Biology subjects

Moeder, W.

Publications and source records attributed to Moeder, W..

5 recordsLinked to original sources

bioRxiv2025

Over-expression of Cyclic Nucleotide-Gated Ion Channel 2 (CNGC2) triggers 1 hypersensitivity to virulent pathogens and elevated Ca2+

The Arabidopsis Cyclic Nucleotide-Gated Ion Channel 2 (CNGC2), also known as Defense No Death 1 (DND1), is the most extensively studied plant CNGC and has been implicated in diverse physiological processes, including floral transition, responses to heat and humidity, and hormone signaling. Its role in immunity has received particular attention due to the autoimmunity phenotype observed in the cngc2/dnd1 knockout mutants. Interestingly, despite this hyperactivation of immunity, the mutant also exhibits impaired hypersensitive cell death--a hallmark of effector-triggered immunity (ETI)--as well as reduced reactive oxygen species (ROS) production and diminished Ca{superscript 2} influx in response to pathogen-associated molecular patterns (PAMPs) such as the bacterial flagellin peptide flg22. These contradictory phenotypes highlight the complex biological functions of CNGC2. To date, most studies have focused on loss-of-function mutants. In this study, we performed a detailed characterization of CNGC2 overexpression lines to gain deeper insight into its role in immunity. Remarkably, overexpression of CNGC2 led to heightened susceptibility to two taxonomically distinct pathogens, despite the plants displaying wild-type morphology. Overexpression of CNGC2 rescued several cngc2 mutant phenotypes, including morphological defects and delayed flowering, yet these plants were also hypersensitive to elevated external Ca{superscript 2} levels. Furthermore, they exhibited attenuated responses to flg22, suggesting that CNGC2 does not act as a simple positive or negative regulator of immunity. Our findings reveal an essential role for CNGC2 where a balanced expression level is critical for maintaining Ca{superscript 2} homeostasis between the apoplast and cytosol, thereby influencing the generation of Ca{superscript 2} signals essential for immune responses.

plant biology↗

bioRxiv2024

Characterization of immunity-inducing rhizobacteria highlights diversity in plant-microbe interactions

The narrow region of soil surrounding roots (rhizosphere) contains an astonishing diversity of microorganisms. Some rhizosphere bacteria can improve plant health and immunity, via direct competition with pathogens or by establishing heightened immunity in aboveground tissues, a phenomenon known as Induced Systemic Resistance (ISR). We screened a bacterial library from agricultural soils to identify strains that, after root treatment, induce immunity in Solanum lycopersicum (tomato) against the fungal pathogen Botrytis cinerea. Here, we report the establishment of a screening method and characterization of a subset of five strains, belonging to the species Bacillus velezensis, Paenibacillus peoriae and Pseudomonas parafulva, that induced systemic resistance in tomato. However interestingly, only two of them triggered canonical ISR in Arabidopsis, indicating plant host specificity and/or alternative modes of actions. Furthermore, some of the strains displayed direct anti-microbial activity. We also found the requirement of the lipid-binding protein DIR1 in ISR establishment, indicating a possible convergence of SAR and ISR signaling. Finally, we found that P. parafulva TP18m, also displayed strong effects on root development. Taken together, we have identified taxonomically diverse immunity-inducing bacteria. Our characterization revealed diverse features, highlighting the complexity of bacteria- host interaction in the rhizosphere. HighlightWe identified taxonomically diverse rhizobacteria that induce systemic resistance in tomato plants to Botrytis after application to the root. These bacteria display diverse modes of action to improve plant health.

plant biology↗

bioRxiv2023

Colour-analyzer: A new dual colour model-based imaging tool to quantify plant disease

Despite major efforts over the last decades, the rising demands of the growing global population makes it of paramount importance to increase crop yields and reduce losses caused by plant pathogens. One way to tackle this is to screen novel resistant genotypes and immunity-inducing agents, which must be conducted in a high-throughput manner. Colour-analyzer is a free web-based tool that can be used to rapidly measure the formation of lesions on leaves. Pixel colour values are often used to distinguish infected from healthy tissues. Some programs employ colour models, such as RGB, HSV or L*a*b*. Colour-analyzer uses two colour models, utilizing both HSV (Hue, Saturation, Value) and L*a*b* values. We found that the a* b* values of the L*a*b* colour model provided the clearest distinction between infected and healthy tissue, while the H and S channels were best to distinguish the leaf area from the background. By combining the a* and b* channels to determine the lesion area, while using the H and S channels to determine the leaf area, Colour-analyzer provides highly accurate information on the size of the lesion as well as the percentage of infected tissue in a high throughput manner and can accelerate the plant immunity research field.

plant biology↗

bioRxiv2020

Phosphorylation of the mitochondrial triphosphate tunnel metalloenzyme TTM1 regulates programmed cell death in senescence

The role of mitochondria in programmed cell death (PCD) during animal growth and development is well documented, but much less is known for plants. We previously showed that the Arabidopsis thaliana triphosphate tunnel metalloenzyme (TTM) proteins TTM1 and TTM2 are tail-anchored proteins that localize in the mitochondrial outer membrane and participate in PCD during senescence and immunity, respectively. Here, we show that TTM1 is specifically involved in senescence induced by abscisic acid (ABA). Moreover, phosphorylation of TTM1 by multiple mitogen-activated protein kinases (MAPKs) regulates its function and turnover. A combination of proteomics and in vitro kinase assays revealed three major phosphorylation sites of TTM1 (S10, S437, and S490), which are phosphorylated upon perception of senescence cues such as ABA and prolonged darkness. S437 is phosphorylated by the MAP kinases MPK3 and MPK4, and S437 phosphorylation is essential for TTM1 function in senescence. These MPKs, together with three additional MAP kinases (MPK1, MPK7, and MPK6), phosphorylate S10 and S490, marking TTM1 for protein turnover, which likely prevents uncontrolled cell death. Taken together, our results show that multiple MPKs regulate the function and turnover of the mitochondrial protein TTM1 during senescence-related PCD, revealing a novel link between mitochondria and PCD. SummaryEmail addresses: purva.karia@mail.utoronto.ca

plant biology↗

bioRxiv2018

A novel role for Cyclic Nucleotide-Gated Ion Channel 2 (DND1) in auxin signaling

Cyclic Nucleotide Gated Ion Channels (CNGCs) have been firmly established as Ca2+-conducting ion channels that regulate a wide variety of physiological responses in plants. CNGC2 has been implicated in plant immunity and Ca2+ signaling due to the autoimmune phenotypes exhibited by null mutants of CNGC2. However, cngc2 mutants display additional phenotypes that are unique among autoimmune mutants, suggesting that CNGC2 has functions beyond defense and generates distinct Ca2+ signals in response to different triggers. In this study we found that cngc2 mutants showed reduced gravitropism, consistent with a defect in auxin signaling. This was mirrored in the diminished auxin response detected by the auxin reporters DR5::GUS and DII-VENUS and in a strongly impaired auxin-induced Ca2+ response. Moreover, the cngc2 mutant exhibits higher levels of the endogenous auxin indole-3-acetic acid (IAA), indicating that excess auxin in cngc2 causes its pleiotropic phenotypes. These auxin signaling defects and the autoimmunity syndrome of cngc2 could be suppressed by loss-of-function mutations in the auxin biosynthesis gene YUCCA6 (YUC6), as determined by identification of the cngc2 suppressor mutant repressor of cngc2 (rdd1) as an allele of YUC6. A loss-of-function mutation in the upstream auxin biosynthesis gene TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS (TAA1, WEAK ETHYLENE INSENSITIVE8) also suppressed the cngc2 phenotypes, further supporting the tight relationship between CNGC2 and the TAA-YUC-dependent auxin biosynthesis pathway. Taking these results together, we propose that the Ca2+ signal generated by CNGC2 is a part of the negative feedback regulation of auxin homeostasis in which CNGC2 balances cellular auxin perception by influencing auxin biosynthesis.

plant biology↗