Analysis Tools
cellular
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• unlike early-passage wild-type MEFs which form colonies in soft agar in the presence of Myc and Ras oncogenes, mutant MEFs cannot be transformed by Ha-rasV12 but can be immortalized by Myc, indicating that oncogenic v-Ha-Ras-dependent transformation is impaired
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• MEFs derived from E12-E13 homozygous mutant embryos show a 50% reduction in growth rate relative to wild-type MEFs, consistent with a reduction in signaling through the MAPK mitogenic pathway
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neoplasm
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• homozygotes are viable and developmentally normal with no detectable histological abnormalities in any major organs up to 1 year of age
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integument
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• after treatment with the phorbol ester TPA, homozygotes display increased alopecia relative to similarly treated wild-type controls
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sparse hair
(
J:84644
)
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• after treatment with the phorbol ester TPA, homozygotes display sparse hair growth relative to similarly treated wild-type controls
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• at P10, the inner root sheath is often separated from the hair shaft, resulting in blisters or cysts
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• homozygotes exhibit disorganized hair follicles as early as 10 days after birth (P10)
• at P10, a significant proportion of mutant hair follicles have a serpentine morphology
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• homozygotes display a defect in hair follicle development, presumably via impairment of EGFR signaling
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• at P10, the inner root sheath is often separated from the hair shaft, resulting in blisters or cysts
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• at P10, mutant hair follicles are disorganized in dermal location and orientation
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• at P10, homozygotes display significantly fewer hair follicles than wild-type littermates
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• at P10, homozygotes display an asynchronous hair growth
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blistering
(
J:84644
)
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• at P10, blisters or cysts are observed in hair follicles in which the inner root sheath has separated from the hair shaft
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