Algal symbiont genera but not coral host genotypes correlate to stony coral tissue loss disease susceptibility among Orbicella faveolata colonies in South Florida

被引:9
作者
Klein, Allison M. [1 ]
Sturm, Alexis B. [1 ]
Eckert, Ryan J. [1 ]
Walker, Brian K. [2 ]
Neely, Karen L. [2 ]
Voss, Joshua D. [1 ]
机构
[1] Florida Atlantic Univ, Oceanog Inst, Harbor Branch, Ft Pierce, FL 34946 USA
[2] Nova Southeastern Univ, Halmos Coll Nat Sci & Oceanog, Davie, FL USA
关键词
SCTLD; coral disease resistance; intraspecies variation; population genetics; Symbiodiniaceae; POPULATION-STRUCTURE; REEF CORAL; GENOME; KEYS;
D O I
10.3389/fmars.2024.1287457
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Stony coral tissue loss disease (SCTLD) has spread throughout the entirety of Florida's Coral Reef (FCR) and across the Caribbean, impacting at least 30 coral species. The threatened hermatypic coral, Orbicella faveolata, demonstrates intraspecific variation in SCTLD affectedness with some colonies experiencing chronic disease lesions, while other nearby O. faveolata colonies appear unaffected with no disease signs over long monitoring periods. This study evaluated potential genotypic underpinnings of variable disease responses to SCTLD by monitoring and sampling 90 O. faveolata colonies from southeast Florida and the lower Florida Keys. High resolution analyses of >11,000 single nucleotide polymorphisms (SNPs) generated from 2bRAD sequencing indicated there were no SNP loci or genetic lineages significantly associated with O. faveolata SCTLD affectedness. Genotypic differences may still contribute to SCTLD susceptibility; however, these differences were not captured using this reduced representation sequencing approach. Algal symbiont community structure characterized from 2bRAD data revealed that the presence of Durusdinium spp. corresponded with SCTLD-affected colonies as compared to unaffected colonies, suggesting that algal symbiont community make-up may play some role in SCTLD resistance. Data generated by this study will be combined with complementary molecular and physiological approaches to further investigate the complex drivers of intraspecific SCTLD susceptibility and resilience.
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