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Pathogen-Induced Shifts in Alternative Splicing Shaping Plant Defense
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DOI：10.1002/fes3.70276.png)
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Abstract
En 中文
Plant immune responses comprise a highly coordinated and dynamic defense network that enables the recognition and containment of diverse microbial pathogens. Alternative splicing (AS), a critical post-transcriptional regulatory mechanism that generates multiple mRNA isoforms from a single pre-mRNA precursor, substantially enhances proteomic diversity and regulatory complexity within the immune system. Pathogen infection triggers extensive AS reprogramming across genes integral to the bipartite immune framework, encompassing pattern-triggered immunity (PTI), which mediates recognition of conserved microbial-associated molecular patterns, and effector-triggered immunity (ETI), which facilitates intracellular detection of pathogen-derived virulence effectors. Despite its recognized importance, the molecular cascades linking pathogen perception to AS reconfiguration remain incompletely understood. Here, we consolidate recent evidence demonstrating how elicitor–receptor interactions promote phosphorylation-dependent modulation of splicing regulators and how pathogen effectors directly bind and modulate host spliceosomal components, thereby altering splice site selection and isoform abundance of immunity-associated transcripts. We further examine the contribution of AS to immune receptor diversification, modulation of signaling amplitude, and functional integration of PTI and ETI, highlighting key mechanistic insights and unresolved questions in the field.
Keywords:
alternative splicing
ETI
NLRs
plant immunity
PRRs
PTI
spliceosome
Journal
IF:
4.5
Papers:
755
Citations:
2.7K
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