Molecular signaling in the response to injury of Trichoderma atroviride

Wound response in multicellular eukaryotes is essential for survival and is highly conserved in plants and animals. In our laboratory, we discovered that the filamentous fungus Trichoderma atroviride responds to injury by triggering hyphal regeneration and the formation of asexual reproductive structures. Transcriptomic analyses revealed that the mechanism of response to this stimulus is similar to that of animals and plants. Furthermore, biochemical data implicate ROS, eATP, and Ca²⁺ as signaling molecules, suggesting that the injury response mechanism is highly conserved in the three eukaryotic kingdoms.

We have recently found that mutants affected in the MAPKs Tmk1 and Tmk3 do not conidiate in response to injury. It is particularly interesting that, in addition to this phenotype, a Dtmk1 mutant does not regenerate. Using this information, we defined a set of regeneration genes based on the transcriptomics analyses of mutants defective in this process, as well as, upon treatment of the wild type strain with drugs that block signaling pathways intervening in regeneration. Furthermore, we evaluated the injury response in mutants of the RNAi synthesis machinery of T. atroviride. The ∆dcr2 and ∆rdr3 strains presented a dramatic defect in regeneration ability and asexual reproduction in response to injury. To understand the molecular processes affected by the absence of the RNAi pathway, we performed transcriptomic analysis of the WT and ∆dcr2 strains subjected to injury, showing that signaling processes, DNA repair and cell cycle progression are essential to overcome this stress and are affected in the ∆dcr2 mutant.