Röse Lars, Kaufmann Stefan H E, Daugelat Sabine
Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 21-22, D-10117 Berlin, Germany.
Microbes Infect. 2004 Sep;6(11):965-71. doi: 10.1016/j.micinf.2004.05.011.
We describe a Mycobacterium smegmatis mutant with impaired biofilm and smegma formation. A gene homologous to Escherichia coli bacA, which has been proposed to play a role as undecaprenyl phosphokinase (Upk) was unmarked in-frame deleted from M. smegmatis. Though Upk is involved in cell wall synthesis, the surface of the mutant strain appeared virtually comparable to that of the wild type by electron microscopy. The absence of Upk influenced colony morphology and bacitracin resistance. The M. smegmatis Deltaupk mutant developed a biofilm characterized by scattered islands of bacteria distinct from the completely covered biofilm surface observed for wild-type bacteria. We further demonstrate biological consequences of upk deletion for smegma development in an in vivo model. These results suggest the upk gene to be essential in biofilm and smegma development.
我们描述了一种耻垢分枝杆菌突变体，其生物膜形成和包皮垢形成受损。在耻垢分枝杆菌中，一个与大肠杆菌bacA同源的基因（该基因被认为作为十一异戊烯磷酸激酶（Upk）发挥作用）被无标记框内缺失。尽管Upk参与细胞壁合成，但通过电子显微镜观察，突变菌株的表面与野生型几乎相当。Upk的缺失影响了菌落形态和对杆菌肽的抗性。耻垢分枝杆菌Deltaupk突变体形成了一种生物膜，其特征是细菌呈分散的岛屿状，与野生型细菌观察到的完全覆盖的生物膜表面不同。我们进一步在体内模型中证明了upk缺失对包皮垢发育的生物学影响。这些结果表明upk基因在生物膜和包皮垢发育中至关重要。
