Depigmentation of Skin and Hair Color in the Somatic Cell Cloned Pig
Depigmentation of Skin and Hair Color in the Somatic Cell Cloned Pig
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DOI：
10.1002/dvdy.21986
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发表时间：
2009-07-01
影响因子：
2.5
通讯作者：
Kim, Jin-Hoi
中科院分区：
文献类型：
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作者：
Hwang, Kyu-Chan;Cho, Scong-Keun;Kim, Jin-Hoi
此前，我们已经成功地使用杜洛克供体细胞克隆了9头小猪。在这些克隆中，有一个在青春期表现出明显的皮肤和头发颜色脱色。在本研究中，我们选择了一个色素脱失的克隆来研究体细胞核移植异常的病因。我们假设与Waardenburg综合征相关的基因(MITF、Pax-3、Sox-10、Slug和Kit)与猪的色素脱失密切相关，猪的脱色起源于体细胞核移植(SCNT)。从发病和未发病的SCNT来源的猪的耳组织中提取总RNA，用逆转录-聚合酶链式反应扩增MITF、Pax-3、Sox-10、Slug和Kit基因的转录本，测序和分析。显示出进行性色素脱失的SCNT猪的cdna序列没有发现这些基因的突变。虽然我们没有发现这些基因的任何突变，但与未受影响的SCNT猪相比，与Waardenburg综合征有关的基因在SCNT猪中的表达严重下调。这种基因表达的下调可能导致一种以前未描述的表型，表现为黑素细胞不稳定，导致色素沉着的进行性丧失。发展动力学238：1701-1708,2009。(C)2009年Wiley-Liss，Inc.
Previously, we have successfully produced nine cloned piglets using Duroc donor cells. Among these clones, one showed distinct depigmentation of the skin and hair color during puberty. In this study, we selected a clone with depigmentation to investigate the etiology of the anomaly in somatic cell nuclear transfer. We hypothesized that genes related to Waardenburg syndrome (Mitf, Pax-3, Sox-10, Slug, and Kit) are closely associated with the depigmentation of pig, which was derived from somatic cell nuclear transfer (scNT). Total RNA was extracted from the ear tissue of affected and unaffected scNT-derived pigs, and the transcripts encoding Mitf, Pax-3, Sox-10, and Slug, together with the Kit gene, were amplified by reverse transcription-polymerase chain reaction, sequenced, and analyzed. The cDNA sequences from the scNT pig that showed progressive depigmentation did not reveal a mutation in these genes. Although we did not find any mutations in these genes, expression of the genes implicated in Waardenburg syndrome was severely down-regulated in the affected scNT pig when compared with unaffected scNT pigs. This down-regulation of gene expression may result in a previously undescribed phenotype that shows melanocyte instability, leading to progressive loss of pigmentation. Developmental Dynamics 238:1701-1708, 2009. (C) 2009 Wiley-Liss, Inc.