Glycogenomics of Mycobacterium tuberculosis

Glycogen is an important energy store of almost all living organisms. It is an alpha linked polymer comprised of thousands of glucose units. In bacteria it is usually synthesized when carbon ions are in excess in the growth medium and its synthesis helps for the survival of the bacteria under such nutritional conditions. Mycobacterium tuberculosis (M. tuberculosis), accumulates glycogen during the adverse condition such as reactive oxygen and nitrogen intermediates, low pH, nutrients and other vital element starvation for their survival in the host. Glycogen also plays a very important role in the pathogenesis of M. tuberculosis. The biosynthesis of glycogens is mediated by glycosyltransferases enzyme which can be divided into two families; glycogen transferase (GT) 3 and glycosyltransferases GT 5. Regulation of glycogen metabolism in bacteria involves a complex mechanism, involving several synthase enzymes such as glycogen synthase A (glgA), glycogen branching enzyme (glgB), and catalytic enzyme (glgC). Another enzyme known as glycogen phosphorylase (glgP), removes extra units of glucose from the non- reducing ends of the glycogen molecule. Several workers have recognized role of glycogen in Mycobacterial pathogenesis, in the recent years. Trehalose-dimycolate (TDM) and trehalose-monomycolate (TMM) present in the cell wall are indeed a precursor of mycolic acid of Mycobacteria, which plays an important role in its invasion and pathogenesis. This review focuses on various cycles and mechanisms involved in the glycogen synthesis in M. tuberculosis and its role in pathogenesis.