ABSTRACT. 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. -KEY WORDS: Marek's disease, p53, RT-PCR, transformation.J. Vet. Med. Sci. 60(8): 923-929, 1998 demyelination of peripheral nerves [23]. The molecular mechanism of transformation by MDV has not been fully understood. Unlike retroviruses, MDV does not have any apparent oncogenes, suggesting that interaction of viral proteins with cellular oncoproteins or activation of cellular oncogenes are important for the transformation mechanism. Recently, it has been reported that Meq, which has a homology with members of the jun/fos oncoprotein family, could be a viral oncogene based on its potential role as a transcription factor [30]. In addition, the Meq protein has been shown to have a potential to interact with p53 [2], suggesting possible involvement of this interaction in the transformation process by MDV. However, no information is available concerning the changes in the p53 gene of host cells related to transformation by MDV. Thus, to determine whether p53 mutations are involved in the neoplastic process of chicken lymphoma, we analyzed the molecular structure of chicken p53 genes and its transcripts in chicken tumor cell lines derived from MD, avian leukosis (AL), reticuloendotheliosis (RE), and field tumors. We here reported that tumor cell lines possess mis-sense mutations and deletion in the p53 transcript.
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