Analyses of cassava phytohormones in biotic responses during South African cassava mosaic virus infection

Abstract

Manihot esculenta Crantz (cassava) is a starch-rich perennial tuber crop that serves as a food source, in addition to having industrial applications. Concerningly, cassava is susceptible to infection by South African cassava mosaic virus, resulting in the development of cassava mosaic disease (CMD). As CMD results in significant losses of cassava yields, it poses a threat to food security. South African cassava mosaic virus (SACMV) encodes for multifunctional proteins that aid in infection and suppress host immune responses, which are coordinated by plant hormones. Phytohormones are activated during a pathogenic infection, and include salicylic acid (SA), jasmonic acid (JA), ethylene (ET), and abscisic acid (ABA). The main aim of this research project was to quantify, using Ultra-High Pressure Liquid Chromatography-Mass Spectrometry (UHPLC-MS), the phytohormone levels of SA, JA, ABA, and ET in the CMD-susceptible T200 and CMD-tolerant TME3 across the three stages of SACMV infection, namely 12-, 32-, and 67-days post infection (dpi). This was to determine if these phytohormones contribute to either susceptibility or recovery, and to relate the hormone levels of the expression of SACMV genes and cassava hormone-related genes, assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Infection trials and subsequent gene expression studies revealed that T200 had a significantly higher SACMV load compared to TME3 at 32- and 67- dpi, and this correlated with the significantly higher expression of SACMV genes in T200. Additionally, the activities of these viral proteins promoted virus fitness in T200 via dysregulation of cell proliferation, promotion of viral replication and transmission, disruption of global metabolism, disruption of plant defences, and the suppression of post-transcriptional gene silencing (PTGS) and transcriptional gene silencing (TGS). Contrastingly, TME3 recovered by 67 dpi and was tolerant to SACMV infection. The quantification of hormone levels and assessment hormone-related gene expression revealed that TME3 relies on an early response of ABA- and JA-mediated PTGS and SA-driven defence, while its recovery is reliant on SA-, ET-, and JA-driven defence responses and the establishment of systemic acquired resistance (SAR). Lastly, following recovery, TME3 tolerates SACMV via induced systemic resistance (ISR) that is reliant on finetuned JA-, ET-, and ABA- signalling.