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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Cma1-cre)ARoer
transgene insertion A, Axel Roers
MGI:3785000
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Stx3Gt(EUCE320f12)1.1Hmgu/Stx3Gt(EUCE320f12)1.1Hmgu
Tg(Cma1-cre)ARoer/0
B6.Cg-Stx3Gt(EUCE320f12)1.1Hmgu Tg(Cma1-cre)ARoer MGI:7469803
cn2
Stx4atm1.1Radac/Stx4atm1.1Radac
Tg(Cma1-cre)ARoer/0
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6J MGI:7469807
cn3
Tg(Cma1-cre)ARoer/0
Tg(Kit*D814V)1Roer/0
involves: C57BL/6 MGI:4942363
cn4
Tg(Cma1-cre)ARoer/0
Tg(Kit*D814V)3Roer/0
involves: C57BL/6 MGI:4942364


Genotype
MGI:7469803
cn1
Allelic
Composition
Stx3Gt(EUCE320f12)1.1Hmgu/Stx3Gt(EUCE320f12)1.1Hmgu
Tg(Cma1-cre)ARoer/0
Genetic
Background
B6.Cg-Stx3Gt(EUCE320f12)1.1Hmgu Tg(Cma1-cre)ARoer
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stx3Gt(EUCE320f12)1.1Hmgu mutation (0 available); any Stx3 mutation (16 available)
Tg(Cma1-cre)ARoer mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• only mast cell (MC)-regulated exocytosis is affected while other MC effector responses remain intact, including the secretion of cytokines via constitutive exocytosis
• no significant differences in the total number, distribution or structure of MCs are observed
• plasma membrane capacitance (Cm) recordings of single peritoneal MCs after stimulation by intracellular dialysis of GTPgammaS and Ca2+ show that MCs achieve the same total increase in plasma membrane area (deltaCm) at a significantly lower rate than control MCs; however, time between cell access and beginning of the exocytic burst is normal
• ~70% of single 'steps' in the Cm curve are equal to or less than 12 fF versus ~35% in control MCs, whereas large steps are almost completely absent, indicating a shift to exocytosis of smaller-sized vesicles; residual exocytosis thus proceeds at a slower pace and is composed primarily of single-vesicle fusion events
• after stimulation with PMA/ionomycin, peritoneal MCs show altered exocytosis-related ultrastructural changes with an intermediate gain in electron lucency of their granules and a nearly complete absence of intracellular multigranular compartments, indicating that MCs are unable to engage multigranular compound exocytosis
• in a model of passive systemic anaphylaxis, mice sensitized i.p. with anti-DNP IgE and challenged i.p. with DNP-HAS exhibit histological evidence that MC degranulation in connective tissues is significantly lower than in control MCs at 90 min post-challenge
• however, the MC-dependent hypothermic response is normal at 50 min post-challenge

hematopoietic system
• plasma membrane capacitance (Cm) recordings of single peritoneal MCs after stimulation by intracellular dialysis of GTPgammaS and Ca2+ show that MCs achieve the same total increase in plasma membrane area (deltaCm) at a significantly lower rate than control MCs; however, time between cell access and beginning of the exocytic burst is normal
• ~70% of single 'steps' in the Cm curve are equal to or less than 12 fF versus ~35% in control MCs, whereas large steps are almost completely absent, indicating a shift to exocytosis of smaller-sized vesicles; residual exocytosis thus proceeds at a slower pace and is composed primarily of single-vesicle fusion events
• after stimulation with PMA/ionomycin, peritoneal MCs show altered exocytosis-related ultrastructural changes with an intermediate gain in electron lucency of their granules and a nearly complete absence of intracellular multigranular compartments, indicating that MCs are unable to engage multigranular compound exocytosis
• in a model of passive systemic anaphylaxis, mice sensitized i.p. with anti-DNP IgE and challenged i.p. with DNP-HAS exhibit histological evidence that MC degranulation in connective tissues is significantly lower than in control MCs at 90 min post-challenge
• however, the MC-dependent hypothermic response is normal at 50 min post-challenge

mortality/aging
N
• mice are viable, grossly normal, and exhibit a normal life span when raised in a specific pathogen-free facility

cellular
• plasma membrane capacitance (Cm) recordings of single peritoneal MCs after stimulation by intracellular dialysis of GTPgammaS and Ca2+ show that MCs achieve the same total increase in plasma membrane area (deltaCm) at a significantly lower rate than control MCs; however, time between cell access and beginning of the exocytic burst is normal
• ~70% of single 'steps' in the Cm curve are equal to or less than 12 fF versus ~35% in control MCs, whereas large steps are almost completely absent, indicating a shift to exocytosis of smaller-sized vesicles; residual exocytosis thus proceeds at a slower pace and is composed primarily of single-vesicle fusion events
• after stimulation with PMA/ionomycin, peritoneal MCs show altered exocytosis-related ultrastructural changes with an intermediate gain in electron lucency of their granules and a nearly complete absence of intracellular multigranular compartments, indicating that MCs are unable to engage multigranular compound exocytosis
• in a model of passive systemic anaphylaxis, mice sensitized i.p. with anti-DNP IgE and challenged i.p. with DNP-HAS exhibit histological evidence that MC degranulation in connective tissues is significantly lower than in control MCs at 90 min post-challenge
• however, the MC-dependent hypothermic response is normal at 50 min post-challenge




Genotype
MGI:7469807
cn2
Allelic
Composition
Stx4atm1.1Radac/Stx4atm1.1Radac
Tg(Cma1-cre)ARoer/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stx4atm1.1Radac mutation (0 available); any Stx4a mutation (20 available)
Tg(Cma1-cre)ARoer mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are viable, grossly normal, and exhibit a normal life span when raised in a specific pathogen-free facility

immune system
N
• plasma membrane capacitance (Cm) recordings of single peritoneal mast cells (MCs) after stimulation by intracellular dialysis of GTPgammaS and Ca2+ show no differences in the magnitude or speed of exocytosis relative to control MCs; time between cell access and beginning of the exocytic burst and frequency distribution of (Cm) step sizes between 1 and 15% of total (deltaCm) are normal
• after stimulation with PMA/ionomycin, peritoneal MCs show normal exocytosis-related ultrastructural changes relative to control MCs
• mice exhibit normal secretion of MC mediators, independent of the mediator measured or the stimuli employed
• no significant differences in the total number, distribution or structure of MCs are observed




Genotype
MGI:4942363
cn3
Allelic
Composition
Tg(Cma1-cre)ARoer/0
Tg(Kit*D814V)1Roer/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Cma1-cre)ARoer mutation (0 available)
Tg(Kit*D814V)1Roer mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• all mice develop intestinal inflammation similar to that in mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn

hematopoietic system
• develop mastocytosis similar to that in mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn
• accumulation of mast cells in the skin and in some cases also in the spleen
• disease symptoms occur later and disease progression is slower compared to mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn

neoplasm
• mast cell tumors are seen in some mice

immune system
• all mice develop intestinal inflammation similar to that in mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn
• develop mastocytosis similar to that in mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn
• accumulation of mast cells in the skin and in some cases also in the spleen
• disease symptoms occur later and disease progression is slower compared to mice carrying Tg(Kit*D814V)1Roer and Tg(Mx1-cre)1Cgn

integument
• mast cell tumors are seen in some mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
mastocytosis DOID:350 OMIM:154800
J:169611




Genotype
MGI:4942364
cn4
Allelic
Composition
Tg(Cma1-cre)ARoer/0
Tg(Kit*D814V)3Roer/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• accumulation of mast cells in the skin and in some cases also in the spleen
• disease symptoms occur later and disease progression is slower compared to mice carrying Tg(Kit*D814V)3Roer and Tg(Mx1-cre)1Cgn
• develop mastocytosis similar to that in mice carrying Tg(Kit*D814V)3Roer and Tg(Mx1-cre)1Cgn

neoplasm
• mast cell tumors are seen in some mice

integument
• mast cell tumors are seen in some mice

immune system
• accumulation of mast cells in the skin and in some cases also in the spleen
• disease symptoms occur later and disease progression is slower compared to mice carrying Tg(Kit*D814V)3Roer and Tg(Mx1-cre)1Cgn
• develop mastocytosis similar to that in mice carrying Tg(Kit*D814V)3Roer and Tg(Mx1-cre)1Cgn

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
mastocytosis DOID:350 OMIM:154800
J:169611





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory