Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection

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 pathogenesi...

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Autores principales:	Anna Golisz, Michal Krzyszton, Monika Stepien, Jakub Dolata, Justyna Piotrowska, Zofia Szweykowska-Kulinska, Artur Jarmolowski, Joanna Kufel
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	alternative splicing biotic stress miRNA PAMPS plant immunity Pst DC3000 Plant culture SB1-1110
Acceso en línea:	https://doaj.org/article/f343dcb567aa43c6a2cbfb66c28b19a1
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spelling	oai:doaj.org-article:f343dcb567aa43c6a2cbfb66c28b19a12021-12-03T06:02:47ZArabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection1664-462X10.3389/fpls.2021.765003https://doaj.org/article/f343dcb567aa43c6a2cbfb66c28b19a12021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fpls.2021.765003/fullhttps://doaj.org/toc/1664-462XSmD3 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.Anna GoliszMichal KrzysztonMonika StepienJakub DolataJustyna PiotrowskaZofia Szweykowska-KulinskaArtur JarmolowskiJoanna KufelFrontiers Media S.A.articlealternative splicingbiotic stressmiRNAPAMPSplant immunityPst DC3000Plant cultureSB1-1110ENFrontiers in Plant Science, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	alternative splicing biotic stress miRNA PAMPS plant immunity Pst DC3000 Plant culture SB1-1110
spellingShingle	alternative splicing biotic stress miRNA PAMPS plant immunity Pst DC3000 Plant culture SB1-1110 Anna Golisz Michal Krzyszton Monika Stepien Jakub Dolata Justyna Piotrowska Zofia Szweykowska-Kulinska Artur Jarmolowski Joanna Kufel Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
description	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.
format	article
author	Anna Golisz Michal Krzyszton Monika Stepien Jakub Dolata Justyna Piotrowska Zofia Szweykowska-Kulinska Artur Jarmolowski Joanna Kufel
author_facet	Anna Golisz Michal Krzyszton Monika Stepien Jakub Dolata Justyna Piotrowska Zofia Szweykowska-Kulinska Artur Jarmolowski Joanna Kufel
author_sort	Anna Golisz
title	Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
title_short	Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
title_full	Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
title_fullStr	Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
title_full_unstemmed	Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection
title_sort	arabidopsis spliceosome factor smd3 modulates immunity to pseudomonas syringae infection
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/f343dcb567aa43c6a2cbfb66c28b19a1
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Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection

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