Phenotypes associated with this allele

• Allele Symbol: Bmal1^tm2Bra
• Allele Name: targeted mutation 1, Chris Bradfield
• Allele ID: MGI:4819968
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Bmal1^tm2Bra/Bmal1^tm2Bra Tg(Pdx1-cre)89.1Dam/0	involves: 129 * C57BL/6 * C57BL/6J * CBA * ICR	MGI:5576883
cn2	Bmal1^tm2Bra/Bmal1^tm2Bra Tg(Tek-cre)12Flv/0	involves: C3H * C57BL/6 * C57BL/6J	MGI:4822129

Genotype
MGI:5576883

cn1

• Allelic Composition: Bmal1^tm2Bra/Bmal1^tm2Bra; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129 * C57BL/6 * C57BL/6J * CBA * ICR

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

homeostasis/metabolism

decreased insulin secretion ( J:162641 )

• 2-4 month old mice show decreased insulin secretion

• islets show diminished insulin responsiveness to glucose, KCL, exendin 4, forskolin and 8-bromo-cAMP, indicating a block in exocytosis

hyperglycemia ( J:162641 )

• 2-4 month old mice show increased ad libitum glucose levels throughout the day

impaired glucose tolerance ( J:162641 )

• 2-4 month old mice show impaired glucose tolerance

endocrine/exocrine glands

abnormal pancreatic beta cell physiology ( J:162641 )

• beta-cell function is defective at the very latest stage of stimulus-secretion coupling

decreased insulin secretion ( J:162641 )

• 2-4 month old mice show decreased insulin secretion

• islets show diminished insulin responsiveness to glucose, KCL, exendin 4, forskolin and 8-bromo-cAMP, indicating a block in exocytosis

behavior/neurological

behavior/neurological phenotype ( J:162641 )

N • mice show normal circadian activity, feeding rhythms and body weight

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
diabetes mellitus		DOID:9351		J:162641

Genotype
MGI:4822129

cn2

• Allelic Composition: Bmal1^tm2Bra/Bmal1^tm2Bra; Tg(Tek-cre)12Flv/0
• Genetic Background: involves: C3H * C57BL/6 * C57BL/6J

behavior/neurological

decreased locomotor activity ( J:155089 )

• in the rest and active phases

cardiovascular system

increased heart rate ( J:155089 )

• in the rest and active phases

decreased mean systemic arterial blood pressure ( J:155089 )

• within the active phase

homeostasis/metabolism

abnormal protein level ( J:155089 )

• mice fail to exhibit circadian alterations in total plasma tissue plasminogen activator (tPA) levels unlike similarly treated wild-type mice

• however, circadian alteration in plasminogen activator inhibitor-1 (PAI-1) levels is normal

abnormal response to injury ( J:155089 )

• time to thrombotic vascular occlusion (TTVO) subsequent to photochemical injury is decreased at zeitgeber time (ZT) 14 unlike in similarly treated wild-type mice