| Summary: | <i>Trichoderma atroviride</i> responds to various environmental stressors through the mitogen-activated protein kinase (MAPK) Tmk3 and MAPK-kinase Pbs2 signaling pathways. In fungi, orthologues to Tmk3 are regulated by a histidine kinase (HK) sensor. However, the role of <i>T. atroviride</i> HKs remains unknown. In this regard, the function of the <i>T. atroviride</i> HK Nik1 was analyzed in response to stressors regulated by Tmk3. The growth of the Δ<i>nik1</i> mutant strains was compromised under hyperosmotic stress; mycelia were less resistant to lysing enzymes than the WT strain, while conidia of Δ<i>nik1</i> were more sensitive to Congo red; however, ∆<i>pbs2</i> and ∆<i>tmk3</i> strains showed a more drastic defect in cell wall stability. Light-regulated <i>blu1</i> and <i>grg2</i> gene expression was induced upon an osmotic shock through Pbs2-Tmk3 but was independent of Nik1. The encoding chitin synthases <i>chs1</i> and <i>chs2</i> genes were downregulated after an osmotic shock in the WT, but <i>chs1</i> and <i>chs3</i> expression were enhanced in ∆<i>nik1</i>, ∆<i>pbs2</i>, and ∆<i>tmk3</i>. The vegetative growth and conidiation by light decreased in ∆<i>nik1</i>, although Nik1 was unrequired to activate the light-responsive genes by Tmk3. Altogether, Nik1 regulates responses related to the Pbs2-Tmk3 pathway and suggests the participation of additional HKs to respond to stress.
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