Elevated -Linolenic Acid Content in Extra-plastidial Membranes of Tomato Accelerates Wound-Induced Jasmonate Generation and Improves Tolerance to the Herbivorous Insects Heliothis peltigera and Spodoptera littoralis

摘要

In tomato, desaturation of linoleic acid (18:2) to -linolenic acid (18:3) is mediated in the plastidial membranes by the -3 fatty acid desaturases 7 (FAD7), and in the ER membrane by its paralog FAD3. According to the prevalent model, the hormone jasmonic acid isoleucine (JA-Ile), which plays a key role in the plant response to various stresses, including wounding and herbivores attack, is derived from 18:3 which is released from the plastidial membrane glycerolipids. The current work aimed at assessing in tomato the effects of ectopic FAD3 over-expression or SlFAD7 silencing on herbivore tolerance and on wound response. The tomato SlFAD7 gene encoding for the plastidial-residing FAD7 was silenced by RNA interference, and enhanced expression of the extra-plastidial ER-residing FAD3 was induced by ectopic expression of BnFAD3. Over-expression of BnFAD3 led to increase, whereas SlFAD7 silencing led to decrease in 18:3 content in the extra-plastidial and plastidial membrane, respectively. As anticipated, silencing SlFAD7 attenuated the accumulation of JA-Ile following wounding, and enhanced susceptibility to two important pest insects: the chewing herbivores Spodoptera littoralis and Heliothis peltigera. Unexpected was the finding that ectopic over-expression of the extra-plastidial ER-residing FAD3 accelerated both wound-induced JA-Ile accumulation and expression of wound-response marker genes. Furthermore, BnFAD3 over-expression significantly improved the tomato tolerance to these two chewing herbivores. The presented information supports the notion that 18:3 derived from extra-plastidial membranes may serve as a substrate for, or as a source for a cue triggering, JA-Ile biosynthesis in response to wounding and insect chewing.