Establishing links between environmental factors, pathogenic microbes and habitat-forming organisms is crucial if we are to understand and protect the health of marine ecosystems. The findings in this paper are the first to demonstrate such links.
Delisea pulchra is a common sub-tidal macroalga in coastal habitats around Sydney, Australia. When in its environment it has much fewer epiphytic bacteria than co-occurring algae, which is attributed to its production of furanones. Furanones are bioactive compounds secreted to the surface of the alga that are similar in structure to acylated homoserine (AHL) quorum sensing molecules, which allows them to act as chemical antagonistics by competitively binding to the quorum sensing response regulator (a LuxR-type protein). Furanone binding to LuxR causes conformational changes such that the furanone-LuxR complex readily undergoes proteolytic degradation, thereby increasing the turnover of the LuxR-type protein and dampens quorum sensing response.
Rugeria sp. R11 (from now on referred to as R11) was isolated from D. pulchra and was used to test the two main hypotheses of this paper; i) bacterium causes bleaching in D. pulchra and ii) temperature and furanone production modulate the incidence of bleaching.
It is possible to manipulate furanone production in D. pulchra in a way that stops the production, but does not affect algal growth or morphology, providing the opportunity to experimentally test the effects of furanones on R11’s interactions with D. pulchra. Minimal cell density required for R11 to effectively colonise was determined. Furanone-free algae were colonised by all tested concentrations (102 – 108 cells/ml), but furanone-producing algae were not colonised by any concentration. The low inoculum concentration required for R11 to colonise is reminiscent of bacteria possessing specific host colonisation mechanisms.
To determine the influence of temperature on R11’s ability to colonise, inoculations were incubated at the local minimum and maximum – 19°C and 24°C respectively. As expected furanone-producing algae was not successfully colonised at either temperature and furanone-free algae was colonised at both temperatures. However, at 19°C the microcolonies were strictly on the surface, they did not, like at 24°C, penetrate into the epidermis. R11 did not infect and cause necrosis of the furanone-free algae at 19°C like it did at 24°C. Some marine pathogens are virulent at temperatures at the upper ranges of their natural habitat. The ability of R11 to colonise is both temperature and furanone dependant.
To test that R11 really is the causative agent of bleaching it was re-isolated from the previous infection assay and identified as Rugeria sp. R11 through 16S rRNA gene sequencing. This isolate was then re-inoculated on furanone-free/producing algae at 24°C, showing the same infection process as before.
It is in the best interest for these macroalga to produce furanones as this chemical defence dampens the quorum sensing in the pathogenic bacteria, meaning it is unable to infect and kill the macroalga.
In conclusion this paper shows bleaching in temperate marine macroalga can be mediated through temperature-enhanced bacterial virulence and depleted algal defences. Declines in macroalgae and other ecosystem engineers such as corals are likely to have significant effects through trophic levels, resulting in potentially severe environmental and economic consequences. This, together with the predicted rise in ocean temperature means the understanding of disease mechanisms and their interplay with environmental changes is critical for the management of natural marine communities.
As previously mentioned this paper id the first to publish such links and I believe that this is only the beginning.
A review of;
Case RJ, Longford SR, Campbell AH, Low A, Tujula N, Steinberg PD and Kjelleberg S (2011) ‘Temperature induced bacterial virulence and bleaching disease in a chemically defended marine macroalga’ Environmental Microbiology. 13(2), 529-537.
Delisea pulchra is a common sub-tidal macroalga in coastal habitats around Sydney, Australia. When in its environment it has much fewer epiphytic bacteria than co-occurring algae, which is attributed to its production of furanones. Furanones are bioactive compounds secreted to the surface of the alga that are similar in structure to acylated homoserine (AHL) quorum sensing molecules, which allows them to act as chemical antagonistics by competitively binding to the quorum sensing response regulator (a LuxR-type protein). Furanone binding to LuxR causes conformational changes such that the furanone-LuxR complex readily undergoes proteolytic degradation, thereby increasing the turnover of the LuxR-type protein and dampens quorum sensing response.
Rugeria sp. R11 (from now on referred to as R11) was isolated from D. pulchra and was used to test the two main hypotheses of this paper; i) bacterium causes bleaching in D. pulchra and ii) temperature and furanone production modulate the incidence of bleaching.
It is possible to manipulate furanone production in D. pulchra in a way that stops the production, but does not affect algal growth or morphology, providing the opportunity to experimentally test the effects of furanones on R11’s interactions with D. pulchra. Minimal cell density required for R11 to effectively colonise was determined. Furanone-free algae were colonised by all tested concentrations (102 – 108 cells/ml), but furanone-producing algae were not colonised by any concentration. The low inoculum concentration required for R11 to colonise is reminiscent of bacteria possessing specific host colonisation mechanisms.
To determine the influence of temperature on R11’s ability to colonise, inoculations were incubated at the local minimum and maximum – 19°C and 24°C respectively. As expected furanone-producing algae was not successfully colonised at either temperature and furanone-free algae was colonised at both temperatures. However, at 19°C the microcolonies were strictly on the surface, they did not, like at 24°C, penetrate into the epidermis. R11 did not infect and cause necrosis of the furanone-free algae at 19°C like it did at 24°C. Some marine pathogens are virulent at temperatures at the upper ranges of their natural habitat. The ability of R11 to colonise is both temperature and furanone dependant.
To test that R11 really is the causative agent of bleaching it was re-isolated from the previous infection assay and identified as Rugeria sp. R11 through 16S rRNA gene sequencing. This isolate was then re-inoculated on furanone-free/producing algae at 24°C, showing the same infection process as before.
It is in the best interest for these macroalga to produce furanones as this chemical defence dampens the quorum sensing in the pathogenic bacteria, meaning it is unable to infect and kill the macroalga.
In conclusion this paper shows bleaching in temperate marine macroalga can be mediated through temperature-enhanced bacterial virulence and depleted algal defences. Declines in macroalgae and other ecosystem engineers such as corals are likely to have significant effects through trophic levels, resulting in potentially severe environmental and economic consequences. This, together with the predicted rise in ocean temperature means the understanding of disease mechanisms and their interplay with environmental changes is critical for the management of natural marine communities.
As previously mentioned this paper id the first to publish such links and I believe that this is only the beginning.
A review of;
Case RJ, Longford SR, Campbell AH, Low A, Tujula N, Steinberg PD and Kjelleberg S (2011) ‘Temperature induced bacterial virulence and bleaching disease in a chemically defended marine macroalga’ Environmental Microbiology. 13(2), 529-537.
1 comment:
I was curious about your comment that the alga could be manipulated so that it doesn't produce the furanone. How was this achieved?
Post a Comment