Phenotypes associated with this allele

• Allele Symbol: Ager^tm1.1Hyam
• Allele Name: targeted mutation 1.1, Hiroshi Yamamoto
• Allele ID: MGI:3692766
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ager^tm1.1Hyam/Ager^tm1.1Hyam	involves: 129P2/OlaHsd * C57BL/6J * CD-1	MGI:3706575
hm2	Ager^tm1.1Hyam/Ager^tm1.1Hyam	involves: 129P2/OlaHsd * CD-1	MGI:3706372
cx3	Ager^tm1.1Hyam/Ager^+ Tg(Ins2-Nos2)40Okam/0	involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA/2	MGI:3706543
cx4	Ager^tm1.1Hyam/Ager^tm1.1Hyam Tg(Ins2-Nos2)40Okam/0	involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA/2	MGI:3706544

Genotype
MGI:3706575

hm1

• Allelic Composition: Ager^tm1.1Hyam/Ager^tm1.1Hyam
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * CD-1

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

growth/size/body

decreased body weight ( J:116507 )

• after induction of diabetes with streptozotocin (STZ) injection, mice show decreased body weight compared to non-diabetic mutants

homeostasis/metabolism

abnormal blood homeostasis ( J:116507 )

• levels of circulating AGE (advanced glycation end products) are higher in diabetic mice than controls, regardless of Ager status

increased circulating glucose level ( J:116507 )

• after induction of diabetes with streptozotocin injection, mice have higher blood glucose levels than untreated controls

cardiovascular system

abnormal angiogenesis ( J:116507 )

• angiogenic response in an in vivo assay using implanted matrigel is similar in STZ-treated Ager-null mice and nondiabetic controls, whereas total cell number and smooth muscle cell number are significantly decreased in STZ-treated wild-type compared to untreated mice

cellular

decreased apoptosis ( J:116507 )

• number of apoptotic cells is decreased in STZ-treated and untreated Ager-null mice compared to STZ-treated wild-type controls

abnormal cell proliferation ( J:116507 )

• in STZ-treated mutants, cell proliferation is similar to untreated mutants or wild-type, whereas a significant decrease is observed in STZ-treated wild-type mice

Genotype
MGI:3706372

hm2

• Allelic Composition: Ager^tm1.1Hyam/Ager^tm1.1Hyam
• Genetic Background: involves: 129P2/OlaHsd * CD-1

normal phenotype

no abnormal phenotype detected ( J:116040 )

• mice grow normally with no gross or microscopic phenotypic abnormalities

Genotype
MGI:3706543

cx3

• Allelic Composition: Ager^tm1.1Hyam/Ager⁺; Tg(Ins2-Nos2)40Okam/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA/2

homeostasis/metabolism

hyperglycemia ( J:116040 )

• mice show sustained hyperglycemia (and display diabetes)

renal/urinary system

abnormal renal glomerulus morphology ( J:116040 )

• glomerular cell number is decreased compared to Ager-sufficient transgenic controls at 4 and 8 months

glomerulosclerosis ( J:116040 )

• progression of sclerosis is intermediate to Ager-sufficient or Ager-null transgenic mice

Genotype
MGI:3706544

cx4

• Allelic Composition: Ager^tm1.1Hyam/Ager^tm1.1Hyam; Tg(Ins2-Nos2)40Okam/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA/2

homeostasis/metabolism

decreased circulating creatinine level ( J:116040 )

• serum creatinine is much lower than in Ager-sufficient transgenic mice at 8 months

hyperglycemia ( J:116040 )

• mice show sustained hyperglycemia (and display diabetes)

albuminuria ( J:116040 )

• urinary albumin/creatinine ratio is much lower than in wild-type transgenic mice or nontransgenic controls at 4 and 8 months

renal/urinary system

albuminuria ( J:116040 )

• urinary albumin/creatinine ratio is much lower than in wild-type transgenic mice or nontransgenic controls at 4 and 8 months

abnormal renal glomerulus morphology ( J:116040 )

glomerulosclerosis ( J:116040 )

• progression of sclerosis is attenuated in mice compared to Ager-sufficient transgenic mice

abnormal kidney size ( J:116040 )

• kidney weight as percentage of body weight is attenuated with Ager-deficiency; kidney weight as percentage of body weight is lower than in wild-type transgenic mice but percentage is still higher than non-transgenic (non-diabetic) mice at 4 and 8 months

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
type 1 diabetes mellitus		DOID:9744	OMIM:222100	J:116040