Analysis Tools
growth/size/body
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• at birth, mutant mice are on average 12% lighter than wild-type newborns
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cellular
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• at 35 days of age, mutant mice show a slightly higher frequency of aberrant spermatocytes than wild-type controls (2% vs 0% respectively), as shown by fragmented sister chromatids and precocious desynapsis of chromosomes of bivalents
• heat treatment increases the frequency of mutant aberrant spermatocytes to 8% but has no significant effect on wild-type mice
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• in vitro oncogenic transformation assays indicate a higher frequency of spontaneous transformants in mutant cells than in wild-type cells
• whereas heat treatment has no effect on spontaneous cellular transformation and very little effect on ionizing radiation (IR)-induced transformation in wild-type cells, heat has a profound effect on both spontaneous and IR-induced transformation in mutant cells
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• after IR treatment, asynchronously growing mutant MEFs display less inhibition of DNA synthesis than wild-type cells
• however, transfection of the Hspa1b gene rescues the radioresistant DNA synthesis observed in mutant MEFs
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• after heat treatment (43C for 30 min), mutant cells exhibit lower mitotic indices than wild-type cells
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• mutant fibroblasts are significantly more sensitive to cell killing by ionizing radiation (IR) than wild-type cells
• mutant cells are significantly more sensitive to cell killing after heat (43C for 30 min) plus IR treatment than wild-type cells
• ectopic expression of Hspa1b rescues the enhanced killing by IR or heat-modulated IR-induced cell killing observed in mutant cells
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• in culture, both early- and late-passage mutant MEFs display significantly slower growth kinetics than wild-type MEFs
• mutant MEFs show a 4-fold decrease in plating efficiency relative to wild-type MEFs
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• in culture, mutant MEFs undergo senescence sooner than wild-type MEFs
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• mutant cells treated with heat plus ionizing radiation (IR) exhibit more S-phase-specific chromosomal aberrations at metaphase than cells treated with IR only, suggesting a defect in S-phase-specific DNA repair
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• heat treatment (41C for 30 min) significantly increases the ratio of normochromatic to polychromatic erythrocytes and micronucleus formation in mutant mice but has no effect on wild-type controls
• heat treatment (41C for 30 min) significantly increases the frequency of chromatid- and chromosome-type gaps and breaks in mutant bone marrow cells but has no effect on wild-type cells
• after heat treatment (43C for 30 min), mutant cells exhibit lower mitotic indices and higher frequencies of S-phase-specific chromatid and chromosomal aberrations at metaphase than wild-type cells
• after heat treatment (43C for 30 min) plus gamma irradiation (2 Gy), mutant cells display significantly higher frequencies of S-phase-specific chromosome aberrations at metaphase than wild-type cells
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• mutant mice display a significantly higher ratio of normochromatic to polychromatic erythrocytes and a higher frequency of spontaneously formed micronuclei relative to wild-type controls, indicating increased spontaneous genomic instability
• mutant bone marrow cells show a higher frequency of chromatid- and chromosome-type gaps and breaks than wild-type cells
• mutant mice have 0.4 chromosomal aberrations per metaphase relative to 0.03 in wild-type mice
• mutant MEFs have ~0.55 chromosome end-to-end associations per metaphase relative to 0.16 in wild-type MEFs
• mutant MEFs show a 2.5-fold-higher frequency of anaphase bridges than wild-type MEFs
• mutant MEFs show a higher frequency of telomere associations and breaks near telomeres than wild-type MEFs
• however, chromosome end-to-end associations are not associated with loss of telomeric repeats at the fusion sites in mutant MEFs
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homeostasis/metabolism
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• increased size of induced myocardial infarction, relative to wild-type, during the late-phase of protection following ischemic preconditioning (IP)
• protection during the early phase of IP remains unaffected
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• mutant cells treated with heat plus ionizing radiation (IR) exhibit more S-phase-specific chromosomal aberrations at metaphase than cells treated with IR only, suggesting a defect in S-phase-specific DNA repair
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• mutant MEFs exhibit a ~2.5-fold decrease in telomerase activity per unit of protein relative to wild-type MEFs
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cardiovascular system
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• increased size of induced myocardial infarction, relative to wild-type, during the late-phase of protection following ischemic preconditioning (IP)
• protection during the early phase of IP remains unaffected
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reproductive system
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• at 35 days of age, mutant mice show a slightly higher frequency of aberrant spermatocytes than wild-type controls (2% vs 0% respectively), as shown by fragmented sister chromatids and precocious desynapsis of chromosomes of bivalents
• heat treatment increases the frequency of mutant aberrant spermatocytes to 8% but has no significant effect on wild-type mice
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