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Ph.D. Yale University
Phone: (818) 677-2950
Fax: (818) 677-2034
Office: Eucalyptus Hall 2205
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
Recent Publications (= equal first author; bold member of Murray Lab)
V Karsten=, SR Murray=, J Pike, K Troy, M Ittensohn, M Kondradzhyan, KB Low, and D Bermudes. 2009. msbB deletion confers acute sensitivity to CO2 in Salmonella enterica serovar Typhimurium that can be suppressed by a loss-of-function mutation in zwf. BMC Microbiol. 9:170.
TC Chu, SR Murray, SF Hsu, Q Vega, and LH Lee. 2011. Temperature-induced activation of freshwater Cyanophage AS-1 prophage. Acta Histochemica 113:294-9.
TC Chu, SR Murray, J Todd, W Perez, JR Yarborough, C Okafor, and LH Lee. 2012. Adaption of Synechococcus sp. IU 625 to growth in the presence of mercuric chloride. Acta Histochemica 114:6-11.
AE Forest=, GG Goldstine=, Y Schrodi, and SR Murray. 2012. Use of bacteria for rapid, pH neutral, hydrolysis of hydrophobic carboxylic acid esters useful in synthetic chemistry. Biocatalysis and Biotransformation 30:435–439.
AT Schredl, YG Perez Mora, A Herrera, MP Cuajungco, SR Murray. 2012. The Caulobacter ctrA P1 promoter is essential for the coordination of cell cycle events that prevent the overinitiation of DNA replication. Microbiology 158:2492-403.
A de Oliveira, SD Adams, LH Lee, SR Murray, SD Hsu, JR Hammond, D Dickinson, P Chen, TC Chu. 2013. Inhibition of Herpes Simplex Virus type 1 with the modified green tea polyphenol palmitoyl-epigallocatechin gallate. Food and Chemical Toxicology. 54:207-215.