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Phenotypes Associated with This Genotype
Genotype
MGI:2672136
Allelic
Composition
Ppm1dtm1Lad/Ppm1dtm1Lad
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation (1 available); any Ppm1d mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only 3 of 20 males survived to 2 years of age
• majority of female null littermates survived to this point, having a similar survival rate as wild-type controls
• fewer than expected number of homozygous mutant pups at birth
• fewer male pups than female, indicating possible selection against male embryos during gestation
• analysis of midgestation embryos failed to show any obvious developmental abnormalities in null mice, authors suggest this may be the result of a portion of the males succumbing to early embryonic defects

cellular
• reduced numbers produced over time, authors suggest as a result of inability to maintain spermatogenesis
• stimulation with LPS resulted in less robust response than wild-type controls
• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls

endocrine/exocrine glands
• some older animals showed reduced thymus size and loss of normal architecture
• extensive vacuolization, loss of normal cellular architecture, and sometimes, absence of mature spermatozoa

growth/size/body
• males only
• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture

hematopoietic system
• stimulation with LPS resulted in less robust response than wild-type controls
• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls
• some older animals showed reduced thymus size and loss of normal architecture
• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture

immune system
• stimulation with LPS resulted in less robust response than wild-type controls
• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls
• some older animals showed reduced thymus size and loss of normal architecture
• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture
• lymph nodes hyperplastic, with infiltration by macrophages, neutrophils, and eosinophils
• organs of older animals showed increased inflammation, particularly in those animals with skin lesions
• increased mortality after infection with mouse-adapted pathogenic influenza virus

reproductive system
• reduced numbers produced over time, authors suggest as a result of inability to maintain spermatogenesis
• extensive vacuolization, loss of normal cellular architecture, and sometimes, absence of mature spermatozoa
• atrophic
• irregular tubules, with abnormal architecture
• few males succeeded in producing offspring

integument
• 5% of animals showed ulcerated skin lesions
• 25% of older mice had fluid-filled neck abscesses


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)
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last database update
05/07/2024
MGI 6.23
The Jackson Laboratory