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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Stk11tm1Tpm
targeted mutation 1, Tomi P Makela
MGI:2387003
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Stk11tm1Tpm/Stk11tm1Tpm Not Specified MGI:3790876
ht2
Stk11tm1Tpm/Stk11+ involves: 129S7/SvEvBrd * C57BL/6 * CD-1 MGI:3790955
ht3
Stk11tm1Tpm/Stk11+ Not Specified MGI:3790954
cx4
Ptgs2tm1Jed/Ptgs2tm1Jed
Stk11tm1Tpm/Stk11+
involves: 129S7/SvEvBrd * C57BL/6 * CD-1 MGI:3790956
cx5
Ptgs2tm1Jed/Ptgs2+
Stk11tm1Tpm/Stk11+
involves: 129S7/SvEvBrd * C57BL/6 * CD-1 MGI:3790958


Genotype
MGI:3790876
hm1
Allelic
Composition
Stk11tm1Tpm/Stk11tm1Tpm
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no viable embryos are observed past E11.0

embryo
• rudimentary vessels are seen between the parietal and visceral leaves of yolk sac; vessels are congested with nucleated embryonic blood cells
• vitelline artery is completely atretic
• large vessels and extensive capillary network fail to develop in mutant yolk sac
• absent in some embryos after E8.25
• hypoplastic in some embryos after E8.25
• after E8.25, failure of embryo turning is observed
• cephalic mesenchyme of E9.5 head folds has lower cell density and fewer capillaries than controls; cell density is result of increased cell death assayed by TUNEL staining and this apoptosis phenotype is limited to the E9.5 embryos
• at E9.5 folds often display large cystic degenerations near dorsal aorta with some containing embryonic blood cells
• defect in neural tube closure is observed after E8.25
• misaligned and contorted along anterior/posterior axis of embryo at E9.25
• somitogenesis is defective resulting in dimorphic protrusive somites at E9.5
• at E9.5, placentas are hemorrhagic and edematous
• blood lacunae have ruptured causing massive hemorrhaging by E10.5
• invasion of placenta by embryonic blood vessels does not occur; at E9.5 lack of fetal blood vessels in rudimentary labyrinth layer is shown by absence of VEGF signal
• less organized than in wild-type and contains larger number of abnormal (flt-1 negative) giant cells
• diameter of placenta is smaller at E9.5
• fusion is delayed in mutant conceptuses compared to controls, but occurs by E9.5

cardiovascular system
• at E8.5, vessel is thin and discontinuous especially in the anterior part
• at E9.5 lumen remains thin with intersomitic branches ending prematurely in the mesenchyme
• blood lacunae have ruptured causing massive hemorrhaging by E10.5
• invasion of placenta by embryonic blood vessels does not occur; at E9.5 lack of fetal blood vessels in rudimentary labyrinth layer is shown by absence of VEGF signal
• rudimentary vessels are seen between the parietal and visceral leaves of yolk sac; vessels are congested with nucleated embryonic blood cells
• vitelline artery is completely atretic
• large vessels and extensive capillary network fail to develop in mutant yolk sac
• complete absence of vascular smooth muscle cell (VSMC) staining is observed in mutant dorsal aorta and somites at E9.5
• strong ectopic VSMC signal is observed in head folds

craniofacial
• absent in some embryos after E8.25
• hypoplastic in some embryos after E8.25

muscle
• complete absence of vascular smooth muscle cell (VSMC) staining is observed in mutant dorsal aorta and somites at E9.5
• strong ectopic VSMC signal is observed in head folds

nervous system
• defect in neural tube closure is observed after E8.25

growth/size/body
• cephalic mesenchyme of E9.5 head folds has lower cell density and fewer capillaries than controls; cell density is result of increased cell death assayed by TUNEL staining and this apoptosis phenotype is limited to the E9.5 embryos




Genotype
MGI:3790955
ht2
Allelic
Composition
Stk11tm1Tpm/Stk11+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• polyposis detected at 4-5 months
• treatment with celecoxib (Ptgs2 inhibitor) between 3.5 and 10 months reduces number of large polyps observed; similar results are obtained when treatment is performed at 6.5-10 months in mice on 129S7/SvEvBrd * CD-1 background
• microvessel density is reduced in polyps with celecoxib treatment
• polyposis detected at 4-5 months
• treatment with celecoxib (Ptgs2 inhibitor) between 3.5 and 10 months reduces number of large polyps observed; similar results are obtained when treatment is performed at 6.5-10 months in mice on 129S7/SvEvBrd * CD-1 background
• microvessel density is reduced in polyps with celecoxib treatment

neoplasm
• 86% decrease in tumor burden is seen at 10 months in mice treated with celecoxib between 3.5 and 10 months compared to untreated controls

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Peutz-Jeghers syndrome DOID:3852 OMIM:175200
J:93361




Genotype
MGI:3790954
ht3
Allelic
Composition
Stk11tm1Tpm/Stk11+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• seen in one animal; incidence similar to age-matched controls

liver/biliary system
• seen in one animal; incidence similar to age-matched controls
• small number of tumors and neoplasias are observed in various organs including multiple liver adenomas in mice 6-20 months of age; incidence similar to age-matched controls

mortality/aging
• 80% die by 16 months of age

growth/size/body
• noted as mice age

digestive/alimentary system
• grossly distended by large polyps
• all mice >6 months of age have macroscopic gastrointestinal polyps; majority are found in glandular stomach with equal distribution in fundus, antrum, and pylorus
• in most animals, 1-3 large polyps (20-30 mm in diameter) originate in pylorus and protrude into duodenum
• all polyps have extensive well-developed smooth muscle component originating from central stalk contiguous with muscularis mucosa
• results from protrusion of large polyps into lumen

neoplasm
• seen in one animal; incidence similar to age-matched controls
• small number of tumors and neoplasias are observed in various organs including multiple liver adenomas in mice 6-20 months of age; incidence similar to age-matched controls
• seen in one animal; incidence similar to age-matched controls
• seen in one animal; incidence similar to age-matched controls

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Peutz-Jeghers syndrome DOID:3852 OMIM:175200
J:79074




Genotype
MGI:3790956
cx4
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Stk11tm1Tpm/Stk11+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (44 available)
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months

neoplasm
• 53-54% decrease in tumor burden is seen at 10 months in mice treated with celecoxib between 3.5 and 10 months compared to untreated controls




Genotype
MGI:3790958
cx5
Allelic
Composition
Ptgs2tm1Jed/Ptgs2+
Stk11tm1Tpm/Stk11+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (44 available)
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months





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last database update
05/15/2018
MGI 6.12
The Jackson Laboratory