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Structure and cooperativity of a T-state mutant of histidine decarboxylase from Lactobacillus 30a
Authors:Worley Scott  Schelp Elisabeth  Monzingo Arthur F  Ernst Stephen  Robertus Jon D
Institution:Institute of Cellular and Molecular Biology, Department of Chemistry and Biochemistry, University of Texas, Austin, Texas 78712, USA.
Abstract:Histidine decarboxylase (HDC) from Lactobacillus 30a converts histidine to histamine, a process that enables the bacteria to maintain the optimum pH range for cell growth. HDC is regulated by pH; it is active at low pH and inactive at neutral to alkaline pH. The X-ray structure of HDC at pH 8 revealed that a helix was disordered, resulting in the disruption of the substrate-binding site. The HDC trimer has also been shown to exhibit cooperative kinetics at neutral pH, that is, histidine can trigger a T-state to R-state transition. The D53,54N mutant of HDC has an elevated Km, even at low pH, indicating that the enzyme assumes the low activity T-state. We have solved the structures of the D53,54N mutant at low pH, with and without the substrate analog histidine methyl ester (HME) bound. Structural analysis shows that the apo-D53,54N mutant is in the inactive or T-state and that binding of the substrate analog induces the enzyme to adopt the active or R-state. A mechanism for the cooperative transition is proposed.
Keywords:histidine decarboxylase  helix disorder  enzyme activation  mutation  cooperativity
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