# Alternative splicing: an underexplored layer in immune receptor regulation, systemic resistance and priming

## TL;DR

This paper explores how alternative splicing may regulate plant immune receptors and contribute to immune memory.

## Contribution

The study proposes that alternative splicing could modulate immune receptor isoforms to enable immune priming without constant defense activation.

## Key findings

- Alternative splicing is reprogrammed during pathogen attack and affects immune receptor expression.
- Priming-associated splicing patterns suggest a role in immune memory formation.
- Computational analysis identifies potential isoform-specific functions in immune receptors.

## Abstract

Plant immunity relies on precise regulation of pattern-recognition receptors (PRRs) and nucleotide-binding leucine-rich repeat receptors (NLRs). Beyond triggering local defenses, these receptors also induce durable systemic resistance, establishing an immune memory or “primed” state that enables faster and stronger responses upon re-infection. While chromatin-based mechanisms are well-recognized contributors to systemic resistance and priming, emerging evidence suggests that alternative splicing (AS) may provide an additional, largely overlooked regulatory layer. AS is reprogrammed during pathogen attack and reshapes both the quantitative and qualitative expression of many defense components, including PRRs, NLRs, downstream kinases, and splicing regulators. In this Perspective, we present a hypothesis-generating computational study based on the integrative reanalysis of publicly available transcriptomic datasets. By combining priming and splicing-associated transcriptomes with an improved isoform-resolved reference transcriptome, we explore AS regulation within PRR and NLR gene families. This approach highlights priming-associated AS patterns affecting subsets of immune receptors, supporting the hypothesis that AS-mediated modulation of receptor isoform pools may contribute to immune priming. We further propose that AS could generate functionally distinct receptor isoforms, providing a mechanism for immune receptors’ plasticity without constitutive defense activation. Finally, we outline experimental strategies required to validate these computational predictions and to define isoform-specific functions of immune receptors in plant immune memory.