FUJINAMI SARCOMA VIRUS AND SARCOMAGENIC, AVIAN ACUTE LEUKEMIA VIRUSES HAVE SIMILAR GENETIC STRUCTURES

Abstract

The structure of the genomic RNAs and the gene products of avian Fujinami sarcoma virus (FSV) and of avian acute leukemia viruses with sarcomagenic potential, i.e., viruses of the myelocytomatosis (MC29)- and erythroblastosis (AEV)-subgroups, are compared. The genome of replication-defective FSV is a 4.5 kilobase (kb) RNA and, like the RNAs of defective acute leukemia viruses, consists of three distinct sections: an internal FSV-specific section flanked by 5′ and 3′ helper-virus-related sequences. Their related terminal sequences identify each of these viruses as belonging to the avian tumor virus group. The internal specific sequences are the structural basis for the distinction of the different subgroups of avian oncogenic viruses, i.e., the MC29-, AEV-, and FSV-subgroups. These sequences are not shared between members of different subgroups, and are not related to the src gene of the Rous subgroup of sarcoma viruses. In each of these viruses, the 5′-gag gene-related and internal specific sequences together form a genetic unit that codes for a nonstructural phosphoprotein which is probably involved in transformation. These genetic units represent less than the total coding capacity of the acute leukemia viral RNAs. However, in the case of FSV, the genetic complexities of the 4.5-kb RNA and of the 140,000-dalton, FSV-specific protein are nearly identical, a fact which excludes the synthesis of other major proteins, in the same reading frame, and suggests that this protein would be sufficient for transforming function. The 140,000-dalton FSV protein is phosphorylated in an in vitro kinase reaction by itself or an associated phosphokinase.