About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Prdm16tm1.1Brsp
targeted mutation 1.1, Bruce M Spiegelman
MGI:5564782
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp B6.129-Prdm16tm1.1Brsp MGI:5564787
cn2
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
B6.Cg-Prdm16tm1.1Brsp A1cfTg(Myh6-cre/Esr1*)1Jmk MGI:7314699
cn3
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(Tnnt2-cre)5Blh/0
involves: 129 * C57BL/6 * C57BL/6J * DBA/2 MGI:7314697
cn4
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(myl7.L-cre)1118Tmhn/0
involves: 129 * C57BL/6J * MF1 MGI:7314277
cn5
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Myf5tm1(cre)Mrc/Myf5+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:6107172
cn6
Mecomtm1Miku/Mecomtm1Miku
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Myf5tm1(cre)Mrc/Myf5+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JCrlj MGI:6107171
cn7
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(Adipoq-cre)1Evdr/0
involves: 129/Sv * C57BL/6 * FVB/N MGI:5564786


Genotype
MGI:5564787
hm1
Allelic
Composition
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Genetic
Background
B6.129-Prdm16tm1.1Brsp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and fertile




Genotype
MGI:7314699
cn2
Allelic
Composition
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Genetic
Background
B6.Cg-Prdm16tm1.1Brsp A1cfTg(Myh6-cre/Esr1*)1Jmk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice do not show overt cardiac phenotypes, even 36 weeks after induction




Genotype
MGI:7314697
cn3
Allelic
Composition
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(Tnnt2-cre)5Blh/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
Tg(Tnnt2-cre)5Blh mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system

mortality/aging
• postnatal lethality before P7




Genotype
MGI:7314277
cn4
Allelic
Composition
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(myl7.L-cre)1118Tmhn/0
Genetic
Background
involves: 129 * C57BL/6J * MF1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
Tg(myl7.L-cre)1118Tmhn mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice exhibit progressive cardiac dysfunction leading to death before P7

cardiovascular system
• thinner left ventricle compact myocardium starting from E15.5
• however, thickness of right ventricle compact myocardium is normal
• mice develop biventricular noncompaction
• mice exhibit clefts at the apices of the hearts as early as E15.5
• thinner interventricular septum starting from E15.5
• however, thickness of right ventricle compact myocardium is not different
• enlarged left ventricle is seen as early as E15.5
• mice exhibit progressive cardiac dysfunction
• severe cardiac contractile dysfunction in P0 to P3 neonates
• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen
• echocardiography shows severe cardiac contractile dysfunction in P0 to P3 neonates, increased left ventricle chamber size, and thinned interventricular septum
• left ventricular noncompaction cardiomyopathy

muscle
• thinner left ventricle compact myocardium starting from E15.5
• however, thickness of right ventricle compact myocardium is normal
• severe cardiac contractile dysfunction in P0 to P3 neonates
• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen
• left ventricular noncompaction cardiomyopathy

cellular
• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
left ventricular noncompaction DOID:0060480 OMIM:604169
J:326525




Genotype
MGI:6107172
cn5
Allelic
Composition
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Myf5tm1(cre)Mrc/Myf5+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myf5tm1(cre)Mrc mutation (1 available); any Myf5 mutation (17 available)
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• pale axillary and cervical brown adipose tissue depots
• however, tissue mass is not altered
• in the interscapular brown adipose tissue of mice older than 6 months
• in the interscapular brown adipose tissue of mice older than 6 months
• whitening in mice older than 6 months with increased size of the tissue, a switch from multilocular to unilocular morphology, and increased lipid content
• in unstimulated interscapular brown adipose tissue
• whitening in mice older than 6 months with increased size of the tissue, a switch from multilocular to unilocular morphology, and increased lipid content
• 3 week old mice fed a high-fat diet exhibit loss of normal brown adipocyte morphology unlike wild-type mice
• in mice older than 6 months
• however, juvenile mice exhibit normal sized brown adipose tissue depots
• precipitous drop in body temperature following exposure to cold
• however, diet-induced thermogenesis is normal

homeostasis/metabolism
• precipitous drop in body temperature following exposure to cold

growth/size/body
• at all ages

cellular
• in unstimulated interscapular brown adipose tissue
• with poorly organized cristae in unstimulated interscapular brown adipose tissue
• reduced basal in interscapular brown adipose tissue




Genotype
MGI:6107171
cn6
Allelic
Composition
Mecomtm1Miku/Mecomtm1Miku
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Myf5tm1(cre)Mrc/Myf5+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mecomtm1Miku mutation (0 available); any Mecom mutation (81 available)
Myf5tm1(cre)Mrc mutation (1 available); any Myf5 mutation (17 available)
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• in the interscapular brown adipose tissue of mice older than 6 months
• pale in 3 month old mice




Genotype
MGI:5564786
cn7
Allelic
Composition
Prdm16tm1.1Brsp/Prdm16tm1.1Brsp
Tg(Adipoq-cre)1Evdr/0
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdm16tm1.1Brsp mutation (1 available); any Prdm16 mutation (72 available)
Tg(Adipoq-cre)1Evdr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• subcutaneous adipose tissue contains larger adipocytes and fewer smaller multiocular UCP1+ adipocytes relative to control mice following cold exposure
• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of crown like structures, however, there are no changes in visceral (abdominal) fat
• subcutaneous adipose tisse from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages
• subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged
• body composition analysis after 16 weeks on high fat diet indicates increased fat mass with no change in lean body mass
• subcutaneous fat mass is doubled as compared to controls after 16 weeks on high fat diet; epididymal and BAT masses are unchanged
• subcutaneous adipocytes from male mice after 18 weeks on high fat diet exhibit a 33% increase in mean adipocyte area
• O2 consumption is reduced in subcutaneous adipose pads, but not in brown adipose pads, at baseline (36% reduced) and following stimulation with a beta-adrenergic agonist (49% reduced)
• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls
• subcutaneous adipocytes exhibit a blunted response to stimuli such as isoproterenol that induce a thermogenic gene program (beige adipocytes)

growth/size/body
• mice exhibit increased weight gain after 16 weeks on high-fat, high-carbohydrate diet relative to control mice

hematopoietic system
• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged

homeostasis/metabolism
• increased fasting plasma insulin levels (55%) in mice after 6 weeks on high fat diet
• unlike controls, mutant mice do not exhibit increased O2 consumption following stimulation with a beta-adrenergic agonist
• mice exhibit an increased respiratory exchange ratio (RER), but no increase in O2 consumption
• a reduced glucose infusion rate (64% of controls) is observed in mice after 6 weeks on high fat diet
• decreased whole body glucose uptake is observed in mice after 6 weeks on high fat diet
• clamped insulin levels do not increase as much as controls in mice after 6 weeks on high fat diet
• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls

immune system
• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged

integument
• subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged

liver/biliary system
• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls
• after 6 weeks on high fat diet

cellular
• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/23/2024
MGI 6.23
The Jackson Laboratory