The Role of Plant Hormones in the Interaction of Colletotrichum Species with Their Host Plants

Abstract

Colletotrichum is a plant pathogenic fungus which is able to infect virtually every economically important plant species. Up to now no common infection mechanism has been identified comparing different plant and Colletotrichum species. Plant hormones play a crucial role in plant-pathogen interactions regardless whether they are symbiotic or pathogenic. In this review we analyze the role of ethylene, abscisic acid, jasmonic acid, auxin and salicylic acid during Colletotrichum infections. Different Colletotrichum strains are capable of auxin production and this might contribute to virulence. In this review the role of different plant hormones in plant-Colletotrichum interactions will be discussed and thereby auxin biosynthetic pathways in Colletotrichum spp. will be proposed.

Keywords: Colletotrichum spp.; abscisic acid; auxin; ethylene; jasmonic acid; plant hormones; salicylic acid.

Figure 1

Ethylene biosynthetic pathways; the ACC pathway is shown in green, KMBA pathway in orange and oxoglutarate pathway in blue.

Figure 2

Abscisic acid biosynthetic pathways; the C₁₅ pathway is indicated by orange arrows.

Figure 3

Tryptophan derived auxin biosynthetic pathway in plants (YUC (green)) and proposed pathways in Colletotrichum spp. (IAM (violet), IPA (black)).

Figure 4

Salicylic acid biosynthesis pathway.

Figure 5

Salicylic acid signal transduction.

Figure 6

Jasmonic acid biosynthesis.

Figure 7

Simplified model of the contribution of different plant hormones to stress response; SA reduces the formation of IAA and induces the expression of non-expressor of pathogenesis related gene 1 (NPR1). Localization of the NPR monomer in the nucleus activates TGA transcription factors (TFs) which can bind pathogenesis related (PR) gene promoters and activate transcription of defense genes. JA is induced upon biotic and abiotic stresses. It is converted to the biologically active form JA-Ile which is perceived by its receptor COI1. COI1 triggers the degradation of JAZ repressors resulting in the release of downstream transcription factors and further induction of JA-responsive genes. JA induces ethylene formation which activates ethylene insensitive 2 (EIN2), a transmembrane protein, which further induces the transcription factor EIN3 leading to expression of ethylene response factors (ERFs) triggering the stress response. ABA induces stress response and autophagy via SNF1-related protein kinase (SnRK) which on the other side inhibits the growth response and the target of rapamycin (TOR) but promotes stress response and autophagy. Auxin leads to the activation of auxin response factors (ARFs) as well as TOR which both trigger growth response.