Arabinosyltransferase A (EmbA), Arabinosyltransferase B (EmbB), Arabinosyltransferase C (EmbC) (EmbA, EmbB, EmbC)

The **arabinosyltransferases EmbA, EmbB, and EmbC** are integral membrane enzymes in the GT-C superfamily, uniquely present in mycobacteria and related genera[2][7]. They catalyze the transfer of arabinofuranosyl residues from the lipid-linked donor decaprenylphosphoryl-D-arabinofuranose (DPA) to growing polysaccharide chains in the cell envelope—specifically, *arabinogalactan* (AG) and *lipoarabinomannan* (LAM), two essential components that give *Mycobacterium tuberculosis* its distinctive and resilient cell wall[1][3][5][7]. *EmbA* and *EmbB* function together in the branching and elongation of the arabinan chain in arabinogalactan, while *EmbC* is principally involved in synthesizing and elongating LAM[2][3][4][7]. All three are targets of the first-line anti-tuberculosis drug **ethambutol**, which inhibits their activity, leading to defective cell wall biosynthesis and, ultimately, bacterial death[3][7][8]. Mutations (particularly in embB) are associated with clinical ethambutol resistance and serve as molecular markers for drug-resistant tuberculosis[4][5]. These enzymes are essential for bacterial viability and have no direct analog in humans, making them prominent and specific therapeutics targets for anti-mycobacterial agents.

Other names

Emb familyEmb arabinosyltransferasesMycobacterial arabinosyltransferase

Inhibition of arabinosyltransferase activity, blocking cell wall arabinan biosynthesis and thus cell wall assembly[3][7][8]. Drug (ethambutol) competes with the natural substrate (decaprenyl-phosphate-arabinose, DPA) at the active site[4][8].