodes

endocrine/exocrine glands

thymus hyperplasia ( J:149560 )

• thymus weight and cellularity is increased by about a third

cellular

increased T cell proliferation ( J:149560 )

• homeostatic CD4⁺ T cell proliferation is increased within the lymph nodes

• allogenic stimulation of CD4⁺ T cells is also increased

Genotype
MGI:3699352

cn4

• Allelic Composition: Gna12^tm1Citb/Gna12^tm1Citb; Gna13^tm2.1Soff/Gna13^tm2.1Soff; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: 129S1/Sv * C57BL/6 * CBA * FVB/N

homeostasis/metabolism

abnormal blood coagulation ( J:99597 )

• platelet thrombus formation is severely impaired ex vivo after treatment of platelets with polyinosinic-polycytidylic acid (PIPC) to induce recombination

• however, initial adhesion of platelets is similar to wild-type

abnormal platelet physiology ( J:99597 )

• serotonin secretion induced by U46619 plus adrenaline or Par-4 peptide exposure is significantly decreased compared to wild-type cells

• however, thrombin-induced serotonin secretion is not impaired

• absence of a shape change in response to low concentration of stimuli compared to wild-type following polyinosinic-polycytidylic acid (PIPC) treatment

• however, shape change is induced with high concentration of stimuli

• potency of agonists to induce aggregation is reduced but aggregation occurs at all agonist concentrations

decreased platelet aggregation ( J:99597 )

• potency of agonists to induce aggregation is reduced but aggregation occurs at all agonist concentrations

increased bleeding time ( J:99597 )

• very large increase in bleeding time in interferon-responsive tissues

• when bone marrow-derived cells PIPC-treated mice are transplanted into irradiated wild-type mice, 4 weeks later mice have greatly prolonged bleeding times (>20 minutes) compared with mice receiving cells from noninduced controls

hematopoietic system

abnormal platelet physiology ( J:99597 )

• serotonin secretion induced by U46619 plus adrenaline or Par-4 peptide exposure is significantly decreased compared to wild-type cells

• however, thrombin-induced serotonin secretion is not impaired

• absence of a shape change in response to low concentration of stimuli compared to wild-type following polyinosinic-polycytidylic acid (PIPC) treatment

• however, shape change is induced with high concentration of stimuli

• potency of agonists to induce aggregation is reduced but aggregation occurs at all agonist concentrations

decreased platelet aggregation ( J:99597 )

• potency of agonists to induce aggregation is reduced but aggregation occurs at all agonist concentrations

Genotype
MGI:3819345

cn5

• Allelic Composition: Gna12^tm1Citb/Gna12^tm1Citb; Gna13^tm2.1Soff/Gna13^tm2.1Soff; X/Tg(Myh11-icre/ERT2)1Soff
• Genetic Background: involves: 129S1/Sv * FVB/N

cardiovascular system

decreased systemic arterial blood pressure ( J:141641 )

♂ • tamoxifen-treated mice exhibit decreased blood pressure following treatment with U46619, 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 vasoconstriction ( J:141641 )

♂ • tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice

muscle

decreased vasoconstriction ( J:141641 )

♂ • tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice

Genotype
MGI:3699351

cn6

• Allelic Composition: Gna13^tm2.1Soff/Gna13^tm2.1Soff; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: C57BL/6 * CBA * FVB/N

homeostasis/metabolism

abnormal blood coagulation ( J:99597 )

• platelet thrombus formation is severely impaired ex vivo after treatment of platelets with polyinosinic-polycytidylic acid (PIPC) to induce recombination

• however, initial adhesion of platelets ex vivo is similar to wild-type

• in wild-type mice transfected with Gna13-deficient bone marrow, after vascular injury no thrombi form

abnormal platelet physiology ( J:99597 )

• impairment in shape change and aggregation induced following polyinosinic-polycytidylic acid (PIPC) treatment is identical to that in mice that are also homozygous for Gna12^tm1Citb

• serotonin secretion induced by U46619 plus adrenaline or Par-4 peptide exposure is significantly decreased compared to wild-type cells

• however, thrombin-induced serotonin secretion is not impaired

• in wild-type mice transfected with Gna13-deficient bone marrow, platelets adhere to subendothelial surface after injury, but with a ~50% reduction in numbers compared to wild-type platelets

increased bleeding time ( J:99597 )

• very large increase in bleeding time in interferon-responsive tissues

• when bone marrow-derived cells PIPC-treated mice are transplanted into irradiated wild-type mice, 4 weeks later mice have greatly prolonged bleeding times (>20 minutes) compared with mice receiving cells from noninduced controls

hematopoietic system

abnormal platelet physiology ( J:99597 )

• impairment in shape change and aggregation induced following polyinosinic-polycytidylic acid (PIPC) treatment is identical to that in mice that are also homozygous for Gna12^tm1Citb

• serotonin secretion induced by U46619 plus adrenaline or Par-4 peptide exposure is significantly decreased compared to wild-type cells

• however, thrombin-induced serotonin secretion is not impaired

• in wild-type mice transfected with Gna13-deficient bone marrow, platelets adhere to subendothelial surface after injury, but with a ~50% reduction in numbers compared to wild-type platelets