Resistance induction based on the understanding of molecular interactions between plant viruses and host plants

Abstract

Background Viral diseases cause significant damage to crop yield and quality. While fungi- and bacteria-induced diseases can be controlled by pesticides, no effective approaches are available to control viruses with chemicals as they use the cellular functions of their host for their infection cycle. The conventional method of viral disease control is to use the inherent resistance of plants through breeding. However, the genetic sources of viral resistance are often limited. Recently, genome editing technology enabled the publication of multiple attempts to artificially induce new resistance types by manipulating host factors necessary for viral infection. Main body In this review, we first outline the two major (R gene-mediated and RNA silencing) viral resistance mechanisms in plants. We also explain the phenomenon of mutations of host factors to function as recessive resistance genes, taking the eIF4E genes as examples. We then focus on a new type of virus resistance that has been repeatedly reported recently due to the widespread use of genome editing technology in plants, facilitating the specific knockdown of host factors. Here, we show that (1) an in-frame mutation of host factors necessary to confer viral resistance, sometimes resulting in resistance to different viruses and that (2) certain host factors exhibit antiviral resistance and viral-supporting (proviral) properties. Conclusion A detailed understanding of the host factor functions would enable the development of strategies for the induction of a new type of viral resistance, taking into account the provision of a broad resistance spectrum and the suppression of the appearance of resistance-breaking strains.

Major Biological Control Strategies for Plant Pathogens

“…In case of host resistance, host R genes typically induce race-specific resistance in response to the Avr genes of pathogens [102,103]. During plant-virus interactions occurring in a single cell, an R gene triggered HR response is vital that kills infected cells and restricts the viral invasion and this phenomenon is associated with several molecular events, such as the activation and expression of salicylic (SA), jasmonic acid (JA), mitogen-activated protein kinase signaling [103], calcium ion influx, callose deposition at the plasmodesmata, membrane permeability modification, pathogenesis-related (PR) protein expression, and immediate accumulation of reactive oxygen species and nitric oxide [104].…”

Perspectives on plant virus diseases in a climate change scenario of elevated temperatures

“…In nature, sophisticated mechanisms are involved in plants' survival when they are under virus attack. The major defense mechanisms of plants against viruses include ETI-mediated resistance and antiviral RNA silencing (Akhter et al 2021;Baruah et al 2020;Gallois et al 2018). Unlike ETI that has long been viewed as an essential antiviral mechanism, pathogen-associated molecular pattern (PAMP) triggered immunity (PTI) was found to be elicited by virus infection only recently (Leonetti et al 2021;Moon and Park 2016;Niehl et al 2016).…”

“…Unlike ETI that has long been viewed as an essential antiviral mechanism, pathogen-associated molecular pattern (PAMP) triggered immunity (PTI) was found to be elicited by virus infection only recently (Leonetti et al 2021;Moon and Park 2016;Niehl et al 2016). Besides those mechanisms, recessive resistance is a type of resistance where host plants are lacking essential factors for viruses to complete their life cycle (Akhter et al 2021). In addition, Quantitative Trait Loci (QTL)-mediated quantitative resistance has been shown to be critical for the durability of plant resistance through modulating the efficiency of major-effect resistance genes (Gallois et al 2018).…”

Aspartic protease inhibitor enhances resistance to potato virus Y and A in transgenic potato plants

“…It enables us to understand better how pathogens attack plants’ immune defenses. Successful interaction between plants and viruses is dependent on complex molecular mechanisms, including the viral hijacking of essential plant factors for infection, plant defense antiviral mechanisms that inhibit viral infections, and viral counter defense mechanisms that circumvent plant defense [ 4 , 5 ]. Depending on the potato cultivars, environmental factors, viral strains, and time of infection, the virus can cause different infection levels with varying outcomes [ 5 ].…”

“…Recessive resistance can occur due to changes in the host factors required for the virus [ 4 , 6 ]. Plant viruses must replicate and translocate through plasmodesmata between cells to spread systemically throughout the plant’s vascular system [ 7 , 8 ].…”