Some of my Acro Collection

runetspike

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Been a minute since we've had a smoothie show!



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CRT The Juice



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CRT Hot Rod



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TGC Bugatti
Boy, you're doing wonders! your acropores are just a surge of emotions
 
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coral reeftank

coral reeftank

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This guy works wonders. Tell me about your light, what do you use?
radions and t5s.
Lighting is only one component, it is your overall husbandry techniques and your fundamental understandings of the organisms that you are taking care of that will lead to your long-term success. Don't chase lighting, I've seen corals that are brilliantly colored with cheaper lights
 
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coral reeftank

coral reeftank

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Well, no eye candy for this post, but a something for the book worms! Here are a list of articles that I've perused through. Here are some of the interesting tidbits that I pulled out. There is a broad range of topics, but plenty of knowledge that we can learn from and apply to our systems! Feel free to read through this compilation and add onto the discussion!

https://www.nature.com/articles/s41467-023-38612-4
Stony coral tissue loss disease induces transcriptional signatures of in situ degradation of dysfunctional Symbiodiniaceae
= disease leads to poor symbiosis

  • one prevailing hypothesis postulates that a growing number of diseases result from environmentally induced microbiome imbalances and a subsequent increase in opportunistic or polymicrobial infections
  • a growing line of evidence implicates viral infection of Symbiodiniaceae in the etiology of this disease based on (1) a reduction or halting of lesion progression in bleached corals19, (2) histopathological examination identifying lytic necrosis of host gastrodermal cells where Symbiodiniaceae reside20, (3) transmission electron microscopy (TEM) detection of filamentous viral-like particles associated with endosymbiont pathology21, and (4) the assembly of putative filamentous viral genomes from SCTLD-affected coral holobiont metatranscriptomes
This article is primarily about sctld, some findings applicable to reefing, as this is not seen in the hobby atm
  • transcriptional evidence of a functional shift in the coral surface mucus layer, the first line of defense against foreign particles and microbes30. Dmbt1, involved in mucosal innate immunity and microbial homeostasis in humans28, exhibited significant overall downregulation in SCTLD-infected corals relative to controls.
  • downregulation of Dmbt1 in SCTLD-infected corals was accompanied by significant shifts in mucus microbiome composition towards dysbiosis in specimens from this same study
    • They get weaker as their immune system is hampered, how can we help strengthen????????
  • These results explain why antibiotic treatment is sufficient to arrest treated SCTLD lesions, but ineffective at preventing new lesion appearance on other parts of the same coral colony
    • The downregulation of Dmbt1 leads to poor microbial homeostasis. Antibiotics will stop the issue at hand but will not prevent further infection. This is because we are not solving the root problem, but really just putting a band-aid on it.
  • Bacterial work on SCTLD suggests that there may be common secondary bacterial infections14,15,16,17, and antibiotic treatment has been shown to halt lesion progression18,32
  • The dramatic shift in symbiont gene expression seen in the exposed corals could represent two things: (1) early symbiont responses to SCTLD infection before the manifestation of visible lesions on the coral, or (2) a successful symbiont response to SCTLD pathogen exposure preventing the onset of disease. Because the expression of many of these orthologs is comparable between control and SCTLD-infected corals, we believe the latter to be true.
  • evidence that (1) viral infection of Symbiodiniaceae is implicated in SCTLD pathology, and (2) disease manifestation is associated with in situ degradation of defective symbionts.

https://www.nature.com/articles/s41598-017-02685-1

Intraspecific differences in molecular stress responses and coral pathobiome contribute to mortality under bacterial challenge in Acropora millepora​


  • Our results suggest that lesions appeared due to changes in the coral pathobiome (multiple bacterial species associated with disease) and general health deterioration after the biotic disturbance, rather than the direct activity of any specific pathogen.
    • It is not the presence of one pathogen that causes issues, rather it is the effect of compounding negative environmental factors and pathogens
    • Poor Environment + Presence of pathogen = disease >>> Common Sense
    • Limiting one of these factors may reduce mortality, but how?
  • Higher constitutive immune activities and responses do not translate into lower mortality rates​

    • Hmm interesting… maybe they are producing the wrong response to the threat? If so, are there any external measures that can be taken to minimize mortality?

  • If diseases in nature arise because of weaknesses in holobiont physiology, instead of the virulence of any single etiological agent, environmental stressors compromising coral condition might play a larger role in disease outbreaks than is currently thought.
    • Bingo!
  • many instances of that coral disease cannot be attributed to a single pathogen. Instead, multiple bacteria appear to act opportunistically during coral disease events
  • One possible explanation is that some corals resist disease by making greater contributions to constitutive or inducible immunity. Coral families that invest more in innate immunity (e.g., production of cytotoxic defenses) are less likely to suffer infectious disease outbreaks
    • Can we induce more contributions to innate immunity? And if so how?
  • Coral genotypes differed significantly in their mortality rates under bacterial challenge (Fig. 1B; p < 0.001). Bacterial treatment significantly increased mortality (p < 0.001) regardless of the genotype
  • Two best-surviving genotypes (22 and 30) had significantly more cyanobacterial and chloroplast-derived OTUs than other genotypes (Supplementary Fig. S7; FDR = 0.001). Chloroplast OTUs were homologous to the green marine algae, Ulvophyceae, a group that includes common endolithic photoautotrophs33. The skeletons of genotypes 22 and 30 were noticeably green (Supplementary Fig. S7), supporting the hypothesis that elevated proportion of chloroplast OTUs in these corals is due to higher loads of endolithic algae.
    • Very interesting, so these corals survived because they had better utilization of symbionts
    • Were the corals able to generate more energy and thus able to combat the threat easier?
  • Seven OTUs varied by survival fraction: Vibrio spp. (OTU250), Streptococcus spp. (OTU409), Chlamydiales (OTU74), Endozoicomonas euniceicola (OTU783), and Corynebacterium spp. (OTU960) were significantly more abundant in corals with higher survival over all treatments. Another two Endozoicomonas species (OTU266 and OTU404) were significantly positively associated with higher mortality. Thirteen OTUs were significantly differentially abundant by bacterial treatment: only one of these (Chlamydiales OTU74, which was only present in genotype 30) was less abundant in treated corals. Four of the OTUs that were significantly enriched by bacterial challenge differed by Vibrio species used: Vibrio spp. (OTU250), Photobacterium spp. (OTU442), Alteromonas spp. (OTU565), and Neptuniibacter caesariensis (OTU781) were all significantly more abundant in V. diazotrophicus-treated corals than in V. owensii-treated corals. Tests for the interaction of bacterial treatment and survival revealed that Vibrio spp. (OTU250), Oleibacter spp. (OTU811), and Rhodobacteraceae (OTU908) were all less abundant in treated corals with high survivorship than in corals with low survivorship.
    • Super interesting, the interplay in the coral holobiont is quite amazing
  • We found that individuals which experienced higher mortality also possessed higher antioxidant or cytotoxic activities, either as a baseline measure in the unchallenged fragments or in response to bacterial challenge (Fig. 2). In contrast, low-mortality corals tended to respond less to the bacterial challenge (Fig. 3), though this relationship was largely driven by a single genotype with 100% survival (Supplementary Fig. S3). The lack of positive correlation between immunity responses and survival suggests that mechanisms other than host immune activity contribute towards the observed variation in robustness to the bacterial challenge in our experiment.
  • Surprisingly few genes involved in stress responses or immunity were upregulated in low-mortality corals in response to bacterial challenge. Instead, these individuals exhibited a more “healthy” gene expression profile: they had elevated glucose-6-phosphate1-dehydrogenase expression that is important for cell growth37, as well as increased levels of fluorescent proteins whose abundances have been linked to health status in corals38, 39. Another signature of lower mortality was the diminished abundance of ubiquitination-related transcripts, e.g., ubiquitin ligases and ubiquitin carboxy-terminal hydrolases. Ubiquitination labels damaged proteins for removal and is a general hallmark of cellular stress40. Ubiquitin has been shown to be upregulated in heat-stressed corals with high levels of damaged proteins41,42,43
    • So the corals with low mortality corals had minimal response. They had elevated glucose, looked healthy and lower signals of heat stress associated transcripts
  • High-mortality corals exhibited abundant changes in gene expression in response to bacterial challenge, including upregulation of matrix metalloproteinases, which are also upregulated in naturally occurring coral disease and bleaching38, 43, and an apoptosis regulator (Fig. 4A). At the same time, gene expression in low-mortality corals responded to bacteria much less if at all
  • Taken together with the lack of elevated immune activity in low-mortality corals (Figs 23), our conclusion is that these corals survived better because they were generally less sensitive to the adverse effects of bacterial challenge, not because they launched a more robust response.
    • Is this similar to an auto-immune disease?
  • Although the proportion of Vibrio spp. was higher in challenged corals than in controls (Fig. 5C), these OTUs remained relatively rare, suggesting that the introduced Vibrio spp. were not the sole cause of lesion formation. This study is not the first instance wherein a simple “one pathogen = one disease” model fails to describe a coral lesion: microbiota of diseased corals often differ dramatically from the microbiota of healthy corals, suggesting that more than one bacterium is involved in deteriorating health10. Likewise, healthy corals often harbor “pathogenic” microbes8.
    • What a head scratcher… there must be some interplay involved that we don’t understand yet
  • The pathobiome describes interactions between pathogenic microbes and healthy microbiota that contribute towards disease processes13. Here, Vibrio treatment caused an increase in the abundance of taxa previously reported to be associated with disease and stress in marine organisms, including Alteromonadaceae11, 44, Pseudoalteromonadaceae11, Rhodobacteraceae45, 46, and, expectably, Vibrionaceae11, 47,48,49, suggesting that the introduced bacteria may have triggered a disturbance in the coral-associated microbiome that facilitated the proliferation of multiple bacterial species which contributed to the disease outcome (i.e., the pathobiome).
    • So it seems that if you screw with the coral’s “default settings” this will lead to issues. Perhaps certain corals have evolved to utilize the specific strains of bacteria that exist in their environment. This could be why seemingly healthy mariculture/wild corals do poorly in the long-run in captivity. It is because they are simply not used to the bacteria strains in our captive systems. Also could be why aquacultured specimens do much better, they’ve simply adapted to their environment better than others.
  • The putative roles of the genes forming the assay provide important insights into potential mechanisms underlying coral disease susceptibility. Deleted in malignant brain tumors 1 (dmbt1) is found in the gut mucosa of humans where it acts as a pattern recognition receptor that maintains mucosal homeostasis by inhibiting bacterial invasion and suppressing inflammation53, 54. Other transcriptomic studies have found that dmbt1 was downregulated in oysters upon bacterial challenge55, upregulated in the Symbiodinium-hosting coral Orbicella faveolata after lipopolysaccharide challenge56, and upregulated in aposymbiotic sponges compared to sponges infected with clade G Symbiodinium, suggesting that dmbt1 may play a role in mediating various marine symbioses57. Elevated dmbt1 in all control fragments and in the low-mortality corals relative to high-mortality, bacterial-challenged corals may signify the role of this protein in maintaining healthy stable symbiotic associations with commensal microbes. The diagnostic gene that was regulated in the opposite direction, a matrix metalloproteinase(mmp), belongs to a family of enzymes with a wide range of functions. The upregulation of MMPs in response to parasitic protists in a gorgonian coral58 and in A. hyacinthus affected with White Syndrome-like symptoms38 suggests an active role of these proteins in the immune response of cnidarians. Changes in dmbt1 and mmp may represent some of the earliest coral responses to immune challenge, as they are detectable even in asymptomatic corals.
    • Very interesting!
  • We found that neither introduced Vibrio species proliferated within the coral host in sampled asymptomatic fragments, but both bacterial treatments triggered the rise of putative opportunistic pathogens in the coral microbiome and subsequent development of disease lesions in corals that exhibited less healthy gene expression profiles. We are not be the first to argue that a coral disease can be caused by opportunistic infection exploiting a compromised host7, and many coral diseases are associated with broad shifts in microbial community composition beyond the rise of a single pathogen10, 11, 59. If coral diseases in nature similarly arise because of weaknesses in holobiont physiology, instead of the virulence of any single etiological agent, environmental stressors compromising coral condition might play a larger role in disease outbreaks than is currently thought.
    • Disease is not caused by just one agent, but the culminating effects of many factors. This is why our best route as reefers is to be proactive and maintain pristine water quality.

https://www.frontiersin.org/articles/10.3389/fmicb.2019.01702/full
Experimental Inoculation of Coral Recruits With Marine Bacteria Indicates Scope for Microbiome Manipulation in Acropora tenuis and Platygyra daedalea


  • At this time point, the cumulative inoculations with the bacterial cocktails had a strong effect on the bacterial community composition in recruits of both coral species. While the location of bacterial cells within the coral hosts was not assessed, metabarcoding using the 16S rRNA gene revealed that two and six of the seven bacterial strains administered through the cocktails were significantly enriched in inoculated recruits of A. tenuis and P. daedalea, respectively, compared to control recruits. Despite being reared in the same environment, A. tenuis and P. daedalea established significantly different bacterial communities, both in terms of taxonomic composition and diversity measurements. These findings indicate that coral host factors as well as the environmental bacterial pool play a role in shaping coral-associated bacterial community composition.
    • So it seems that the corals can actively select which bacteria they culture. This is already known. However, knowing that different coral hosts select different strains is important! It could be the reason why certain people can’t keep a certain coral alive in their system.
  • In another laboratory experiment, bacterial strains were selected for putatively beneficial traits including nutrient cycling, antioxidative capacities, and antagonistic activities against pathogens (Rosado et al., 2018). Inoculation of Pocillopora damicornisnubbins with the resulting consortium was able to partially mitigate coral bleaching and alleviate pathogenic infection (Rosado et al., 2018). Thus, coral bacterial community composition seems to be flexible to some extent and adjustable to benefit the host. Finally, a single exposure of coral larvae to the mucus-associated microbes of four different coral species resulted in divergent prokaryotic communities after 4 months of rearing in filter-sterilized seawater (Damjanovic et al., 2017). Even though the initial inoculum composition was not characterized, this experiment showed that coral-associated microbiomes could be influenced to develop in distinct directions following microbial dosing.
  • The observed differences in bacterial communities retrieved from corals versus those from the surrounding water column are compelling evidence that coral-bacteria associations are non-random and subject to selective mechanisms (Sunagawa et al., 2010; Sweet et al., 2010).
  • By exposing coral recruits to a chosen bacterial consortium, we were able to significantly modify their microbiome (Figure 3). Several bacterial strains in the inocula (i.e., two in the case of A. tenuis and six for P. daedalea) were statistically significantly enriched in the inoculated recruits (Figure 5). Bacteria used in the inocula were also among the major ASVs driving the separation of bacterial communities associated with control and inoculated recruits (Table 3). Effective inoculations were thus not precluded by using bacteria isolated from non-coral organisms, which demonstrates a degree of flexibility in the coral microbiome. Altogether, this study supports the proof-of-concept for the feasibility of manipulating coral-associated prokaryotes
    • So we can manipulate the microbiome, but how to do so effectively is still unknown. This could be why methods such as carbon dosing/kz/aquaforest see great success. By promoting the growth of preexisting beneficial microbes we may be able to strengthen the corals!

https://www.nature.com/articles/s41467-023-38502-9

Ecology of Endozoicomonadaceae in three coral genera across the Pacific Ocean​


  • Coral-associated bacteria contribute significantly to the health of the host by participating in nutrient acquisition, metabolic (re)cycling, and protection against pathogens6,7,12,13. Understanding the composition, the diversity and the functions of coral-associated microorganisms can thus provide clues about the health status, but also the resilience and adaptive capabilities of corals14.
  • The question of host-specificity remains open, however, since some Endozoicomonadaceae types could be shared between different hosts41, different Endozoicomonadaceae types can dominate within a same host43, and changes in their relative abundance seems to be independent of the symbiotic algae46. If the host is not the driver of microbiome composition, external factors could play a role47. Endozoicomonadaceaecommunities could be shaped by environmental factors as they were shown to be less abundant in Acropora millepora at lower seawater pH48,49, or during increased temperatures and subsequent bleaching31,50, as well as anthropogenic impact and habitat suitability44,51.
  • These findings suggest that Endozoicomonas are underrepresented in stressed corals14, however, it’s not always the case. In Pocillopora verrucosa and Acropora hemprichii, although Endozoicomonadaceae decreased at sites impacted by sedimentation, they increased at sites impacted by municipal wastewater39. Endozoicomonadaceae also increased in abundance in Porites spp. under lower pH53, and under natural stressful conditions of shallow hydrothermal vent54, and were not impacted by coral bleaching or severe tissue sloughing in P. verrucosa in response to eutrophication55. Endozoicomonadaceae also proliferated after warm summer months in French Polynesia42. These contrasted observations between individual studies conducted locally illustrate the need for a large-scale approach on multiple coral species to unveil Endozoicomonadaceaediversity and biogeography, and better understand the factors controlling their presence and community composition
    • Very interesting to see when these bacteria flourish and when they do not!
  • A comparative analysis of several Endozoicomonadaceae genomes showed an enrichment of genes associated with carbon sugar transport and utilization, protein secretion, and synthesis of amino acids that could potentially be transferred to the host43. In addition, Endozoicomonas acroporae has the potential to degrade dimethylsulfoniopropionate (DMSP), which bacteria could use as a carbon source24. Various studies also suggested that Endozoicomonadaceae play a role in regulating the overall microbiome structure either by direct competition with other bacteria, or by producing antimicrobial compounds48,59.
    • So Endozoicomonadaceae helps the coral gather and create energy, compete with other microbes and potentially create antiseptic compounds that can ward off pathogens
  • Overall, Endozoicomonadaceae ASVs were detected in 99% of the coral samples (n = 2447). Despite their prevalence, their relative abundance varied greatly between samples (Fig. 1b). Pocillopora had the highest proportion of ASVs affiliated to Endozoicomonadaceae (53% of all Pocillopora sequences) followed by Porites (30%) and then Millepora (11%).
  • At any given site, the presence of Endozoicomonadaceae in one coral genus was not predictive of its presence in the other genera (e.g., Rapa Nui I04 or Moorea I07), although at other sites, Endozoicomonadaceaewere present and abundant in all three coral genera (e.g., Chesterfield I20 and New Caledonia I21).
    • Very interesting as to why they are not present on all the corals even when the Endozoicomonadaceae is present in that environment
  • Endozoicomonadaceae sequences were detected in the water, but their relative abundance decreased rapidly with increasing distance from the colonies (Fig. 3a). While Endozoicomonadaceae represented on average 30% of the bacteria in Pocillopora, their relative abundances decreased to ~0.5% in coral surrounding water, 0.05% in surface water over the reef, and 0.001% in surface water off the island (Fig. 3a). Additionally, we observed a significant positive correlation (r = 0.52) between the relative abundance of Endozoicomonadaceae in Pocillopora and in the colony surrounding water (Fig. 3b). The Endozoicomonadaceae ASVs that were abundant in Pocillopora were also detected in the water, but in varying proportions (Fig. 3c). When moving away from the Pocillopora colonies, the proportion of typical Pocillopora Endozoicomonadaceae (asv0000001, asv0000003 and asv0000020) decreased, while the proportion of other Endozoicomonadaceae increased. In some cases, Endozoicomonadaceae were not detected at all in the surface water off the island.
    • The Endozoicomonadaceae species present on the coral must be actively selected and cultured by the coral given their lack of presence in the surrounding water.
    • This also reinforces the hypothesis of why corals from certain regions do not fare well in captivity. Even though they may be the same species, the environment that they grew in can be drastically different. This leads to the coral selecting the “optimal tools for the job”. If we remove these tools they are forced to rapidly adapt and can lead to microbes exploiting the open niche. Imagine that for your whole life you’ve been trained to trained to read left to right.
  • There was no strong correlation between Endozoicomonadaceae relative abundance at the family level and chlorophyll a, pH, phosphate, silanol, sea surface salinity and temperature in Pocillopora and Millepora (Fig. 4a). In Porites, Endozoicomonadaceae had the highest correlation to salinity. At the ASV level, however, all correlation values were low, but there were differences within coral genera. In Pocillopora, asv0000001 had the strongest positive correlation to sea surface temperature and was negatively associated with pH, while asv0000003 and asv0000020 had the highest correlations to salinity and were negatively correlated to SiOH (Fig. 4a). In Porites, asv0000007 had the highest positive correlation to salinity, while asv0000028 and asv0000038 only had very low correlation values to environmental conditions. In Millepora, asv0000024 had the highest positive correlation to SiOH and asv0000110 only had low correlation values
    • Many abiotic factors can influence the microbial compositions of these corals, that’s why environmental stress factors lead to microbial dysbiosis and can lead to coral mortality. These shifts destabilize the coral holobiont and lead to unpredictable events. That’s why we shoot for “stability”
  • Among the pathways common to all Endozoicomonadaceae we noted the Embden-Meyerhof pathway, the pyruvate dehydrogenase, the citrate cycle, the non-oxidative phase of the pentose phosphate pathway, and the Type I, II secretion systems. Sequences coding for subunits of the DmsABC enzyme, which catalyzes the reduction of dimethylsulfoxide (DMSO) to dimethyl sulfide (DMS), were also detected in all Endozoicomonadaceae (Fig. 6, Supplementary Fig. 8). Most Endozoicomonadaceae encoded different eukaryotic-like proteins (ankyrin, leucine-rich, tetratricopeptide, HEAT and WD40 repeats). We did not find any genes involved in the assimilation of nitrate in the E. pocilloporae, P. poriteae, and E. milleporae, species, but they were present in E. acroporae and P. haliclonae
  • Most of the Endozoicomonadaceae genomes had genes for the biosynthesis of riboflavin (vitamin B2). E. milleporae and P. poriteae had the potential to export riboflavin, but not E. pocilloporae
  • Genes involved in the uptake of the L-Ascorbate (vitamin C) and its anaerobic degradation in D-Xylulose-5P were found in E. milleporae and P. poriteae only
  • Our clade A corresponded to an abundant Pocillopora OTU that did not decrease in abundance under elevated nitrate and urea concentrations in the Pacific Ocean (Moorea) or the Red Sea42,55, although it decreased under excess dissolved organic carbon (OTU255) and elevated temperature (OTU-Endo62). The success of E. pocilloporae clade A may thus, in part, rely on its tolerance to specific environmental perturbations, but it could also benefit from its ability to disperse and effectively colonize corals. We found it abundant in the plankton surrounding the coral colonies, or ‘coral ecosphere’22, and as far away as in water off the islands, yet in lower abundances
  • The host-bacteria association could thus reflect an interplay between co-evolution that is strongly marked in isolated islands, such as Easter Island, and other selection factors leading to mixed communities, potentially via ‘shuffling’ of abundant Endozoicomonasphylotypes71 in more interconnected islands.
    • So it does seem that corals select specific bacteria to do a certain job, while these are all Endozoicomonadaceae, they vary in their ability to do certain processes
  • In our study, the environmental parameters did not strongly explain the variability of Endozoicomonas in Millepora. Regarding potential metabolisms, E. milleporae, contrary to E. pocilloporae and P. poriteae, did not have the potential to use GlcNac polymer, cellobiose or starch, but could use peptidoglycans from other bacteria.
  • Our results draw a fine picture of the patterns of Endozoicomonadaceae abundance in corals across the Pacific Ocean with implications for our understanding of the ecology and evolution of host-symbiont relationships. We show that the ecology of this widespread symbiont should be considered at the lineage level to understand the factors structuring communities and infer associated metabolic contributions. Our data suggest that different coral species exhibit distinct host-Endozoicomonadaceae relationships ranging from a strong association illustrated by the global, and abundant presence of Endozoicomonas in Pocillopora, to a rather weak association with a rare and scattered presence in Millepora. In all corals, the environment had generally only a small structuring effect on Endozoicomonadaceae community composition, while the genetic lineage of the host was important in some corals, arguing for a high level of host specificity putatively shaped by long co-evolutionary histories. Thus, coral-bacterial association at large may range from stable co-dependent relationships that arose through evolutionary time to opportunistic associations that are flexible and determined by the prevailing environment.
    • Coevolution at work! Adapting to a new environment is hard work ladies and gents, it’s our job to smoothen this process, but how!?

https://floridadep.gov/sites/default/files/DEP Report 2020 Task 2 and 3 8.31.20 (1).pdf




Development of probiotics and alternative treatments for stony coral tissue loss disease

Results summary and future directions:


  • A total of 400 out of 2,000 isolates show antibacterial activity against putative pathogens
  • Chemical analysis of McH1-7 and Of7M-16 shows they both produce three different antibacterial compounds
  • McH1-7 has proven effective at treating M. cavernosa colonies but is less effective with C. natans and possibly P. strigosa
  • Significant slowing of the disease process on C. natans does suggest that probiotics are a possible treatment, but more species-specific strains are needed
  • Of7M-16 does not seem effective at treating infected O. faveolata or M. cavernosa colonies and will no longer be pursued as a probiotic treatment
  • Combinational probiotic treatments have not yet been more successful than McH1-7 at treating SCTLD; different combinations will be pursued in the future
  • Essential oils may not be a safe alternative treatment for SCTLD as they appear to cause harm to the coral fragments and will no longer be pursued
  • The presence of Vibrio coralliilyticus on disease lesions is associated with faster lesion progression rate and mortality on M. cavernosa regardless of location along the FRT. Probiotics with the ability to combat this bacterium will be targeted in the future
  • Metabolomics has been an important advance to speeding up the identification of known antibiotics in our probiotic bacteria and identifying compound classes that may be biomarkers for SCTLD



Microbiome and Metabolome Contributions to Coral Health and Disease​

https://www.journals.uchicago.edu/doi/full/10.1086/720971

  • focuses on the coral microbiome and the coral host’s potential to utilize microbial symbionts for disease resistance,
  • During coral stress, healthy or beneficial microbial groups that regulate the coral metabolome may become compromised, changing the concentration and output of metabolites within the coral holobiont
  • These studies demonstrate that beneficial microorganisms for corals (BMCs) have the ability to contribute antimicrobial activity against potential pathogens and that corals likely contain a plethora of these microbial groups that may contribute to host immunity and other essential functions.
  • During a trial of elevated salinity, an increase in the compound floridoside emitted by Symbiodinium effectively lowered ROSs and decreased bleaching susceptibility. Photoprotective compounds produced by photosynthetic organisms can also reduce ROS damage (Dunlap and Shick, 1998; Nielsen et al., 2018). Cyanobacteria, heterotrophic bacteria, and microalgae produce mycosporine-like amino acids that act as a natural photoprotective compound by absorbing UV radiation (Ravindran et al., 2013).
    • Why dosing Flourine is important!
  • The BMC treated corals showed significantly different bacterial community structure than placebo treated corals during heat stress. However, microbial communities were more similar between treatment times during the recovery period from heat stress. Additionally, BMC treated corals showed signs of DMSP degradation, lipid maintenance, and ROS mitigation, contributing to an overall higher survival rate compared to placebo treated corals. This study emphasizes that BMC consortium is more readily taken by the coral host as it experiences stress and attempts to restructure the microbiome to a pre-stress state.
  • This leads to questions about probiotic application time frames, because it is unclear how long BMC communities will remain in the coral host. Morgans et al. (2020) inoculated Acropora milleporacorals with Symbiodiniaceae probiotics after experimentally exposing corals to heat stress. Corals that contained the inoculant showed higher resistance to heat stress and bleach compared to corals that did not receive the inoculant (Morgans et al., 2020). However, unlike the study by Santoro et al., the species of Symbiodiniaceae applied were not detected during microbial analysis of the coral tissues. This is because the inoculant may instead be indirectly supplementing heterotrophic nutrition to the coral, thus providing the coral with nutrients needed to mitigate thermal stress.
    • Similar to my method/explains the probiotic/bacterial method. They aid in the transfer of energy through a system. This allows for better access and utilization of resources which leads to higher stress tolerances
 

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