BIOINFORMATICS<-->STRUCTURE
Jerusalem, Israel, November 17-21, 1996

Abstract


Molecular modelling and site diected mutagenesis of the active site of endothelin converting enzyme

C.E. Sansom, V.M. Hoang and A.J. Turner

Department of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, West Yorkshire, UK.

ces@bmb.leeds.ac.uk


Mammalian endothelin-converting enzyme (ECE) is a membrane-bound zinc metalloprotease, and a member of the neprilysin sub-family. Its C-terminal domain has about 20% sequence identity to the bacterial metalloprotease, thermolysin, and contains sequence motifs characteristic of zinc metallo- proteases. From the sequence alignment of ECE with neprilysin and thermolysin, the structure of thermolysin and functional studies we constructed a preliminary molecular model of those residues likely to form the active site of ECE (Sansom et al. (1995), J. Cardiovasc. Pharmacol. 26S3, S75-S77). We examined those residues expected to be important for substrate and inhibitor binding using site directed mutagenesis with rat ECE-1.

A conserved N-A-Ar-Ar motif (residues 550-553# ; Ar = any aromatic) believed to form part of the S1 and S2 subsites is very important for activity. Changing N550 to Q or Y552 to F (the latter as in neprilysin or thermolysin) reduced specific activity to 17-20% of wild type. In thermolysin, the equivalent residue to Tyrosine 553 binds substrate or inhibitor through a water-mediated hydrogen bond from its backbone NH group. Removing this putative backbone interaction in rat ECE-1 by mutating Y553 to proline completely removes activity.

There is a conserved IGG motif N-terminal of the zinc-binding HExxH motif. Mutating G583 to Alanine has no measurable effect, but mutating G584 to Alanine removes almost all activity. Residue 589 is Valine in all ECE-1 sequences, but Methionine in bovine ECE-2. (This is the only change in any active site residue in ECE-2). Mutating this residue to Methionine in ECE-1 increases specific activity to about 350% of wild type. Tyrosine 633 is the most likely equivalent residue to Y157 in thermolysin, which can form hydrogen-bonds to a substrate or inhibitor. Mutating this residue to Phenylalanine reduces specific activity by about 20%. This change is compatible with the loss of a single hydrogen bond.

#: all numbering from rat ECE-1


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