MaCts1, an Endochitinase, Is Involved in Conidial Germination, Conidial Yield, Stress Tolerances and Microcycle Conidiation in Metarhizium acridum

SIMPLE SUMMARY: Entomopathogenic fungi are promising biocontrol agents. Microcycle conidiation has shown great potential in enhancing the conidial yield and quality of entomopathogenic fungi. Elucidating the regulatory mechanisms underlying the induction of microcycle conidiation will be helpful for genetic improvement of entomopathogenic fungi. This work focused on the connection of an endochitinase, MaCts1, to the biocontrol potential of the entomopathogenic fungus Metarhizium acridum. MaCts1, an endochitinase gene of M. acridum, was shown to be involved in conidial germination, conidial yield and fungal resistance to UV-B irradiation and heat-shock. Interestingly, disruption of MaCts1 led to maintenance of typical conidiation on the microcycle conidiation induction medium, SYA, which may not be dependent on the MOR/RAM pathway. This work provided insight into the regulatory mechanisms governing the shift to microcycle conidiation in M. acridum. ABSTRACT: Entomopathogenic fungi are promising biocontrol agents of insect-mediated crop damage. Microcycle conidiation has shown great potential in enhancing the conidial yield and quality of entomopathogenic fungi. Homologs of Cts1, an endochitinase of Saccharomyces cerevisiae, participate in cell separation in several fungal spp. and may contribute to the morphological differences that occur during the shift to microcycle conidiation. However, the precise functions of Cts1 in entomopathogenic fungi remain unclear. Herein, the endochitinase gene, MaCts1, was characterized in the model entomopathogen, Metarhizium acridum. A loss of function line for MaCts1 led to a delay of 1 h in the median germination time, a 28% reduction in conidial yield and significant defects in fungal resistances to UV-irradiation (18%) and heat-shock (15%), while fungal tolerances to cell wall stressors, oxidative and hyperosmotic stresses and virulence remained unchanged. The MaCts1-disruption strain displayed typical conidiation on the microcycle conidiation induction medium, SYA. In contrast, deletion of key genes in the morphogenesis-related NDR kinase network (MOR pathway)/regulation of Ace2 and morphogenesis (RAM pathway) did not affect the SYA-induction of microcycle conidiation. This indicates that MaCts1 makes contributions to the microcycle conidiation, which may not be dependent on the MOR/RAM pathway in M. acridum.