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Host-microbe interactions in reef building coral

Coral reefs are biologically and economically important ecosystems underpinned by corals that are able to flourish in oligotrophic waters due to their mutualistic association with dinoflagellate symbionts (genus Symbiodinium). Symbiodinium are strictly intracellular, residing within the gastrodermal tissues of the coral host, and contributing the majority of the coral’s energy requirements. Coral reefs are in rapid decline due to a range of threats such as local human influences, bleaching (loss of Symbiodnium and/or reduction of pigment), disease and ocean acidification, to which links to climate change have been made. The close association of corals and a diverse community of microbes led to development of the coral holobiont hypothesis, in which a range of microorganisms (e.g Bacteria) form a functionally-relevant mutualistic relationship with corals and Symbiodinium. This thesis aimed to fill knowledge gaps in the coral holobiont hypothesis and the host-microbe interactions within this system, including pathogen interactions and coral immune system functioning. This thesis revealed that host-microbe interactions in corals are complex, and that the underlying mechanisms of immunity and symbiosis may be similar. The findings corroborate the idea that corals maintain specific bacterial communities that have potential probiotic and nutritional value. In particular, a group of common coral associates were identified, and it is suggested that members of this group are globally occurring key associates. Corals affected by a disease previously described as “White Syndrome” were observed to undergo pronounced changes in their microbial community structure in comparison to healthy colonies. However, in contrast to previous findings, no single pathogen could be identified as the causative agent of the disease syndrome, and it is speculated that corals experiencing altered health status result in a breakdown of the resident associated microbial community structure. Culturable bacterial isolates from corals were shown to affect the growth of each other and in particular some species had great inhibitory properties. Hence, the presence of some bacterial species has the potential to influence the all over structure of the coral associated microbial community. It was also shown that changed environmental conditions may alter the growth conditions for coral associated bacteria in mucus. It is suggested that increased replication is needed in studies of bacterial assemblages on corals, as variability between coral species and sites were observed. In addition, studies of the role of coral microbial communities in health and disease should broaden their focus to more thoroughly consider the role of the coral holobiont, especially with regards to the coral host. This thesis identified the first functional Pattern Recognition Protein (PRP), a C-type lectin named Millectin, in scleractinian corals. Millectin was isolated by affinity chromatography and was shown to bind to bacterial pathogens as well as coral Symbiodinium symbionts. Gene expression of Millectin was upregulated in response to immune stimuli and the lectin was further abundantly expressed in the tissues of corals, suggesting a major role for this protein in system functioning and immunity. Further research into Millectin and a complement factor C3 homolog suggested that these molecules may have been co-opted into the equally important role of symbiont recruitment. Gene expression analysis of C3 also indicated this molecule may be involved in responses to tissue trauma. Millectin shows variability in the binding region, and hence, is the earliest evolutionary representative to date of a variable PRP. This finding, and the observed ancestral relation with vertebrate homologs, provided further information on the evolution of the innate immune system and gives further insight into invertebrate immunity.

Identiferoai:union.ndltd.org:ADTP/279168
CreatorsEva Charlotte Kvennefors
Source SetsAustraliasian Digital Theses Program
Detected LanguageEnglish

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