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Meyer, J. L.

Publications and source records attributed to Meyer, J. L..

5 recordsLinked to original sources

Baseline microbiomes of the pillar coral Dendrogyra cylindrus reveal novel taxa and regional differences

The pillar coral Dendrogyra cylindrus is a rare but iconic member of Caribbean reefs that has suffered range-wide losses. D. cylindrus is highly susceptible to stony coral tissue loss disease (SCTLD), and the outbreak has contributed to the functional extinction of Floridas population of pillar corals. The coral microbiome can impact the health and disease resistance of coral colonies, yet little is known about what constitutes the core microbiome of D. cylindrus. This information is crucial for comparisons of healthy and diseased tissue in pathogen identification studies and can be applied to restoration efforts as a coral health metric. Therefore, we characterized the microbiomes of D. cylindrus colonies ahead of the SCTLD disease front in Belize and Curacao. The most prevalent members of the D. cylindrus microbial community were bacteria for which taxonomy could not be assigned confidently beyond the level of domain as well as the putatively endosymbiotic genera Endozoicomonas, Ca. Amoebophilus, and Spiroplasma. The coral reefs of Belize and Curacao represent distinct Caribbean marine ecoregions, and we documented regional differences in strains among predominant bacterial taxa. The understudied microbiome of D. cylindrus harbors unique bacterial lineages that are in danger of extinction along with its critically endangered coral host, and these bacterial lineages may be important bioindicators during restoration efforts. IMPORTANCETropical corals face global extinction if average temperatures rise by 2{degrees}C (3.6{degrees}F), which may occur as soon as 2050. Included in the loss of charismatic macrofauna like the majestic pillar coral is the loss of the biological and genetic diversity of its symbionts. Here we examined the bacterial and archaeal communities associated with Caribbean pillar corals and found that the microbiome was dominated by taxonomically unclassified and putatively endosymbiotic taxa. Endosymbiotic bacteria, which live inside the coral tissue, are likely to have evolved unique adaptations to become symbionts and may be important to the health and success of pillar corals in ecosystem restoration efforts.

microbiology↗

Shifts in the coral microbiome in response to in situ experimental deoxygenation

Global climate change impacts ocean communities through rising surface temperatures, ocean acidification, and deoxygenation. While the response of the coral holobiont to the first two effects has been relatively well studied, little is known about the response of the coral microbiome to deoxygenation. In this study, we investigated the response of the microbiome to hypoxia in two coral species that differ in their relative tolerance to hypoxia. We conducted in situ oxygen manipulations on a coral reef in Bahia Almirante, Panama, which has previously experienced episodes of low dissolved oxygen concentrations. Naive coral colonies (previously unexposed to hypoxia) of massive starlet coral (Siderastrea siderea) and Lamarcks sheet coral (Agaricia lamarcki) were transplanted to a reef and either enclosed in chambers that created hypoxic conditions or left at ambient oxygen levels. We collected samples of surface mucus and tissue after 48 hours of exposure and characterized the microbiome by sequencing 16S rRNA genes. We found that the microbiomes of the two coral species were distinct from one another and remained so after exhibiting similar shifts in microbiome composition in response to hypoxia. There was an increase in both abundance and number of taxa of anaerobic microbes after exposure to hypoxia. Some of these taxa may play beneficial roles in the coral holobiont by detoxifying the surrounding environment during hypoxic stress. This work describes the first characterization of the coral microbiome under hypoxia and is an initial step toward identifying potential beneficial bacteria for corals facing this environmental stressor. ImportanceMarine hypoxia is a threat for corals but has remained understudied in tropical regions where coral reefs are abundant. Deoxygenation on coral reefs will worsen with ongoing climate change, acidification, and eutrophication. We do not yet understand the response of the coral microbiome to hypoxia, and whether this reaction may have a beneficial or harmful role in the coral holobiont. To understand how the coral microbial community structure responds during hypoxic stress, we experimentally lowered the oxygen levels around corals in the field to observe changes in the composition of the coral microbiome. We documented the increase of anaerobic and pathogenic bacteria in the microbiomes of the massive starlet coral (Siderastrea siderea) and Lamarcks sheet coral (Agaricia lamarcki) in 48 hours. This work provides fundamental knowledge of the microbial response in the coral holobiont during hypoxia and may provide insight to holobiont function during stress.

ecology↗

A meta-analysis of the stony coral tissue loss disease microbiome finds key bacteria in lesions and unaffected tissue of diseased colonies

Stony coral tissue loss disease (SCTLD) has been causing significant whole colony mortality on reefs in Florida and the Caribbean. The cause of SCTLD remains unknown, with limited concurrence of SCTLD-associated bacteria among studies. We conducted a meta-analysis of SSU 16S ribosomal RNA gene datasets generated by 16 field and laboratory SCTLD studies to find consistent bacteria associated with SCTLD across disease zones (vulnerable, endemic, and epidemic), coral species, coral compartments (mucus, tissue, and skeleton), and disease states (apparently healthy colony tissue [AH], and unaffected [DU] and lesion [DL] tissue from diseased colonies). We also evaluated bacteria in seawater and sediment, which may be sources of SCTLD transmission. Although AH colonies in endemic and epidemic zones harbor bacteria associated with SCTLD lesions, and aquaria and field samples had distinct microbial compositions, there were still clear differences in the microbial composition among AH, DU, and DL in the combined dataset. Alpha diversity between AH and DL was not different; however, DU showed increased alpha diversity compared to AH, indicating that, prior to lesion formation, corals may undergo a disturbance to the microbiome. This disturbance may be driven by Flavobacteriales, which were especially enriched in DU. While Rhodobacterales and Peptostreptococcales-Tissierellales were prominent in structuring microbial interactions in DL. Peptostreptococcales-Tissierellales specifically may contribute to lesion progression through an alpha-toxin. We provide a consensus of SCTLD-associated bacteria both prior to and during lesion progression and identify how these taxa vary across studies, coral species, coral compartments, seawater, and sediment.

microbiology↗

Plcg2M28L interacts with high fat-high sugar diet to accelerate Alzheimers disease-relevant phenotypes in mice

Obesity is recognized as a significant risk factor for Alzheimers disease (AD). Studies have supported the notion that obesity accelerates AD-related pathophysiology in mouse models of AD. The majority of studies to date have focused on the use of early-onset AD models. Here we evaluate the impact of genetic risk factors on late-onset AD (LOAD) in mice fed a high fat/high sugar diet. We focused on three mouse models created through the IU/JAX/Pitt MODEL-AD Center, LOAD1, LOAD1.Plcg2M28L and LOAD1.Mthfr677C>T. At 2 months of age, animals were placed on a high fat/high sugar diet (HFD) that induces obesity, or a control diet (CD) that does not, until 12 months of age. Throughout the study, blood was collected to assess cholesterol and glucose. Positron emission tomography/computed tomography (PET/CT) was completed prior to sacrifice to image for glucose utilization and brain perfusion. At the completion of the study, blood and brains were collected for analysis. As expected, animals fed the HFD, regardless of genotype or sex, showed a significant increase in body weight compared to those fed the CD. Glucose and cholesterol increased as a function of HFD as well. Interestingly, LOAD1.Plcg2M28L demonstrated an increase in microglia density as well as alterations in regional brain glucose and perfusion when on a HFD. These changes were not observed in LOAD1 or LOAD1.Mthfr677C>T animals when fed a HFD. Furthermore, LOAD1.Plcg2M28L but not LOAD1.Mthfr677C>T or LOAD1 animals showed transcriptomics correlations to human AD modules. Our results show HFD affects brain health in a genotype-specific manner. Further insight into this process may have significant implications in the development of lifestyle interventions for treatment of AD.

neuroscience↗

Microbial community shifts associated with the ongoing stony coral tissue loss disease outbreak on the Florida Reef Tract

As many as 22 of the 45 coral species on the Florida Reef Tract are currently affected by stony coral tissue loss disease (SCTLD). The ongoing disease outbreak was first observed in 2014 in Southeast Florida near Miami and as of early 2019 has been documented from the northernmost reaches of the reef tract in Martin County down to Key West. We examined the microbiota associated with disease lesions and apparently healthy tissue on diseased colonies of Montastraea cavernosa, Orbicella faveolata, Diploria labyrinthiformis, and Dichocoenia stokesii. Analysis of differentially abundant taxa between disease lesions and apparently healthy tissue identified five unique amplicon sequence variants enriched in the diseased tissue in three of the coral species, namely an unclassified genus of Flavobacteriales and sequences identified as Fusibacter (Clostridiales), Planktotalea (Rhodobacterales), Algicola (Alteromonadales), and Vibrio (Vibrionales). In addition, several groups of likely opportunistic or saprophytic colonizers such as Epsilonbacteraeota, Patescibacteria, Clostridiales, Bacteroidetes, and Rhodobacterales were also enriched in SCTLD disease lesions. This work represents the first microbiological characterization of SCTLD, as an initial step toward identifying the potential pathogen(s) responsible for SCTLD.

microbiology↗