Abstract

Small plant populations are more prone to extinction due to the loss of genetic variation through random genetic drift, increased selfing, and mating among related individuals. To date, most researchers dealing with genetic erosion in fragmented plant populations have focused on threatened or rare species. We raise the question whether common plant species are as susceptible to habitat fragmentation as rare species. We conducted a formal meta-analysis of habitat fragmentation studies that reported both population size and population genetic diversity. We estimated the overall weighted mean and variance of the correlation coefficients among four different measures of genetic diversity and plant population size. We then tested whether rarity, mating system, and plant longevity are potential moderators of the relationship between population size and genetic diversity. Mean gene diversity, percent polymorphic loci, and allelic richness across studies were positively and highly significantly correlated with population size, whereas no significant relationship was found between population size and the inbreeding coefficient. Genetic diversity of self-compatible species was less affected by decreasing population size than that of obligate outcrossing and self-compatible but mainly outcrossing species. Longevity did not affect the population genetic response to fragmentation. Our most important finding, however, was that common species were as, or more, susceptible to the population genetic consequences of habitat fragmentation than rare species, even when historically or naturally rare species were excluded from the analysis. These results are dramatic in that many more plant species than previously assumed may be vulnerable to genetic erosion and loss of genetic diversity as a result of ongoing fragmentation processes. This implies that many fragmented habitats have become unable to support plant populations that are large enough to maintain a mutation-drift balance and that occupied habitat fragments have become too isolated to allow sufficient gene flow to enable replenishment of lost alleles.

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