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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Spry2tm1.1Mrt
targeted mutation 1.1, Gail R Martin
MGI:3578633
Summary 10 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Spry2tm1.1Mrt/Spry2tm1.1Mrt involves: 129P2/OlaHsd MGI:3702557
hm2
Spry2tm1.1Mrt/Spry2tm1.1Mrt involves: 129/Sv * 129P2/OlaHsd * Black Swiss * C57BL/6 * FVB/N MGI:3581224
cn3
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5467304
cn4
Ptentm2.1Ppp/Pten+
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5467305
cn5
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N MGI:3716399
cx6
Ednrbs-36Pub/Ednrb+
Spry2tm1.1Mrt/Spry2+
involves: 101/Rl * 129P2/OlaHsd * C3H/Rl * C57BL/6J MGI:3759579
cx7
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Spry4tm1.2Mrt/Spry4+
involves: 129P2/OlaHsd MGI:7309963
cx8
Spry2tm1.1Mrt/Spry2+
Spry4tm1.2Mrt/Spry4tm1.2Mrt
involves: 129P2/OlaHsd MGI:6209558
cx9
Fgfr1tm1.1Jpa/Fgfr1+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:3702559
cx10
Fgfr2tm1.1Dor/Fgfr2+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
involves: 129P2/OlaHsd * 129X1/SvJ MGI:3702560


Genotype
MGI:3702557
hm1
Allelic
Composition
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• all craniofacial bones are thinner compared to wild-type controls
• density of craniofacial bones is reduced as early as E18.5
• enlarged intermaxillary spaces or extended sutures at 9 weeks of age
• higher cranial vault
• more rounded skull with a higher cranial vault
• skull centroid sizes become more similar to wild-type controls with age suggesting a delay in ontogenetic development
• relatively longer, appearing to compensate for decreased length of the nasal and supraoccipital bones
• relatively longer, appearing to compensate for decreased length of the nasal and supraoccipital bones
• relatively shorter compared to wild-type controls
• lack the opening normally seen in the temporal bone
• decrease in the length of individual bones in the skull vault
• rather than regressing as in wild-type mice, diastema tooth buds survive
• thinning is especially evident in suture forming areas
• an ectopic tooth is found rostrally of the first molar in the mandibular diastema region or the first molar is expanded with a rostral ectopic cusp
• on the anterior end of M1, the cusps are farther apart resulting in shortening of M1
• however, other molar cups are essentially normal, unlike in other mice with supernumerary teeth
• rather than regressing as in wild-type mice, diastema tooth buds survive
• in the mandible 92% of mice have bilateral diastema teeth, 5% unilateral and 3% no diastema teeth (J:119280)
• less than 5% of mice have supernumerary teeth in the maxilla (J:119280)
• rudimentary tooth bud is present at E14.5 in the diastemal area in the mandible (J:315670)
• mandibular and maxillary molars do not properly occlude
• abnormally shaped mandibular notches
• mandibles tend to have longer toothrow, longer and backward shifted processus coronoideus, slightly shorter incisors, and shortened angular process compared to wild-type controls
• abnormally shaped
• irregular articular cartilage surfaces throughout the condyle
• vomeronasal bones display posterior curvature that prevents formation of the vomeromaxillary suture within the palatine process of the maxilla
• relatively shorter nasal bone compared to wild-type controls
• complete and incomplete cleft palates are seen

cellular
• axoneme elongation is seen in postnatal but not prenatal tibial and mandibular condyle chondrocytes

digestive/alimentary system
• vomeronasal bones display posterior curvature that prevents formation of the vomeromaxillary suture within the palatine process of the maxilla
• complete and incomplete cleft palates are seen

skeleton
• all craniofacial bones are thinner compared to wild-type controls
• density of craniofacial bones is reduced as early as E18.5
• enlarged intermaxillary spaces or extended sutures at 9 weeks of age
• higher cranial vault
• more rounded skull with a higher cranial vault
• skull centroid sizes become more similar to wild-type controls with age suggesting a delay in ontogenetic development
• relatively longer, appearing to compensate for decreased length of the nasal and supraoccipital bones
• relatively longer, appearing to compensate for decreased length of the nasal and supraoccipital bones
• relatively shorter compared to wild-type controls
• lack the opening normally seen in the temporal bone
• decrease in the length of individual bones in the skull vault
• rather than regressing as in wild-type mice, diastema tooth buds survive
• thinning is especially evident in suture forming areas
• an ectopic tooth is found rostrally of the first molar in the mandibular diastema region or the first molar is expanded with a rostral ectopic cusp
• on the anterior end of M1, the cusps are farther apart resulting in shortening of M1
• however, other molar cups are essentially normal, unlike in other mice with supernumerary teeth
• rather than regressing as in wild-type mice, diastema tooth buds survive
• in the mandible 92% of mice have bilateral diastema teeth, 5% unilateral and 3% no diastema teeth (J:119280)
• less than 5% of mice have supernumerary teeth in the maxilla (J:119280)
• rudimentary tooth bud is present at E14.5 in the diastemal area in the mandible (J:315670)
• mandibular and maxillary molars do not properly occlude
• abnormally shaped mandibular notches
• mandibles tend to have longer toothrow, longer and backward shifted processus coronoideus, slightly shorter incisors, and shortened angular process compared to wild-type controls
• abnormally shaped
• irregular articular cartilage surfaces throughout the condyle
• vomeronasal bones display posterior curvature that prevents formation of the vomeromaxillary suture within the palatine process of the maxilla
• relatively shorter nasal bone compared to wild-type controls
• in the tibia the growth plate is extended compared to wild-type controls
• reduced in size
• bone thickness is reduced in all areas along the vertebral column
• reduced size is especially noticeable in the vertebral processes and most pronounced in the processus spinosus
• the transverse process of the atlas/axis is not fully formed and the transverse foramen is not closed at the caudal aspect in some cases
• reduced in size
• bone thickness is reduced in all areas of the vertebral column
• spinal stenosis
• density of craniofacial bones is reduced as early as E18.5
• axoneme elongation is seen in primary cilia of postnatal but not prenatal tibial and mandibular condyle chondrocytes

growth/size/body
• an ectopic tooth is found rostrally of the first molar in the mandibular diastema region or the first molar is expanded with a rostral ectopic cusp
• on the anterior end of M1, the cusps are farther apart resulting in shortening of M1
• however, other molar cups are essentially normal, unlike in other mice with supernumerary teeth
• rather than regressing as in wild-type mice, diastema tooth buds survive
• in the mandible 92% of mice have bilateral diastema teeth, 5% unilateral and 3% no diastema teeth (J:119280)
• less than 5% of mice have supernumerary teeth in the maxilla (J:119280)
• rudimentary tooth bud is present at E14.5 in the diastemal area in the mandible (J:315670)
• mandibular and maxillary molars do not properly occlude
• vomeronasal bones display posterior curvature that prevents formation of the vomeromaxillary suture within the palatine process of the maxilla
• relatively shorter nasal bone compared to wild-type controls
• complete and incomplete cleft palates are seen

respiratory system
• relatively shorter nasal bone compared to wild-type controls

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
ciliopathy DOID:0060340 J:315670




Genotype
MGI:3581224
hm2
Allelic
Composition
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * Black Swiss * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• almost half of the homozygous null mice died by weaning

hearing/vestibular/ear
• multiple regions with more supporting Claudius' cells at P0-P5
• extra outer hair cells found in patches alternating with regions containing the normal three rows at P0-P5
• extra Deiters' supporting cell underlying the extra outer hair cell at P0-P5
• had an ectopic third pillar cell at P5-P10 but not at P0-P5, resulting in the formation of an aberrant, second tunnel of Corti-like space between it and the normal outer pillar cell
• absence of a wave in response in ABR test
• auditory brainstem response (ABR) tests showed that homozygous null mice have intermediate to severe hearing loss at P21 (and at 7, 10, or 19 weeks of age), with click-evoked ABR thresholds averaging 76 decibles sound pressure level (dB SPL) compared to 11 dB SPL in controls

growth/size/body

digestive/alimentary system
• abnormalities in gastrointestinal tract function

nervous system
• extra outer hair cells found in patches alternating with regions containing the normal three rows at P0-P5




Genotype
MGI:5467304
cn3
Allelic
Composition
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry1tm1.1Jdli mutation (0 available); any Spry1 mutation (15 available)
Spry1tm1Jdli mutation (1 available); any Spry1 mutation (15 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
Spry2tm1Mrt mutation (1 available); any Spry2 mutation (24 available)
Tg(Osr1-cre)4Mrt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• at 8 months of age, multiple small focal areas of ductal hyperplasia with increased epithelial cell number and stratification without dysplastic features are seen in the prostate
• by 14 months of age, ductal hyperplasia is seen in all mutant prostates and ducts occasionally show multilayered epithelium with atypical cells and nuclear pleomorphism typical of low-grade PIN

reproductive system
• at 8 months of age, multiple small focal areas of ductal hyperplasia with increased epithelial cell number and stratification without dysplastic features are seen in the prostate
• by 14 months of age, ductal hyperplasia is seen in all mutant prostates and ducts occasionally show multilayered epithelium with atypical cells and nuclear pleomorphism typical of low-grade PIN

neoplasm
• by 14 months of age, ductal hyperplasia is seen in all mutant prostates and ducts occasionally show multilayered epithelium with atypical cells and nuclear pleomorphism typical of low-grade PIN




Genotype
MGI:5467305
cn4
Allelic
Composition
Ptentm2.1Ppp/Pten+
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (81 available)
Spry1tm1.1Jdli mutation (0 available); any Spry1 mutation (15 available)
Spry1tm1Jdli mutation (1 available); any Spry1 mutation (15 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
Spry2tm1Mrt mutation (1 available); any Spry2 mutation (24 available)
Tg(Osr1-cre)4Mrt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN

reproductive system
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN

endocrine/exocrine glands
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN




Genotype
MGI:3716399
cn5
Allelic
Composition
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (76 available)
Meox2tm1(cre)Sor mutation (3 available); any Meox2 mutation (18 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lungs at E12.5 show increased branching compared to Kras; Meox2-cre, Spry2-wild-type lungs; bronchi number is increased, but is still less than age-matched wild-type




Genotype
MGI:3759579
cx6
Allelic
Composition
Ednrbs-36Pub/Ednrb+
Spry2tm1.1Mrt/Spry2+
Genetic
Background
involves: 101/Rl * 129P2/OlaHsd * C3H/Rl * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednrbs-36Pub mutation (0 available); any Ednrb mutation (103 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• rugae morphology is disorganized and fragmented in cleft palate, whereas wild-type palates exhibit orderly array of 7-9 rugae
• compound mutants display 35% incidence of cleft secondary palate

digestive/alimentary system
• rugae morphology is disorganized and fragmented in cleft palate, whereas wild-type palates exhibit orderly array of 7-9 rugae
• compound mutants display 35% incidence of cleft secondary palate

growth/size/body
• rugae morphology is disorganized and fragmented in cleft palate, whereas wild-type palates exhibit orderly array of 7-9 rugae
• compound mutants display 35% incidence of cleft secondary palate




Genotype
MGI:7309963
cx7
Allelic
Composition
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Spry4tm1.2Mrt/Spry4+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
Spry4tm1.2Mrt mutation (1 available); any Spry4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• display ciliopathy-like limb phenotypes
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate

limbs/digits/tail
• defects in autopodium patterning
• display variable forms and combinations of forelimb abnormalities, including polydactyly, brachydactyly, and syndactyly

neoplasm
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
ciliopathy DOID:0060340 J:315670




Genotype
MGI:6209558
cx8
Allelic
Composition
Spry2tm1.1Mrt/Spry2+
Spry4tm1.2Mrt/Spry4tm1.2Mrt
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
Spry4tm1.2Mrt mutation (1 available); any Spry4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• display ciliopathy-like limb long bone phenotypes
• at E18.5
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate
• axoneme elongation is seen in primary cilia of prenatal tibial chondrocytes

limbs/digits/tail
• defects in autopodium patterning
• display variable forms and combinations of forelimb abnormalities, including polydactyly, brachydactyly, and syndactyly
• at E18.5

cellular
• axoneme elongation is seen in prenatal tibial chondrocytes

neoplasm
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate
• located in ossified central areas of ribs and in the distal zone of long limb bones adjacent to disarranged growth plate

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
ciliopathy DOID:0060340 J:315670




Genotype
MGI:3702559
cx9
Allelic
Composition
Fgfr1tm1.1Jpa/Fgfr1+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1.1Jpa mutation (0 available); any Fgfr1 mutation (221 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• frequency of diastema tooth formation is reduced to 60% compared to almost 100% in mice homozygous for the Spry2 allele alone

growth/size/body
• frequency of diastema tooth formation is reduced to 60% compared to almost 100% in mice homozygous for the Spry2 allele alone

skeleton
• frequency of diastema tooth formation is reduced to 60% compared to almost 100% in mice homozygous for the Spry2 allele alone




Genotype
MGI:3702560
cx10
Allelic
Composition
Fgfr2tm1.1Dor/Fgfr2+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr2tm1.1Dor mutation (0 available); any Fgfr2 mutation (87 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
N
• unlike in mice homozygous for the Spry2 allele alone, no diastema tooth formation is seen





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