TY - JOUR
T1 - Structures of RNA polymerase-antibiotic complexes
AU - Ho, Mary X.
AU - Hudson, Brian P.
AU - Das, Kalyan
AU - Arnold, Eddy
AU - Ebright, Richard H.
N1 - Funding Information:
We thank Tom Eck, Mira Patel, Noam Fine, and Yulia Frenkel for assistance with generation of the homology model of M. tuberculosis RNAP and for discussion. Preparation of this report was supported by NIH grant AI072766 to RHE and EA and a HHMI Investigatorship to RHE.
PY - 2009/12
Y1 - 2009/12
N2 - Inhibition of bacterial RNA polymerase (RNAP) is an established strategy for antituberculosis therapy and broad-spectrum antibacterial therapy. Crystal structures of RNAP-inhibitor complexes are available for four classes of antibiotics: rifamycins, sorangicin, streptolydigin, and myxopyronin. The structures define three different targets, and three different mechanisms, for inhibition of bacterial RNAP: (1) rifamycins and sorangicin bind near the RNAP active center and block extension of RNA products; (2) streptolydigin interacts with a target that overlaps the RNAP active center and inhibits conformational cycling of the RNAP active center; and (3) myxopyronin interacts with a target remote from the RNAP active center and functions by interfering with opening of the RNAP active-center cleft to permit entry and unwinding of DNA and/or by interfering with interactions between RNAP and the DNA template strand. The structures enable construction of homology models of pathogen RNAP-antibiotic complexes, enable in silico screening for new antibacterial agents, and enable rational design of improved antibacterial agents.
AB - Inhibition of bacterial RNA polymerase (RNAP) is an established strategy for antituberculosis therapy and broad-spectrum antibacterial therapy. Crystal structures of RNAP-inhibitor complexes are available for four classes of antibiotics: rifamycins, sorangicin, streptolydigin, and myxopyronin. The structures define three different targets, and three different mechanisms, for inhibition of bacterial RNAP: (1) rifamycins and sorangicin bind near the RNAP active center and block extension of RNA products; (2) streptolydigin interacts with a target that overlaps the RNAP active center and inhibits conformational cycling of the RNAP active center; and (3) myxopyronin interacts with a target remote from the RNAP active center and functions by interfering with opening of the RNAP active-center cleft to permit entry and unwinding of DNA and/or by interfering with interactions between RNAP and the DNA template strand. The structures enable construction of homology models of pathogen RNAP-antibiotic complexes, enable in silico screening for new antibacterial agents, and enable rational design of improved antibacterial agents.
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U2 - 10.1016/j.sbi.2009.10.010
DO - 10.1016/j.sbi.2009.10.010
M3 - Review article
C2 - 19926275
AN - SCOPUS:70549114083
SN - 0959-440X
VL - 19
SP - 715
EP - 723
JO - Current Opinion in Structural Biology
JF - Current Opinion in Structural Biology
IS - 6
ER -