Overview

Sirtuin 1 KO mice may be useful for studying the endothelial expression of genes involved in angiogenesis and endothelial homeostasis, and postnatal vascular growth.

Donating Investigator

Leonard P Guarente, Massachusetts Institute of Technology

Genetic overview

Genetic Background	Generation

Sirt1^tm1Mcby

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Sirt1	sirtuin 1

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Research Applications

Developmental Biology Research
Cardiovascular Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

A hygro cassette replaces exons 5-6 of the sirtuin 1 (Sirt1) gene, abolishing gene expression. Heterozygous mice are viable and fertile. Homozygotes are perinatal lethal on inbred backgrounds. The donating investigator reports that F1 crosses of B6 heterozygotes and FVB heterozygotes produces homozygotes at Mendelian ratios. Homozygous F1 offspring are infertile. SIRT1 is a protein deacetylase involved with telomere deacetylation, DNA repair, energy homeostasis. As such SIRT1 plays roles in telomere length maintenance, tumor growth, aging, and improved metabolic syndrome caused by high fat diets. Mice have craniofacial defects, increased apoptosis spermatocytes, and they fail to ovulate. They exhibit micropthalmia, and respiratory, cardiovascular, and immune defects. Some mice develop nephrogenic diabetes insipidus (NDI) characterized by production of large amounts of dilute urine due to the inability of the kidney to concentrate the urine.

Development

A targeting vector was designed to replace exons 5-6 of the sirtuin 1 (Sirt1) gene with a hyrgomycin resistance (hygro) cassette. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl⁺-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into CD1 blastocysts and the resulting chimeric males were bred to 129/Sv females. Mice were then backcrossed at least 10 generations to C57BL/6J background. Upon arrival at The Jackson Laboratory, mice were bred to C57BL/6J (Stock No. 000664) for at least one generation to establish the colony.

Control Suggestions

Wild-type from the colony

Approximate Controls

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

McBurney MW; Yang X; Jardine K; Hixon M; Boekelheide K; Webb JR; Lansdorp PM; Lemieux M. 2003. The mammalian SIR2alpha protein has a role in embryogenesis and gametogenesis. Mol Cell Biol 23(1):38-54PubMed: 12482959 MGI: J:81010

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Genetics

Sirt1^tm1Mcby

Allele Symbol: Sirt1^tm1Mcby

Allele Name	targeted mutation 1, Michael W McBurney
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Sir2-; sir2alpha null; Sirt1 KO; SIRT1^-
Gene Symbol and Name	Sirt1, sirtuin 1
Gene Synonym(s)
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Chromosome	10
Molecular Note	The gene was disrupted by replacement of exons 5 and 6, which encode a large portion of the catalytic domain, with a hygromycin resistance cassette via homologous recombination. Northern blot analysis of RNA from homozygous mutant E12.5 embryos and adult tissues did not detect gene expression.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

nephrogenic diabetes insipidus

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Developmental Biology Research
- Internal/Organ Defects
  - kidney
  - heart: vasculature
  - lung
  - heart
- Embryonic Lethality (Homozygous)
- Eye Defects
Cardiovascular Research
- Vascular Defects
- Heart Abnormalities

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129

cardiovascular system phenotype

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

hematopoietic system phenotype

decreased CD8-positive, alpha-beta T cell number
- there is a decreased number of CD8 T cells in the spleen

homeostasis/metabolism phenotype

pulmonary edema
- frequently observed in mice

immune system phenotype

decreased CD8-positive, alpha-beta T cell number
- there is a decreased number of CD8 T cells in the spleen

interstitial pneumonia
- occurs consistently in mice

lung inflammation
- lungs are infiltrated with neutrophils suggesting chronic pulmonary infection

limbs/digits/tail phenotype

abnormal digit development
- mineralization of digits is delayed relative to their wild-type littermates

mortality/aging

perinatal lethality, incomplete penetrance
- only half the expected number of homozygotes are found one day after birth
- the expected Mendelian ratio is observed in E18.5 embryos indicating the pups die shortly before or after birth

postnatal lethality, complete penetrance
- all mice die within one month of birth

muscle phenotype

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

craniofacial phenotype

short snout
- many mice have a short or deviated snout

respiratory system phenotype

interstitial pneumonia
- occurs consistently in mice

lung inflammation
- lungs are infiltrated with neutrophils suggesting chronic pulmonary infection

pulmonary edema
- frequently observed in mice

vision/eye phenotype

eyelids fail to open
- eyelids remain closed for entire lifespan

microphthalmia
- in some mice the eyes are smaller possibly as result of failure of eyelids to open

digestive/alimentary phenotype

exocrine pancreas atrophy
- the pancreas shows patchy atrophy of the exocrine epithelium

embryo phenotype

decreased embryo size
- embryos are visibly smaller than controls starting at E12.5

endocrine/exocrine gland phenotype

exocrine pancreas atrophy
- the pancreas shows patchy atrophy of the exocrine epithelium

growth/size/body region phenotype

decreased body weight
- mice weigh smaller at birth compared to wild-type littermates and continue to be under weight until their premature death

decreased embryo size
- embryos are visibly smaller than controls starting at E12.5

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

short snout
- many mice have a short or deviated snout

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129S1/Sv * 129X1/SvJ * CD-1

adipose tissue phenotype

abnormal inguinal fat pad morphology
- a calorie restricted diet for 25-28 weeks decreases fat pad weight to a higher degree than in wild-type mice
- inguinal fat pads are 34% smaller at 3-5 months of age and 52% smaller in mice between 1-2 years of age

cellular phenotype

abnormal cellular respiration
- liver but not skeletal mitochondria produce less ATP and have a lower proton motive force under both phosphorylating and non-phosphorylating conditions
- liver mitochondria also produce less reactive oxygen species

abnormal male germ cell apoptosis
- all mice have increased levels of spermatocyte apoptosis

abnormal sperm flagellum morphology
- many of the sperm have flagellas that are fine and lack associated cell bodies

abnormal spermatid morphology
- multi-nucleated germ cells occasionally occur
- retention of highly condensed spermatids occurs in most mice with some spermatids sharing acrosomes and other being larger than normal
- there are decreased number of mature spermatids and increased numbers of retained elongated spermatids in the testis of some mice

asthenozoospermia
- virtually none of the mature sperm cells are motile

globozoospermia
- majority of sperm are abnormal with small, rounded cell bodies
- many sperm retain cytoplasm around their nucleus

oligozoospermia
- there are 20-fold less mature sperm in the seminal fluid compared to wild-type littermates

teratozoospermia
- majority of sperm are abnormal with small, rounded cell bodies and blunted or absent hooks in the tail

craniofacial phenotype

short snout
- many mice have a short or deviated snout

digestive/alimentary phenotype

exocrine pancreas atrophy
- the pancreas shows patchy atrophy of the exocrine epithelium

embryo phenotype

decreased embryo size
- embryos are visibly smaller than controls starting at E12.5

endocrine/exocrine gland phenotype

abnormal seminiferous tubule epithelium morphology
- there is an increase in the number and size of vacuoles within the seminiferous epithelium

absent corpus luteum
- corpora lutea are absent possibly due to failure to ovulate

decreased testis weight
- testis are subnormal in weight

exocrine pancreas atrophy
- the pancreas shows patchy atrophy of the exocrine epithelium

increased insulin secretion
- insulin levels rise 3-fold higher than in wild-type mice in response to refeeding after overnight fast

small ovary
- ovaries are smaller than wild-type littermates

behavior/neurological phenotype

abnormal nursing
- the female mouse able to produce offspring failed to nurse her pups

hypoactivity
- mice 3-6 months of age are 50% less active than controls with the biggest differences occurring during the dark phase
- older mice are about 33% less active than controls

polydipsia

polyphagia
- mice older than a year in age consume 46% more calories when normalized to bodyweight
- mice under a year in age comsume 20% more calories when normalized to body weight

growth/size/body region phenotype

decreased body weight
- mice weigh smaller at birth compared to wild-type littermates and continue to be under weight well into adulthood
- starting at 30 days of age, many mice reach weights that is similar to controls

decreased embryo size
- embryos are visibly smaller than controls starting at E12.5

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

short snout
- many mice have a short or deviated snout

slow postnatal weight gain
- as they get older, weight differences increase to 30% at 5-8 months of age and 40% at 13-20 months of age
- mice are 25% smaller at 2-4 months of age

hematopoietic system phenotype

decreased CD8-positive, alpha-beta T cell number
- there is a decreased number of CD8 T cells in the spleen

increased immunoglobulin level
- sinusoids of the liver show deposits

homeostasis/metabolism phenotype

abnormal glucose tolerance
- serum glucose levels in fasted mice are almost 30% lower than in wild-type mice
- upon refeeding, glucose levels increase to a level comparable to wild-type mice

decreased circulating thyroxine level
- circulating levels of thyroxine are 20% less than in controls

decreased urine osmolality
- several 18-22 month old mice excrete large volumes of urine with low osmolarity

increased insulin secretion
- insulin levels rise 3-fold higher than in wild-type mice in response to refeeding after overnight fast

increased oxygen consumption
- mice have a 20% higher oxygen consumption as measured by percent relative cumulative frequency of VO2 normalized to body weight
- mice increase their oxygen consumption to a higher degree than in wild-type mice when on a calorie-restricted diet for over 25 weeks
- respiratory exchange ratios indicate that mice rely more on oxidation of fatty lipids during the 6-8 hours prior to onset of the dark period
- the largest differences occur during the light period when mice are inactive

increased urine antidiuretic hormone level
- urine vasopressin concentration is increased

pulmonary edema
- frequently observed in mice

immune system phenotype

decreased CD8-positive, alpha-beta T cell number
- there is a decreased number of CD8 T cells in the spleen

glomerulonephritis
- immunoglobulin deposits in the kidney

increased anti-nuclear antigen antibody level
- 73% of mice have anti-nuclear antibodies

increased immunoglobulin level
- sinusoids of the liver show deposits

interstitial pneumonia
- occurs consistently in mice

lung inflammation
- lungs are infiltrated with neutrophils suggesting chronic pulmonary infection

limbs/digits/tail phenotype

abnormal digit development
- mineralization of digits is delayed relative to their wild-type littermates

mortality/aging

perinatal lethality, incomplete penetrance
- only half the expected number of homozygotes are found one day after birth
- the expected Mendelian ratio is observed in E18.5 embryos indicating the pups die shortly before or after birth

muscle phenotype

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

nervous system phenotype

decreased brain weight
- the brain weight is 20% smaller in both younger and older mice

renal/urinary system phenotype

abnormal renal glomerulus morphology
- the glomeruli of 24 month old animals are hypercellular with evidence of reduced vascularity

decreased urine osmolality
- several 18-22 month old mice excrete large volumes of urine with low osmolarity

glomerulonephritis
- immunoglobulin deposits in the kidney

increased urine antidiuretic hormone level
- urine vasopressin concentration is increased

renal glomerular immunoglobulin deposits

reproductive system phenotype

abnormal estrous cycle
- defects in estrous cycle can be overcome by injections with gonadotropin and choriogonadotropin
- female mice are arrested in diestrus and do not ovulate

abnormal male germ cell apoptosis
- all mice have increased levels of spermatocyte apoptosis

abnormal seminiferous tubule epithelium morphology
- there is an increase in the number and size of vacuoles within the seminiferous epithelium

abnormal sperm flagellum morphology
- many of the sperm have flagellas that are fine and lack associated cell bodies

abnormal spermatid morphology
- multi-nucleated germ cells occasionally occur
- retention of highly condensed spermatids occurs in most mice with some spermatids sharing acrosomes and other being larger than normal
- there are decreased number of mature spermatids and increased numbers of retained elongated spermatids in the testis of some mice

abnormal uterus size
- uterus is thin walled

absent corpus luteum
- corpora lutea are absent possibly due to failure to ovulate

absent estrous cycle
- females do not appear to cycle efficiently through estrus

anovulation
- ovaries from female mice are able to form follicles but fail to ovulate
- ovulation will occur after injections with gonadotropin and choriogonadotropin

asthenozoospermia
- virtually none of the mature sperm cells are motile

decreased testis weight
- testis are subnormal in weight

globozoospermia
- majority of sperm are abnormal with small, rounded cell bodies
- many sperm retain cytoplasm around their nucleus

male infertility
- male mice are unable to produce sire with wild-type females

oligozoospermia
- there are 20-fold less mature sperm in the seminal fluid compared to wild-type littermates

reduced female fertility
- only one female out of seven was able to produce offspring with a wild-type male

small ovary
- ovaries are smaller than wild-type littermates

teratozoospermia
- majority of sperm are abnormal with small, rounded cell bodies and blunted or absent hooks in the tail

respiratory system phenotype

interstitial pneumonia
- occurs consistently in mice

lung inflammation
- lungs are infiltrated with neutrophils suggesting chronic pulmonary infection

pulmonary edema
- frequently observed in mice

cardiovascular system phenotype

heart right ventricle hypertrophy
- occurs as a result of lung inflammation

vision/eye phenotype

eyelids fail to open
- eyelids remain closed for at least several months and sometimes for entire lifespan

microphthalmia
- in some mice the eyes are smaller possibly as result of failure of eyelids to open

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
129/Sv-Sirt1

cellular phenotype

abnormal male germ cell apoptosis
- at 3 weeks of age, TUNEL analysis indicates abundant apoptosis of pachytene spermatocytes

abnormal spermatid morphology
- at 3 weeks of age, male homozygotes show severely reduced numbers or a total absence of spermatids

abnormal spermatocyte morphology
- at 3 weeks of age, male homozygotes display numerous multinucleate or abnormally large spermatocytes in the seminiferous tubules, indicating degenerating or dying spermatocytes

multinucleated giant male germ cells

growth/size/body region phenotype

decreased body size
- at 3 weeks of age, male homozygotes are significantly smaller than wild-type controls

postnatal growth retardation
- at 3 weeks of age, male homozygotes display a severely reduced growth relative to wild-type controls

homeostasis/metabolism phenotype

decreased circulating follicle stimulating hormone level
- at P12, serum FSH levels in mutant male mice are reduced by ~50% relative to wild-type levels

decreased circulating luteinizing hormone level
- at 3 weeks of age, serum LH leves in mutant male mice are below the detection limit of the RIA

mammalian phenotype

reproductive system phenotype
- Normal - at postnatal day 1 (P1), neonatal male homozygotes display normal fetal testis, Leydig cell, and Sertoli cell development relative to wild-type controls
- Normal - in addition, spermatogonial multiplication and stem cell renewal appear unaffected

mortality/aging

premature death
- after 14-18 backcrosses on a 129/Sv background, most homozygotes die at around 3 or 4 weeks of age; only rare homozygotes survive up to 6 weeks of age
- Background Sensitivity - unlike homozygotes that are backcrossed on a 129/Sv strain, homozygotes generated on a C57BL/6 background or an outbred background involving 129/Sv and CD-1 can survive into adulthood

reproductive system phenotype

abnormal adult Leydig cell differentiation
- at 3 weeks of age, mutant testes show absence of differentiating Leydig cells with an oval-to-round-shaped nucleus morphology, typical of maturing wild-type Leydig cells
- instead, clusters of fetal-type Leydig cells and some early spindle-shaped progenitor cells are found close to the seminiferous tubules and blood vessels

abnormal male germ cell apoptosis
- at 3 weeks of age, TUNEL analysis indicates abundant apoptosis of pachytene spermatocytes

abnormal seminiferous tubule morphology
- at 3 weeks of age, only 3% of mutant seminiferous tubules exhibit a tubular lumen vs 99% of wild-type tubules

abnormal Sertoli cell development
- at 3 weeks of age, mutant Sertoli cell nuclei often contain several smaller nucleoli instead of one single nucleolus, indicating defective Sertoli cell maturation

abnormal spermatid morphology
- at 3 weeks of age, male homozygotes show severely reduced numbers or a total absence of spermatids

abnormal spermatocyte morphology
- at 3 weeks of age, male homozygotes display numerous multinucleate or abnormally large spermatocytes in the seminiferous tubules, indicating degenerating or dying spermatocytes

abnormal testes secretion
- at P27, male homozygotes display a >5-fold decrease in intratesticular testosterone levels relative to wild-type controls

arrest of male meiosis
- Normal - however, germ cell proliferation is not significantly decreased
- the first round of spermatogenesis arrests in late-meiotic prophase; as a result, only rare round spermatids are observed

arrest of spermatogenesis
- Background Sensitivity - unlike homozygotes that are backcrossed on a 129/Sv strain, homozygotes generated on a C57BL/6 background or an outbred background involving 129/Sv and CD-1 display defective rather than arrested spermatogenesis

Leydig cell hypoplasia
- at 3 weeks of age, male homozygotes display a severely reduced number of developing adult-type Leydig cells relative to wild-type controls

male infertility
- male infertility is attributed to dysregulated hypothalamic-pituitary gonadotropin signaling

multinucleated giant male germ cells

small seminiferous tubules
- at 3 weeks of age, the average mutant seminiferous tubular diameter is reduced ~40% relative to the wild-type

endocrine/exocrine gland phenotype

abnormal adult Leydig cell differentiation
- at 3 weeks of age, mutant testes show absence of differentiating Leydig cells with an oval-to-round-shaped nucleus morphology, typical of maturing wild-type Leydig cells
- instead, clusters of fetal-type Leydig cells and some early spindle-shaped progenitor cells are found close to the seminiferous tubules and blood vessels

abnormal seminiferous tubule morphology
- at 3 weeks of age, only 3% of mutant seminiferous tubules exhibit a tubular lumen vs 99% of wild-type tubules

abnormal Sertoli cell development
- at 3 weeks of age, mutant Sertoli cell nuclei often contain several smaller nucleoli instead of one single nucleolus, indicating defective Sertoli cell maturation

abnormal testes secretion
- at P27, male homozygotes display a >5-fold decrease in intratesticular testosterone levels relative to wild-type controls

Leydig cell hypoplasia
- at 3 weeks of age, male homozygotes display a severely reduced number of developing adult-type Leydig cells relative to wild-type controls

small seminiferous tubules
- at 3 weeks of age, the average mutant seminiferous tubular diameter is reduced ~40% relative to the wild-type

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129S1/Sv * 129X1/SvJ

behavior/neurological phenotype

lethargy

immune system phenotype

increased autoantibody level
- increased levels of La and Ro autoantibodies

mortality/aging

perinatal lethality
- high levels of perinatal lethality

reproductive system phenotype

female infertility

male infertility

respiratory system phenotype

hyperpnea
- elevated respiration

craniofacial phenotype

abnormal palatal rugae morphology
- rugae of the hard palate are disorganized

short snout

vision/eye phenotype

abnormal eyelid morphology

abnormal lacrimal gland morphology
- lymphoid infiltration of lacrimal gland in almost all mice; infiltration is more extensive than in Sirt1^tm3.1 mice

eyelids fail to open

ocular hypotelorism
- interorbital distance is reduced

digestive/alimentary phenotype

abnormal palatal rugae morphology
- rugae of the hard palate are disorganized

abnormal salivary gland morphology
- lymphoid infiltration of salivary gland in almost all mice; infiltration is more extensive than in Sirt1^tm3.1 mice

endocrine/exocrine gland phenotype

abnormal lacrimal gland morphology
- lymphoid infiltration of lacrimal gland in almost all mice; infiltration is more extensive than in Sirt1^tm3.1 mice

abnormal salivary gland morphology
- lymphoid infiltration of salivary gland in almost all mice; infiltration is more extensive than in Sirt1^tm3.1 mice

growth/size/body region phenotype

abnormal palatal rugae morphology
- rugae of the hard palate are disorganized

decreased body size

decreased body weight

short snout

References

McBurney MW; Yang X; Jardine K; Hixon M; Boekelheide K; Webb JR; Lansdorp PM; Lemieux M. 2003. The mammalian SIR2alpha protein has a role in embryogenesis and gametogenesis. Mol Cell Biol 23(1):38-54PubMed: 12482959 MGI: J:81010

Additional - Sirt1^tm1Mcby related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Sirt1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, heterozygous mice may be bred to wildtype mice from the colony, or to C57BL/6J inbred mice (Stock No. 000664). Homozygotes are perinatal lethal on an inbred background. The donating investigator reports that an F1 cross of B6 heterozygotes and FVB heterozygotes produces homozygotes at Mendelian ratios. Homozygous F1 offspring are infertile.
- Additional Breeding and Husbandry Support
Citation
When using the B6.129-Sirt1^tm1Mcby/LguJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #026009 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or wildtype for -Sirt1<tm1Mcby>

Related Products and Services

Frozen Mouse Embryo	B6.129-Sirt1<tm1Mcby>/LguJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129-Sirt1<tm1Mcby>/LguJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129-Sirt1<tm1Mcby>/LguJ Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6.129-Sirt1<tm1Mcby>/LguJ Frozen Embryo	$3373.50

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Sirt1tm1Mcby

Allele Symbol: Sirt1tm1Mcby

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Sirt1tm1Mcby/Sirt1tm1Mcbyinvolves: 129

cardiovascular system phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

limbs/digits/tail phenotype

mortality/aging

muscle phenotype

craniofacial phenotype

respiratory system phenotype

vision/eye phenotype

digestive/alimentary phenotype

embryo phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

Genotype: Sirt1tm1Mcby/Sirt1tm1Mcbyinvolves: 129S1/Sv * 129X1/SvJ * CD-1

adipose tissue phenotype

cellular phenotype

craniofacial phenotype

digestive/alimentary phenotype

embryo phenotype

endocrine/exocrine gland phenotype

behavior/neurological phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

limbs/digits/tail phenotype

mortality/aging

muscle phenotype

nervous system phenotype

renal/urinary system phenotype

reproductive system phenotype

respiratory system phenotype

cardiovascular system phenotype

vision/eye phenotype

Genotype: Sirt1tm1Mcby/Sirt1tm1Mcby129/Sv-Sirt1

cellular phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mammalian phenotype

mortality/aging

reproductive system phenotype

endocrine/exocrine gland phenotype

Genotype: Sirt1tm1Mcby/Sirt1tm1Mcbyinvolves: 129S1/Sv * 129X1/SvJ

behavior/neurological phenotype

immune system phenotype

mortality/aging

reproductive system phenotype

respiratory system phenotype

craniofacial phenotype

vision/eye phenotype

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

References

Additional - Sirt1tm1Mcby related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Sirt1^tm1Mcby

Allele Symbol: Sirt1^tm1Mcby

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129S1/Sv * 129X1/SvJ * CD-1

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
129/Sv-Sirt1

Genotype: Sirt1^tm1Mcby/Sirt1^tm1Mcby
involves: 129S1/Sv * 129X1/SvJ

Additional - Sirt1^tm1Mcby related