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Dongus, J. A.

Publications and source records attributed to Dongus, J. A..

7 recordsLinked to original sources

Natural variation in DXR expression is associated with apical hook bending under NaCl stress in Arabidopsis thaliana

Successful soil emergence requires apical hook establishment during skotomorphogenesis. Soil salinity disrupts this process, but the mechanisms linking environmental stress to hook growth remain unclear. Here, we employed a genome-wide association study (GWAS) across Arabidopsis thaliana accessions to identify a locus associated with variation in the salt-induced reduction of apical hook curvature. Fine mapping reveals genetic variation in the promoter of 1-DEOXY-D-XYLULOSE 5-PHOSPHATE REDUCTOISOMERASE (DXR), encoding the first committed enzyme of the plastid-localized methylerythritol phosphate (MEP) pathway. Accessions carrying an alternative promoter haplotype exhibit elevated DXR expression and a stronger hook bending under salt. Salt treatment and loss of transcriptional repressor PHYTOCHROME INTERACTING FACTOR1 (PIF1) additively increase DXR transcript levels, and pif1-2 seedlings exhibit higher apical hook angles under salt stress. This phenotype is suppressed by inhibition of DXR activity, indicating that an increased MEP pathway flux reduces salt sensitivity in pif1-2 seedlings. Across accessions, DXR expression positively correlates with hook curvature under salt stress, further strengthening the link between DXR and modulation of hook bending under salt stress. Together, these findings identify plastid metabolism as a regulatory layer linking environmental stress to altered skotmomorphogenis, and raise important questions about how etioplast-derived signals interact with growth-control networks in the dark. HighlightA genome wide association study in Arabidopsis reveals that variation in DXR expression, encoding an essential enzyme in the MEP pathway, drives salt-induced repression of apical hook formation darkness.

plant biology↗

The SAUERKRAUT transposable element acceleratesArabidopsis floral transition

Salt stress alters plant development, including the floral transition, but regulation of timing of flowering by salt is poorly understood at the molecular level. To identify genetic loci regulating the floral transition under high soil salinity, we performed a genome-wide association study (GWAS) in Arabidopsis thaliana and identified natural variation at the UGT74E1-UGT74E2-BT3 (UUB) locus that correlates with bolting time specifically in response to salt stress. Genetic analysis revealed BT3 as a novel repressor of the floral transition in control conditions. Similarly, the putative IBA glycosylases UGT74E1 & UGT74E2 delay the floral transition in control conditions. Furthermore, we identified that IBA homeostasis regulators TOB1 and ECH2/IBR10 play a key role in the floral transition, and that ECH2/IBR10 are required for the early flowering phenotype of the ugt74e1/ugt74e2 double mutant, indicating that UGT74E1 & UGT74E2 delay flowering by altering IBA homeostasis. A pangenome analysis of the UUB locus revealed variation in the occurrence of the DNA transposon SAUERKRAUT (SKRT). CRISPR-mediated SKRT deletion in Col-0 affected gene expression both within and outside the UUB locus and caused a salt-dependent delayed floral transition. The delayed bolting phenotype of the skrt-2 mutant also depends on ECH2/IBR10 function, indicating that SKRT accelerates the floral transition by altering IBA homeostasis. Finally, targeted demethylation of SKRT resulted in delayed floral transition under salt stress. Taken together, our data show a role for SKRT and its DNA methylation levels in the salt-dependent bolting time response in Arabidopsis, revealing a novel molecular mechanism to control flowering in adverse conditions.

plant biology↗

SeedMatExplorer: The transcriptome atlas of Arabidopsis seed maturation

BackgroundSeed maturation is a critical developmental phase during which seeds acquire traits essential for nutritional value, desiccation tolerance, and long-term survival. Abscisic acid (ABA) signalling is a key regulator of this process, coordinating gene expression programs underlying the acquisition of seed quality traits. However, the molecular regulation of many of these traits remains poorly understood. To address this, we performed a comprehensive analysis of seed maturation in Arabidopsis thaliana, combining physiological and transcriptomic approaches across wild-type plants and mutants affected in ABA biosynthesis, signalling, and catabolism. ResultsWe generated a high-resolution transcriptome dataset covering seed development from 12 days after pollination to the dry seed stage in wild-type and ten mutant lines. In parallel, we characterized the temporal acquisition of multiple seed traits, including germination capacity, dormancy, chlorophyll fluorescence, longevity and desiccation tolerance. Integration of these datasets using weighted gene co-expression network analysis (WGCNA) identified gene modules associated with specific trait acquisition patterns. This approach enabled the identification of coordinated transcriptional programs linked to distinct seed quality traits, extending beyond individual gene-level analyses. Notably, modules associated with desiccation tolerance and longevity were enriched for genes involved in stress responses and ABA-regulated pathways, highlighting the complex and multifactorial regulation of these traits. ConclusionsThis study provides a comprehensive physiological and transcriptomic framework for understanding seed maturation and the acquisition of key seed quality traits in Arabidopsis thaliana. By linking gene expression dynamics to trait development, our work offers new insights into the regulatory networks underlying seed resilience and storage capacity. The dataset is made accessible through SeedMatExplorer (https://www.bioinformatics.nl/SeedMatExplorer), an open-access web platform that enables interactive exploration and supports hypothesis generation. Together, this resource represents a valuable tool for advancing research on seed biology and improving seed performance in agricultural contexts.

plant biology↗

Differential EDS1 requirement for cell death activities of plant TIR-domain proteins

Toll/interleukin-1 Receptor (TIR) domains are integral to immune systems across all domains of life. TIRs exist as single-domain and as larger receptor or adaptor proteins. In plants, TIRs constitute N-terminal domains of nucleotide-binding leucine-rich repeat (NLR) immune receptors. Although TIR-NLR and TIR signaling requires the Enhanced disease susceptibility 1 (EDS1) protein family, TIR domains persist in species that have incomplete or no EDS1 members. To assess whether particular TIR groups appear with EDS1, we searched for TIR-EDS1 co-occurrence patterns. Using a large-scale phylogenetic analysis of TIR domains from 39 algae and land plant species, we identify four conserved TIR groups, two of which are TIR-NLRs present in eudicots and two are more widespread. Presence of one TIR-only protein group is highly correlated with EDS1 and members of this group elicit EDS1-dependent cell death. By contrast, a more widely represented TIR group of TIR-NB-WD40/TPR (TNP) proteins (formerly called XTNX) has at least one member which can induce EDS1-independent cell death. Our data provide a new phylogeny-based plant TIR classification and identify TIR groups that appear to have evolved with and are dependent on EDS1, while others have EDS1-independent activity. One sentence summaryLand plants have evolved four conserved TIR groups

plant biology↗

Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity

Plants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 "helper" NLRs (RNLs), cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). However, the mechanism of RNL/EDS1-family protein cooperation is poorly understood. Here, we provide genetic and molecular evidence for exclusive EDS1/SAG101/NRG1 and EDS1/PAD4/ADR1 co-functions in TNL immunity. Using immunoprecipitation and mass spectrometry, we show effector recognition-dependent association of NRG1 with EDS1 and SAG101, but not PAD4. An EDS1-SAG101 complex associates with NRG1, and EDS1-PAD4 associates with ADR1, only in an immune-activated state. NRG1 requires an intact nucleotide-binding P-loop motif, and EDS1 a functional EP domain and its partner SAG101, for induced association and immunity. Thus, two distinct modules (NRG1/EDS1/SAG101 and ADR1/EDS1/PAD4) are required to execute TNL receptor defence signalling.

plant biology↗

Arabidopsis PAD4 lipase-like domain is a minimal functional unit in resistance to green peach aphid

Plants have evolved mechanisms to attract beneficial microbes and insects while protecting themselves against pathogenic microbes and pests. In Arabidopsis, the immune regulator PAD4 functions with its cognate partner EDS1 to limit pathogen growth. PAD4, independently of EDS1, reduces infestation by Green Peach Aphid (GPA). How PAD4 regulates these defense outputs is unclear. By expressing the N-terminal PAD4-lipase-like domain (LLD) without its C-terminal EDS1-PAD4 (EP) domain, we interrogated PAD4 functions in plant defense. Here we show that transgenic expression of PAD4LLD in Arabidopsis is sufficient for limiting GPA infestation, but not for conferring basal and effector-triggered pathogen immunity. This suggests that the C-terminal PAD4-EP domain is necessary for EDS1-dependent immune functions. Moreover, PAD4LLD is not sufficient to interact with EDS1, indicating the PAD4-EP domain is required for heterodimerisation. These data provide molecular evidence that PAD4 has domain specific functions.

plant biology↗

A coevolved EDS1-SAG101-NRG1 module mediates cell death signaling by TIR-domain immune receptors

Plant intracellular nucleotide-binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-Interleukin1-receptor (TIR)-domain NLRs (TNLs) converge on the Enhanced Disease Susceptibility1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis TNL immunity, AtEDS1 heterodimers with Phytoalexin Deficient4 (AtPAD4) transcriptionally boost basal defense pathways. AtEDS1 uses the same surface to interact with PAD4-related Senescence-Associated Gene101 (AtSAG101), but the role of AtEDS1-AtSAG101 heterodimers was unclear. We show that AtEDS1-AtSAG101 function together with AtNRG1 coiled-coil domain helper NLRs as a coevolved TNL cell death signaling module. AtEDS1-AtSAG101-AtNRG1 cell death activity is transferable to the solanaceous species, Nicotiana benthamiana, and cannot be substituted by AtEDS1-AtPAD4 with AtNRG1 or AtEDS1-AtSAG101 with endogenous NbNRG1. Analysis of EDS1-family evolutionary rate variation and heterodimer structure-guided phenotyping of AtEDS1 variants or AtPAD4-AtSAG101 chimeras identify closely aligned -helical coil surfaces in the AtEDS1-AtSAG101 partner C-terminal domains that are necessary for TNL cell death signaling. Our data suggest that TNL-triggered cell death and pathogen growth restriction are determined by distinctive features of EDS1-SAG101 and EDS1-PAD4 complexes and that these signaling machineries coevolved with further components within plant species or clades to regulate downstream pathways in TNL immunity.

plant biology↗