During recent decades, many tropical reefs have transitioned from coral to macroalgal dominance. These community shifts increase the frequency of algal-coral interactions and may suppress coral recovery following both anthropogenic and natural disturbance. However, the extent to which macroalgae damage corals directly, the mechanisms involved, and the species specificity of algal-coral interactions remain uncertain. Here, we conducted field experiments demonstrating that numerous macroalgae directly damage corals by transfer of hydrophobic allelochemicals present on algal surfaces. These hydrophobic compounds caused bleaching, decreased photosynthesis, and occasionally death of corals in 79% of the 24 interactions assayed (three corals and eight algae). Coral damage generally was limited to sites of algal contact, but algae were unaffected by contact with corals. Artificial mimics for shading and abrasion produced no impact on corals, and effects of hydrophobic surface extracts from macroalgae paralleled effects of whole algae; both findings suggest that local effects are generated by allelochemical rather than physical mechanisms. Rankings of macroalgae from most to least allelopathic were similar across the three coral genera tested. However, corals varied markedly in susceptibility to allelopathic algae, with globally declining corals such as Acropora more strongly affected. Bioassay-guided fractionation of extracts from two allelopathic algae led to identification of two loliolide derivatives from the red alga Galaxaura filamentosa and two acetylated diterpenes from the green alga Chlorodesmis fastigiata as potent allelochemicals. Our results highlight a newly demonstrated but potentially widespread competitive mechanism to help explain the lack of coral recovery on many present-day reefs.allelopathy | chemical ecology | competition | phase shift C orals are structurally complex foundation species that generate and maintain tropical reef biodiversity. However, the direct and interactive effects of climate-induced coral bleaching (1, 2), ocean acidification (2, 3), coral disease (4), coastal overfishing, and eutrophication (5-8) have led to coral decline over wide areas. On many reefs, dramatic declines in coral cover have co-occurred with significant increases in fleshy macroalgae (9-11). Once established, macroalgae can inhibit coral recruitment and decrease herbivore grazing, producing negative feedbacks that reinforce phase shifts and further diminish reef function (12-14). Thus, local (e.g., overfishing) and global (e.g., climate) stresses may interact in complex ways to suppress coral cover, promote algal proliferation, and compromise reef resilience; such complexities provide both challenges and opportunities for managing these dynamic ecosystems (11, 13).As corals decline and macroalgae proliferate, the frequency of algal-coral interactions will increase, potentially affecting the survivorship, growth, and reproduction of remnant adult corals and new coral recruits (12, 13). However, the consequences ...

Organism surfaces represent signaling sites for attraction of allies and defense against enemies. However, our understanding of these signals has been impeded by methodological limitations that have precluded direct fine-scale evaluation of compounds on native surfaces. Here, we asked whether natural products from the red macroalga Callophycus serratus act in surface-mediated defense against pathogenic microbes. Bromophycolides and callophycoic acids from algal extracts inhibited growth of Lindra thalassiae, a marine fungal pathogen, and represent the largest group of algal antifungal chemical defenses reported to date. Desorption electrospray ionization mass spectrometry (DESI-MS) imaging revealed that surface-associated bromophycolides were found exclusively in association with distinct surface patches at concentrations sufficient for fungal inhibition; DESI-MS also indicated the presence of bromophycolides within internal algal tissue. This is among the first examples of natural product imaging on biological surfaces, suggesting the importance of secondary metabolites in localized ecological interactions, and illustrating the potential of DESI-MS in understanding chemically-mediated biological processes.imaging mass spectrometry ͉ macroalga ͉ natural product ͉ surface-associated

Interactions among microscopic planktonic organisms underpin the functioning of open ocean ecosystems. With few exceptions, these organisms lack advanced eyes and thus rely largely on chemical sensing to perceive their surroundings. However, few of the signaling molecules involved in interactions among marine plankton have been identified. We report a group of eight small molecules released by copepods, the most abundant zooplankton in the sea, which play a central role in food webs and biogeochemical cycles. The compounds, named copepodamides, are polar lipids connecting taurine via an amide to isoprenoid fatty acid conjugate of varying composition. The bloom-forming dinoflagellate Alexandrium minutum responds to pico- to nanomolar concentrations of copepodamides with up to a 20-fold increase in production of paralytic shellfish toxins. Different copepod species exude distinct copepodamide blends that contribute to the species-specific defensive responses observed in phytoplankton. The signaling system described here has far reaching implications for marine ecosystems by redirecting grazing pressure and facilitating the formation of large scale harmful algal blooms.

Monospecific blooms of phytoplankton can disrupt pelagic communities and negatively affect human health and economies. Interspecific competition may play an important role in promoting blooms, and so we tested (1) whether the outcome of competition between the red tide dinoflagellate Karenia brevis (ex Gymnodinium breve) and 12 cooccurring phytoplankters could be explained by allelopathic effects of compounds released by K. brevis and (2) whether waterborne, lipophilic molecules, including brevetoxins, are involved. Nine of 12 phytoplankton species were suppressed when grown with live K. brevis at bloom concentrations. K. brevis extracellular filtrates or lipophilic extracts of filtrates inhibited six of these nine species, indicating allelopathy. However, these inhibitory effects were weaker than those experienced by competitors exposed to live K. brevis. Brevetoxins at ecologically reasonable waterborne concentrations accounted for the modest inhibition by K. brevis of only one competitor, Skeletonema costatum. The addition of brevetoxins also caused significant autoinhibition, reducing the maximum concentration of K. brevis. Allelopathy is one mechanism by which K. brevis appears to exhibit competitive advantage over some sympatric phytoplankters, although unidentified compounds other than brevetoxins must be involved, in most cases. K. brevis was also susceptible to competitive exclusion by several species, including Odontella aurita and Prorocentrum minimum, known to thrive during K. brevis blooms. Although field experiments are required to assess whether allelopathy plays a fundamental role in bloom dynamics, our results indicate that allelopathy occurs widely but with species-specific consequences.Competition is one of the dominant forces structuring communities, including marine pelagic communities (Hutchinson 1961). The production and release of compounds that inhibit competitors, a process known as allelopathy, is a mechanism of interference competition that is hypothesized to be important among phytoplankton (Smayda 1997), affecting species succession (Keating 1977), especially under eutrophic conditions (Maestrini and Bonin 1981). Allelopathy may be a successful strategy for phytoplankton species that occur in dense blooms, maximizing the concentration of allelopathic compound(s) exposed to competitors and mini-1 Corresponding author (julia.kubanek@biology.gatech.edu). AcknowledgmentsThis research was supported by NSF grant OCE-0134843 to J.K. M.K.H. was supported as a summer undergraduate research assistant by the Camille and Henry Dreyfus Foundation Environmental Chemistry Program. Nutrient analyses were funded by NOAA MERHAB grant MER 02-627A to T.A.V., and ELISA analyses were funded by COP-NOAA MERHAB, NIEHS PO1 ES10594-03, and the CDC-FDOH U50/CCU423360-01 to J.N. We thank P. Tester, R. Pierce, M. Hay, and E. Litchman for advice in planning experiments and two anonymous reviewers for suggestions that improved the manuscript. We also thank E. Prince, A. Prusak, E. John, D. Collins, and A....