The wild tobacco species Nicotiana attenuata needs to tailor its defense responses against herbivores and pathogens most efficiently, requiring sophisticated signaling systems to distinguish its individual attackers. One of these signaling components is the phytohormone jasmonic acid (JA) which is produced by N. attenuata in response to e.g. Manduca sexta herbivory. This JA biosynthesis is initialized by the chloroplastic glycerolipase NaGLA1 which hydrolizes trienoic fatty acids from membrane lipids. Using transgenic N. attenuata genotypes stably silenced in NaGLA1 gene expression, this thesis work could show that NaGLA1 is the major lipase in N. attenuata involved in JA biosynthesis after wounding and simulated M. sexta herbivory, however not during infection with Phytophthora parasitica. Instead, NaGLA1 participates in the generation of potential signaling molecules different from JA in the latter interaction NaHSPRO, was found to be a potential regulator of early N. attenuata responses to M. sexta herbivory due to its transcript accumulation pattern. To test this hypothesis, transgenic N. attenuata genotypes stably silenced in NaHSPRO expression were generated. Although no involvement of NaHSPRO in N. attenuata´s resistance to M. sexta could be demonstrated, a role of NaHSPRO in N. attenuata tolerance rather than resistance or in the trade-off process between these defense mechanisms is well possible. Plant tolerance is mediated by SnRK1 and it is known for NaHSPRO homologs from Arabidopsis that they are able to interact with this kinase complex. This thesis work could show that NaHSPRO negatively regulates growth promotion of N. attenuata seedlings mediated by the mutualistic fungus Piriformospora indica via SnRK1 signaling, thus supporting also other hyptheses based on a NaHSPRO function via SnRK1 involving mechanisms.