Biochemical and structural basis for inhibition of Enterococcus faecalis hydroxymethylglutaryl-CoA synthase, mvaS, by hymeglusin.
Biochemical and structural basis for inhibition of Enterococcus faecalis hydroxymethylglutaryl-CoA synthase, mvaS, by hymeglusin.
复制标题
DOI:
10.1021/bi300037k
复制
发表时间:
2012-06-12
期刊:
影响因子:
2.9
通讯作者:
Miziorko HM
中科院分区:
文献类型:
--
作者:
Skaff DA;Ramyar KX;McWhorter WJ;Barta ML;Geisbrecht BV;Miziorko HM
Hymeglusin (1233A; F244; L-659-699) is established as a specific beta lactone inhibitor of eukaryotic hydroxymethylglutaryl-CoA synthase (HMGCS). Inhibition results from formation of a thioester adduct to the active site cysteine. In contrast, hymeglusin’s effects on bacterial HMG-CoA synthase, mvaS, have been minimally characterized. Hymeglusin blocks growth of Enterococcus faecalis. After removal of inhibitor from culture media, a growth curve inflection point at 3.1 hr is observed (versus 0.7 hr for uninhibited control). Upon hymeglusin inactivation of purified E. faecalis mvaS, the thioester adduct is more stable than that measured for human HMGCS. Hydroxylamine cleaves the thioester adduct; substantial enzyme activity is restored at a rate that is 8-fold faster for human HMGCS than for mvaS. Structural results explain these differences in enzyme-inhibitor thioester adduct stability/solvent accessibility. The E. faecalis mvaS-hymeglusin co-crystal structure (1.95 Å) reveals virtually complete occlusion of bound inhibitor in a narrow tunnel that is largely occluded from bulk solvent. In contrast, eukaryotic (Brassica juncea) HMGCS binds hymeglusin in a more solvent exposed cavity.