TY - JOUR
T1 - Symbiodinium associations with diseased and healthy scleractinian corals
AU - Correa, A. M.S.
AU - Brandt, M. E.
AU - Smith, T. B.
AU - Thornhill, D. J.
AU - Baker, A. C.
N1 - Funding Information:
and Wildlife Collection/Export Permit No. STT017-07 (to TBS). We thank Joanne Delaney and Brian Keller for FKNMS permit support and Bill Valley and the Florida Keys National Marine Sanctuary for boat use. We thank William K. Fitt, Gregory W. Schmidt, and Dustin W. Kemp for their contributions to sample collection and molecular analysis. We are grateful to Mark D. Fitchett for his advice on statistical analysis. We thank Craig Starger for sequencing work and Rob DeSalle and George Amato for sequencing support through the Sac-kler Institute for Comparative Genomics at the American Museum of Natural History. We are grateful to Mary Alice Coffroth, Peter Glynn and three anonymous reviewers, whose comments improved previous versions of this manuscript. A Columbia University Graduate Fellowship (to AMSC) supported this work, with additional support from the National Science Foundation (BIO-OCE 0099301 and 0547169 to ACB), a Seed Grant from Columbia University’s Center for Environmental Research and Conservation (to ACB and J. Danoff-Burg), and grants from the Wildlife Conservation Society (to ACB).
Funding Information:
Acknowledgments This work was conducted in the Florida Keys under National Marine Sanctuary permits FKNMS-2006-013-A1 (to AMSC) and FKNMS-2001-030 (to ACB), and under Florida Fish and Wildlife Conservation Commission permit 01S-620 (to ACB). Collections in the US Virgin Islands were made under Division of Fish
PY - 2009/6
Y1 - 2009/6
N2 - Despite recent advances in identifying the causative agents of disease in corals and understanding the impact of epizootics on reef communities, little is known regarding the interactions among diseases, corals, and their dinoflagellate endosymbionts (Symbiodinium spp.). Since the genotypes of both corals and their resident Symbiodinium contribute to colony-level phenotypes, such as thermotolerance, symbiont genotypes might also contribute to the resistance or susceptibility of coral colonies to disease. To explore this, Symbiodinium were identified using the internal transcribed spacer-2 region of ribosomal DNA from diseased and healthy tissues within individual coral colonies infected with black band disease (BB), dark spot syndrome (DSS), white plague disease (WP), or yellow blotch disease (YB) in the Florida Keys (USA) and the US Virgin Islands. Most of the diseased colonies sampled contained B1, B5a, or C1 (depending on host species), while apparently healthy colonies of the same coral species frequently hosted these types and/or additional symbiont diversity. No potentially "parasitic" Symbiodinium types, uniquely associated with diseased coral tissue, were detected. Within most individual colonies, the same dominant Symbiodinium type was detected in diseased and visually healthy tissues. These data indicate that specific Symbiodinium types are not correlated with the infected tissues of diseased colonies and that DSS and WP onset do not trigger symbiont shuffling within infected tissues. However, few diseased colonies contained clade D symbionts suggesting a negative correlation between hosting Symbiodinium clade D and disease incidence in scleractinian corals. Understanding the influence of Symbiodinium diversity on colony phenotypes may play a critical role in predicting disease resistance and susceptibility in scleractinian corals.
AB - Despite recent advances in identifying the causative agents of disease in corals and understanding the impact of epizootics on reef communities, little is known regarding the interactions among diseases, corals, and their dinoflagellate endosymbionts (Symbiodinium spp.). Since the genotypes of both corals and their resident Symbiodinium contribute to colony-level phenotypes, such as thermotolerance, symbiont genotypes might also contribute to the resistance or susceptibility of coral colonies to disease. To explore this, Symbiodinium were identified using the internal transcribed spacer-2 region of ribosomal DNA from diseased and healthy tissues within individual coral colonies infected with black band disease (BB), dark spot syndrome (DSS), white plague disease (WP), or yellow blotch disease (YB) in the Florida Keys (USA) and the US Virgin Islands. Most of the diseased colonies sampled contained B1, B5a, or C1 (depending on host species), while apparently healthy colonies of the same coral species frequently hosted these types and/or additional symbiont diversity. No potentially "parasitic" Symbiodinium types, uniquely associated with diseased coral tissue, were detected. Within most individual colonies, the same dominant Symbiodinium type was detected in diseased and visually healthy tissues. These data indicate that specific Symbiodinium types are not correlated with the infected tissues of diseased colonies and that DSS and WP onset do not trigger symbiont shuffling within infected tissues. However, few diseased colonies contained clade D symbionts suggesting a negative correlation between hosting Symbiodinium clade D and disease incidence in scleractinian corals. Understanding the influence of Symbiodinium diversity on colony phenotypes may play a critical role in predicting disease resistance and susceptibility in scleractinian corals.
KW - Coral
KW - Dark spot syndrome
KW - Disease
KW - Internal transcribed spacer-2 (ITS-2)
KW - White plague disease
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U2 - 10.1007/s00338-008-0464-6
DO - 10.1007/s00338-008-0464-6
M3 - Article
AN - SCOPUS:67349091693
VL - 28
SP - 437
EP - 448
JO - Coral Reefs
JF - Coral Reefs
SN - 0722-4028
IS - 2
ER -