Protease-catalyzed splicing of peptide bond


 

Principal Investigator :    Rajendra P Roy

Research Associate
M V S Sivaram

PhD students
R Sudha
S R Balajee
Lavanya Anantharaman

The two major themes of the project are A) understanding the structural and mechanistic imperatives of peptide ligation reactions catalyzed by proteases and, B) engineering of new and novel hemoglobin tetramers to delineate intermolecular interactions in the sickle hemoglobin fiber.

A.    Protease-catalyzed splicing of native peptide fragments

Model studies on reverse proteolytic condensation reactions utilizing natural or designer peptide segments is the objective of the research.

In the reporting year, we explored if the volume exclusion effect or the ability of the crowding molecules to strengthen the associative interactions between non-covalently held segments could facilitate the splicing of discontiguity sites in fragment complementing systems. RNase A and triosephosphate isomerase (TIM) were chosen as model system for this study. The respective proteins were proteolyzed by subtilisin in dilute aqueous solution and their re-formation followed in the presence of crowded media such as polyethyleneglycol (PEG) and dextran. The ligation reactions were also carried out in the presence of organic cosolvents to serve as controls.

The multiply nicked (six or more fragments) TIM was converted into intact TIM in the presence of dextran or PEG albeit with slower kinetics as compared with that observed in the presence of aqueous-acetonitrile solution. Interestingly, a single nick in RNase A could not be ligated under similar conditions in the crowded milieu. The control reaction in the presence of glycerol proceeded smoothly. The failure of synthesis in the case of RNase A suggest that conversion of RNase S to RNase A may not be accompanied by sufficient reduction in volume exclusion. This is consistent with the fact that the crystal structures of RNase S and RNase A are almost superimposable. In contrast, considerable compaction, and consequently large volume reduction is attained in the case of TIM re-formation.

B.    Chemo-enzymic engineering of proteins

Site-specific incorporation of natural and/or nonstandard amino acids in hemoglobin to probe the intermolecular interactions in sickle hemoglobin (HbS) fiber is the objective of this work.

In the reporting year, further studies on the polymerization of HbS twin peaks [HbS (a113His®Leu)] were done with the idea to delineate the quinary interactions of a113 site in the HbS fiber. Towards this, we constructed HbA Twin Peaks and carried out co-polymerization studies. The rationale of the study was based on the fact that while a deoxygenated stoichiometric mix of HbA twin peaks and HbS would be largely populated by tetramers with a113 site in the trans configuration, a similar mixture containing HbS twin peaks and HbA would be dominated by tetramers with the mutant site in the cis orientation. Thus a comparative analysis of equilibrium solubility (Csat) of these mixtures with that of the HbS/HbA mixture would provide insights into the relative contributions of the cis/trans stereochemistry of the a113 site in the polymerization of HbS. The Csat value of the ‘trans’ mixture was found to be similar to that of the control HbA/HbS mixture suggesting that the site was inactive in the trans configuration. Consistent with this, the ‘cis’ mixture yielded a Csat that was significantly higher than the control sample. These results establish that a113 site facilitates the fiber assembly only when present in the cis orientation i.e in the same ab dimer that contains the ‘active’ val6b.

We earlier reported the studies on the interactions between a113 with a16 or a23 amino acid residues, proximal sites located in the AB-GH region of the molecule. We observed that the inhibitory effect of a113 was additive with a16 but not with a23. In our continued efforts to delineate interaction-linkage map of participating residues, we initiated studies to examine concerted interactions, if any, between two well separated a-chain contact sites. Two sites, a16 (AB) and a78 (EF) were chosen for this study. We intended to use the chemo-enzymatic strategy for the construction of a-globin mutants, namely, the propensity of V8 protease to catalyze the ligation of complementary fragments, a1-30 and a31-141 to generate a full-length a-globin (a1-141). We wished to introduce mutation at a16 through a synthetic a1-30 segment and that at a78 by using the a31-141 fragment from the a-chain of Hanuman Langur (Presbytis entellus) hemoglobin. The reported sequence of the a-chain of langur differs from human at only three sites; a19Ala®Gly, a21Ala®Gly, and a78Asn®His.

The Hb samples from Langur, surprisingly, yielded two chromatographically distinct a-chains. The mass spectrometric analysis, tryptic peptide mapping and amino acid sequencing of the tryptic peptides lead to the identification of a variant that differed from the documented sequence only at a78 site (His®Gln). The discovery of this new variant provided us with an opportunity to probe the influence of the microenvironment of this site on the polymerization reaction. Accodingly, we prepared respective hybrid tetramers of the two chains with the bs-chain. Both the HbS hybrid tetramers (a2 78Asn®His b2S, and a2 78Asn®Gln b2S) displayed near UV and soret region CD spectra that was very similar to native HbS. The oxygen binding properties as reflected by the P50 (half-maximal binding) value was found to be normal. However, preliminary results of polymerization studies appear to reveal differences in the behavior of the two hybrids. Detailed studies on kinetics of polymerization and equilibrium solubility of the hybrids and the preparation of the double (a16, a78) mutant HbS are in progress.

Publications

Original peer-reviewed articles

1.     *Sivaram MVS, Sudha R and Roy RP (2001) A role for a113 (GH1) amino acid residue in the polymerization of sickle hemoglobin: Evaluation of its inhibitory strength and interaction linkage with two fiber contact sites (a16/23) in the AB region of the a-chain. J Biol Chem 276:18209-18215 (*in press last year, since published).