Analysis Tools
mortality/aging
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• none of the homozygotes surviving to term live beyond this time
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• only ~50% of homozygotes survive to term
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digestive/alimentary system
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• at 18.5 dpc, homozygotes display a smaller gastrointestinal tract relative to wild-type
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anal atresia
(
J:62158
)
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• at 18.5 dpc, all homozygotes have an imperforate anus
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• at 18.5 dpc, all homozygotes display an obvious malrotation of the gut, in the absence of reversions in gut situs
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• at 18.5 dpc, the mutant esophagus tissue is reduced and fused to the trachea
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• at 18.5 dpc, the mutant trachea and esophagus are fused to form a fistula-like fusion of the alimentary and respiratory tract
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• at 18.5 dpc, the mutant colon ends in a blind dilation that is not fused to the surface ectoderm; however, no aganglionic colon is observed
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• at 18.5 dpc, homozygotes show a 21% reduction in thickness of the circular smooth muscle layer along the small intestine; however, no intestinal dilation is observed
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• at 18.5 dpc, 67% of homozygotes display occlusion of the duodenum by overgrown villi, resembling duodenal stenosis
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• at 18.5 dpc, the mutant glandular epithelium displays histologic features that resemble intestinal metaplasia
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• at 18.5 dpc, all homozygotes display a significant overgrowth of stomach epithelium, in spite of normal rates of cell proliferation in the stomach
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• at 18.5 dpc, all homozygotes exhibit intestinal transformation of the stomach epithelium
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respiratory system
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• poorly vascularized airways
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• at 18.5 dpc, the mutant trachea and esophagus are fused to form a fistula-like fusion of the alimentary and respiratory tract
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• in mutant trachea, the layer of smooth muscle that normally lines the proximal epithelium is absent
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• although left and right buds form, mutant lungs fail to undergo lobation or subsequent extensive branching
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• at 12.5 dpc, mutant lungs fail to branch or display one abnormally positioned branch point
• in organ culture, mutant lungs fail to grow or branch extensively; bronchial mesenchyme cells detach from the endodermal epithelium
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• by 18.5 dpc, only a few air sacs are present
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• mutant lungs fail to undergo lobation
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• at 18.5 dpc, homozygotes display a rudimentary respiratory organ with a few large, poorly vascularized airways
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• in mutant trachea, cartilaginous rings are present but appear disorganized
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muscle
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• at 18.5 dpc, homozygotes show a 21% reduction in thickness of the circular smooth muscle layer along the small intestine
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• in mutant trachea, the layer of smooth muscle that normally lines the proximal epithelium is absent
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growth/size/body
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• at 18.5 dpc, mutant embryos have an overall reduced size relative to wild-type embryos
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endocrine/exocrine glands
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• at 18.5 dpc, 85% of homozygotes exhibit an annular pancreas
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nervous system
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• at 18.5 dpc, homozygotes show excessive and abnormally located neurons that differentiate under the epithelium and into the villi
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skeleton
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• in mutant trachea, cartilaginous rings are present but appear disorganized
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integument
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• at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type, with no difference observed in apoptosis
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• skin grafts of mutant skin (epidermis and dermis) transplanted onto nude mice generate hairless, pigmented skin
• some keratinized pigmented material resembling hair matrix is present, but no hair is formed
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• skin grafts of mutant skin transplanted onto nude mice show abnormal ingrowth of the epidermis and consequently aberrant morphogenesis of the hair shaft
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• at 15.5 dpc, mutant hair follicles form a smaller hair plug; however, epidermal expansion into the dermis and dermal condensation of mesenchyme at the base of the hair plug occur normally
• at 15.5 dpc, wild-type hair follicles have progressed to stage 2, whereas mutant follicles at still at stage 1 or 0
• skin grafts of mutant skin transplanted onto nude mice exhibit giant disorganized hair-bud-like structures, some with hair-shaft-like material, in the vicinity of epidermis
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• homozygotes display delayed hair folliculoenesis: embryonic follicles are arrested shortly after induction and fail to progress beyond stage 2
• at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type; no difference is observed in apoptosis
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• mutant hair follicles fail to initiate development of the inner root sheath from the hair matrix (stages 3-5)
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• mutant hair buds fail to exhibit an obvious polarity; in contrast, wild-type follicles show a typical polarized development along the anterior-posterior axis
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• by 18.5 dpc, homozygotes show a severe reduction in the number of induced hair follicles relative to wild-type mice
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• skin grafts of mutant skin transplanted onto nude mice exhibit a reduced dermal fat layer
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• mutant skin displays only a rudimentary dermal papilla, indicating abnormal epithelial-mesenchymal interactions
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• skin grafts of mutant skin transplanted onto nude mice display hyperplasia and abnormal keratin expression in interfollicular epidermis
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• skin grafts of mutant skin transplanted onto nude mice exhibit a thickened epidermis with large disorganized ingrowths
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cardiovascular system
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• poorly vascularized airways
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cellular
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• at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type, with no difference observed in apoptosis
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