Abnormal keratinization in the pupoid fetus (pf/pf) mutant mouse epidermis.
Abnormal keratinization in the pupoid fetus (pf/pf) mutant mouse epidermis.
复制标题
蛹状胎儿 (pf/pf) 突变小鼠表皮角化异常。
DOI：
10.1016/0012-1606(84)90194-5
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发表时间：
1984
影响因子：
2.7
通讯作者：
Kollar,EJ
中科院分区：
文献类型：
--
作者：
Fisher,C;Dale,BA;Kollar,EJ
在其发育过程中，pf - pf突变小鼠的表皮受到下层真皮细胞的侵袭。这些入侵的细胞在整个表皮上建立了一个细胞网络，包括成纤维细胞、内皮细胞和神经纤维。在这些事件之后，角透明蛋白，聚丝蛋白，急剧减少，角化无法发生。异型组织重组表明pf基因在皮肤中不表达。在简单地移植整个突变背皮肤后，开始了聚丝蛋白的合成，并实现了有序的表皮分化过程。这些结果表明，pf基因的作用是系统性的，突变体表皮分化失败是继发于表皮组织异常。
During its development the epidermis of the pf pf mutant mouse is invaded by cells from the underlying dermis. These invading cells establish a network of cells including fibroblasts, endothelial cells, and nerve fibers, throughout the epidermis. Subsequent to these events the keratohyalin protein, filaggrin, is drastically reduced and keratinization fails to occur. Heterotypic tissue recombinations indicate that the pf gene is not expressed in the skin. After simply grafting whole mutant dorsal skin, filaggrin synthesis is initiated and an orderly process of epidermal differentiation is achieved. These results suggest that the pf gene acts systemically and that the failure of epidermal differentiation in the mutant occurs secondary to abnormal epidermal organization.