Deretic V, Martin D W, Schurr M J, Mudd M H, Hibler N S, Curcic R, Boucher J C
Department of Microbiology, University of Texas Health Science Center, San Antonio 78284-7758.
Biotechnology (N Y). 1993 Oct;11(10):1133-6. doi: 10.1038/nbt1093-1133.
Chronic respiratory complications in cystic fibrosis, compounded by recurring infections with mucoid Pseudomonas aeruginosa and the associated inflammation, are the primary cause of high mortality in this inheritable disease. Since the conversion of P. aeruginosa into the exopolysaccharide alginate overproducing strains plays a critical role in the establishment of chronic infection, studies are directed towards understanding the processes underlying this phenomenon. The genes (algU, mucA, and mucB) and genetic alterations responsible for conversion to mucoidy have been recently characterized. The mutations leading to the emergence of mucoid strains are superimposed on a regulatory system with elements that resemble those controlling other aspects of bacterial developmental physiology.
囊性纤维化中的慢性呼吸并发症，再加上黏液样铜绿假单胞菌反复感染及相关炎症，是这种遗传性疾病高死亡率的主要原因。由于铜绿假单胞菌转变为过量产生胞外多糖藻酸盐的菌株在慢性感染的形成中起关键作用，因此研究方向是了解这一现象背后的过程。最近已对导致转变为黏液样的基因（algU、mucA和mucB）及基因改变进行了表征。导致黏液样菌株出现的突变叠加在一个调控系统上，该系统的元件类似于控制细菌发育生理学其他方面的元件。
