| Botrytis cinerea causes gray mould disease on various important vegetables,fruits,and crops.The disease causes a significant economic loss pre-and post-harvest.This problem can be generally solved upon usage of chemical fungicides.However,most of them are expensive,non-environmentally friendly,and ineffective for long term use.This is due the ability of B.cinerea on development of the pathogen resistant to those chemicals.Alternatively,determination the pathogenesis of B.cinerea on the molecular levels emerged as effective and environmental benign approach for gray mould diseases.Heme is an essential molecule as the prosthetic group of many proteins for numerous living organisms,participates in many physiological processes.Heme is also involved in regulating gene expression through the action of specific transcriptional regulatory factors.Hemoproteins and multiple heme synthetic steps can sense O2 concentration,therefore heme plays central roles in O2 sensing and utilization in many living organisms.The heme biosynthesis pathway(HBSP)is well conserved among diverse organisms from bacteria,fungi,plants,animals to human.The involvement of the heme biosynthesis pathway(HBSP)in microbial virulence remains very obscure.Here,we demonstrate that Botrytis cinerea employ HBSP for their host infection.During the pathogen in hypoxia or host infection,key components in their HBSP were significantly up-regulated.Depletion of five,including ALS1?PBD1?URD1?CPO1?FEC1,out of the eight enzymes in HBSP in the pathogen resulted in dramatic pathogenicity reduction,sensitivity H2O2 and light.Heme could partially restore the mutants' attenuated pathogenicity,sensitivity to H2O2,but not light.These findings provide novel insights into our understanding of fungal pathogen employment of HBSP for successful host infection and survival via speedup of their growth,removal of infection environmental photosensitizer(uro)porphyrin,scavenging of reactive oxygen species. |
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