In this work, I describe the activation and regulation of oxylipin signaling pathways in Nicotiana attenuata in response to herbivory. When the tobacco hornworm, Manduca sexta, feeds on N. attenuata, the plant perceives fatty acid-amino acid conjugates like 18:3-Glu present in the insect’s oral secretions. After contact with wounded leaf tissue, 18:3-Glu is rapidly modified into active and inactive metabolites catalyzed by LOX2. This metabolism of 18:3-Glu may play a role in the fine tuning of plant responses to insect herbivory. In response to herbivory, the plant induces the jasmonic acid (JA) biosynthesis. Here, 18:3-Glu together with the regulatory factors salicylate induced protein kinase (SIPK) and nonexpressor of PR-1 (NPR1) affect JA biosynthesis by enhancing the supply of α-linolenic acid through glycerolipase A1 (GLA1) whereas wound induced protein kinase (WIPK) affect basal allene oxide synthase (AOS) activity. After stimulus, the produced JA is conjugated to isoleucine by JASMONATE RESISTANT 4 and 6 (JAR4/6) to form JA-Ile. JA-Ile binds to SCFCOI which participates in the activation of defense response against insect herbivores. The plants’ capacity to mediate this JA signaling is essential to survive in nature. Besides the activation of JA biosynthesis, leaf wounding and insect herbivory does also results in the generation of green leaf volatiles such as (3Z)-hexenal and C12 molecules such as (9Z)-traumatin through the cleavage of e.g. 13-OOH-18:3 by hydroperoxy lyase (HPL). 98% of the (9Z)-traumatin formed is converted into 9-OH-traumatin: two-thirds by product recycling through LOX2 and one-third by non-enzymatic oxidation. In summary I showed that metabolism of insect elicitors at the wound site can tune the induction of oxylipin signaling pathways, how these pathways are activated upon insect herbivore attack and which function these signaling pathways fulfill in nature.