ANALYSIS OF TUMOR-SUPPRESSOR GENE P53 IN CHICKEN LYMPHOBLASTOID TUMOR-CELL LINES AND FIELD TUMORS

To determine whether there is any abnormalities of the p53 gene in chi cken lymphoblastoid tumor cell lines derived from Mareks disease (MD), lymphoid leukosis, reticuloendotheliosis, and field tumors, some port ions of p53 cDNA corresponding to core and C-terminal domains (nucleot ide positions 277-1104 in the p53 open reading frame (ORF)) were seque nced. Several mutations were identified in both cell lines and field t umors. 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 t ranscriptional level. This deletion could cause a frame shift of the e ncoding p53 protein, possibly resulting in the generation of a functio nally different p53 protein. However, we confirmed that p53 mRNA witho ut deletion is also present in each of these cell lines. These mutatio ns of the p53 gene and deletion in the p53 transcript may be ones of m olecular changes specific to the transformation induced by MD virus.