Dubey Vinod S, Sirakova Tatiana D, Cynamon Michael H, Kolattukudy Pappachan E
Biomolecular Science Center, University of Central Florida, Orlando, Florida 32816, USA.
J Bacteriol. 2003 Aug;185(15):4620-5. doi: 10.1128/JB.185.15.4620-4625.2003.
We show that the disruption of one of the mycocerosic acid synthase (mas)-like genes, msl5 (pks8 plus pks17) in Mycobacterium tuberculosis H37Rv generates a mutant incapable of producing monomethyl branched unsaturated C(16) to C(20) fatty acids that are minor constituents of acyltrehaloses and sulfolipids. The msl5 mutation did not cause any significant change in the acyl lipid composition and also did not affect growth in culture, in mouse alveolar macrophage cell line MH-S, or in the murine lung.
我们发现,结核分枝杆菌H37Rv中一个类霉菌酸合酶(mas)样基因msl5(pks8加pks17)的破坏产生了一个突变体,该突变体无法产生单甲基支链不饱和C(16)至C(20)脂肪酸,这些脂肪酸是酰基海藻糖和硫脂的次要成分。msl5突变在酰基脂质组成上没有引起任何显著变化,也不影响在培养基中、小鼠肺泡巨噬细胞系MH-S或小鼠肺中的生长。