MycoSec a database for Mycobacterium secretome analysis
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Why MycoSec


Members of the genus Mycobacterium are aerobic, unicellular, non motile, gram +ve bacteria in nature with characteristic high G+C content. The  members of this family  are  highly pathogenic  causing lethal diseases in various living forms (De Voss et al., 2000). Mycobacterium extends across a varied range of host niche ranging from human and animal hosts to environmental domains (Cole et al., 2001). Mycobacteria not only includes obligate pathogens like M. tuberculosis and M. leprae but also oppurtunistic pathogens like M. abscessusM. ulcerans that visit human host under compromised conditions (Zumla and Grange, 2002).
Some eco-friendly non-pathogenic, free-living strains like M. vanbaalenii and Mycobacterium sp. strains JLS, KMS etc show the ability to degrade high and low molecular weight compounds in soil (Miller et al., 2004).
Mycobacterial infections are difficult to treat due to their cell wall, which is neither truly Gram- negative nor positive (De Voss et al., 2000). Additionally, they are naturally resistant to a number of antibiotics that disrupt cell-wall biosynthesis, such as penicillin. They can survive for a long period on exposure to acids, alkalis, detergents, oxidative bursts, lysis by complement, and many antibiotics due to their unique notorious cell wall (Goude and Parish, 2008). Most mycobacteria are susceptible to the antibiotics clarithromycin and rifamycin. Depending upon diagnosis and treatment, Mycobacteria can be classified into several major groups: M. tuberculosis complex, which can cause tuberculosis: M. tuberculosis, M. bovis, M. africanum, and M. microti; M. leprae, which causes Hansen's disease or leprosy; Nontuberculous mycobacteria (NTM) are the other members, which can cause pulmonary disease resembling tuberculosis, lymphadenitis, skin disease, or disseminated disease (Garcia et al., 2010; Niederweis et al., 2010; van Soolingen et al., 1991).
Successful mycobacterial infections depend a lot on apposite protein secretion into the extracellular environment. Thus proper research on mycobacterial "secretome" can answer various riddles pertaining to mycobacterial infection strategy and proper host-microbe interaction [8]. Secretome is popularly coined as the group of proteins secreted by a cell and has a wide range of functions ranging from cellular cross-talks to even successful pathogenesis (Bonin-Debs et al., 2004; Ranganathan and Garg, 2009).
Secreted protein represents a distinct group of proteins with respect to their structure and function and also their contribution to virulence. They are very much important for vaccine development because of their immunogenicity and potential to be recognized in early infection (Tjalsma et al., 2004; von Heijne, 1984, 1989, 1990).
In future this work will definitely help researchers in this field to study various others aspects of Mycobacterium like exploring 

  • About virulence, pathogen infection and host-pathogen interactions.

  • Help in studying localization of proteins.

  • Generation and characterization of new recombinant vaccines containing immunodominant  antigens  can be done by comparing the secretomes .

  • Knowledge of the host cell response to pathogenic microrganism is important to understand the disease process.



BONIN-DEBS, A.L., BOCHE, I., GILLE, H., and BRINKMANN, U. (2004). Development of secreted proteins as biotherapeutic agents. Expert opinion on biological therapy 4, 551-558.

COLE, S.T., EIGLMEIER, K., PARKHILL, J., JAMES, K.D., THOMSON, N.R., WHEELER, P.R., et al. (2001). Massive gene decay in the leprosy bacillus. Nature 409, 1007-1011.

DE VOSS, J.J., RUTTER, K., SCHROEDER, B.G., SU, H., ZHU, Y.Q., and BARRY, C.E. (2000). The salicylate-derived mycobactin siderophores of Mycobacterium tuberculosis are essential for growth in macrophages. Proceedings of the National Academy of Sciences 97, 1252-1257.

GARCIA, J.C., RESTREPO, S., and ZAMBRANO, M.M. (2010). Comparative analysis of six Mycobacterium tuberculosis complex genomes. Biomedica 30, 23-31.

GOUDE, R., and PARISH, T. (2008). The genetics of cell wall biosynthesis in Mycobacterium tuberculosis. Future Microbiology 3, 299-313.

MILLER, C.D., HALL, K., LIANG, Y.N., NIEMAN, K., SORENSEN, D., ISSA, B., et al. (2004). Isolation and Characterization of Polycyclic Aromatic Hydrocarbon Degrading Mycobacterium Isolates from Soil. Microbial ecology 48, 230-238.

NIEDERWEIS, M., DANILCHANKA, O., HUFF, J., HOFFMANN, C., and ENGELHARDT, H. (2010). Mycobacterial outer membranes: in search of proteins. Trends in microbiology 18, 109-116.

RANGANATHAN, S., and GARG, G. (2009). Secretome: clues into pathogen infection and clinical applications. Genome Med 1, 113.

TJALSMA, H., ANTELMANN, H., JONGBLOED, J.D.H., BRAUN, P.G., DARMON, E., DORENBOS, R., et al. (2004). Proteomics of protein secretion by Bacillus subtilis: separating the "secrets" of the secretome. Microbiology and molecular biology reviews 68, 207-233.

VAN SOOLINGEN, D., HERMANS, P.W., DE HAAS, P.E., SOLL, D.R., and VAN EMBDEN, J.D. (1991). Occurrence and stability of insertion sequences in Mycobacterium tuberculosis complex strains: evaluation of an insertion sequence-dependent DNA polymorphism as a tool in the epidemiology of tuberculosis. Journal of clinical microbiology 29, 2578-2586.

VON HEIJNE, G. (1984). How signal sequences maintain cleavage specificity. Journal of molecular biology 173, 243.

VON HEIJNE, G. (1989). The structure of signal peptides from bacterial lipoproteins. Protein engineering 2, 531-534.

VON HEIJNE, G. (1990). The signal peptide. Journal of Membrane Biology 115, 195-201.

ZUMLA, A.I., and GRANGE, J. (2002). Non-tuberculous mycobacterial pulmonary infections. Clinics in chest medicine 23, 369-376.



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