Molecular analysis of the c-myc locus in normal tissue and in avian leukosis virus-induced lymphomas.
We isolated molecular clones of the provirus-host cell junctions (tumor junction fragments) from two avian leukosis virus-induced lymphomas and compared the structures of these clones with a clone of the normal c-myc gene. Restriction mapping and DNA sequencing demonstrated that normal proviral integration events occurred adjacent to c-myc in both tumors, without gross structural alteration of c-myc. The right long terminal repeat of an avian leukosis virus provirus is integrated upstream from the bulk of the c-myc coding sequences and oriented such that transcription can initiate within the long terminal repeat and proceed downstream into c-myc. A comparison of a tumor junction fragment with the v-myc gene showed that there are two regions of v-myc-related sequences (which are probably exons) separated by 1 kilobase of sequences unrelated to v-myc (probably an intron). A DNA sequence analysis of the tumor junction fragments suggested that integration had occurred in exons adjacent to splice donor sites. This suggests that there are additional exons and introns in c-myc. Based on these findings, a model is proposed for the genesis of the tumor-specific RNAs containing viral-5' and c-myc information in avian leukosis virus-induced lymphomas.
D000818:Animals; D001353:Avian Leukosis / Q000235:genetics / Q000382:microbiology; D001354:Avian Leukosis Virus / Q000235:genetics*; D001483:Base Sequence; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D002645:Chickens / Q000235:genetics; D003001:Cloning, Molecular; D004262:DNA Restriction Enzymes; D005796:Genes; D005814:Genes, Viral; D008223:Lymphoma / Q000235:genetics / Q000382:microbiology*; D011995:Recombination, Genetic; D012091:Repetitive Sequences, Nucleic Acid
D004262:DNA Restriction Enzymes