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Mechanical vulnerability explains size-dependent mortality of reef corals

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madin2014ecologylett1008.pdf (551.8Kb)
Date
02/07/2014
Author
Madin, J.S.
Baird, A.H.
Dornelas, Maria
Connolly, S.R.
Funder
European Research Council
Grant ID
250189
Keywords
Biomechanics
Colonial
Demography
Disturbance
Life history
Mortality
Reef coral
GC Oceanography
BDC
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Abstract
Understanding life history and demographic variation among species within communities is a central ecological goal. Mortality schedules are especially important in ecosystems where disturbance plays a major role in structuring communities, such as coral reefs. Here, we test whether a trait-based, mechanistic model of mechanical vulnerability in corals can explain mortality schedules. Specifically, we ask whether species that become increasingly vulnerable to hydrodynamic dislodgment as they grow have bathtub-shaped mortality curves, whereas species that remain mechanically stable have decreasing mortality rates with size, as predicted by classical life history theory for reef corals. We find that size-dependent mortality is highly consistent between species with the same growth form and that the shape of size-dependent mortality for each growth form can be explained by mechanical vulnerability. Our findings highlight the feasibility of predicting assemblage-scale mortality patterns on coral reefs with trait-based approaches.
Citation
Madin , J S , Baird , A H , Dornelas , M & Connolly , S R 2014 , ' Mechanical vulnerability explains size-dependent mortality of reef corals ' , Ecology Letters , vol. 17 , no. 8 , pp. 1008-1015 . https://doi.org/10.1111/ele.12306
Publication
Ecology Letters
Status
Peer reviewed
DOI
https://doi.org/10.1111/ele.12306
ISSN
1461-023X
Type
Journal article
Rights
Copyright © 2014 The Authors. Ecology Letters published by John Wiley & Sons Ltd and CNRS. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Description
JM, AB and SC were supported by fellowships from the Australian Research Council (FT110100609, FT0990652 and DP0880544 respectively). MD was supported by the ERC (BioTIME 250189) and the Scottish Funding Council (MASTS - HR09011).
Collections
  • University of St Andrews Research
URI
http://hdl.handle.net/10023/4981

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