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Profile of Richard P. Novick PROFILE Profile of Richard P. Novick acteria are infinitely versatile, occupying every imaginable ecological niche, from miles- B deep ice cores to fuming hot springs to high-pressure cauldrons of the deep. Much of their versatility results from a remarkable ability to exchange genetic material between relatives as well as total biological strangers. To do this, they use ‘‘mobile genetic elements’’ (MGEs), which carry from one to sev- eral hundred specialization genes and maintain the ability to self-replicate and transfer themselves from one bacterium to another. Although MGEs have helped bacteria diversify, they are also responsible for virtually all lethal bacte- rial toxins, for most resistance to antibi- otics, and for much of the ability of bacteria to attach to body surfaces. Richard Novick, Professor of Microbi- ology and Medicine at New York Uni- versity (NYU, New York, NY), has Richard Novick made critical discoveries about MGEs in staphylococci. In his Inaugural Article published in this issue, Novick, who was other mouse, which it would then at- head of medicine, Paul Beeson. Beeson’s elected to the National Academy of Sci- tack,’’ says Novick. research on endocarditis and infectious ences in 2006, details the mechanism of Despite a growing interest in biology disease inspired Novick and piqued a replication of a fascinating member of and research, after graduating from lifelong interest in how microbes cause the MGE family (1). Yale in 1954, Novick entered medical disease. school at NYU, still unsure of a career Then, in 1960, Novick crossed the Reluctant Biologist goal. ‘‘Although I went to medical Atlantic to the National Institute for Medical Research in London for a post- Born and raised in New York City, Nov- school because of its rough ballpark fo- doctoral fellowship, working with micro- ick developed a love of nature during cus on science,’’ he says, ‘‘I still did not bial biochemist Martin Pollock. During weekends and summers at his family’s quite understand that my calling was research rather than medical practice.’’ his two years in London, the threads of second home in Westport, Connecticut. interest in bacterial genetics and regula- ‘‘I became an outdoor biologist very After his first year of medical school, Novick entered the laboratory of tion, plus infectious diseases, combined early,’’ says Novick. ‘‘My mom would Charles Gilvarg, with whom he would into a career-determining focus on the have a fit when she wanted to take a work for two summers on basic bacterial genetics and biology of the staphylo- bath, only to find a frog or an eel in the biochemistry. As his interest in research cocci. Pollock had put him to work on bathtub.’’ However, he did not realize became clearer, Novick considered leav- ␤-lactamase, a bacterial enzyme respon- that biology was his calling until much ing medical school to pursue a doctorate sible for staphylococcal resistance to ␤ later. In high school, he focused more at The Rockefeller University (New -lactam antibiotics, the penicillins and on the ‘‘hard’’ sciences, such as mathe- York, NY). He did not do it. Instead, he cephalosporins. Researchers had just matics, physics, and chemistry. ‘‘In those took advantage of a newly established synthesized a new penicillin drug, days, a very long time ago, biology was ‘‘Honors Program’’ at NYU that allowed called methicillin. Pollock wanted Nov- ␤ counting flies and photographing ferns,’’ medical students to take a year off to ick to test whether he could get the - he quips. ‘‘I didn’t even take the course conduct research. Novick spent his year lactamase gene in Staphylococcus to in high school because it was for sis- in the laboratory of Werner Maas, mutate to become resistant to methicil- sies.’’ His perspective changed as an un- where he studied genetic regulation of lin. ‘‘This was ethically slightly dubious; dergraduate at Yale (New Haven, CT). the arginine biosynthetic pathway in one might think twice about encourag- ‘‘I took a very inspiring biology course Escherichia coli. The experience ‘‘initi- ing resistance to a critically important with Norman Giles, which focused on ated a lifelong interest in gene regula- new antibiotic,’’ Novick says. ‘‘In the genetics and evolution,’’ he recalls. tion,’’ Novick says. course of those experiments, which ‘‘From that, I developed an interest in failed by the way, I discovered that the Rather than giving up on medicine ␤ the human mind, resulting in a major in entirely, Novick completed his medical -lactamase gene in staph was carried psychology.’’ Novick got his first taste of degree in 1959. ‘‘Then I did a series of by a plasmid,’’ he says (2). Joshua Lederberg discovered plas- serious research when he worked on a what I call ‘yo-yo’ bounces, back and mids, arguably the most important and senior thesis project with biopsychologist forth between clinical medicine and ba- Frank Beach, titled ‘‘Reward value of sic science and couldn’t quite decide aggression in mice.’’ ‘‘As I remember which way to go,’’ he says. In his first This is a Profile of a recently elected member of the National with some satisfaction, a mouse, most clinical bounce, Novick went to Yale– Academy of Sciences to accompany the member’s Inaugural likely male, would learn to perform New Haven Medical Center for an in- Article on page 14182. some task in order to gain access to an- ternship under the direction of Yale’s © 2007 by The National Academy of Sciences of the USA www.pnas.org͞cgi͞doi͞10.1073͞pnas.0707438104 PNAS ͉ September 4, 2007 ͉ vol. 104 ͉ no. 36 ͉ 14179–14181 Downloaded by guest on September 29, 2021 widespread class of MGEs, in the late spected would not acknowledge anything mids regulate their own replication (8). 1940s, determining that they were the novel in our work unless it had been He then identified a plasmid-encoded mediators of bacterial conjugation (mat- confirmed with E. coli. Then they would protein responsible for initiating plasmid ing) in E. coli. However, at the time of quote the E. coli results and not bother replication (9) and demonstrated that an Novick’s discovery, they were still poorly referring to ours. That has been a thorn anti-sense RNA molecule (10) controls understood and had been identified in in my side throughout my career.’’ replication by attenuating production of only a handful of bacterial species. ‘‘This the initiator protein (11). This protein was the first plasmid discovered in Probing Plasmids limited the rate of plasmid replication. Gram-positive bacteria,’’ says Novick. After completing the fellowship with Novick’s studies also led him to suspect ‘‘It was a discovery that was instrumen- Hotchkiss in 1965, Novick began his inde- that this regulation could work only if tal in the development of my career.’’ pendent research career at New York’s the protein were inactivated after use, Before recognition of the plasmid’s bio- Public Health Research Institute (PHRI), a hypothesis later confirmed by Avi Ra- logical significance, clinicians assumed a private, nonprofit institute founded by sooly, a postdoctoral fellow in Novick’s that conventional mutations caused clini- the city to provide a venue for basic re- laboratory (12). cal antibiotic resistance, Novick recalls. ‘‘I search on infectious diseases connected to In parallel with its plasmid studies, was taught in medical school that two the city health department. At PHRI, the Novick laboratory cloned the plas- antibiotics should always be used in treat- Novick discovered that, in addition to an- mid-encoded gene for lysostaphin, an ment since the probability of simultaneous tibiotic resistance, plasmids also carried enzyme that effectively degrades the mutations causing resistance to both was genes for resistance to toxic inorganic ions staphylococcal cell wall (13). Lyso- vanishingly small.’’ However, adds Novick, including cadmium, arsenate, arsenite, and staphin’s ability to lyse staphylococci ‘‘a remarkable observation by the late lead, which could help the bacteria sur- made it a useful reagent for laboratories Tsutomo Watanabe that the dysentery vive in a polluted environment (5). He researching the bacteria. It also sug- bacillus could become resistant to three also demonstrated the in vivo transmission gested that the enzyme could be used to or four antibiotics simultaneously during of plasmid-encoded antibiotic resistance treat staphylococcal infections. Indeed, treatment with only one, and that acquisi- among staphylococcal strains in infected Mead Johnson initiated the develop- tion of a plasmid was responsible, radically mouse kidneys (6) and began a series of ment of lysostaphin as a therapeutic changed this view and led to the realiza- studies of plasmid replication and its agent in the 1960s but quickly dropped tion that plasmids were a major source of control. it for fear that it could spark an immu- antibiotic resistance in bacteria.’’ The theory at the time was that a nological reaction, says Novick. ‘‘I didn’t This finding was ample encourage- plasmid had to be attached to the cell agree with their dropping it,’’ he says. ment for Novick to pursue the study of membrane to replicate. If this was true, ‘‘We thought it could be used therapeu- plasmids and antibiotic resistance in it would mean that the host cell con- tically even if allergenic. It was, mole- staphylococci during his time in Pol- trolled plasmid replication. Researchers for-mole, 100-fold more effective than lock’s laboratory. He developed a also thought then that the plasmid was penicillin for curing an infection in mice number of tools for the study of staphy- an accessory to the bacterial genome, (his unpublished data).’’ ‘‘It’s never lococcal genetics, including a highly sen- merely the provider of useful gene func- really gotten a fair trial,’’ he adds. In sitive assay for ␤-lactamase (3), which tions that were not encoded in the chro- addition, given the growing threat of enabled him to demonstrate that, con- mosomes.
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