A.
sydowii produces proteases which aid in colonisation of the host
by breaking down host tissue to release nutrients for the fungus and by
disrupting the immune function of the host. Meanwhile, healthy colonies of G. ventalina produce protease inhibitor
to act against pathogen proteases and prevent colonisation by the fungal
pathogen. A study by Mann et al.
(2014) aims to demonstrate how environmental conditions, such as increased
temperatures, can alter the balance of a relationship between host and pathogen,
such as the “arms race” between A.
sydowii and G. ventalina and
result in the outbreak of infection and disease.
Five strains of A.
sydowii were analysed: three from various tropical reefs, one from a human
and another from stock spore solutions. A
sydowii was cultured and protease activity quantified by calculating a
ratio from the measurement of both colony growth and the clear zone around a
colony, where the casein protein in the media had been broken down. Ten healthy
and ten diseased G. ventalina samples
were taken from healthy and diseased colonies reefs in the Florida Keys, at a
range of depths between 3-6 m. Diseased coral samples were taken from
purple-coloured lesions and healthy samples were taken at least 10cm from a
lesion site. Coral health was determined visually. The sea fan colonies were gradually
exposed over 2 hours to artificially elevated temperatures of 30-32°C
for 14 days, with controls being exposed to 26-28 °C. In
addition, the sea fan colonies were exposed to three different types of commercially-
and fungal-derived proteases. Protease and protease inhibitors were determined
with assays and quantified with a microplate reader.
The results revealed that there was a significant
increase in extracellular protease activity with elevated temperature for all
fungal strains, with those fungal strains at the highest temperatures producing
the greatest protease activity. Overall, inhibitor activity in G. ventalina did not significantly increase
with temperature stress. Protease inhibitor activity was higher in healthy sea
fan colonies as opposed to diseased ones. There was inhibition of all three
proteases by the sea fan colonies, however, this protease inhibition was lower within
the lesion area of diseased colonies than in healthy tissues of diseased and
healthy sea fan samples.
The fact that sea fan colonies have protease inhibitors
that work effectively against a range of proteases, including non-fungal ones,
suggests that sea fans may have the capacity to resist infection by A. sydowii. Nevertheless, elevated
temperatures may tip the balance in favour of A. sydowii, as protease inhibitor activity may not be sufficient to
counteract the effect of increased protease production by the pathogenic
fungus. Another line of defence for G.
ventalina may be the microbial holobiont associated with the coral, which may
produce antimicrobial compounds that inhibit pathogens such as A. sydowii. The authors acknowledged
that the coral extracts used contained all of the associated microbes which may
influence this pathogen-host interaction. This needs to be considered when
analysing these results, yet I feel that removing this holobiont would be
counter-productive and unrealistic in terms of the environmental conditions that
sea fan colonies inhabit.
Reference:
Mann, W.T., Beach-Letendre,
J. and Mydlarz, L. (2014) Interplay between proteases and protease inhibitors in the sea fan - Aspergillus pathosystem, Marine Biology,
161, 2213-2220.http://link.springer.com.plymouth.idm.oclc.org/article/10.1007/s00227-014-2499-2
Hi Anita, Great read... am I right in thinking the coral shows purple tissue if it is infected? Also it was interesting that they used Aspergillus sydowii from a human. Did they find anything different with this? I wouldn't of thought a human pathogen would be capable of harming a marine species or was this more for a control? Thanks
ReplyDeleteHi Elyssa
ReplyDeleteThank you, yes you are correct in thinking that diseased coral tissue is observed as a purple lesion. Yes, Aspergillus is pathogenic to many organisms including humans, where it can cause infections for people with cystic fibrosis. They used the human strain as a comparison to see how it would perform against the strains from the sea fans and it did produce much less protease than the sea fan strains when grown on the PYG media across a 26-32 degree temperature range. I suppose it goes to show how virulent this fungus can be and how adaptable it can be as a pathogen, infecting a range of different hosts.
Thanks for your questions! :)
Hi Anita,
ReplyDeleteA question about the methods: What do you exactely mean with that the colonies were exposed to elevated temperatures? Did this happen insitu (not sure if that would work) of the whole seafan or were the samples taken from the colonies exposed to elevated temperatures in the lab? I definately agree with you that removing the holobiont is critical. In general I think lab-based experiments need to be handled with care (if you read my latest post they found something completely different in the environment to what was previously found in incubation experiments). Thanks :)
Hi Tabea
ReplyDeleteYes, they removed samples of the sea fan colonies and artificially raised the temperature of the samples in the lab. I agree that lab-based experiments can yield different results to those in situ but I suppose by removing some of the additional factors and external conditions that the organisms experience can help simplify and clarify the situation. Definitely, caution is needed when interpreting these sort of results.