Characterisation of guided entry of tail-anchored proteins in Magnaporthe oryzae

Summary

Rice blast disease caused by the fungus Magnaporthe oryzae threatens global rice production. This study identified and studied five proteins (GET components) that help the fungus insert special proteins into cell membranes, a process essential for the fungus to infect rice plants. Researchers found that two of these proteins are critical for the fungus to grow, reproduce, and cause disease, while a third one actually reduces the fungus’s ability to infect plants. This discovery could lead to new strategies to control rice blast disease.

Background

Rice blast disease caused by Magnaporthe oryzae is a devastating fungal disease affecting global rice production with annual yield losses around 30%. Tail-anchored (TA) proteins are conserved across organisms and require post-translational insertion into membranes. The Guided Entry of Tail-anchored (GET) complex has been extensively studied in yeast and mammals but remains unexplored in pathogenic fungi.

Objective

To identify and characterize GET pathway components in M. oryzae and determine their roles in vegetative growth, asexual reproduction, stress response, cell wall integrity, and pathogenesis of the rice blast fungus.

Results

MoGet1 and MoGet2 are essential for vegetative growth, conidiation, and pathogenesis, with ER localization required for DTT-induced ER stress response. MoGet3 negatively regulates hyphal growth, asexual development, and pathogenesis. MoGet4 and MoSgt2 deletions showed no effect on fungal development. MoGet2 is critical for osmotic stress response and cell wall integrity, while MoGet1, MoGet2, and MoGet3 physically interact.

Conclusion

The GET pathway components play differential roles in M. oryzae pathogenesis, with MoGet1 and MoGet2 being critical for virulence-related traits. This study provides valuable insights into GET complex functions in plant fungal pathogens and demonstrates the importance of TA protein trafficking in fungal pathogenesis.
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