ABSTRACT
Filamentous fungi produce a number of secondary metabolic compounds that have been shown to be both of great value (i.e., antibiotics and anti-hypercholesterolemics) and great harm (i.e., aflatoxins and trichothecenes). Since the initial discovery of clustered genes involved in the biosynthesis of penicllin in Penicillium chrysogenum and Aspergillus nidulans (Diez et al. 1990; MacCabe et al. 1990), a number of secondary metabolic gene clusters have been identified and characterized in filamentous fungi at the molecular level [reviewed in Cary et al. (2001); Keller and Hohn (1997)]. In general, fungal secondary metabolic pathway gene clusters share common genetic components with respect to function. In addition to the structural genes encoding the biosynthetic enzymes the pathway cluster can also contain a gene(s) required for regulation of expression of the other pathway genes (Chang et al. 1995b; Pedley and Walton 2001; Proctor 2000) and a gene(s) required for export of the metabolite or “self protection” to the metabolite (Alexander et al. 1999; Pitkin et al. 1996). A common question that inevitably arises during the study of fungal gene clusters has been why are the genes for these biosynthetic pathways maintained as a cluster(s) in the genome and what advantage does this impart on the fungus? This is especially perplexing in light of the fact that all of the secondary metabolic gene clusters studied appear to be “dispensible” with respect to their metabolic functions and advantage imparted to the producing organism. Keller and Hohn (1997) used the term “dispensable metabolic pathways” for those primary and secondary metabolic pathways “that either are not required for growth or are only required for growth under a limited range of conditions.”
