4.2 Article

The Dickeya dadantii biofilm matrix consists of cellulose nanofibres, and is an emergent property dependent upon the type Ill secretion system and the cellulose synthesis operon

期刊

MICROBIOLOGY-SGM
卷 157, 期 -, 页码 2733-2744

出版社

MICROBIOLOGY SOC
DOI: 10.1099/mic.0.051003-0

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资金

  1. US Department of Agriculture (USDA) National Research Initiative (NRI) [2006-35319-17396]
  2. USDA [WIS01072, 2001-52100-11316]
  3. National Science Foundation (NSF) [0412599]
  4. Direct For Biological Sciences
  5. Emerging Frontiers [0412599] Funding Source: National Science Foundation

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Dickeya dadantii is a plant-pathogenic bacterium that produces cellulose-containing biofilms, called pellicles, at the air-liquid interface of liquid cultures. D. dadantii pellicle formation appears to be an emergent property dependent upon at least three gene clusters, including cellulose synthesis, type Ill secretion system (T3SS) and flagellar genes. The D. dadantii cellulose synthesis operon is homologous to that of Gluconacetobacter xylinus, which is used for industrial cellulose production, and the cellulose nanofibres produced by D. dadantii were similar in diameter and branching pattern to those produced by G. xylinus. Salmonella enterica, an enterobacterium closely related to D. dadantii, encodes a second type of cellulose synthesis operon, and it produced biofilm strands that differed in width and branching pattern from those of D. dadantii and G. xylinus. Unlike any previously described cellulose fibre, the D. dadantii cellulose nanofibres were decorated with bead-like structures. Mutation of the cellulose synthesis operon genes resulted in loss of cellulose synthesis and production of a cellulase-resistant biofilm. Mutation of other genes required for pellicle formation, including those encoding FliA (a sigma factor that regulates flagella production), HrpL (a sigma factor that regulates the T3SS), and AdrA, a GGDEF protein, affected both biofilm and cell morphology. Mutation of the cellulose synthase bcsA or of bcsC resulted in decreased accumulation of the T3SS-secreted protein HrpN.

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