Arabidopsi s Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
Anna Golisz1, Michal Krzyszton1, Monika Stepien1
1Faculty of Biology, Institute of Genetics and Biotechnology, University of Warsaw, Warsaw, Poland.
Abstract:
SmD3 is a core component of the small nuclear ribonucleoprotein (snRNP) that is essential for pre-mRNA splicing. The role of Arabidopsis SmD3 in plant immunity was assessed by testing sensitivity of smd3a and smd3b mutants to Pseudomonas syringae pv. tomato (Pst) DC3000 infection and its pathogenesis effectors flagellin (flg22), EF-Tu (elf18) and coronatine (COR). Both smd3 mutants exhibited enhanced susceptibility to Pst accompanied by marked changes in the expression of key pathogenesis markers. mRNA levels of major biotic stress response factors were also altered upon treatment with Pseudomonas effectors. Our genome-wide transcriptome analysis of the smd3b-1 mutant infected with Pst, verified by northern and RT-qPCR, showed that lack of SmD3-b protein deregulates defense against Pst infection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. Importantly, we show that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. We propose that it is the malfunction of the stomata that is the primary cause of an altered mutant response to the pathogen. Other changes in the smd3b-1 mutant involved enhanced elf18- and flg22-induced callose deposition, reduction of flg22-triggered production of early ROS and boost of secondary ROS caused by Pst infection. Together, our data indicate that SmD3 contributes to the plant immune response possibly via regulation of mRNA splicing of key pathogenesis factors.
Insights
SmD3 protein is crucial for plant immunity, affecting pre-mRNA splicing and stomatal development. Mutants show increased susceptibility to Pseudomonas syringae, indicating SmD3
Area of Science:
- Plant molecular biology
- Plant pathology
- Plant immunity
Background:
- SmD3 is a key component of small nuclear ribonucleoproteins (snRNPs), essential for pre-mRNA splicing.
- The function of SmD3 in plant immunity is not well understood.
Purpose of the Study:
- To investigate the role of Arabidopsis SmD3 in plant defense against Pseudomonas syringae pv. tomato (Pst) DC3000.
- To determine the molecular mechanisms underlying SmD3's contribution to plant immunity.
Main Methods:
- Analysis of smd3a and smd3b mutants' sensitivity to Pst DC3000 infection and its effectors (flg22, elf18, COR).
- Genome-wide transcriptome analysis (RNA-seq) of smd3b-1 mutant infected with Pst.
- Verification of gene expression changes using Northern blot and RT-qPCR.
- Assessment of stomatal development and function.
Main Results:
- smd3 mutants exhibit enhanced susceptibility to Pst infection and altered expression of pathogenesis markers.
- SmD3-b deficiency deregulates plant defense at transcriptional and posttranscriptional levels, including splicing defects.
- SmD3-b dysfunction primarily impairs stomatal immunity due to defects in stomatal development.
- Mutants show altered responses to Pst effectors, including callose deposition and reactive oxygen species (ROS) production.
Conclusions:
- SmD3 plays a significant role in Arabidopsis immunity, particularly in stomatal defense.
- SmD3 regulates plant immune responses through the splicing of key pathogenesis-related factors.
- Defects in stomatal development and function are a primary cause of altered mutant responses to pathogens.
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