Brachycladium were found. A single report on the toxicity of culture extracts of Pleospora for cell lines was reviewed (Ge et al. 2005), but it was not helpful in evaluating the potential risks of infection of humans or animals. If those fungi are shown to be thermotolerant (that is, able to grow efficiently at human body temperature, 37°C), there would be a theoretical risk that increasing their amounts in the environment might lead to infection in immunocompromised humans and animals. However, on the basis of the absence of any case reports, the likelihood appears quite low.

MUTATION

The potential for mycoherbicides to mutate is similar to that of fungi in general, as described in Chapter 4. The diversity of fungal genotypes also is affected by sexual recombination within species. Many fungi that have not been observed to reproduce sexually may do so cryptically, judging from populationgenetics evidence (Taylor et al. 2000). In some cases, population-genetics evidence on sex has led to confirmation by laboratory mating (O’Gorman et al. 2009). New genetic variation can become established in fungal populations by natural selection or by chance. Adaptation to new environments, for example, to new plant hosts or to new cultivars of crop plants can be accelerated by outbreeding and recombination due to sexual reproduction (Goddard et al. 2005; Zhan et al. 2007; Sommerhalder et al. 2010). All those processes could affect Crivellia or Brachycladium species.

However, there is little basic genetic information on C. papaveracea or B. papaveris, so only a generalization about the potential for mutation can be made. There is no reason to expect that the mutation rate of these fungi would be different from that of other filamentous fungi or that they would be more or less susceptible to gene gain, gene duplication, or horizontal gene transfer. C. papaveracea outbreeds by sexual reproduction. B. papaveris reproduces sexually but is homothallic (self-mating) and need not produce recombined progeny (Farr et al. 2000). Thus, adaptation involving virulence or host range could be accelerated by genetic recombination in the case of C. papaveracea but not necessarily in the case of B. papaveris.

Mutation could play a role in determining the toxicity (with respect to secondary metabolites produced) of a mycoherbicide to the extent that mutation results in changes in the amount of toxin produced or the environmental conditions under which the toxins are produced. Concerns about mutationrelated changes in the toxicity of C. papaveracea or B. papaveris are all but impossible to assess because very little research has been performed. As noted earlier, the available data are insufficient to determine what secondary metabolites are produced by C. papaveracea or B. papaveris, let alone in what quantities or how production would be affected by mutations.



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