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Rifamycins do not function by allosteric modulation of binding of Mg2+ to the RNA polymerase active center.


ABSTRACT: Rifamycin antibacterial agents inhibit bacterial RNA polymerase (RNAP) by binding to a site adjacent to the RNAP active center and preventing synthesis of RNA products >2-3 nt in length. Recently, Artsimovitch et al. [(2005) Cell 122:351-363] proposed that rifamycins function by allosteric modulation of binding of Mg(2+) to the RNAP active center and presented three lines of biochemical evidence consistent with this proposal. Here, we show that rifamycins do not affect the affinity of binding of Mg(2+) to the RNAP active center, and we reassess the three lines of biochemical evidence, obtaining results not supportive of the proposal. We conclude that rifamycins do not function by allosteric modulation of binding of Mg(2+) to the RNAP active center.

SUBMITTER: Feklistov A 

PROVIDER: S-EPMC2567451 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature

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Rifamycins do not function by allosteric modulation of binding of Mg2+ to the RNA polymerase active center.

Feklistov Andrey A   Mekler Vladimir V   Jiang Qiaorong Q   Westblade Lars F LF   Irschik Herbert H   Jansen Rolf R   Mustaev Arkady A   Darst Seth A SA   Ebright Richard H RH  

Proceedings of the National Academy of Sciences of the United States of America 20080911 39


Rifamycin antibacterial agents inhibit bacterial RNA polymerase (RNAP) by binding to a site adjacent to the RNAP active center and preventing synthesis of RNA products >2-3 nt in length. Recently, Artsimovitch et al. [(2005) Cell 122:351-363] proposed that rifamycins function by allosteric modulation of binding of Mg(2+) to the RNAP active center and presented three lines of biochemical evidence consistent with this proposal. Here, we show that rifamycins do not affect the affinity of binding of  ...[more]

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