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Piotrowska, J.

Publications and source records attributed to Piotrowska, J..

2 recordsLinked to original sources

The Arabidopsis deNADding enzyme DXO1 modulates the plant immunity response.

O_LIDXO1, the only DXO homolog in Arabidopsis, due to its plant-specific features, has a strong deNADding enzymatic activity but no apparent role in 5'QC. Most molecular and morphological changes observed so far in dxo1 mutant plants depended on the plant-specific N-terminal domain of the protein. C_LIO_LIOur investigation revealed the importance of DXO1 enzymatic activity in the plant immune response. We observed that dxo1-2 knockout mutant and transgenic dxo1-2 lines expressing a DXO1 variant either catalytically inactive or lacking the N-terminal domain exhibited enhanced resistance to Pseudomonas syringae, accompanied by marked changes in the expression of key pathogenesis markers. Other markers of plant immunity, such as callose deposition and production of ROS, were strongly induced by elf18 and flg22. C_LIO_LIOur results strongly suggest that both DXO1 features, the N-terminal domain and its catalytic site, contribute to regulating plant immunity. This is the first observation revealing the involvement of the DXO1 enzymatic activity in plant physiology. C_LIO_LIMoreover, our analyses showed that dxo1-2 mutation altered the expression of a large group of defense-related genes, affected their mRNAs stability, and delayed activation of MAP kinases. Therefore, we postulate that DXO1 protein deregulates defense against Pst infection at both the transcriptional and post-transcriptional level. C_LI

molecular biology↗

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 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 these factors were also altered upon treatment with Pseudomonas effectors. We showed that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. Our genome-wide transcriptome analysis of the smd3b-1 mutant infected with Pst revealed that lack of SmD3-b deregulates defense against Pst infection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. 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.

molecular biology↗