The CaSCH9 deletion mutant was attenuated in virulence

However, it was significantly reduced in virulence on flowering wheat heads and corn silks. Although SCH9 orthologs are well-conserved in plant pathogenic fungi or filamentous ascomyctes, none of them have been characterized. However, its ortholog is known to be important for virulence in human pathogens C. albicans and C. neoformans. The CaSCH9 deletion mutant was attenuated in virulence in a mouse mode of systemic candidiasis due to its defects in yeast Liproxstatin-1 growth and filamentation. In C. neoformans, the SCH9 ortholog functions both independently of and in conjunction with the cAMP-PKA pathway in pathogenesis. In F. graminearum, DON is an important virulence factor and the DFgsch9 mutant was significantly reduced in DON production in infected wheat kernels. In addition, the DFgsch9 mutant had a reduced growth rate and increased sensitivity to oxidative and other stresses. All these factors may contribute to the defects of the DFgsch9 mutant in plant infection. The DFgsch9 mutant had increased sensitivity to cell wall stresses, indicating defects in cell wall integrity. However, unlike the mgv1 mutant, deletion of FgSCH9 had no effect on Maytansinol hyphal fusion in F. graminearum. Interestingly, old hyphae of the DFgsch9 mutant often had empty, dead intercalary compartments, likely due to its defects in cell wall integrity. In some of them, new, narrow hyphae were produced from the middle of septa and grew into the empty, dead old hyphae. It appears that the DFgsch9 mutant can plug up the septal pore when hyphal compartments become damaged. However, it is defective in this process and somehow can regain polarized growth through the plugged septal pore areas. To our knowledge, this phenomenon of new hyphal growth inside old hyphal compartments has not been reported in F. graminearum. Recently, we found that the tub2 deletion mutant also had similar defects. It will be interesting to determine the molecular mechanisms involved in the regulation of septal pore plugging and further growth inside empty hyphal fragments or re-establishment of hyphal tip growth at the septal pore.

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