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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Pdx1tm1Cvw
targeted mutation 1, Christopher VE Wright
MGI:2181360
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Pdx1tm1Cvw/Pdx1tm1Cvw involves: 129S1/Sv * 129X1/SvJ * Black Swiss MGI:3583984
ht2
Pdx1tm1Cvw/Pdx1+ involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:4837260
ht3
Pdx1tm1Cvw/Pdx1tm1.1Stof involves: 129/Sv * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:4359484
cn4
Pdx1tm1Cvw/Pdx1tm4Cvw
Tg(Ins2-cre)25Mgn/0
involves: 129S1/Sv * 129X1/SvJ * Black Swiss * C57BL/6 * DBA MGI:3774583
cn5
Nkx6-1tm1.1Msan/Nkx6-1+
Pdx1tm1Cvw/Pdx1+
Tg(Neurog3-cre)C1Able/0
involves: 129/Sv * C57BL/6 * SJL MGI:5501187
cx6
Pdx1tm1Cvw/Pdx1+
SpopGt(BGB118)Byg/Spop+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:4837259
cx7
Pdx1tm1Cvw/Pdx1+
Pbx1tm1Mlc/Pbx1+
involves: 129S6/SvEvTac * C57BL/6 MGI:3052685


Genotype
MGI:3583984
hm1
Allelic
Composition
Pdx1tm1Cvw/Pdx1tm1Cvw
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygotes can survive until at least 6.5 days post-partum (P6.5), but are not maintained longer for ethical reasons

digestive/alimentary system
• homozygotes show impaired posterior foregut development
• homozygotes show a blockage in differentiation of acinar cells
• homozygotes exhibit normal initial generation and outgrowth of dorsal and ventral pancreatic ducts
• however, at 11.5 dpc, homozygotes lack the discrete outgrowth derived from the ventral pancreatic duct
• also at 11.5 dpc, the dorsal pancreatic outgrowth is replaced by an extra short ductular structure which persists into perinatal stages and undergoes limited proliferation and outgrowth as well as abnormal branching
• this ductular tree lacks insulin and amylase-positive cells and contains glucagons-expressing cells instead
• at P1, mutant small intestines contain no milky gut contents and appear empty
• at 18.5 dpc and P1, homozygotes exhibit a malformed stomach/duodenum junction relative to wild-type mice
• in most mutants, the rostral-most duodenum forms an undulated cavity lacking villi, and mature Brunner's glands, with a smooth cuboidal (rather than columnar) epithelium lining that is continuous with the common bile duct and dorsal pancreatic ductule
• a few mutants lack this undulated cavity but still contain abnormal smooth cuboidal epithelium
• 5 of 6 homozygotes show altered gut lumen architecture with a spiraled (rather than fairly straight) tube and several tight lumen constrictions
• just distal to the malformed rostral duodenum, homozygotes contain apparently normal villi, enterocytes and most enteroendocrine cell types; however, the numbers of enteroendocrine cells are markedly reduced in mutant villi
• homozygotes exhibit a "duodenal" gut tube of wild-type length; no extensive cell death is detected at any stage of development
• at P6.5, many homozygotes display a stomach/duodenal obstruction, as shown by stomach distension and failure of gastric emptying
• at 18.5 dpc and P1, the mutant pyloric sphincter appears twisted despite normal smooth muscle bands

endocrine/exocrine glands
• homozygotes show a blockage in differentiation of acinar cells
• homozygotes exhibit normal initial generation and outgrowth of dorsal and ventral pancreatic ducts
• however, at 11.5 dpc, homozygotes lack the discrete outgrowth derived from the ventral pancreatic duct
• also at 11.5 dpc, the dorsal pancreatic outgrowth is replaced by an extra short ductular structure which persists into perinatal stages and undergoes limited proliferation and outgrowth as well as abnormal branching
• this ductular tree lacks insulin and amylase-positive cells and contains glucagons-expressing cells instead
• at 11.5 dpc, the common bile duct is severely reduced in size
• homozygotes show a blockage in differentiation of islets
• homozygotes show a blockage in differentiation of mature beta-cells
• at 18.5 dpc, homozygotes display complete lack of pancreatic tissues
• in contrast, the liver, gall bladder, spleen, stomach, common bile duct, and other viscera are present and normal

growth/size/body
• although P6.5 homozygotes contain milk in their stomachs, they weigh ~60% less than wild-type littermates
• homozygotes appear normal immediately after birth but show signs of growth retardation as early as P1

homeostasis/metabolism
• homozygotes show signs of dehydration as early as P1
• by P6.5, homozygotes are severely dehydrated

liver/biliary system
• at 11.5 dpc, the common bile duct is severely reduced in size
• at 11.5 dpc, the mutant liver primordium is juxtaposed to the duodenum

integument
• at P6.5, homozygotes have very little fur relative to wild-type mice
• at P6.5, homozygotes have a thin and cracking skin

muscle
• at 18.5 dpc and P1, the mutant pyloric sphincter appears twisted despite normal smooth muscle bands

cellular
• homozygotes show a blockage in differentiation of mature beta-cells




Genotype
MGI:4837260
ht2
Allelic
Composition
Pdx1tm1Cvw/Pdx1+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• beta cell size is normal
• mice exhibit an increase in the number of small islets with a decrease in medium and large sized islets compared with wild-type mice
• beta cells exhibit increased endoplasmic reticulum stress that results in apoptosis unlike in wild-type mice
• beta cell replication and apoptosis are increased compared to in wild-type mice
• mice exhibit beta cell apoptosis unlike in wild-type mice
• in response to glucose in mice and isolated cells

homeostasis/metabolism
• in response to glucose in mice and isolated cells

cellular
• mice exhibit beta cell apoptosis unlike in wild-type mice




Genotype
MGI:4359484
ht3
Allelic
Composition
Pdx1tm1Cvw/Pdx1tm1.1Stof
Genetic
Background
involves: 129/Sv * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdx1tm1.1Stof mutation (0 available); any Pdx1 mutation (15 available)
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• small compared to in wild-type mice but not as small as in Pdx1tm1Cvw homozygotes
• decreased weight compared to in wild-type mice but not as much as in Pdx1tm1Cvw homozygotes

homeostasis/metabolism
• at birth




Genotype
MGI:3774583
cn4
Allelic
Composition
Pdx1tm1Cvw/Pdx1tm4Cvw
Tg(Ins2-cre)25Mgn/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * Black Swiss * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
Pdx1tm4Cvw mutation (1 available); any Pdx1 mutation (15 available)
Tg(Ins2-cre)25Mgn mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• proliferation of Pdx1- cells is decreased compared to in wild-type pancreas
• beginning at E18.5, the number of glucagon+ cells is increased
• by one month of age mice are overtly diabetic with increased numbers of glucagon+ cells
• proliferation of glucagon+ cells is increased
• the number of insulin+ cells decreases as the number of glucagon+ cells increases
• the proliferation of insulin+ cells is decreased
• by one month of age mice are overtly diabetic with decreased insulin immunoreactivity in remaining insulin+ cells
• by one month of age mice are overtly diabetic with increased numbers of somatostatin+ cells
• glucagon+ and somatostatin+ cells are scattered throughout the islet instead of localized to the periphery as in wild-type mice

homeostasis/metabolism
• insulin levels following administration of glucose are lower in males and females compared to wild-type mice
• unlike male mice, females exhibit only mild glucose intolerance compared to wild-type females

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:130389




Genotype
MGI:5501187
cn5
Allelic
Composition
Nkx6-1tm1.1Msan/Nkx6-1+
Pdx1tm1Cvw/Pdx1+
Tg(Neurog3-cre)C1Able/0
Genetic
Background
involves: 129/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx6-1tm1.1Msan mutation (1 available); any Nkx6-1 mutation (2 available)
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
Tg(Neurog3-cre)C1Able mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice exhibit an increase in the glucagon to insulin cell ratio as in Pdx1tm1Cvw heterozygotes
• as in Pdx1tm1Cvw heterozygotes
• as in Pdx1tm1Cvw heterozygotes




Genotype
MGI:4837259
cx6
Allelic
Composition
Pdx1tm1Cvw/Pdx1+
SpopGt(BGB118)Byg/Spop+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
SpopGt(BGB118)Byg mutation (0 available); any Spop mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• beta cell mass and the distribution of islet size are normalized unlike in either single heterozygote
• mice do not exhibit beta cell apoptosis unlike either single heterozygote
• beta cell size is decreased compared to in wild-type mice or either single heterozygote
• endoplasmic reticulum stress is reduced compared to in Pdx1tm1Cvw heterozygote
• beta cell replication is increased compared to in wild-type mice
• glucose-stimulated insulin secretion is reduced compared to in wild-type mice but not as severely as in Pdx1tm1Cvw heterozygote

homeostasis/metabolism
• glucose-stimulated insulin secretion is reduced compared to in wild-type mice but not as severely as in Pdx1tm1Cvw heterozygote
• compared with Pdx1tm1Cvw heterozygote




Genotype
MGI:3052685
cx7
Allelic
Composition
Pdx1tm1Cvw/Pdx1+
Pbx1tm1Mlc/Pbx1+
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pbx1tm1Mlc mutation (0 available); any Pbx1 mutation (24 available)
Pdx1tm1Cvw mutation (1 available); any Pdx1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• disrupted architecture, inappropriate cell types interspersed with beta cells

growth/size/body
• 9-10 weeks

homeostasis/metabolism
• onset between 9-10 weeks, progresses to overt diabetes

renal/urinary system

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Noninsulin-Dependent; NIDDM 125853 J:75811





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last database update
08/17/2016
MGI 6.05
The Jackson Laboratory