“…D-Alanyl esters of WTA, which have a lower content of D-alanine, are derived from those of D-alanyl-LTA (Perego et al, 1995;Neuhaus and Baddiley, 2003). Studies of dlt mutants have shown that D-alanyl ester depletion of TA affects a variety of phenotypes of Gram-positive bacteria including biofilm formation (Gross et al, 2001), adherence (Abachin et al, 2002;Kristian et al, 2005), co-aggregation (Clemans et al, 1999), acid tolerance (Boyd et al, 2000;Kristian et al, 2005), autolysis (Wecke et al, 1996;Kristian et al, 2005;Steen et al, 2005;Palumbo et al, 2006), resistance to cationic peptides including defensins (Peschel et al, 1999;Poyart et al, 2003;Kristian et al, 2005;Kovács et al, 2006), and virulence (Abachin et al, 2002;Collins et al, 2002;Poyart et al, 2003). Because of their increased negative cell surface charge, dlt mutants bind positively charged compounds such as autolysins and antimicrobial peptides (defensins) more avidly, resulting in increased cell lysis and sensitivity respectively (Wecke et al, 1996;Peschel et al, 1999;Poyart et al, 2003;Kristian et al, 2005;Steen et al, 2005;Kovács et al, 2006;Palumbo et al, 2006).…”