作者: Anne Edwards , Marijke Frederix , Florence Wisniewski-Dyé , Jacob Jones , Angeles Zorreguieta
DOI: 10.1128/JB.01650-08
关键词: Mutant 、 Biology 、 Quorum sensing 、 Rhizobium 、 Rhizobium leguminosarum 、 Regulation of gene expression 、 Homoserine 、 Biochemistry 、 Cell biology 、 Gene expression 、 Regulator gene
摘要: To understand how the Rhizobium leguminosarum raiI-raiR quorum-sensing system is regulated, we identified mutants with decreased levels of RaiI-made N-acyl homoserine lactones (AHLs). A LuxR-type regulator, ExpR, required for raiR expression, and RaiR to induce raiI. Since (and raiI) expression also reduced in cinI cinR mutants, thought CinI-made AHLs may activate ExpR raiR. However, added did not a mutant. The was due lack cinS immediately downstream cinI. encodes 67-residue protein, translationally coupled CinI, acts expR induction. Cloned R. caused an unusual collapse colony structure, this delayed by mutation expR. phenotype looked like loss exopolysaccharide (EPS) integrity; mutations cinI, cinR, cinS, all plyB, encoding EPS glycanase, plyB abolished effect cloned on morphology. We conclude that CinS act increase PlyB levels, thereby influencing bacterial surface. conserved other rhizobia, including etli; previously observed decreasing swarming strain primarily rather than AHL. mediates regulation because it coregulated AHL synthase demonstrate its regulatory effects can occur absence AHLs.