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Stony coral tissue loss disease induces transcriptional signatures of in situ degradation of dysfunctional Symbiodiniaceae

  • Kelsey M. Beavers
  • , Emily W. Van Buren
  • , Ashley M. Rossin
  • , Madison A. Emery
  • , Alex J. Veglia
  • , Carly E. Karrick
  • , Nicholas J. MacKnight
  • , Bradford A. Dimos
  • , Sonora S. Meiling
  • , Tyler B. Smith
  • , Amy Apprill
  • , Erinn M. Muller
  • , Daniel M. Holstein
  • , Adrienne M.S. Correa
  • , Marilyn E. Brandt
  • , Laura D. Mydlarz
  • University of Texas at Arlington
  • Louisiana State University
  • Rice University
  • University of the Virgin Islands
  • Woods Hole Oceanographic Institution
  • Mote Marine Laboratory

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

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.

Original languageEnglish
Article number2915
JournalNature Communications
Volume14
Issue number1
DOIs
StatePublished - Dec 2023

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