01842nas a2200301   4500000000100000008004100001260000900042653002600051653003100077653001400108653001600122653001100138653002400149653002000173653002200193653002800215653001800243653001800261653001800279653003100297100001600328700001400344245003400358300001000392490000700402520111700409022001401526       1995                            d  c199510aCarbohydrate Sequence10aCell Membrane Permeability10aCell Wall10aGlycolipids10aHumans10aLipopolysaccharides10aMembrane Lipids10aMembrane Proteins10aMolecular Sequence Data10aMycobacterium10aMycolic Acids10aPeptidoglycan10aPolysaccharides, Bacterial1 aBrennan P J1 aNikaido H00aThe envelope of mycobacteria.  a29-630 v643 a<p>Mycobacteria, members of which cause tuberculosis and leprosy, produce cell walls of unusually low permeability, which contribute to their resistance to therapeutic agents. Their cell walls contain large amounts of C60-C90 fatty acids, mycolic acids, that are covalently linked to arabinogalactan. Recent studies clarified the unusual structures of arabinogalactan as well as of extractable cell wall lipids, such as trehalose-based lipooligosaccharides, phenolic glycolipids, and glycopeptidolipids. Most of the hydrocarbon chains of these lipids assemble to produce an asymmetric bilayer of exceptional thickness. Structural considerations suggest that the fluidity is exceptionally low in the innermost part of bilayer, gradually increasing toward the outer surface. Differences in mycolic acid structure may affect the fluidity and permeability of the bilayer, and may explain the different sensitivity levels of various mycobacterial species to lipophilic inhibitors. Hydrophilic nutrients and inhibitors, in contrast, traverse the cell wall presumably through channels of recently discovered porins.</p>  a0066-4154