Specificity of disease induced by M-MuLV chimeric retroviruses containing v-myc or v-src is not determined by the LTR.
The long terminal repeats (LTRs) of defective Moloney Murine Leukemia Virus (M-MuLV) containing the avian v-myc and v-src oncogenes were exchanged for LTRs from murine retroviruses inducing myeloid and erythroid disease, in an attempt to retarget disease specificity. Chimeric MuLVs containing either the Myeloproliferative sarcoma virus or the Rauscher mink cell focus-inducing virus LTRs induced the same disease as the parental viruses, suggesting that for these viruses the v-myc and v-src oncogenes are the major determinants in the disease specificity. However, substitution of the LTRs did affect the efficiency of tumorigenesis.
Department of Medicine, UCLA School of Medicine.
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Feuer
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Lee
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Pattengale
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Fan
D000818:Animals; D001358:Avian Sarcoma Viruses / Q000235:genetics; D002478:Cells, Cultured; D002678:Chimera; D003001:Cloning, Molecular; D004273:DNA, Neoplasm / Q000235:genetics; D016259:Genes, myc; D016391:Genes, src; D007942:Leukemia, Experimental / Q000209:etiology* / Q000382:microbiology; D051379:Mice; D008979:Moloney murine leukemia virus / Q000235:genetics / Q000502:physiology*; D011925:Rauscher Virus / Q000235:genetics; D012091:Repetitive Sequences, Nucleic Acid
D004273:DNA, Neoplasm