Fibroblast-dependent Proliferation of Mast Cells

肥大细胞的成纤维细胞依赖性增殖由成纤维细胞产生的干细胞因子（SCF）和肥大细胞表面表达的c-kit受体（KIT）介导。Ws从各种观点研究了SCF-KIT系统，并获得了以下结果。1）。尽管在小鼠中发现了许多KIT突变体，但在大鼠中还不知道KIT突变体。我们在大鼠中描述了第一个KIT突变体。我们描述了编码KIT的大鼠的Ws（白色斑点）位点。我们比较了小鼠KIT突变体的分子性质与其皮肤中肥大细胞的数量。3）。我们研究了被命名为Wsh的独特KIT突变。虽然Wsh突变等位基因位于W位点，但我们在KIT基因编码区未发现任何异常。由于KIT在来源于Wsh/Wsh小鼠骨髓的培养肥大细胞中不转录，因此认为Wsh突变是调节区的突变。由于KIT在Wsh/Wsh小鼠的成红细胞和生殖细胞中转录，因此KIT转录异常似乎具有细胞类型特异性。此外，我们还发现Wsh/Wsh小鼠肥大细胞中KIT的转录受年龄的影响。虽然在Wsh/Wsh胚胎的皮肤中发现了相当数量的肥大细胞，但由于KIT转录的废除，肥大细胞在出生后迅速减少。4）。小鼠mi基因座编码碱性螺旋-环-螺旋亮氨酸拉链家族的转录因子。我们证明，在mi/mi小鼠肥大细胞中观察到的表型异常可归因于多种蛋白质的转录缺陷。

Fibroblast-dependent proliferation of mast cells is mediated by stem cell factor (SCF) produced by fibroblasts and c-kit receptor (KIT) expressed on the surface of mast cells. Ws studied the SCF-KIT system from various viewpoints and obtained the following results. 1). Although many KIT mutants have been found in mice, KIT mutants were not known in rats. We described the first KIT mutants in rats. We characterized the Ws (White spotting) locus of rats which encoded the KIT.2). We compared the molecular nature of murine KIT mutants with the number of mast cells in thier skin. 3). We studied the unique KIT mutation designated as Wsh. Although the Wsh mutant allele is located at the W locus, we could not find any abnormalities in the coding region of KIT gene. Since KIT was not transcribed in cultured mast cells derived from the bone marrow of Wsh/Wsh mice, the Wsh mutation was considered to be a mutation at the regulatory region. Since KIT was transcribed in erythroblasts and germ cells of Wsh/Wsh mice, the abnormality of KIT transcription appeared to be cell type specific. Moreover, we found the KIT transcription was influenced by the age in mast cells of Wsh/Wsh mice. Although an appreciable number of mast cells was found in the skin of Wsh/Wsh embryos, mast cells decreased rapidly after birth due to the abolishment of KIT transcription. 4). The mi locus of mice encodes a transcription factor of basic helix-loop-helix leucine zipper family. We demonstrated that the phenotypic abnormalities observed in mast cells of mi/mi mice was attributable to the deficeint transcription of various proteins.