title: Cerebrosides A and C, sphingolipid elicitors of hypersensitive cell death and phytoalexin accumulation in rice plants.
abstract: When plants interact with certain pathogens, they protect themselves by generating various chemical and physical barriers called the hypersensitive response. These barriers are induced by molecules called elicitors that are produced by pathogens. In the present study, the most active elicitors of the hypersensitive response in rice were isolated from the rice pathogenic fungus Magnaporthe grisea, and their structures were identified as cerebrosides A and C, sphingolipids that were previously isolated as inducers of cell differentiation in the fungus Schizophyllum commune. Treatment of rice leaves with cerebroside A induced the accumulation of antimicrobial compounds (phytoalexins), cell death, and increased resistance to subsequent infection by compatible pathogens. The degradation products of cerebroside A (fatty acid methyl ester, sphingoid base, and glucosyl sphingoid base) showed no elicitor activity. Hydrogenation of the 8E-double bond in the sphingoid base moiety or the 3E-double bond in the fatty acid moiety of cerebroside A did not alter the elicitor activity, whereas hydrogenation of the 4E-double bond in the sphingoid base moiety led to a 12-fold decrease in elicitor activity. Furthermore, glucocerebrosides from Gaucher's spleen consisting of (E)-4-sphingenine and cerebrosides from rice bran mainly consisting of (4E,8E)-4,8-sphingadienine and (4E,8Z)-4,8-sphingadienine showed no elicitor activity. These results indicate that the methyl group at C-9 and the 4E-double bond in the sphingoid base moiety of cerebrosides A and C are the key elements determining the elicitor activity of these compounds. This study is the first to show that sphingolipids have elicitor activity in plants.
authors.affiliation: Bio Science Laboratories, Meiji Seika Kaisha, Ltd., 5-3-1, Chiyoda, Sakado-shi, Saitama 350-0289, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Koga
authors.forename: T
authors.initials: T
authors.lastname: Yamauchi
authors.forename: M
authors.initials: M
authors.lastname: Shimura
authors.forename: N
authors.initials: N
authors.lastname: Ogawa
authors.forename: K
authors.initials: K
authors.lastname: Oshima
authors.forename: K
authors.initials: K
authors.lastname: Umemura
authors.forename: M
authors.initials: M
authors.lastname: Kikuchi
authors.forename: N
authors.initials: N
authors.lastname: Ogasawara
mesh_terms: D000890:Anti-Infective Agents / Q000378:metabolism*; D016923:Cell Death / Q000187:drug effects; D002554:Cerebrosides / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology*; D004224:Diterpenes / Q000378:metabolism; D005776:Gaucher Disease / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D015394:Molecular Structure; D012275:Oryza / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010936:Plant Extracts / Q000096:biosynthesis*; D018515:Plant Leaves; D012567:Schizophyllum / Q000737:chemistry / Q000502:physiology; D012717:Sesquiterpenes; D013107:Sphingolipids / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology*; D013154:Spleen / Q000737:chemistry; D013729:Terpenes; D000094162:Phytoalexins
chemical_list: D000890:Anti-Infective Agents; D002554:Cerebrosides; D004224:Diterpenes; D010936:Plant Extracts; D012717:Sesquiterpenes; D013107:Sphingolipids; D013729:Terpenes; C116024:cerebroside A; C116025:cerebroside C; C116023:momilactone A; D000094162:Phytoalexins