Analysis Tools
vision/eye
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• mutant mice develop severe corneal inflammation shortly after birth due to a lack of protection by the abnormal eyelids
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• mutant embryos show no formation of eyelid protrusive tips at E14.5
• no extension of the upper or lower eyelids is observed at E15.5
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• although rudimentary eyelid tips may be observed at E16.5, they extend only slightly and do not cover the entire cornea even by E19.5
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• the eyes of adult mutant mice are often smaller than normal
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• mutant mice are born with a wide oval gap between the eyelids due to a failure of eyelid epithelial migration around E15
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eye opacity
(
J:84743
)
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• the eyes of adult mutant mice are often opaque
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homeostasis/metabolism
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• whereas wild-type full-thickness skin wounds typically require 11 days for full closure, those in mutant mice are fully closed after 14 days due to impaired reepithelialization
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• at 4 days after cutaneous wounding, the mutant leading edge epidermis is clearly malformed and fails to migrate or invade into the fibrin clot properly, despite normal keratinocyte proliferation
• impaired reepithelialization is associated with decreased expression levels of keratin-6 and PTK2 protein tyrosine kinase 2 (FAK), and a large reduction in activation of the EGF receptor at the leading edge of mutant wounds
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immune system
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• mutant mice develop severe corneal inflammation shortly after birth due to a lack of protection by the abnormal eyelids
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integument
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• in an in vitro scratch assay, mutant keratinocytes appear less elongated and show a striking fragmentation of actin stress fibers at the leading edge of the wound, unlike wild-type cells where stress fibers accumulate in the anterior lamellipodia towards the wound
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• in vitro, mutant keratinocytes cultured in the presence of mitomycin C fail to migrate or elongate properly at the border of scratch assays, unlike wild-type keratinocytes which migrate into the gap in an EGF-dependent manner and achieve wound closure within 14 hrs
• in an in vitro scratch assay, mutant keratinocytes show no EGF receptor activation and display significantly less focal adhesions than wild-type keratinocytes at the front of leading edge cells
• addition of HB-EGF (an EGF ligand) into the mutant cell growth medium rescues the keratinocyte migration defect and induces phosphorylation of EGF receptor
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• in culture, primary keratinocytes isolated from newborn mutant mice display significantly reduced EGF-induced proliferation relative to wild-type controls
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cellular
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• in culture, primary keratinocytes isolated from newborn mutant mice display significantly reduced EGF-induced proliferation relative to wild-type controls
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