Alternative splicing for a world with more resilient crops – GIMM Alternative splicing for a world with more resilient crops – GIMM

  January 31, 2025

Alternative splicing for a world with more resilient crops

Much like animals, plants are susceptible to a broad range of pathogens. Every year, up to 40% of global crop production is lost to infections caused by these pathogens, with substantial economic impact. The Paula Duque Lab at GIMM, dedicated to Plant Molecular Biology, uses the flowering plant Arabidopsis thaliana as a model organism to study posttranscriptional regulation of plant stress responses. While the team has primarily focused on abiotic factors such as drought and high salinity, a new research line within the lab explores the interaction between Arabidopsis and Pseudomonas syringae, a pathogenic bacterium that poses a major threat to crops.

Plant immunity (yes, plants also have immune responses!) is a complex and tailored response to a wide variety of pathogens. Plants employ two main mechanisms to recognize pathogens: pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is activated when receptors located on the surface of plant cells recognize molecular patterns associated with a broad range of pathogens. By contrast, ETI occurs inside the cells, where immune receptors recognize specific proteins (effectors) released by the pathogen. This mechanism triggers a stronger and often more targeted defense response. Furthermore, when a pathogen is detected, many plant genes are either activated or repressed, initiating different defense signaling pathways. While some mechanisms and pathways are general and effective against multiple pathogens, many components of the plant immune response are specific to a certain pathogen. For instance, in ETI, each intracellular receptor recognizes a particular effector protein produced by the pathogen.

Given the importance of pathogen resistance in crop production, much is known about the genes involved in plant immunity and the metabolites they produce. However, despite this extensive knowledge of how the expression of genes changes during pathogen attack, the subsequent mechanisms that regulate these responses remain poorly understood. In fact, gene regulation also occurs after transcription — the process by which a gene is copied from DNA. One example of these posttranscriptional mechanisms is the alternative splicing of RNA. Plants orchestrate complex and highly specific immune responses with a relatively limited genome, and alternative splicing allows the same transcript to encode multiple proteins by rearranging or removing parts of the molecule. This is a key example of how posttranscriptional mechanisms can expand the genome’s encoding capacity. Such flexibility enables plants to mount tailored immune responses. While it is well recognized that alternative splicing is important in plant immunity, the mechanisms driving differential splicing upon pathogen infection have remained largely unexplored until recently.

In the past few years, advances in the field have shed new light on the posttranscriptional regulation of plant immunity, as reviewed by the Paula Duque lab here (Godinho et al., Trends in Plant Science). Key recent discoveries indicate that, during PTI, the recognition of pathogens by plant receptors on the surface of their cells triggers a response that affects the function of the plant’s splicing machinery, leading to altered alternative splicing. Remarkably, some pathogens appear to manipulate the splicing of plant immunity-related genes to their advantage through direct interactions between their effector molecules and the plant’s splicing machinery. These findings are revealing the mechanisms driving alternative splicing of plant genes during pathogen infection, opening new research opportunities to understand how plants fine-tune their immune responses at the molecular level. Several critical questions remain, such as: How do different pathogens trigger specific splicing changes? Can plants reverse the splicing changes induced by pathogen effectors? And what role does splicing play in the interaction between PTI and ETI?

Nevertheless, it is becoming increasingly clear that the modulation of alternative splicing in plant immunity is driven by complex interactions between pathogen molecules and host splicing factors. In this context, SR proteins — a key family of conserved alternative splicing regulators involved in plant development and abiotic stress responses — are likely crucial players in plant-pathogen interactions. The Duque Lab is now focusing on these splicing regulators to investigate how they influence the plant’s response to pathogen infection. The goal is to address unresolved questions in the field and contribute significantly to understanding the molecular dynamics of plant-pathogen interactions. This research not only promises to deepen our knowledge of how plants fine-tune their immune responses through splicing but also holds potential for uncovering novel strategies to improve pathogen resistance in crops, offering solutions to a major global challenge.

This article was written by Diogo P. Godinho, postdoctoral researcher in the Paula Duque Lab, and Paula Duque. 

0 0 votes
Article Rating
Subscribe
Notify of
guest
0 Comments
Inline Feedbacks
View all comments
0
Would love your thoughts, please comment.x
()
x