Takagi M, Ohashi K, Morimura T, Sugimoto C, Onuma M
Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
J Vet Med Sci. 1998 Aug;60(8):923-9. doi: 10.1292/jvms.60.923.
To determine whether there is any abnormalities of the p53 gene in chicken lymphoblastoid tumor cell lines derived from Marek's disease (MD), lymphoid leukosis, reticuloendotheliosis, and field tumors, some portions of p53 cDNA corresponding to core and C-terminal domains (nucleotide positions 277-1104 in the p53 open reading frame (ORF)) were sequenced. Several mutations were identified in both cell lines and field tumors. However, none of these mutations is localized at the "hot spot", which has been reported as the site for transformation-activating mutations. Moreover, partial cDNA clones with a 122-bp deletion in the p53 ORF were identified in two cell lines, MSB1 and MTB1 derived from MD tumors. Southern blot analysis showed that no deletion occurred in the genome of p53 in MSB1, indicating that deletion occurred at the transcriptional level. This deletion could cause a frame shift of the encoding p53 protein, possibly resulting in the generation of a functionally different p53 protein. However, we confirmed that p53 mRNA without deletion is also present in each of these cell lines. These mutations of the p53 gene and deletion in the p53 transcript may be ones of molecular changes specific to the transformation induced by MD virus.
为了确定源自马立克氏病（MD）、淋巴细胞白血病、网状内皮增生症和田间肿瘤的鸡淋巴母细胞肿瘤细胞系中p53基因是否存在任何异常，对与核心和C末端结构域相对应的p53 cDNA的某些部分（p53开放阅读框（ORF）中的核苷酸位置277 - 1104）进行了测序。在细胞系和田间肿瘤中均鉴定出了几种突变。然而，这些突变均未定位在“热点”区域，该区域已被报道为转化激活突变的位点。此外，在源自MD肿瘤的两个细胞系MSB1和MTB1中鉴定出了在p53 ORF中存在122 bp缺失的部分cDNA克隆。Southern印迹分析表明，MSB1中p53基因组未发生缺失，表明缺失发生在转录水平。这种缺失可能导致编码的p53蛋白发生移码，可能产生功能不同的p53蛋白。然而，我们证实这些细胞系中的每一个中也都存在无缺失的p53 mRNA。p53基因的这些突变和p53转录本中的缺失可能是MD病毒诱导转化所特有的分子变化之一。
