Unveiling the underlying complexities in breeding for disease resistance in crop plants: review

Abstract

Biotic stress significantly contributes to global crop losses, posing a major threat to food security and agricultural sustainability. While conventional plant breeding techniques have successfully enhanced crop resistance to pathogens, the perpetual emergence of new pathogens and the need to develop varieties with effective, stable, and broad-spectrum resistance in the shortest feasible time remain formidable challenges. The rapid delivery of these technologies to stakeholders further underscores the urgency for innovative approaches. This review delves into the complexities of breeding for disease resistance in crop plants, tracing its historical evolution and highlighting recent advancements in genetic and genomic technologies. These advancements have significantly deepened our understanding of host-pathogen interactions, enabling the identification of key genes and mechanisms governing resistance. We aim to offer insights into how historical perspectives and cutting-edge innovations can guide breeders in designing robust resistance strategies. Ultimately, this work seeks to empower breeders with actionable knowledge and tools to address the dynamic challenges posed by pathogens, paving the way for a more resilient and adaptable agricultural landscape.

Keywords: Flor’s hypothesis; RLP/RLK; pathogen; pathogenesis; plant breeding; plant disease; plant immunity; resistance.

Figure 1

Milestones in genetics of disease resistance.

Figure 2

Plant pathogen interaction and development of disease resistance mechanisms (Flor’s hypothesis).

Figure 3

Variable phenotypic expression observed in qualitative and quantitative resistance reaction.

Figure 4

Schematic representation of plant immunity: pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) (Jones et al., 2024; Yu et al., 2024; Nguyen et al., 2021; Doughari, 2015). The first line of defence, PTI (marked by red arrows), is triggered when pattern recognition receptors (PRRs) detect pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). This activates a cascade of signalling events, including mitogen-activated protein kinase (MAPK) activation, Ca²⁺ influx, and the production of reactive oxygen species (ROS). To suppress PTI, pathogens release effectors. When these effectors are recognized by nucleotide-binding (NB) and leucine-rich-repeat (LRR)-containing receptors (NLRs), the second layer of immunity, ETI (marked by blue arrows), is activated. This recognition induces conformational changes in NLRs, initiating intracellular signalling that leads to the hypersensitive response (HR) or systemic acquired resistance (SAR). SAR further activates key hormonal pathways, such as salicylic acid (SA) and jasmonic acid (JA) signalling. Research suggests that PTI and ETI are interconnected, working together to amplify immune responses (Nguyen et al., 2021).

Figure 5

Epi-breeding design for crop disease resistance improvement. Epigenetic variations are either derived from natural populations, or induced by stresses, chemical treatments, mutations in epigenetic machinery, induced gene-specific DNA methylation, and epigenome editing (Zhi and Chang, 2021).

Figure 6

Schematic diagram of SDN1, SDN2, and SDN3. Nucleases such as ZFNs, TALENs, and CRISPR/Cas9 bind with target DNA to cause DSBs that are repaired by two different mechanisms. SDN1 does not need a template and results in gene disruptions through indels (small insertions or deletions of bases). SDN2 utilizes a homologous template and results in gene correction or modification at one or more positions. SDN3 requires a full gene as a template, and leads to gene replacement or foreign DNA insertion.