Gene flow

The gene or genotype flow, or the process through which particular alleles or individuals are exchanged among separate populations (McDonald and Linde, 2002), is another evolutionary force. While considered as a unifying force that usually prevents populations from diverging by breaking down the geographical or other boundaries that could otherwise isolate populations, this evolutionary force could lead to the increased incidence or severity of a disease or even to a new disease. It tends to modify pathosystems involving pathogens that produce propagules with the natural potential of long-distance dispersal, such as powdery mildew and rust fungi, but also applies to pathogens with the potential of short-distance spreading because of dispersal by anthropogenic movement. Depending on the distribution of populations and the environmental conditions, which are influenced by climate change, gene flow leads to an increase in population diversity or to the introduction of a new population in new ecological niches, depending on the presence or otherwise of another population of the same species in the introduction area. The evolutionary potential resulting from gene flow allows for a variation in host resistance and pathogen virulence, as well as new disease or pathogen emergence.

In the newly colonized area, specific interactions could lead to very diverse situations. The introduction of the Asian chestnut tree blight fungus, Cryphonectria parasitica, led to the extermination of the American chestnut, Castanea dentata, from eastern USA forests (Anagnostakis, 1987). Similarly, the introduction of the aggressive pathogen Ophiostoma novo-ulmi sp. nov. in North America caused the extermination of many elms that had survived the original epidemic by Ophiostoma ulmi. Dutch elm disease epidemics that resulted from the movement of Ophiostoma species between and across continents illustrate the dangers of moving plant material around the world (Brasier, 1991). Climate change was not the cause of the gene flow or its consequence in this case, but these examples illustrate the high risks of introducing pathogen genotypes into new ecological niches where favourable interactions allow the development of new epidemics. The role played by wild oat populations in driving virulence evolution in the pathogen populations of oat rusts (Puccinia graminis f. sp. avenae and Puccinia coronata) on oats in Australia also shows that interactions at the agroecological interface through gene flow between cultivated and wild host plant populations could also alter pathosystems (Burdon and Thrall, 2008).

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