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A Developmental Role for Fatty Acids in Eukaryotes

Public Library of Science
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  • Medicine


PLBI0209_1243-1277.indd PLoS Biology | 1243 Open access, freely available online September 2004 | Volume 2 | Issue 9 | e292 Research Digest Synopses of Research Articles Evolution of a Primate Defense against Intragenomic Infi ltrators DOI: 10.1371/journal.pbio.0020292 Anyone who uses a word processor is likely thankful for the spell checker program. But that autocorrect function can introduce errors, “correcting” the spelling of words to fi t its stored repertoire, which is decidedly limited. Take that one step further and imagine a rogue program that destroys the coherence and meaning of your prose by swapping out one letter for another throughout the document. That’s the situation retroviruses like the human immunodefi ciency virus (HIV) face during the course of their infectious cycle, when a protein encoded by the host genome slips into the virus, mutates the virus’s genetic material, and alters the viral genome. The gene, APOBEC3G, belongs to a family of primate genes that produce enzymes (in this case, APOBEC3G) that “edit” DNA and RNA, by slipping into viral particles and inducing mutations that replace one base (cytosine) with another (uracil) as the virus undergoes reverse transcription in the host cell’s cytoplasm. The edited virus fails to replicate. HIV, in turn, generates a protein called Vif that binds to the APOBEC3G enzyme and targets it for degradation, thereby eliminating its antiviral activity. Since the protein-binding regions that govern these interactions have a direct effect on the fi tness of both virus and host, one would expect to see the proteins angling for advantage, with Vif maximizing its ability to recognize APOBEC3G and APOBEC3G doing its best to evade Vif. Such battles are thought to result in frequent mutations that alter the amino acids involved in the interaction; the perpetuation of such advantageous mutations is called positive selection. In this issue of PLoS Biology, Sara Saw

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