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Background    Mycobacterium tuberculosis  ( M.tb ), the pathogen that causes tuberculosis, is capable of staying asymptomatically in a latent form, persisting for years in very low replicating state, before getting reactivated to cause active infection. It is therefore important to study  M.tb  chromosome replication, specifically its initiation and regulation. While the region between  dnaA  and  dnaN  gene is capable of autonomous replication, little is known about the interaction between DnaA initiator protein,  oriC  origin of replication sequences and their negative effectors of replication.    Methodology/Principal Findings  By KMnO 4  mapping assays the sequences involved in open complex formation within  oriC , mediated by  M.tb  DnaA protein, were mapped to position −500 to −518 with respect to the  dnaN  gene. Contrary to  E. coli , the  M.tb  DnaA in the presence of non-hydrolysable analogue of ATP (ATPγS) was unable to participate in helix opening thereby pointing to the importance of ATP hydrolysis. Interestingly, ATPase activity in the presence of supercoiled template was higher than that observed for DnaA box alone.  M.tb  rRv1985c, a homologue of  E.coli  IciA ( I nhibitor of  c hromosomal  i nitiation) protein, could inhibit DnaA-mediated  in-vitro  helix opening by specifically binding to A+T rich region of  oriC , provided the open complex formation had not initiated. rIciA could also inhibit  in-vitro  replication of plasmid carrying the  M.tb  origin of replication.    Conclusions/Significance  These results have a bearing on the functional role of the important regulator of  M.tb  chromosomal replication belonging to the LysR family of bacterial regulatory proteins in the context of latency.

In-Vitro Helix Opening of M. tuberculosis oriC by DnaA Occurs at Precise Location and Is Inhibited by IciA Like Protein