Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr3tm1Jch mutation
(0 available);
any
S1pr3 mutation
(24 available)
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mortality/aging
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• mutants are protected from LPS lethality
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homeostasis/metabolism
immune system
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• increase in IL-1beta levels in mesenteric lymph nodes but reduced levels in the lungs after LPS challenge
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• mesenteric lymph nodes are 3 times larger than in wild-type 18 hours after LPS challenge
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• mutants are protected from lipopolysaccharide (LPS) induced lethality
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr3tm1Jch mutation
(0 available);
any
S1pr3 mutation
(24 available)
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reproductive system
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• litter sizes from homozygous intercrosses are significantly smaller than those from crosses between heterozygous males and wild-type females (5.6 vs 7.5 pups/litter)
• however, homozygotes exhibit normal embryonic development, general health, body weight, fertility, hematology, tissue histology and longevity relative to wild-type mice
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cellular
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• MEFs obtained from E14 mutant embryos exhibit significant decreases in phospholipase C activation, slight decreases in adenylyl cyclase inhibition, and no change in Rho activation relative to wild-type MEFs
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respiratory system
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• resistant to pulmonary edema induced by intratracheal injection of sphingosine 1 phosphate
• lung epithelial cells maintain tight junctions between one another after sphingosine 1 phosphate treatment whereas control cells will retract from one another opening clear paracellular gaps between the airway surface and the subepithelial extracellular matrix
• TNF effect to enhance pulmonary edema is blocked
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hearing/vestibular/ear
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• homozygotes display a normal startle reflex, responding to acoustic stimuli >90-100 dB
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr2tm1Jch mutation
(1 available);
any
S1pr2 mutation
(46 available)
S1pr3tm1Jch mutation
(0 available);
any
S1pr3 mutation
(24 available)
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mortality/aging
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• more than half of pups born from crosses between homozygotes are dead within one week, mostly within 24 hours
• surviving pups grow up normally with no obvious abnormalities at young ages
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behavior/neurological
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• older double homozygotes become disoriented and often experience a delay in contact righting behavior
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• as early as 4 weeks of age, all double homozygotes completely lack a startle reflex to acoustic stimuli >90-100 dB
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• as early as 2 months, double homozygotes suspended by the tail curl upward, often landing on their heads when returned to the ground
• this behavior shows an age-related increase in penetrance and occurs uniformly by 6 months of age
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• double homozygotes show a progressive loss of swimming ability and are almost uniformly deficient by 18 weeks of age
• in contrast, very young double mutant mice (4 weeks) display no difficulty in the forced swim test
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• at >6 months, double homozygotes display consistent postural defects indicative of vestibular dysfunction
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• at >6 months, double homozygotes show a persistent head tilt
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• at 12-14 weeks of age, double homozygotes show a significant decrease in rearing frequency, fail to maintain balance on their hindlimbs, and arch their backs to elevate their noses
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• perinatal death of pups due to maternal neglect
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reproductive system
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• vastly reduced number of progeny from crosses between double null parents
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hearing/vestibular/ear
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• at >2 weeks, double homozygotes display progressive IHC degeneration in a basal-to-apical pattern that is almost complete by 4 months of age
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• at >2 weeks, double homozygotes display progressive OHC degeneration in a basal-to-apical pattern that is almost complete by 4 months of age
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• at >2 weeks, double homozygotes display progressive degeneration of supporting cells that is almost complete by 4 months of age
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• at >2 weeks of age, double homozygotes show progressive degeneration of the organ of Corti in a basal-to-apical pattern
• however, cochlear hair cell stereociliary bundle morphology is normal at P4, and cochlear histology remains intact until at least 2 weeks of age
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• starting at >4 weeks, double homozygotes exhibit a progressive disorganization of the sensory epithelium of vestibular maculas that becomes prominent at 4 months
• by 8 months, the epithelial layer is significantly disorganized and lacks afferent calyces and stereocilia
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• older double homozygotes show complete loss of vestibular stereocilia
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• double homozygotes exhibit progressive loss of vestibular function, as shown by impaired swimming, rearing behavior and contact righting
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nervous system
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• at >2 weeks, double homozygotes display progressive IHC degeneration in a basal-to-apical pattern that is almost complete by 4 months of age
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• at >2 weeks, double homozygotes display progressive OHC degeneration in a basal-to-apical pattern that is almost complete by 4 months of age
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• older double homozygotes show complete loss of vestibular stereocilia
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• at >2 weeks, double homozygotes exhibit a striking degeneration of afferent neurons in the spiral ganglia, in a basal-to-apical pattern
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr2tm1Jch mutation
(1 available);
any
S1pr2 mutation
(46 available)
S1pr3tm1Jch mutation
(0 available);
any
S1pr3 mutation
(24 available)
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behavior/neurological
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• as early as 4 weeks of age, all mutant mice homozygous for Edg5tm1Jch and heterozygous for Edg3tm1Jch completely lack a startle reflex to acoustic stimuli >90-100 dB
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Analysis Tools