Abstract
The Gram-negative bacterium Flavobacterium johnsoniae employs gliding motility to move rapidly over solid surfaces. Gliding involves the movement of the adhesin SprB along the cell surface. F. johnsoniae spreads on nutrient-poor 1% agar-PY2, forming a thin film-like colony. We used electron microscopy and time-lapse fluorescence microscopy to investigate the structure of colonies formed by wild-type (WT) F. johnsoniae and by the sprB mutant (ΔsprB). In both cases, the bacteria were buried in the extracellular polymeric matrix (EPM) covering the top of the colony. In the spreading WT colonies, the EPM included a thick fiber framework and vesicles, revealing the formation of a biofilm, which is probably required for the spreading movement. Specific paths that were followed by bacterial clusters were observed at the leading edge of colonies, and abundant vesicle secretion and subsequent matrix formation were suggested. EPM-free channels were formed in upward biofilm protrusions, probably for cell migration. In the nonspreading ΔsprB colonies, cells were tightly packed in layers and the intercellular space was occupied by less matrix, indicating immature biofilm. This result suggests that SprB is not necessary for biofilm formation. We conclude that F. johnsoniae cells use gliding motility to spread and maturate biofilms.
Highlights
Flavobacterium johnsoniae is a Gram-negative rod-shaped aerobic bacterium commonly found in soil and fresh water
The cells of this bacterium move rapidly over solid surfaces by gliding motility and form thin spreading colonies on agar [1,2]. This characteristic motility is shared by many other members of the Bacteroidetes phylum that lack bacterial motility organelles, such as flagella or pili. Their movements depend on a complex motility-specific apparatus that has been intensively studied in F. johnsoniae, which is a model system [3,4]
SprB filaments were observed on WT cells using ammonium molybdate staining and transmission electron microscopy (TEM), but were not present on sprB mutant (∆sprB) cells [6]
Summary
Keiko Sato 1,*, Masami Naya 2, Yuri Hatano 2, Yoshio Kondo 3, Mari Sato 2, Keiji Nagano 4, Shicheng Chen 5 , Mariko Naito 1 and Chikara Sato 2,*. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
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