Mortality structures population size characteristics of juvenile yellowtail kingfish Seriola lalandi reared at different densitiesExport / Share PlumX View Altmetrics View AltmetricsMoran, D., Smith, C. K., Lee, P. S. and Pether, S. J. (2011) Mortality structures population size characteristics of juvenile yellowtail kingfish Seriola lalandi reared at different densities. Aquatic Biology, 11 (3). pp. 229-238. Full text not currently attached. Access may be available via the Publisher's website or OpenAccess link. Article Link: http://doi.org/10.3354/ab00314 Publisher URL: http://www.int-res.com/abstracts/ab/v11/n3/p229-238/ AbstractA study was undertaken to measure the effects of conspecific density on the growth, mortality and deformity rate of yellowtail kingfish <i>Seriola lalandi</i> Valenciennes during the first feeding period. Newly hatched larvae were stocked in replicate tanks at initial densities of 40, 60 and 100 ind. l<sup>–1</sup> until 30 d post-hatch (DPH). Live prey was administered at frequent intervals in an effort to maintain absolute prey density for all treatments. There was a negative relationship between conspecific density and mean individual length during the first half of the trial, which was attributed to food depletion between supplementary feedings at higher conspecific densities. The effect size (partial eta-squared) of conspecific density decreased considerably during the trial, to the point where the initial stocking density had no discernible effect on cohort growth or mortality rate. The apparent morphological deformity rate ranged from 17 to 32%, but did not differ between treatments. Jaw malformations were the most commonly observed deformity (12 to 30%). The weights of juveniles at the end of the trial were log-normally distributed, with some disproportionately large individuals skewing the weight distributions. There was substantial variation in mortality between and within treatments (74 to 97%), and the conspecific densities of each replicate at 30 DPH did not reflect the relative ordering of the initial treatments. Median individual weight was highly correlated with mortality and weight variance, and the positive skewness of populations decreased as mortality increased. Both trends indicated a strong population size-structuring mechanism. Given the controlled experimental conditions the size-structuring mechanism was not predation or cannibalism. Differential feeding success and an unidentified size-specific mortality agent are hypothesized to be the mechanisms by which mortality was able to strongly influence population size distributions.
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