Fisheries-induced selection as a driver of biodiversity change in exploited populations

Heino, M. ORCID: & Dieckmann, U. ORCID: (2007). Fisheries-induced selection as a driver of biodiversity change in exploited populations. In: ICES CM Documents 2007 - ICES Annual Science Conference, 17-21 September 2007.

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Today, fishing is the dominant source of mortality in most commercially exploited fish stocks. Life-history theory predicts that changes in mortality regime cause selection on life-history traits. In particular, increased mortality can strongly favour earlier maturation. Indeed, commercially exploited fish stocks often show trends towards earlier maturation. However, earlier maturation may also simply reflect phenotypic plasticity triggered, for example, by improved individual growth when stock abundance is diminished. Until recently, the difficulties involved in disentangling plastic and evolutionary components of life-history changes have hindered understanding the nature of phenotypic maturity changes. Introduction of probabilistic reaction norms for age and size at maturation have helped to combat this problem: by estimating maturation reaction norms, one can control for growth-related phenotypic plasticity and changes in mortality. A suite of methods for estimating these reaction norms is now available. Addressing different types of data, these methods have been applied to about 20 stocks, representing 10 different species of marine and freshwater fish. All but three of these studies suggest that a significant evolutionary component has contributed to the observed trends in age and size at maturation. Remarkably, this component is often detectable at time scales as short as a couple of decades.

Item Type: Conference or Workshop Item (UNSPECIFIED)
Research Programs: Evolution and Ecology (EEP)
Bibliographic Reference: In:; ICES CM Documents 2007 - ICES Annual Science Conference; 17-21 September 2007, Helsinki, Finland
Depositing User: IIASA Import
Date Deposited: 15 Jan 2016 08:40
Last Modified: 27 Aug 2021 17:20

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