Proton-coupled antiporter flippase that catalyzes the translocation, from the inner to the outer leaflet of the cell membrane, of the lipid-linked disaccharide (anchor-LLD) that anchors lipoteichoic acids (LTA) to the cell membrane (PubMed:32367070, PubMed:17209021). Displays high selectivity towards the headgroup of its substrate (PubMed:32367070). Plays an important role during infection (PubMed:17209021). Contributes to S.aureus survival under physiological acidic conditions (PubMed:32367070). Flipping activity is inhibited by increasing concentrations of gentiobiose, a disaccharide with the same chemical composition and conformation as the anchor-LLD headgroup. Not inhibited by other disaccharides such as lactose, sucrose and trehalose at a similar concentration. Cell wall biogenesis; lipoteichoic acid biosynthesis. Interacts with YpfP/UgtP, LtaS, and with numerous cell division and peptidoglycan synthesis proteins. Distributed all around the membrane. The N-terminal hydrophilic pocket is crucial for flipping activity. The central cavity of LtaA shows a unique amphiphilic architecture. Deletion mutant does not show a growth defect at high pH, but it shows very strong growth retardation at low pH (PubMed:32367070). At low pH, mutant displays aberrant cell morphologies, including enlarged cells, defects in the formation and localization of the division septum and abnormal cell-wall shape (PubMed:32367070). Inactivation of the gene causes structural changes in staphylococcal LTA but does not affect glycolipid synthesis (PubMed:17209021). Mutants lacking this gene display a virulence defect in a murine abscess model (PubMed:17209021). Belongs to the major facilitator superfamily. LtaA family.