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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tardbptm1.1Pcw
targeted mutation 1.1, Philip C Wong
MGI:4834273
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Tardbptm1.1Pcw/Tardbp+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:4834589
cn2
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:4834592
cn3
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbptm1.1Pcw
involves: 129 * C57BL/6 * SJL MGI:4834587
cn4
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbp+
involves: 129 * C57BL/6 * SJL MGI:4834588
cn5
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(Stra8-icre)1Reb/0
involves: C57BL/6 * FVB/NJ * SJL MGI:7266812


Genotype
MGI:4834589
cn1
Allelic
Composition
Tardbptm1.1Pcw/Tardbp+
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (60 available)
Tg(CAG-cre/Esr1*)5Amc mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• after cre induction by tamoxifen, mice show decrease in body weight relative to controls

adipose tissue
• absence of fatty acid vacuoles in adipocytes in interscapular brown fat is detected
• reduction of fatty acid vacuoles in adipocytes in subcutaneous fat is detected




Genotype
MGI:4834592
cn2
Allelic
Composition
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (60 available)
Tg(CAG-cre/Esr1*)5Amc mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• after cre induction by tamoxifen, mice show decrease in body relative to controls

cellular
• increased fat oxidation after loss of Tardbp results in fat loss in adipocytes

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass
• absence of fatty acid vacuoles in adipocytes in interscapular brown fat is detected
• adipocytes are present in brown fat, but lack of stored fat within adipocytes results in loss of fat content in animals after induction by tamoxifen
• dramatic fat loss is observed
• reduction of fatty acid vacuoles in adipocytes in subcutaneous fat is detected
• adipocytes are present in white fat, but lack of stored fat within adipocytes results in loss of fat content in animals after induction by tamoxifen

homeostasis/metabolism
• increased fat oxidation after loss of Tardbp results in fat loss in adipocytes




Genotype
MGI:4834587
cn3
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (3 available); any Gt(ROSA)26Sor mutation (942 available)
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (60 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when cre expression is induced with a tamoxifen-containing diet (400 mg/kg of chow), mice die by day 9 post-introduction of tamoxifen

growth/size/body
• during the initial 3 days after cre induction by tamoxifen, all mice show decrease in body weight due to decreased food intake, but whereas controls regain recover some weight, experimental mice do not
• mice show a cumulative loss of body weight compared to controls following cre induction, but energy intake (cumulative food intake) is similar to controls

homeostasis/metabolism
N
• without induction of cre by tamoxifen treatment, animals are indistinguishable from controls
• increased fat oxidation after induction is basis for increased weight loss
• following cre induction, animals exhibit a decreased respiratory exchange ratio (RER) indicative of pure fat oxidation compared to controls by day 6

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass

cellular
• increased fat oxidation after induction is basis for increased weight loss

behavior/neurological
• energy intake on day 7 is significantly higher than on day 1 after cre induction




Genotype
MGI:4834588
cn4
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbp+
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (3 available); any Gt(ROSA)26Sor mutation (942 available)
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (60 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• during the initial 3 days after cre induction by tamoxifen, all mice show decrease in body weight due to decreased food intake, but whereas controls regain recover some weight, experimental mice do not

homeostasis/metabolism
• following cre induction, animals exhibit a decreased respiratory exchange ratio (RER) indicative of pure fat oxidation compared to controls by day 6

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass




Genotype
MGI:7266812
cn5
Allelic
Composition
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(Stra8-icre)1Reb/0
Genetic
Background
involves: C57BL/6 * FVB/NJ * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (60 available)
Tg(Stra8-icre)1Reb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• most cauda epididymal sperm are morphologically abnormal
• ~55% of sperm tails are curved/bent
• roughly 50% of cauda sperm show deformed or detached heads
• ~55% of sperm show head and midpiece bent over the principal piece of the tail
• headless sperm are observed
• extensive male germ cell depletion is observed at P35
• germ cell depletion is progressively worse at 3, 7, and 21 months of age
• males exhibit 7.4 times less cauda epididymal sperm than control males
• TUNEL staining showed a significant increase in spermatocyte apoptosis
• vacuole formation is observed within the seminiferous epithelium at P35
• at advanced ages, the seminiferous epithelium only consists of Sertoli cells
• onset of seminiferous epithelium pathology with reduced cellularity is at P12
• at P35, the seminiferous tubule diameter appears narrower than in control males
• a 1.6-fold reduction in tubule cross-section diameter is seen at 3 months of age
• atrophy of the seminiferous tubules, germ cell loss, and vacuole formation are observed at P35
• vacuole formation is progressively worse at 3, 7, and 21 months of age
• testis size is severely decreased at P35
• a 2.9-fold reduction in testis weight is seen at 3 months of age
• diplotene-like spermatocytes display nonhomologous chromosome synapsis
• zygotene-like spermatocytes show nonhomologous chromosome synapsis, short chromosome length, and abnormal number of chromosomes
• pachytene-like spermatocytes show nonhomologous chromosome synapsis, with persistent gammaH2AX flares/foci on autosomes likely indicating unrepaired double-strand DNA breaks
• at P35, spermatogonia and a few meiotic cells can be seen but no round spermatids are detected
• at 3-4 months of age, flow cytometry data showed a significant decrease in 1N cells (round spermatids) and an increase in 2N (spermatogonia, Sertoli, peritubular, and Leydig cells) and 4N (primary spermatocytes) cells, indicating arrest in meiosis
• spermatocytes show failure to complete prophase I of meiosis with arrest at the mid-pachytene stage
• 3-month-old males are severely subfertile, producing a significantly lower number of litters than control males over a 6-month period (0.6 litters versus 6 litters, respectively)

cellular
• most cauda epididymal sperm are morphologically abnormal
• ~55% of sperm tails are curved/bent
• roughly 50% of cauda sperm show deformed or detached heads
• ~55% of sperm show head and midpiece bent over the principal piece of the tail
• headless sperm are observed
• extensive male germ cell depletion is observed at P35
• germ cell depletion is progressively worse at 3, 7, and 21 months of age
• males exhibit 7.4 times less cauda epididymal sperm than control males
• zygotene-like spermatocytes show short chromosome length and abnormal number of chromosomes
• some pachytene-like spermatocytes show abnormally long chromosomes
• zygotene-like spermatocytes show abnormal number of chromosomes likely due to abnormal synapsis between nonhomologous chromosomes
• TUNEL staining showed a significant increase in spermatocyte apoptosis
• pachytene-like spermatocytes with synapsis defects show gammaH2AX foci/flares on autosomes, indicating delayed DSB repair

endocrine/exocrine glands
• vacuole formation is observed within the seminiferous epithelium at P35
• at advanced ages, the seminiferous epithelium only consists of Sertoli cells
• onset of seminiferous epithelium pathology with reduced cellularity is at P12
• at P35, the seminiferous tubule diameter appears narrower than in control males
• a 1.6-fold reduction in tubule cross-section diameter is seen at 3 months of age
• atrophy of the seminiferous tubules, germ cell loss, and vacuole formation are observed at P35
• vacuole formation is progressively worse at 3, 7, and 21 months of age
• testis size is severely decreased at P35
• a 2.9-fold reduction in testis weight is seen at 3 months of age

homeostasis/metabolism
• pachytene-like spermatocytes with synapsis defects show gammaH2AX foci/flares on autosomes, indicating delayed DSB repair





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory