C. parasitica has a remarkable ability to colonize bark wounds on chestnut trees followed by the formation of a specialized structure called the hyphal fan, which efficiently penetrates through chemical and physical defense barriers and invades healthy cambial tissue under the bark. The fungus erupts from the bark after the formation of stromata, in which asexual and sexual fruiting bodies develop, releasing orange-pigmented spores to infect other trees. C. parasitica is also a tractable experimental organism for both classical and molecular genetics. It can mate in the laboratory, which facilitates genetic linkage analysis, and can be transformed with high efficiency. The level of homologous recombination during DNA-mediated transformation of spheroplasts has been increased to 85% with the development of a C. parasitica mutant strain defective in non-homologous end joining DNA repair. Because C. parasitica is haploid and asexual spores are uninucleate, gene disruption and selection of homokaryons after transformation is efficient. C. parasitica has been shown to support the replication of well-characterized viruses representing five different families: Hypoviridae, Reoviridae, Narnaviridae, Partitiviridae and Chrysoviridae. The development of infectious cDNA clones of several hypoviruses has provided a powerful system for the study of virus-host interactions and presented the means for engineering hypoviruses to enhance biological control potential. Completion of the C. parasitica genome sequence will provide insights into the mechanisms underlying fungal colonization and penetration of tree host defense barriers. It will contribute to a molecular understanding of the vegetative incompatibility system, which will have significant implications for enhancing mycovirus-based biological control potential. It will also increase utility of a tractable experimental system for advancing studies on a wide variety of important biological processes. These range from signal transduction pathways underlying fungal development, secondary metabolism and pathogenesis to self-nonself recognition and programmed cell death.
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