Glucosyltransferase that uses UDP-glucose as the sugar donor to elongate alpha-(1->4)-glucans. Is involved in the biosynthesis of both 6-O-methylglucosyl lipopolysaccharides (MGLP) and glycogen. May also use ADP-glucose as substrate. [(1->4)-alpha-D-glucosyl](n) + UDP-alpha-D-glucose = [(1->4)-alpha-D-glucosyl](n+1) + H(+) + UDP Glycan biosynthesis; glycogen biosynthesis. Inactivation of Rv3032 affects the production of both glycogen (two-fold reduction) and 6-O-methylglucosyl lipopolysaccharides (MGLP), but not that of capsular alpha-D-glucan. Cells lacking this gene are not affected in their multiplication or persistence in the BALB/c mouse infection model. They also show a slightly slower growth than that of wild-type at 37 degrees Celsius and a completely abolished growth at 39 degrees Celsius. Moreover, in contrast to wild-type, they are exceptionally sensitive to the TreS inhibitor validamycin A; the sensitivity is abolished by overexpression of TreS. Attempts to disrupt both the Rv3032 gene and glgA in order to create a mutant simultaneously deficient in both alpha-1,4-glucosyltransferases turned out to be unsuccessful. Thus, M.tuberculosis H37Rv requires a functional copy of at least one of these two genes for growth. Moreover, it is not possible to inactivate Rv3032 in a mutant lacking treS, suggesting the joint essentiality of the different alpha-(1->4)-glucans biosynthesis pathways involving these two genes. Belongs to the glycosyltransferase group 1 family.