Abstract

The widespread occurrence of genet fragmentation among modular, clonal organisms results in size—dependent life history patterns that are often independent of clonal age. In this study the size dependence of clonal growth rates was experimentally evaluated using two common coral reef cnidarians that inhabit shallow reef environments at Discovery Bay, Jamaica. As a result of the turbulent conditions associated with storms, these organisms commonly undergo fragmentation. The growth of aggregations of these clonal fragments in three small size classes (ranging over three orders of magnitude) was statistically evaluated against a null, exponential model that predicts that relative growth rates of small aggregations are size independent. Growth rates for Zoanthus solanderi were consistent with this model. Z. sociatus, on the other hand, exhibited size—dependent relative growth rates. The smallest aggregations of this species had the higher relative growth rates, which were sufficiently high to more than compensate for losses due to mortality. These results are consistent with other life history and distributional differences between these two species. Zoanthus sociatus has a higher rate of mortality, does not undergo sexual reproduction until reaching a larger aggregation size, and commonly has a higher vertical distribution (which may represent a spatial refuge from subtidal predators) than does Z. solanderi. The comparatively rapid relative growth rates of small aggregations of Z. sociatus may be the result of spatial constraints on growth in large aggregations and/or of higher relative energy allocations to growth in small aggregations. The incorporation of fragmentation into the life history strategy of clonal organisms has a range of predicted consequences. Among some organisms, fragmentation and associated adaptations may be rare and of little consequence. Among organisms that frequently fragment as a result of physical disturbances, natural selection should favor repair and regenerative processes as well as resistance to this source of mortality. At the extreme, fragmentation need not be associated with death and injury. Adaptations at the developmental and physiological level may involve genetically programmed production of asexual fragments and size—dependent shifts in energy allocations to growth, sexual reproduction, and energy reserves. The degree of interdependence of the processes controlling the dynamics of genets and fragmented modules may well depend on the relative importance of such adaptations.

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