TY - JOUR
T1 - Adaptive radiation of Pseudomonas fluorescens SBW25 in experimental microcosms provides an understanding of the evolutionary ecology and molecular biology of A-L interface biofilm formation
AU - Koza, Anna
AU - Kuśmierska, Anna
AU - McLaughlin, Kimberley
AU - Moshynets, Olena
AU - Spiers, Andrew J.
PY - 2017/7/3
Y1 - 2017/7/3
N2 - Combined experimental evolutionary and molecular biology approaches have been used to investigate the adaptive radiation of Pseudomonas fluorescens SBW25 in static microcosms leading to the colonisation of the air-liquid interface by biofilm–forming mutants such as the Wrinkly Spreader. In these microcosms, the ecosystem engineering of the early wild-type colonists establish the niche space for subsequent WS evolution and colonisation. Random WS mutations occurring in the developing population that de-regulate diguanylate cyclases and c-di-GMP homeostasis result in cellulose-based biofilms at the air-liquid interface. These structures allow Wrinkly Spreaders to intercept O2 diffusing into the liquid column and limit the growth of competitors lower down. As the biofilm matures, competition increasingly occurs between WS lineages, and niche divergence within the biofilm may support further diversification before system failure when the structure finally sinks. A combination of pleiotropic and epistasis effects, as well as secondary mutations, may explain variations in WS phenotype and fitness. Understanding how mutations subvert regulatory networks to express intrinsic genome potential and key innovations providing a selective advantage in novel environments is key to understanding the versatility of bacteria, and how selection and ecological opportunity can rapidly lead to substantive changes in phenotype and in community structure and function.
AB - Combined experimental evolutionary and molecular biology approaches have been used to investigate the adaptive radiation of Pseudomonas fluorescens SBW25 in static microcosms leading to the colonisation of the air-liquid interface by biofilm–forming mutants such as the Wrinkly Spreader. In these microcosms, the ecosystem engineering of the early wild-type colonists establish the niche space for subsequent WS evolution and colonisation. Random WS mutations occurring in the developing population that de-regulate diguanylate cyclases and c-di-GMP homeostasis result in cellulose-based biofilms at the air-liquid interface. These structures allow Wrinkly Spreaders to intercept O2 diffusing into the liquid column and limit the growth of competitors lower down. As the biofilm matures, competition increasingly occurs between WS lineages, and niche divergence within the biofilm may support further diversification before system failure when the structure finally sinks. A combination of pleiotropic and epistasis effects, as well as secondary mutations, may explain variations in WS phenotype and fitness. Understanding how mutations subvert regulatory networks to express intrinsic genome potential and key innovations providing a selective advantage in novel environments is key to understanding the versatility of bacteria, and how selection and ecological opportunity can rapidly lead to substantive changes in phenotype and in community structure and function.
U2 - 10.1093/femsle/fnx109
DO - 10.1093/femsle/fnx109
M3 - Article
VL - 364
JO - FEMS Microbiology Letters
JF - FEMS Microbiology Letters
SN - 0378-1097
IS - 12
M1 - fnx109
ER -