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18111 Nordhoff Street
Northridge, CA 91330-8303
Phone: (818) 677-3356
Fax: (818) 677-2034
Email:biology.dept@csun.edu
Office Location:
Eucalyptus Hall 2102
Hours:
Mon-Fri: 8:00am-5:00pm

Assistant Professor
Ph.D. Yale University
email: sean.murray@csun.edu
Phone: (818) 677-2950
Fax: (818) 677-2034
Office: Eucalyptus Hall 2229
The dimorphic bacterium Caulobacter crescentus is a model organism for studying the bacterial cell cycle. Its asymmetric cell division results in one swarmer and one stalked cell progeny. Motile swarmer cells can not undergo DNA replication until they differentiate into stationary stalked cells. If sufficient nutrients are available, swarmer cells eject their polar flagellum and build a stalk (with adhesive at its end; for attaching to a surface near nutrients) at the same pole formerly occupied by the flagellum. Stalked cells are competent for DNA replication and cell division. During cell division, a flagellum is placed at the pole opposite that of the stalk. Caulobacter's obligate cell cycle is controlled by oscillating master regulators that control different genetic modules in space and time. As a result of this carefully orchestrated process, a flagellum is synthesized only when needed (just prior to cell division) and is placed at the pole opposite that of the stalk. Likewise, a new stalk is synthesized only at the pole previously occupied by a flagellum. Our lab studies the roles of lipid biosynthesis in this process, using pharmacological, genetic, and molecular approaches. Only by further elucidating the control mechanisms of bacterial cell division can we advance the development of new antimicrobial compounds. Lipid biosynthesis is essential for cell viability and bacterial fatty acid synthetic enzymes have been suggested as antibiotic targets. In fact, compounds specific to bacterial fatty acid biosynthetic compounds have been generated. Most previous studies on bacterial lipid metabolism have focused on E. coli, a gamma-proteobacteria. Caulobacter in contrast, as an alpha-proteobacteria, is closely related to human pathogenic bacteria, such as Brucella and Rickettsia.
Additional Academic History:
1997 B.S., Biology and Psychology, Summa Cum Laude, Montclair State University, NJ
1999 M.S., Biology,Yale University, New Haven, CT
2000 M.Phil., Biology, Yale University, New Haven, CT
2003-2007 Postdoctoral Fellow in Dr. Lucy Shapiro’s laboratory at Developmental Biology Department, Stanford University, Stanford, CA
2004 J. Spangler Nicholas Prize for best Ph.D. thesis in Molecular, Cellular and Developmental Biology at Yale University
Representative Publications:
LH Lee, B Lustigman, S Murray, S Koepp. 1999. Effect of selenium on the growth of the Cyanobacterium Anacystis nidulans. Bull. Environ. Contam. Toxicol. 62: 591-599.
SR Murray, D Bermudes, K Suwwan de Felipe, and KB Low. 2001. Extragenic suppressors of growth defects in msbB Salmonella. J. Bacteriol. 183: 5554-5561.
LH Lee, B Lustigman, SR Murray. 2002. Combined effect of mercuric chloride and selenium dioxide on the growth of the Cyanobacteria Anacystis nidulans. Bull. Environ. Contam. Toxicol. 69: 900-907.
SR Murray, K Suwwan de Felipe, PL Obuchowski, J Pike, D Bermudes and KB Low. 2004. Hot spot for a large deletion in the 18-19 Cs region confers a multiple phenotype in Salmonella enterica serovar Typhimurium strain ATCC 14028. J. Bacteriol. 186: 8516-23.
Collier J, SR Murray, and L Shapiro. 2006. DnaA couples DNA replication and the expression of two cell cycle master regulators. EMBO J. 25: 346-356.
SR Murray, RK Ernst, D Bermudes, SI Miller, and KB Low. 2007. PmrA(Con) confers pmrHFIJKL-dependent EGTA and polymyxin resistance on msbB Salmonella by decorating lipid A with phosphoethanolamine. J. Bacteriol. 189:5161-5169.