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The FNR‐type transcriptional regulator SinR controls maturation of Agrobacterium tumefaciens biofilms
Author(s) -
Ramey Bronwyn E.,
Matthysse Ann G.,
Fuqua Clay
Publication year - 2004
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2004.04079.x
Subject(s) - agrobacterium tumefaciens , biofilm , biology , mutant , regulator , microbiology and biotechnology , transcription (linguistics) , wild type , transcription factor , gene , bacteria , genetics , transformation (genetics) , linguistics , philosophy
Summary Agrobacterium tumefaciens is a plant pathogen that persists as surface‐associated populations on plants or soil particles. A genetic screen for A. tumefaciens mutants deficient for surface interactions identified a mutant that forms thin, sparsely populated biofilms, but is proficient for initial attachment. The mutant is disrupted in a gene designated sinR , encoding a member of the DNR subfamily of FNR‐type transcription regulators. SinR is required for normal maturation of A. tumefaciens biofilms on both inert surfaces and plant tissues, and elevated sinR expression results in accelerated biofilm formation. Expression of sinR is increased close to 30‐fold in cultures grown in oxygen‐limited environments and is also induced within biofilms grown under oxic conditions. A consensus FNR box, the presumptive binding site for FNR‐type proteins, is located upstream of the sinR promoter. FnrN, a second A. tumefaciens FNR‐like regulator, is required for induction of sinR in oxygen‐limited cultures, whereas SinR negatively influences its own expression. FnrN influences biofilm formation, but its effects are less dramatic than those of SinR. We propose a model in which a signal cascade, responsive to oxygen limitation and initiated by FnrN, activates sinR expression in response to decreased oxygen levels, and influences the formation of A. tumefaciens biofilms.