Reef Sediments Can Act As a Stony Coral Tissue Loss Disease Vector

Stony coral tissue loss disease (SCTLD) was first observed in 2014 near Virginia Key in Miami-Dade County, Florida. Field sampling, lab experiments, and modeling approaches have suggested that reef sediments may play a role in SCTLD transmission, though a positive link has not been tested experimentally. We conducted an ex situ transmission assay using a statistically-independent disease apparatus to test whether reef sediments can transmit SCTLD in the absence of direct contact between diseased and healthy coral tissue. We evaluated two methods of sediment inoculation: batch inoculation of sediments collected from southeast Florida using whole colonies of diseased Montastraea cavernosa, and individual inoculations of sediments following independent, secondary infections of similar to 5 cm(2) coral fragments. Healthy fragments of the coral species Orbicella faveolata and M. cavernosa were exposed to these diseased sediment treatments, as well as direct disease contact and healthy sediment controls. SCTLD transmission was observed for both batch and individual diseased sediment inoculation treatments, albeit with lower proportions of infected individuals as compared to disease contact controls. The time to onset of lesions was significantly different between species and among disease treatments, with the most striking infections occurring in the individual diseased sediment treatment in under 24 h. Following infection, tissue samples were confirmed for the presence of SCTLD signs via histological examination, and sediment subsamples were analyzed for microbial community variation between treatments, identifying 16 SCTLD indicator taxa in sediments associated with corals experiencing tissue loss. This study demonstrated that reef sediments can indeed transmit SCTLD through indirect exposure between diseased and healthy corals, and adds credence to the assertion that SCTLD transmission occurs via an infectious agent or agents. This study emphasizes the critical need to understand the roles that sediment microbial communities and coastal development activities may have on the persistence of SCTLD throughout the endemic zone, especially in the context of management and conservation strategies in Florida and the wider Caribbean

Ordering of localized moments in Kondo lattice models

We describe the transition from a ferromagnetic phase, to a disordered para- magnetic phase, which occurs in one-dimensional Kondo lattice models with partial conduction band filling. The transition is the quantum order-disorder transition of the transverse-field Ising chain, and reflects double-exchange ordered regions of localized spins being gradually destroyed as the coupling to the conduction electrons is reduced. For incommensurate conduction band filling, the low-energy properties of the localized spins near the transition are dominated by anomalous ordered (disordered) regions of localized spins which survive into the paramagnetic (ferromagnetic) phase. Many interesting properties follow, including a diverging susceptibility for a finite range of couplings into the paramagnetic phase. Our critical line equation, together with numerically determined transition points, are used to determine the range of the double-exchange interaction. Models we consider are the spin 1/2 Kondo lattices with antiferromagnetic (Kondo) coupling, with ferromagnetic (Hund's rule) coupling, and the Kondo lattice with repulsive interactions between the conduction electrons.Comment: 18 pages, 6 embedded eps figures. To appear in Phys Rev

Expansion of a single transposable element family is associated with genome-size increase and radiation in the genus Hydra

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.Transposable elements are one of the major contributors to genome-size differences in metazoans. Despite this, relatively little is known about the evolutionary patterns of element expansions and the element families involved. Here we report a broad genomic sampling within the genus Hydra, a freshwater cnidarian at the focal point of diverse research in regeneration, symbiosis, biogeography, and aging. We find that the genome of Hydra is the result of an expansion event involving long interspersed nuclear elements and in particular a single family of the chicken repeat 1 (CR1) class. This expansion is unique to a subgroup of the genus Hydra, the brown hydras, and is absent in the green hydra, which has a repeat landscape similar to that of other cnidarians. These features of the genome make Hydra attractive for studies of transposon-driven genome expansions and speciation

Experimental transmission of Stony Coral Tissue Loss Disease results in differential microbial responses within coral mucus and tissue

© The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Huntley, N., Brandt, M., Becker, C., Miller, C., Meiling, S., Correa, A., Holstein, D., Muller, E., Mydlarz, L., Smith, T., & Apprill, A. Experimental transmission of Stony Coral Tissue Loss Disease results in differential microbial responses within coral mucus and tissue. ISME Communications, 2(1), (2022): 46, https://doi.org/10.1038/s43705-022-00126-3.Stony coral tissue loss disease (SCTLD) is a widespread and deadly disease that affects nearly half of Caribbean coral species. To understand the microbial community response to this disease, we performed a disease transmission experiment on US Virgin Island (USVI) corals, exposing six species of coral with varying susceptibility to SCTLD. The microbial community of the surface mucus and tissue layers were examined separately using a small subunit ribosomal RNA gene-based sequencing approach, and data were analyzed to identify microbial community shifts following disease acquisition, potential causative pathogens, as well as compare microbiota composition to field-based corals from the USVI and Florida outbreaks. While all species displayed similar microbiome composition with disease acquisition, microbiome similarity patterns differed by both species and mucus or tissue microhabitat. Further, disease exposed but not lesioned corals harbored a mucus microbial community similar to those showing disease signs, suggesting that mucus may serve as an early warning detection for the onset of SCTLD. Like other SCTLD studies in Florida, Rhodobacteraceae, Arcobacteraceae, Desulfovibrionaceae, Peptostreptococcaceae, Fusibacter, Marinifilaceae, and Vibrionaceae dominated diseased corals. This study demonstrates the differential response of the mucus and tissue microorganisms to SCTLD and suggests that mucus microorganisms may be diagnostic for early disease exposure.This work was funded by an International Coral Reef Society student grant to N.H., National Science Foundation (NSF) VI EPSCoR 0814417 and 1946412 and NSF (Biological Oceanography) award numbers 1928753 to MEB and TBS, 1928609 to AMSC, 1928817 to EMM, 19228771 to LDM, 1927277 to DMH as well as 1928761 and 1938112 to AA, NSF EEID award number 2109622 to MEB, AA, LDM, and AMSC, and a NOAA OAR Cooperative Institutes award to AA (#NA19OAR4320074). Samples were collected under permit #DFW19057U authorized by the Department of Planning and Natural Resources Coastal Zone Management

Alphaflexivirus genomes in stony coral tissue loss disease-affected, disease-exposed, and disease-unexposed coral colonies in the U.S. Virgin Islands

© The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Veglia, A., Beavers, K., Van Buren, E., Meiling, S., Muller, E., Smith, T., Holstein, D., Apprill, A., Brandt, M., Mydlarz, L., & Correa, A. Alphaflexivirus genomes in stony coral tissue loss disease-affected, disease-exposed, and disease-unexposed coral colonies in the U.S. Virgin Islands. Microbiology Resource Announcements, 11(2), (2022): e01199–e01121, https://doi.org/10.1128/mra.01199-21.Stony coral tissue loss disease (SCTLD) is decimating Caribbean corals. Here, through the metatranscriptomic assembly and annotation of two alphaflexivirus-like strains, we provide genomic evidence of filamentous viruses in SCTLD-affected, -exposed, and -unexposed coral colonies. These data will assist in clarifying the roles of viruses in SCTLD.This work was supported by the National Science Foundation (Biological Oceanography) award numbers 1928753 to M.E.B. and T.B.S., 1928609 to A.M.S.C., 1928817 to E.M.M., 19228771 to L.D.M., 1927277 to D.M.H., and 1928761 to A.A., as well as by VI EPSCoR (NSF numbers 0814417 and 1946412)

Variable species responses to experimental stony coral tissue loss disease (SCTLD) exposure

© The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Meiling, S. S., Muller, E. M., Lasseigne, D., Rossin, A., Veglia, A. J., MacKnight, N., Dimos, B., Huntley, N., Correa, A. M. S., Smith, T. B., Holstein, D. M., Mydlarz, L. D., Apprill, A., & Brandt, M. E. Variable species responses to experimental stony coral tissue loss disease (SCTLD) exposure. Frontiers in Marine Science, 8, (2021): 670829, https://doi.org/10.3389/fmars.2021.670829.Stony coral tissue loss disease (SCTLD) was initially documented in Florida in 2014 and outbreaks with similar characteristics have since appeared in disparate areas throughout the northern Caribbean, causing significant declines in coral communities. SCTLD is characterized by focal or multifocal lesions of denuded skeleton caused by rapid tissue loss and affects at least 22 reef-building species of Caribbean corals. A tissue-loss disease consistent with the case definition of SCTLD was first observed in the U.S. Virgin Islands (USVI) in January of 2019 off the south shore of St. Thomas at Flat Cay. The objective of the present study was to characterize species susceptibility to the disease present in St. Thomas in a controlled laboratory transmission experiment. Fragments of six species of corals (Colpophyllia natans, Montastraea cavernosa, Orbicella annularis, Porites astreoides, Pseudodiploria strigosa, and Siderastrea siderea) were simultaneously incubated with (but did not physically contact) SCTLD-affected colonies of Diploria labyrinthiformis and monitored for lesion appearance over an 8 day experimental period. Paired fragments from each corresponding coral genotype were equivalently exposed to apparently healthy colonies of D. labyrinthiformis to serve as controls; none of these fragments developed lesions throughout the experiment. When tissue-loss lesions appeared and progressed in a disease treatment, the affected coral fragment, and its corresponding control genet, were removed and preserved for future analysis. Based on measures including disease prevalence and incidence, relative risk of lesion development, and lesion progression rates, O. annularis, C. natans, and S. siderea showed the greatest susceptibility to SCTLD in the USVI. These species exhibited earlier average development of lesions, higher relative risk of lesion development, greater lesion prevalence, and faster lesion progression rates compared with the other species, some of which are considered to be more susceptible based on field observations (e.g., P. strigosa). The average transmission rate in the present study was comparable to tank studies in Florida, even though disease donor species differed. Our findings suggest that the tissue loss disease affecting reefs of the USVI has a similar epizootiology to that observed in other regions, particularly Florida.This work was supported by the National Science Foundation (Biological Oceanography) award number 1928753 to MB and TS, 1928609 to AC, 1928817 to EM, 19228771 to LM, 1927277 to DH, and 1928761 to AA as well as by VI EPSCoR (NSF #0814417 and NSF #1946412)

Electronic states, Mott localization, electron-lattice coupling, and dimerization for correlated one-dimensional systems. II

We discuss physical properties of strongly correlated electron states for a linear chain obtained with the help of the recently proposed new method combining the exact diagonalization in the Fock space with an ab initio readjustment of the single-particle orbitals in the correlated state. The method extends the current discussion of the correlated states since the properties are obtained with varying lattice spacing. The finite system of N atoms evolves with the increasing interatomic distance from a Fermi-liquid-like state into the Mott insulator. The criteria of the localization are discussed in detail since the results are already convergent for N>=8. During this process the Fermi-Dirac distribution gets smeared out, the effective band mass increases by ~50%, and the spin-spin correlation functions reduce to those for the Heisenberg antiferromagnet. Values of the microscopic parameters such as the hopping and the kinetic-exchange integrals, as well as the magnitude of both intra- and inter-atomic Coulomb and exchange interactions are calculated. We also determine the values of various local electron-lattice couplings and show that they are comparable to the kinetic exchange contribution in the strong-correlation limit. The magnitudes of the dimerization and the zero-point motion are also discussed. Our results provide a canonical example of a tractable strongly correlated system with a precise, first-principle description as a function of interatomic distance of a model system involving all hopping integrals, all pair-site interactions, and the exact one-band Wannier functions.Comment: 18 pages, REVTEX, submitted to Phys. Rev.

Dynamical renormalization group approach to transport in ultrarelativistic plasmas: the electrical conductivity in high temperature QED

The DC electrical conductivity of an ultrarelativistic QED plasma is studied in real time by implementing the dynamical renormalization group. The conductivity is obtained from the realtime dependence of a dissipative kernel related to the retarded photon polarization. Pinch singularities in the imaginary part of the polarization are manifest as growing secular terms that in the perturbative expansion of this kernel. The leading secular terms are studied explicitly and it is shown that they are insensitive to the anomalous damping of hard fermions as a result of a cancellation between self-energy and vertex corrections. The resummation of the secular terms via the dynamical renormalization group leads directly to a renormalization group equation in real time, which is the Boltzmann equation for the (gauge invariant) fermion distribution function. A direct correspondence between the perturbative expansion and the linearized Boltzmann equation is established, allowing a direct identification of the self energy and vertex contributions to the collision term.We obtain a Fokker-Planck equation in momentum space that describes the dynamics of the departure from equilibrium to leading logarithmic order in the coupling.This determines that the transport time scale is given by t_{tr}=(24 pi)/[e^4 T \ln(1/e)}]. The solution of the Fokker-Planck equation approaches asymptotically the steady- state solution as sim e^{-t/(4.038 t_{tr})}.The steady-state solution leads to the conductivity sigma = 15.698 T/[e^2 ln(1/e)] to leading logarithmic order. We discuss the contributions beyond leading logarithms as well as beyond the Boltzmann equation. The dynamical renormalization group provides a link between linear response in quantum field theory and kinetic theory.Comment: LaTex, 48 pages, 14 .ps figures, final version to appear in Phys. Rev.

Stony coral tissue loss disease: a review of emergence, impacts, etiology, diagnostics, and intervention

Stony coral tissue loss disease (SCTLD) is destructive and poses a significant threat to Caribbean coral reef ecosystems. Characterized by the acute loss of coral tissue, SCTLD has impacted over 22 stony coral species across the Caribbean region, leading to visible declines in reef health. Based on the duration, lethality, host range, and spread of this disease, SCTLD is considered the most devastating coral disease outbreak ever recorded. Researchers are actively investigating the cause and transmission of SCTLD, but the exact mechanisms, triggers, and etiological agent(s) remain elusive. If left unchecked, SCTLD could have profound implications for the health and resilience of coral reefs worldwide. To summarize what is known about this disease and identify potential knowledge gaps, this review provides a holistic overview of SCTLD research, including species susceptibility, disease transmission, ecological impacts, etiology, diagnostic tools, host defense mechanisms, and treatments. Additionally, future research avenues are highlighted, which are also relevant for other coral diseases. As SCTLD continues to spread, collaborative efforts are necessary to develop effective strategies for mitigating its impacts on critical coral reef ecosystems. These collaborative efforts need to include researchers from diverse backgrounds and underrepresented groups to provide additional perspectives for a disease that requires creative and urgent solutions