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1.
BMC Genomics ; 25(1): 226, 2024 Feb 29.
Artigo em Inglês | MEDLINE | ID: mdl-38424480

RESUMO

Long-read sequencing is revolutionizing de-novo genome assemblies, with continued advancements making it more readily available for previously understudied, non-model organisms. Stony corals are one such example, with long-read de-novo genome assemblies now starting to be publicly available, opening the door for a wide array of 'omics-based research. Here we present a new de-novo genome assembly for the endangered Caribbean star coral, Orbicella faveolata, using PacBio circular consensus reads. Our genome assembly improved the contiguity (51 versus 1,933 contigs) and complete and single copy BUSCO orthologs (93.6% versus 85.3%, database metazoa_odb10), compared to the currently available reference genome generated using short-read methodologies. Our new de-novo assembled genome also showed comparable quality metrics to other coral long-read genomes. Telomeric repeat analysis identified putative chromosomes in our scaffolded assembly, with these repeats at either one, or both ends, of scaffolded contigs. We identified 32,172 protein coding genes in our assembly through use of long-read RNA sequencing (ISO-seq) of additional O. faveolata fragments exposed to a range of abiotic and biotic treatments, and publicly available short-read RNA-seq data. With anthropogenic influences heavily affecting O. faveolata, as well as its increasing incorporation into reef restoration activities, this updated genome resource can be used for population genomics and other 'omics analyses to aid in the conservation of this species.


Assuntos
Antozoários , Transcriptoma , Animais , Análise de Sequência de DNA/métodos , Antozoários/genética , Genoma , Região do Caribe , Sequenciamento de Nucleotídeos em Larga Escala/métodos
2.
Nat Commun ; 14(1): 2915, 2023 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-37217477

RESUMO

Stony coral tissue loss disease (SCTLD), one of the most pervasive and virulent coral diseases on record, affects over 22 species of reef-building coral and is decimating reefs throughout the Caribbean. To understand how different coral species and their algal symbionts (family Symbiodiniaceae) respond to this disease, we examine the gene expression profiles of colonies of five species of coral from a SCTLD transmission experiment. The included species vary in their purported susceptibilities to SCTLD, and we use this to inform gene expression analyses of both the coral animal and their Symbiodiniaceae. We identify orthologous coral genes exhibiting lineage-specific differences in expression that correlate to disease susceptibility, as well as genes that are differentially expressed in all coral species in response to SCTLD infection. We find that SCTLD infection induces increased expression of rab7, an established marker of in situ degradation of dysfunctional Symbiodiniaceae, in all coral species accompanied by genus-level shifts in Symbiodiniaceae photosystem and metabolism gene expression. Overall, our results indicate that SCTLD infection induces symbiophagy across coral species and that the severity of disease is influenced by Symbiodiniaceae identity.


Assuntos
Antozoários , Dinoflagellida , Animais , Antozoários/fisiologia , Recifes de Corais , Dinoflagellida/genética , Transcriptoma , Perfilação da Expressão Gênica , Simbiose/genética
3.
Sci Adv ; 8(39): eabo6153, 2022 09 30.
Artigo em Inglês | MEDLINE | ID: mdl-36179017

RESUMO

Infectious diseases are an increasing threat to coral reefs, resulting in altered community structure and hindering the functional contributions of disease-susceptible species. We exposed seven reef-building coral species from the Caribbean to white plague disease and determined processes involved in (i) lesion progression, (ii) within-species gene expression plasticity, and (iii) expression-level adaptation among species that lead to differences in disease risk. Gene expression networks enriched in immune genes and cytoskeletal arrangement processes were correlated to lesion progression rates. Whether or not a coral developed a lesion was mediated by plasticity in genes involved in extracellular matrix maintenance, autophagy, and apoptosis, while resistant coral species had constitutively higher expression of intracellular protein trafficking. This study offers insight into the process involved in lesion progression and within- and between-species dynamics that lead to differences in disease risk that is evident on current Caribbean reefs.


Assuntos
Antozoários , Animais , Antozoários/genética , Recifes de Corais , Resistência à Doença/genética , Plásticos , Transcriptoma
4.
Commun Biol ; 4(1): 679, 2021 06 03.
Artigo em Inglês | MEDLINE | ID: mdl-34083722

RESUMO

Disease outbreaks have caused significant declines of keystone coral species. While forecasting disease outbreaks based on environmental factors has progressed, we still lack a comparative understanding of susceptibility among coral species that would help predict disease impacts on coral communities. The present study compared the phenotypic and microbial responses of seven Caribbean coral species with diverse life-history strategies after exposure to white plague disease. Disease incidence and lesion progression rates were evaluated over a seven-day exposure. Coral microbiomes were sampled after lesion appearance or at the end of the experiment if no disease signs appeared. A spectrum of disease susceptibility was observed among the coral species that corresponded to microbial dysbiosis. This dysbiosis promotes greater disease susceptiblity in coral perhaps through different tolerant thresholds for change in the microbiome. The different disease susceptibility can affect coral's ecological function and ultimately shape reef ecosystems.


Assuntos
Antozoários/microbiologia , Recifes de Corais , Disbiose/microbiologia , Microbiota/fisiologia , Animais , Antozoários/classificação , Bactérias/classificação , Bactérias/genética , Biodiversidade , Região do Caribe , Resistência à Doença , Ecossistema , Microbiota/genética , RNA Ribossômico 16S/genética , Água do Mar/microbiologia , Análise de Sequência de DNA/métodos , Especificidade da Espécie
5.
Integr Comp Biol ; 59(4): 819-829, 2019 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-31236558

RESUMO

Historically mechanisms with which basal animals such as reef-building corals use to respond to changing and increasingly stressful environments have remained elusive. However, the increasing availability of genomic and transcriptomic data from these organisms has provided fundamental insights into the biology of these critically important ecosystem engineers. Notably, insights into cnidarians gained in the post-genomics age have revealed a surprisingly complex immune system which bears a surprising level of similarity with the vertebrate innate immune system. This system has been critically linked to how corals respond to the two most prominent threats on a global scale, emerging coral diseases and increasing water temperature, which are recognized cellularly as either foreign or domestic threats, respectively. These threats can arise from pathogenic microbes or internal cellular dysfunction, underscoring the need to further understand mechanisms corals use to sense and respond to threats to their cellular integrity. In this investigation and meta-analysis, we utilize resources only recently available in the post-genomic era to identify and characterize members of an underexplored class of molecules known as NOD-like receptors in the endangered Caribbean coral Orbicella faveolata. We then leverage these data to identify pathways possibly mediated by NLRs in both O. faveolata and the ecologically important branching coral Acropora digitifera. Overall, we find support that this class of proteins may provide a mechanistic link to how reef-building corals respond to threats both foreign and domestic.


Assuntos
Antozoários/genética , Antozoários/imunologia , Imunidade Inata/genética , Proteínas NLR/imunologia , Animais , Espécies em Perigo de Extinção , Evolução Molecular , Imunidade Inata/imunologia , Proteínas NLR/genética , Estresse Fisiológico
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