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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Pou3f2tm1Rsd
targeted mutation 1, Michael G Rosenfeld
MGI:1857996
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Pou3f2tm1Rsd/Pou3f2tm1Rsd involves: 129S4/SvJae * C57BL/6 MGI:2660736
cx2
Pou3f2tm1Rsd/Pou3f2tm1Rsd
Pou3f3tm1Rmc/Pou3f3tm1Rmc
involves: 129S4/SvJae * C57BL/6 MGI:2660729


Genotype
MGI:2660736
hm1
Allelic
Composition
Pou3f2tm1Rsd/Pou3f2tm1Rsd
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pou3f2tm1Rsd mutation (1 available); any Pou3f2 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 90% of homozygotes died before P6
• the remaining 10% died between P9 and P10

adipose tissue
• most homozygotes showed a significant decrease in brown adipose tissue, consistent with severe malnutrition

endocrine/exocrine glands
N
• the adrenal glands and cerebral cortex of homozygous mutant mice appeared normal
• by E19, homozygotes displayed complete loss of pituicytes and a fold of the intermediate lobe filled the space normally occupied by the posterior lobe
• homozygotes displayed loss of the posterior lobe of the pituitary gland; the anterior and intermediate lobes appeared normal
• the developing posterior pituitary gland appeared normal until E16.5, when axonal projections from magnocellular neurons failed to make contact
• complete loss of pituicytes by E19

growth/size/body
• homozygotes were born normally but displayed a reduction in size and weight from P3
• by P6, mutants were 50-60% smaller than age-matched wild-type mice

nervous system
N
• homozygotes showed no abnormalities in the cortex, hippocampal formation, or other structures outside the hypothalamus
• by E19, homozygotes displayed complete loss of pituicytes and a fold of the intermediate lobe filled the space normally occupied by the posterior lobe
• homozygotes displayed loss of the posterior lobe of the pituitary gland; the anterior and intermediate lobes appeared normal
• the developing posterior pituitary gland appeared normal until E16.5, when axonal projections from magnocellular neurons failed to make contact
• complete loss of pituicytes by E19
• homozygotes displayed loss of endocrine hypothalamic nuclei
• starting at E15-E16, mutants showed a progressive loss of the parvocellular and magnocellular neurons of the paraventricular hypothalamic (PVH) and supraoptic nuclei in a dorsal-ventral pattern, with most cells lost by E17
• by E19.5, mutant neonates showed a striking neuronal loss only in the hypothalamic supraoptic and paraventricular nuclei

integument
• by P6, mutants displayed epidermal hyperkeratosis
• by P6, mutants had a flaking epidermis




Genotype
MGI:2660729
cx2
Allelic
Composition
Pou3f2tm1Rsd/Pou3f2tm1Rsd
Pou3f3tm1Rmc/Pou3f3tm1Rmc
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pou3f2tm1Rsd mutation (1 available); any Pou3f2 mutation (19 available)
Pou3f3tm1Rmc mutation (0 available); any Pou3f3 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• double homozygotes were not viable at birth

nervous system
• double homozygotes displayed abnormalities in axonal outgrowth and projection in the forebrain
• double homozygotes displayed abnormal organization of cortical lamination with delayed radial migration of layers II/III
• double homozygotes displayed inversion of cortical layers II-V through aberrant regulation of the p39/p35 regulatory components of CDK5





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory