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Transcription Factor PFB1 Is Required for the Botrytis cinerea Effector BcSCR1-Mediated Pathogenesis

Summary

Researchers discovered how a fungal disease (grey mould) spreads by identifying a toxic protein it produces that disables a plant’s defense system. The fungal protein BcSCR1 sneaks into plant cells and targets a control switch called PFB1 that normally turns on genes protecting plants from infection. By blocking this control switch, the fungus weakens the plant’s immune defenses and establishes infection more easily.

Background

Botrytis cinerea is a necrotrophic fungus infecting over 200 plant species worldwide, causing significant economic losses through grey mould disease. The fungus employs secreted effector proteins to suppress plant immune defenses, though the mechanisms remain largely unexplored. This study identifies a novel effector protein BcSCR1 and its role in plant pathogenesis.

Objective

To identify and characterize the function of the Botrytis cinerea effector BcSCR1 and its interaction with the Arabidopsis transcription factor PFB1 in mediating pathogenesis. The study aims to elucidate how this effector suppresses plant immunity through transcriptional regulation.

Results

BcSCR1 physically interacts with PFB1 and functions as a secreted effector that promotes B. cinerea virulence. Deletion of BcSCR1 reduced fungal aggressiveness, while ectopic expression in plants enhanced susceptibility. BcSCR1 binding to PFB1 represses its transcriptional activation of defense genes OPR3 and WRKY33, reducing plant resistance.

Conclusion

B. cinerea employs the secreted effector BcSCR1 to suppress plant immunity by targeting the transcription factor PFB1, thereby repressing expression of jasmonic acid synthesis and signaling genes essential for plant defense. This reveals a novel mechanism of fungal pathogenesis mediated through transcriptional suppression of host defense responses.
  • Published in:Molecular Plant Pathology,
  • Study Type:Experimental Research,
  • Source: 41514501
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