bioRxiv Science⌕ Search

Biology subjects

Zubillaga, A. L.

Publications and source records attributed to Zubillaga, A. L..

2 recordsLinked to original sources

Genomic characterization reveals high clonal redundancy in two Acropora cervicornis nurseries in the Dominican Republic

Acropora cervicornis is often propagated through fragmentation (i.e., clonal propagation), a common practice implemented by restoration projects. Known as asexual propagation, this strategy may rapidly increase coral cover but reduces genetic variation. We used 2b-RAD sequencing to characterize multilocus genotypic variation among 45 A. cervicornis colonies maintained in two in-situ nurseries (Cap Cana, Acuario) in Punta Cana, Dominican Republic. After reference-based SNP discovery and filtering, 2,515 high-quality SNPs were retained in the dataset. Principal coordinate analysis (PCoA), hierarchical clustering, identity-by-state (IBS) distances, and relatedness estimates identified only three multilocus genets among the 45 colonies (AC1, AC2, and AC3). Of these, AC2 was the most abundant (n = 23; 51.1%), followed by AC3 (n = 14; 31.1%) and lastly AC1 (n = 8; 17.8%). Within-genet IBS distances (0.153-0.227) did not overlap with between-genet distances (0.406-0.497). AC1 and AC2 were detected in both nurseries, whereas AC3 was limited to Acuario. These results reveal substantial clonal redundancy among sampled nursery colonies that determines local reef conservation efforts. These data highlight the value of incorporating genotype identification in nursery-based coral restoration projects.

ecology↗

Stony coral tissue loss disease (SCTLD) destabilizes the coral microbiome

Stony coral tissue loss disease (SCTLD) is a rapidly spreading lethal coral disease, the etiology of which remains poorly understood. In this study, using deep metagenomic sequencing, we investigate microbial and viral community dynamics associated with SCTLD progression in the Caribbean stony coral Diploria labyrinthiformis. We assembled 264 metagenome-assembled genomes (MAGs) and correlated their abundance with disease phenotypes, revealing significant shifts in both the prokaryotic microbiome and virome. Our results provide clear evidence of microbial destabilization in diseased corals, suggesting that microbial dysbiosis is an outcome of SCTLD progression. We identified DNA viruses that increase in abundance in infected corals and are present in SCTLD-affected corals at other sites. In addition, we identify the first putative instance of asymptomatic/resistant SCTLD-affected colonies, suggesting potential microbial induced resilience (i.e., beneficial microbiome). Finally, we propose a mechanistic model of SCTLD progression, in which viral dynamics may contribute to a microbiome collapse. These findings provide novel insights into SCTLD pathogenesis and offer consistent molecular signals of disease across diverse geographic sites, presenting new opportunities for disease monitoring and mitigation.

microbiology↗