|Nishimura, Marc - CARNEGIE, STANFORD, CA|
|Stein, Monica - CARNEGIE, STANFORD, CA|
|Hou, Bi-Huei - CARNEGIE, STANFORD, CA|
|Edwards, Herb - WESTERN ILLINOIS UNIV|
|Somerville, Shauna - CARNEGIE, STANFORD, CA|
Submitted to: Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 8, 2003
Publication Date: August 15, 2003
Citation: Nishimura, M.T., Stein, M., Hou, B., Vogel, J.P., Edwards, H., Somerville, S.C. 2003. Loss of a callose synthase results in salicylic acid dependent disease resistance. Science. 301:969-972. Interpretive Summary: This paper describes the cloning of a plant gene, PMR4, that is responsible for biosynthesis of callose, a polysaccharide component of the plant cell wall. Callose deposition is typically observed in response to pathogen attack and wounding and is thought to play a role in defense. Surprisingly, mutations in pmr4 that no longer produce callose in response to pathogen attack or wounding are resitant to powdery mildew disease. This resistance is dependent on the activation of the well described salicylic acid-dependent defense pathway. These results indicate that callose or callose synthase negatively regulates the salicylic acid pathway.
Technical 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.