The major sources of D-AAs in bacteria are extracellular or periplasmic biomolecules:
D-Ala and D-Glu are routinely found in the peptidoglycan cell wall of bacteria and may contribute to antibiotic resistance in some bacteria.
D-AAs play a role in bacterial cell wall formation during stationary phase.
Many diverse bacterial phyla synthesize and release D-AAs, including D-Met and D-Leu. These D-AAs regulate cell wall remodeling in stationary phase and cause biofilm dispersal in aging bacterial communities. The primary mode of variation between peptidoglycan structures is in the length and composition of the interpeptide bridge that can contain: D-Ala, D-Glu, D-Ser, D-Asp, D-Asn, D-Lys and D-Orn.
D-AAs in cell culture supernatant impact PG functionality through their incorporation in PG: paracrine regulators in microbial communities. The bacteria release and use D-AAs to decrease cell wall formation when resources are scarce. Thus, the D-AAs help bacteria adapt to adverse environmental conditions.
Periplasmic or extracellular transpeptidases are responsible for incorporation of D-AAs into mature PGs.
D-AAs are proposed to disassemble biofilms, to inhibit spore germination and to be produced depending on stress response-related sigma factor RpS (in V. cholera).
It has been postulated that marine invertebrates (e.g., crab, shrimp, lobster) may use D-AAs for osmoregulation and/or a source of L-AAs under adverse conditions. D-Asp was found in all microalgae, but D-Ala was only present in the marine diatoms.
The platypus, funnel web spider, and cone snail all have D-AAs in their venom. Isomerases in these organisms are thought to produce the D-AAs needed for the venom (Allan et al., 2005).
0,2-8% relative to L-AAs.
Plants contain a D-AA level