The plant disease resistance gene Asc-1 prevents disruption of sphingolipid metabolism during AAL-toxin-induced programmed cell death.
The nectrotrophic fungus Alternaria alternata f.sp. lycopersici infects tomato plants of the genotype asc/asc by utilizing a host-selective toxin, AAL-toxin, that kills the host cells by inducing programmed cell death. Asc-1 is homologous to genes found in most eukaryotes from yeast to humans, suggesting a conserved function. A yeast strain with deletions in the homologous genes LAG1 and LAC1 was functionally complemented by Asc-1, indicating that Asc-1 functions in an analogous manner to the yeast homologues. Examination of the yeast sphingolipids, which are almost absent in the lag1Deltalac1Delta mutant, showed that Asc-1 was able to restore the synthesis of sphingolipids. We therefore examined the biosynthesis of sphingolipids in tomato by labeling leaf discs with l-[3-3H]serine. In the absence of AAL-toxin, there was no detectable difference in sphingolipid labeling between leaf discs from Asc/Asc or asc/asc leaves. In the presence of pathologically significant concentrations of AAL-toxin however, asc/asc leaf discs showed severely reduced labeling of sphingolipids and increased label in dihydrosphingosine (DHS) and 3-ketodihydrosphingosine (3-KDHS). Leaf discs from Asc/Asc leaves responded to AAL-toxin treatment by incorporating label into different sphingolipid species. The effects of AAL-toxin on asc/asc leaflets could be partially blocked by the simultaneous application of AAL-toxin and myriocin. Leaf discs simultaneously treated with AAL-toxin and myriocin showed no incorporation of label into sphingolipids or long-chain bases as expected. These results indicate that the presence of Asc-1 is able to relieve an AAL-toxin-induced block on sphingolipid synthesis that would otherwise lead to programmed cell death.
Spassieva
Stefka D
SD
Department of Molecular Biology of Plants, Research School GBB, University of Groningen, Kerklaan 30, 9751NN Haren, the Netherlands.
Markham
Jonathan E
JE
Hille
Jacques
J
D000528:Alternaria / Q000502:physiology; D017209:Apoptosis / Q000187:drug effects*; D017353:Gene Deletion; D005800:Genes, Fungal / Q000235:genetics; D017343:Genes, Plant / Q000235:genetics*; D005816:Genetic Complementation Test; D020022:Genetic Predisposition to Disease; D018551:Solanum lycopersicum / Q000166:cytology* / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D008969:Molecular Sequence Data; D015394:Molecular Structure; D009183:Mycotoxins / Q000633:toxicity*; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D030821:Plants, Genetically Modified; D013107:Sphingolipids / Q000378:metabolism*
D009183:Mycotoxins; D013107:Sphingolipids