Transcytosis shuts the door for an unwanted guest.
ABSTRACT Penetration resistance is a well-described plant defense process, in which SOLUBLE N-ETHYLMALEIMIDE-SENSITIVE-FACTOR ATTACHMENT RECEPTOR (SNARE) proteins have essential roles in membrane fusion processes. Strong focal accumulation of these proteins at the site of attack by powdery mildew fungi has been considered important for their function. However, recent insight indicates that transcytosis, leading to the formation of exosomes, has an important role in this defense and, furthermore, that strong accumulation of these SNARE proteins with the exosomes is biologically irrelevant. These findings alter the established function of SNAREs in penetration resistance; therefore, in this opinion, we propose that PEN1 and its SNARE partners function on an endosome in their control of penetration resistance.
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ABSTRACT: Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.Science 09/2003; 301(5635):969-72. · 31.20 Impact Factor