Phenotypes associated with this allele

• Allele Symbol: F2r^tm1Pago
• Allele Name: targeted mutation 1, Patricia Andrade-Gordon
• Allele ID: MGI:3038377
• Summary: 5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	F2r^tm1Pago/F2r^tm1Pago	B6.129P2-F2r^tm1Pago	MGI:3826826
hm2	F2r^tm1Pago/F2r^tm1Pago	involves: 129P2/OlaHsd	MGI:4822460
hm3	F2r^tm1Pago/F2r^tm1Pago	involves: 129P2/OlaHsd * C57BL/6	MGI:3038598
cx4	F2r^tm1Pago/F2r^tm1Pago F3^tm1.1Dwr/F3^tm1.1Dwr	B6.129-F3^tm1.1Dwr F2r^tm1Pago	MGI:4829887
cx5	F2r^tm1Pago/F2r^tm1Pago Tg(MMTV-PyVT)634Mul/0	B6.Cg-F2r^tm1Pago Tg(MMTV-PyVT)634Mul	MGI:4821159

Genotype
MGI:3826826

hm1

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago
• Genetic Background: B6.129P2-F2r^tm1Pago

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

cardiovascular system

cardiovascular system phenotype ( J:135087 )

N • retinal neoangiogenesis after oxygen induced retinopathy is similar to wild-type mice

abnormal heart left ventricle morphology ( J:142990 )

• although the size of cardiac infarctions is unaffected, the extent of left ventricular dilation after infarction and recovery is reduced

abnormal response to cardiac infarction ( J:142990 )

• less impairment of left ventricular function after cardiac infarction and recovery

homeostasis/metabolism

abnormal response to cardiac infarction ( J:142990 )

• less impairment of left ventricular function after cardiac infarction and recovery

immune system

immune system phenotype ( J:88245 )

N • mice show no differences in high dose (100% lethal challenge) lipopolysaccharide (LPS)-induced inflammation and lethality compared to controls

Genotype
MGI:4822460

hm2

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago
• Genetic Background: involves: 129P2/OlaHsd

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:133917 )

• mutants exhibit increased survival over wild-type mice after 90%, but not 100%, lethal LPS challenge

homeostasis/metabolism

abnormal cytokine level ( J:133917 )

• decrease in IL-6 and IL-1beta levels six hours after 90% lethal LPS challenge

• increase in IL-1beta levels in mesenteric lymph nodes but reduced levels in the lungs after LPS challenge

immune system

abnormal cytokine level ( J:133917 )

• decrease in IL-6 and IL-1beta levels six hours after 90% lethal LPS challenge

• increase in IL-1beta levels in mesenteric lymph nodes but reduced levels in the lungs after LPS challenge

abnormal lymph node morphology ( J:133917 )

• 18 hours after LPS challenge, lymph nodes exhibit abundant fibrin throughout the parenchyma compared to staining within lymphatic ducts in wild-type

enlarged mesenteric lymph nodes ( J:133917 )

• mesenteric lymph nodes are 3 times larger than in wild-type 18 hours after LPS challenge

decreased susceptibility to endotoxin shock ( J:133917 )

• mutants exhibit a similar level of initial development of inflammation as wild-type mice in response to severe challenge with lipopolysaccharide (LPS), however attenuation of the inflammation occurs 12-18 hours after challenge while wild-type mice succumb to the infection

Genotype
MGI:3038598

hm3

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance ( J:38032 )

• a large portion of embryos are resorbed after E10, though some mice develop normally and survive to adulthood

cardiovascular system

cardiovascular system phenotype ( J:38032 , J:124465 )

N • mice that survive to adulthood exhibit normal platelet number and function, coagulation parameters, basal heart rate, and arterial blood pressure (J:38032)

N • mutants exhibit normal pulmonary vasoreactivity to vasoactive mediators (J:124465)

abnormal carotid artery morphology ( J:103347 )

• cell density is greater in normal carotids from mutants than in wild-type mice

abnormal blood pressure regulation ( J:38032 )

• mutants exhibit a reduction of the hypertensive response to the selective thrombin receptor activating peptide, SFLLRN-NH2, before and after L-NAME (an inhibitor of nitric oxide synthesis) and absence of hypertension in the presence of L-NAME

abnormal systemic arterial blood pressure regulation ( J:38032 )

• mutants show absence of an arterial pressure response to the selective thrombin receptor activating peptide, TFLLRNPNDK-NH2

abnormal systemic arterial blood pressure ( J:96312 )

• the hypertensive response and heart rate decrease in response to TFLLRNPNDK, a F2r (PAR-1) selective activating peptide, is absent

• SFLLRN, a nonselective receptor activating peptide, was able to induce hypotension in mutants as in wild-type mice but the heart rate decrease and secondary hypotension following L-NAME are absent

decreased vascular permeability ( J:124465 )

• the thrombin-induced increase in pulmonary microvessel permeability seen in controls is absent in mutants

abnormal vascular wound healing ( J:103347 )

• vessel diameter is unchanged and lumen diameter decreases following vascular injury unlike in wild-type mice in which vessel and lumen diameters increase following injury

• area of neointima formation following vascular injury is slightly less than in wild-type mice

• however, medial cell loss, incidence of thrombosis, endothelial regrowth, and medial thickening after injury are similar to wild-type

reproductive system

abnormal fertility/fecundity ( J:38032 )

• matings between homozygous mice occur infrequently and produce less than 3 offspring

homeostasis/metabolism

abnormal vascular wound healing ( J:103347 )

• vessel diameter is unchanged and lumen diameter decreases following vascular injury unlike in wild-type mice in which vessel and lumen diameters increase following injury

• area of neointima formation following vascular injury is slightly less than in wild-type mice

• however, medial cell loss, incidence of thrombosis, endothelial regrowth, and medial thickening after injury are similar to wild-type

digestive/alimentary system

abnormal intestine physiology ( J:96182 )

• mutants have a lower baseline short-circuit current in the colon than wild-type mice but no difference in the short-circuit current response to electrical field stimulation, indicating abnormal basal ion secretion in the colon

decreased susceptibility to induced colitis ( J:94420 )

• trinitrobenzene sulfonic acid (TNBS) induced colitis is less severe in mutants than in wild-type mice

immune system

decreased inflammatory response ( J:124648 )

• absence of human trypsin IV and rat p23 induced edema and granulocyte infiltration after intraplantar injection

decreased susceptibility to induced colitis ( J:94420 )

• trinitrobenzene sulfonic acid (TNBS) induced colitis is less severe in mutants than in wild-type mice

Genotype
MGI:4829887

cx4

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago; F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: B6.129-F3^tm1.1Dwr F2r^tm1Pago

cardiovascular system

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

vision/eye

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

Genotype
MGI:4821159

cx5

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago; Tg(MMTV-PyVT)634Mul/0
• Genetic Background: B6.Cg-F2r^tm1Pago Tg(MMTV-PyVT)634Mul

neoplasm

increased mammary adenocarcinoma incidence ( J:138924 )

• progression of mammary adenocarcinoma development occurs to a similar extent as in Tg(MMTV-PyVT)634Mul mice

increased adenoma incidence ( J:138924 )

• adenomas develop by 9 weeks of age, at similar time and rate as in Tg(MMTV-PyVT)634Mul mice

integument

increased mammary adenocarcinoma incidence ( J:138924 )

• progression of mammary adenocarcinoma development occurs to a similar extent as in Tg(MMTV-PyVT)634Mul mice

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:138924 )

• progression of mammary adenocarcinoma development occurs to a similar extent as in Tg(MMTV-PyVT)634Mul mice