The Discovery of Reverse Transcriptase
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چکیده
In 1961, Howard Temin began to gather evidence that was inconsistant with the central dogma. Temin, who devoted his life to studying RNA tumor viruses (now known as retroviruses), focused his early work on Rous sarcoma virus (RSV). This RNA virus is capable of transforming normal cells into cancerous cells. Temin felt the best explanation for the virus’s behavior was a model whereby the virus remains in a dormant, or proviral, state in the cell. However, since RNA is notoriously unstable, Temin proposed that the RNA genome of RSV is converted into a DNA provirus. With this model in mind, he set out to prove his hypothesis. He amassed data showing that RSV is sensitive to inhibitors of DNA synthesis and suggesting that DNA, complementary to the RSV genomic RNA, is present in transformed cells. Other researchers, however, remained unconvinced. A definitive experiment would be required to finally prove his model. Meanwhile, another virologist, David Baltimore, had been studying the replication of viruses. He was taking a biochemical approach, looking directly for RNA and DNA synthesis in the virions themselves. Previously he had isolated an RNA-dependent RNA polymerase activity in virions of vesicular stomatitis virus, a nontumorigenic RNA virus. His attention then turned to the RNA tumor viruses, finally settling on the Rauscher murine leukemia virus (R-MLV). With this organism, he would independently prove Temin’s model.
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