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High density populations of the crown-of-thorns seastar, Acanthaster planci, are a major contributor to the decline of coral reefs, however the causes behind periodic outbreaks of this species are not understood. The enhanced nutrients hypothesis posits that pulses of enhanced larval food in eutrophic waters facilitate metamorphic success with a flow-on effect for population growth. The larval resilience hypothesis suggests that A. planci larvae naturally thrive in tropical oligotrophic waters. Both hypotheses remain to be tested empirically. We raised A. planci larvae in a range of food regimes from starvation (no food) to satiation (excess food). Algal cell concentration and chlorophyll levels were used to reflect phytoplankton conditions in nature for oligotrophic waters (0-100 cells ml(-1); 0-0.01 μg chl a L(-1)), natural background levels of nutrients on the Great Barrier Reef (GBR) (1,000-10,000 cells ml(-1); 0.1-1.0 μg chl a L(-1)), and enhanced eutrophic conditions following runoff events (100,000 cells ml(-1); 10 μg chl a L(-1)). We determine how these food levels affected larval growth and survival, and the metamorphic link between larval experience and juvenile quality (size) in experiments where food ration per larvae was carefully controlled. Phytoplankton levels of 1 μg chl a L(-1), close to background levels for some reefs on the GBR and following flood events, were optimal for larval success. Development was less successful above and below this food treatment. Enhanced larval performance at 1 μg chl a L(-1) provides empirical support for the enhanced nutrients hypothesis, but up to a limit, and emphasizes the need for appropriate mitigation strategies to reduce eutrophication and the consequent risk of A. planci outbreaks.
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25790074
???displayArticle.pmcLink???PMC4366153 ???displayArticle.link???PLoS One
Fig 1. Regions on the Great Barrier Reef where hotspots of Acanthaster planci outbreaks occur (Wet Tropics, Burdekin, Fitzroy), with indication of coastal, mid-shelf and offshore reefs.The ‘initiation box’ for A. planci outbreaks between Cooktown and Cairns [12] is indicated by the rectangle.
Fig 2. Examples of development of Acanthaster planci larvae.(a) Brachiolaria (day 16) with rudiment (r), (b) late-bipinnaria (day 7), (c) early-bipinnaria (day 4), (d-f) abnormal, distorted or arrested development.
Fig 3. Levels of chl a (μg L-1) on the Great Barrier Reef where hotspots of Acanthaster planci outbreaks occur (Wet Tropics, Burdekin and Fitzroy), when larvae would be expected in the plankton (November-March).Average (a) natural chl a from 2011–2014 (n = 20; ±se), and (b) mean and (c) maximum chl a recorded for the week following major cyclone or flood events between 2009–2014 (n = 7; ±se). Data sourced from eReefs (http://www.bom.gov.au/marinewaterquality/).
Fig 4. Larval (a) length and (b) width for Acanthaster planci reared in five algal concentrations, represented as chl a concentration (μg L-1) on days 4, 7 and 10 (n = 10).Boxes represent the interquartile range (25 and 75th percentile), the horizontal line is the median, and the whiskers represent the data range. Tukey’s HSD test: levels not connected by the same letter are significantly different (within each day).
Fig 5. Average percent abnormality (±se) of Acanthaster planci reared in five algal concentrations, represented as chl a concentration (μg L-1) on days 4, 7 and 10 (n = 10).
Fig 6. Average (a) percent settlement and (b) size of recently settled Acanthaster planci juveniles at day 18, following rearing larval rearing in five algal concentrations represented as chl a concentration (μg L-1) across all settlement assays (±se).Tukey’s HSD test: levels not connected by the same letter are significantly different.
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