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The cnidarian–dinoflagellate symbiosis relies on the regulation of resident symbiont populations to maintain biomass stability; however, the relative importance of host regulatory mechanisms [cell-cycle arrest (CC), apoptosis (AP), autophagy (AU), and expulsion (EX)] during symbiosis onset and maintenance is largely unknown. Here, we inoculated a symbiont-free (aposymbiotic) model cnidarian (Exaiptasia diaphana: “Aiptasia”) with either its native symbiont Breviolum minutum or one of three non-native symbionts: Symbiodinium microadriaticum, Cladocopium goreaui, and Durusdinium trenchii. We then measured and compared host AP, host AU, symbiont EX, and symbiont cell-cycle phase for up to a year with these different symbionts and used these discrete measurements to inform comparative models of symbiont population regulation. Our models showed a general pattern, where regulation through AP and AU is reduced after onset, followed by an overshoot of the symbiont population that requires a strong regulatory response, dealt with by strong CC and increased EX. As colonization progresses into symbiosis maintenance, CC remains crucial for achieving steady-state symbiont populations, with our models estimating that CC regulates 10-fold more cells (60 to 90%) relative to the other mechanisms. Notably though, our models also revealed that D. trenchii is less tightly regulated than B. minutum, consistent with D. trenchii’s reputation as a suboptimal partner for this cnidarian. Overall, our models suggest that single regulatory mechanisms do not accurately replicate observed symbiont colonization patterns, reflecting the importance of all mechanisms working concomitantly. This ultimately sheds light on the cell biology underpinning the stability of this ecologically significant symbiosis. 

ABSTRACT Crown‐of‐thorns sea star (CoTS) outbreaks are a main cause of hard coral cover decline across the Indo‐Pacific, posing a major threat to the resilience of coral reefs. However, the drivers underlying CoTS feeding on preferred (e.g.,Acroporaspecies) versus non‐preferred (e.g.,Poritesspecies) are poorly understood. We hypothesised that coral venom may influence CoTS prey preferences. To investigate this hypothesis, we compared the coral venom toxin families across the genomes of preferred (A. digitifera,A. hyacinthus,A. milleporaandA. tenuis) and non‐preferred (P. australiensis,P. compressa,P. luteaandP. rus) prey species of CoTS. We also included one species from each genus inhabiting the Caribbean, where CoTS are absent (A. cervicornisandP. astreoides), to broaden our identification of venom constituents shared within each genus and investigate geographic differences. We collected known cnidarian toxins, and along with the cnidarian Tox‐Prot database, used these to identify putative toxins and investigate their phylogeny. The most abundant toxins across all coral species included neurotoxins (kunitz‐type and SCRiPS) and pore‐forming toxins (actinoporins and MAC‐PFs). We found genera‐specific differences with jellyfish toxins (CFXs) only present inPoritesspecies. Similarly, onlyAcroporaspecies harboured pore‐forming toxins with the aerolysin domain. Two toxin homologues only present in Indo‐Pacific corals (CFX and MAC‐PF homologues) showed evidence of positive selection, suggesting their evolution is shaped by environmental pressures, including exposure to CoTS. These findings provide a foundation for future studies of scleractinian venoms, which have direct applications to assessing reef coral's susceptibility to future CoTS outbreaks and active reef management.