The improvement of biopesticides for use in the agriculture industry requires an understanding of the biological- and ecological principles underlying their behavior in natural environments. The nuclear genomes of members of the genus Trichoderma, which are representative fungal biocontrol agents, have been actively studied in relation to the unique characteristics of these species as effective producers of CAZymes/secondary metabolites and biopesticides, but their mitochondrial genomes have received much less attention. In this study, the mitochondrial genome of Trichoderma atroviride (Hypocreales, Sordariomycetes), which targets wood-decaying fungal pathogens and has the ability to degrade chemical fungicides, was assembled de novo. A 32,758 bp circular DNA molecule was revealed with specific features, such as a few more protein CDS and trn genes, two homing endonucleases (LAGLIDADG-/GIY-YIG-type), and even a putative overlapping tRNA gene, on a closer phylogenetic relationship with T. gamsii among hypocrealean fungi. Particularly, introns were observed with several footprints likely to be evolutionarily associated with the intron dynamics of the Trichoderma mitochondrial genomes. This study is the first to report the complete de novo mitochondrial genome of T. atroviride, while comparative analyses of Trichoderma mitochondrial genomes were also conducted from the perspective of mitochondrial evolution for the first time.

Invasive aspergillosis is a life-threatening mycosis caused by the pathogenic fungus Aspergillus. The predominant causal species is Aspergillus fumigatus, and azole drugs are the treatment of choice. Azole drugs approved for clinical use include itraconazole, voriconazole, posaconazole, and the recently added isavuconazole. However, epidemiological research has indicated that the prevalence of azole-resistant A. fumigatus isolates has increased significantly over the last decade. What is worse is that azole-resistant strains are likely to have emerged not only in response to long-term drug treatment but also because of exposure to azole fungicides in the environment. Resistance mechanisms include amino acid substitutions in the target Cyp51A protein, tandem repeat sequence insertions at the cyp51A promoter, and overexpression of the ABC transporter Cdr1B. Environmental azole-resistant strains harboring the association of a tandem repeat sequence and punctual mutation of the Cyp51A gene (TR34/L98H and TR46/Y121F/T289A) have become widely disseminated across the world within a short time period. The epidemiological data also suggests that the number of Aspergillus spp. other than A. fumigatus isolated has risen. Some non-fumigatus species intrinsically show low susceptibility to azole drugs, imposing the need for accurate identification, and drug susceptibility testing in most clinical cases. Currently, our knowledge of azole resistance mechanisms in non-fumigatus Aspergillus species such as A. flavus, A. niger, A. tubingensis, A. terreus, A. fischeri, A. lentulus, A. udagawae, and A. calidoustus is limited. In this review, we present recent advances in our understanding of azole resistance mechanisms particularly in A. fumigatus. We then provide an overview of the genome sequences of non-fumigatus species, focusing on the proteins related to azole resistance mechanisms.