Biology subjects

Schmitz-Thom, I.

Publications and source records attributed to Schmitz-Thom, I..

3 recordsLinked to original sources

bioRxiv2023

A bi-kinase module sensitizes and potentiates plant immune signaling

Systemic signaling is an essential hallmark of multicellular life. Pathogen encounter occurs locally but triggers organ-scale and organismic immune responses. In plants, elicitor perception provokes systemically expanding Ca2+ and H2O2 signals conferring immunity. Here, we identify a Ca2+ sensing bi-kinase module as becoming super-activated through mutual trans-phosphorylation and imposing synergistically enhanced NADPH oxidase activation. A combined two-layer bi-kinase/substrate phospho-code allows for sensitized signaling initiation already by near-resting elevations of Ca2+ concentration at the infection site. Subsequently, it facilitates further signal wave proliferation with minimal amplitude requirement, triggering protective defense responses throughout the plant. Our study reveals how plants build and perpetuate trans-cellular immune signal proliferation while avoiding disturbance of ongoing cellular signaling along the path of response dissemination. One sentence summaryMutual trans-activation of a Ca2+ sensing bi-kinase module potentiates NADPH oxidase activation to facilitate systemic immunity.

plant biology↗

bioRxiv2020

A mechanism for sensing of and adaptation to K+ deprivation in plants

Potassium ions (K+) are essential for manifold cellular processes. Organismal K+ homoeostasis requires sensing of K+ availability, efficient uptake and defined distribution. Roots are the organ for K+ uptake in plants and soil K+ availability shapes root growth and architecture1. Important channels and transporters conveying cellular K+ fluxes have been described2,3. Understanding K+ sensing and the mechanisms that orchestrate downstream responses exemplifies how environmental conditions integrate with root development and is essential to advance plant nutrition for sustainable agriculture. Here, we report where plants sense K+ deprivation and how this translates into spatially defined ROS signals to trigger HAK5 K+ uptake transporter induction and accelerated maturation of the Casparian strip (CS) paracellular barrier. We define the organ scale K+ pattern of roots and identify a postmeristematic K+-sensing niche (KSN) defined by rapid K+ decline and Ca2+ signals. We discover a Ca2+-triggered bifurcating low-K+ signalling (LKS) axis in that LK-enhanced CIF peptide signalling reinforces SGN3-LKS4/SGN1 receptor kinase complex activation. As consequence, activation of the NOXs RBOHC and RBOHD conveys transcriptome adaptation including HAK5 induction and accelerated CS maturation superimposed on the RBOHF-executed default CS formation. These mechanisms synchronise developmental differentiation and transcriptome reprogramming for maintaining K+ homoeostasis and optimising nutrient foraging by roots.

plant biology↗

bioRxiv2018

The Ca2+ sensor protein CMI1 fine tunes root development, auxin distribution and responses

Signaling cross-talks between auxin, a regulator of plant development and Ca2+, a universal second messenger have been proposed to modulate developmental plasticity in plants. However, the underlying molecular mechanisms are largely unknown. Here we report that in Arabidopsis roots, auxin elicits specific Ca2+ signaling pattern that spatially coincide with the expression pattern of auxin-regulated genes. We identified the EF-hand protein CMI1 (Ca2+ sensor Modulator of ICR1) as an interactor of the ROP effector ICR1 (Interactor of Constitutively active ROP). CMI1 is monomeric in solution, changes its secondary structure at Ca2+ concentrations ranging from 10-9 to 10-8 M and its interaction with ICR1 is Ca2+ dependent, involving a conserved hydrophobic pocket. cmi1 mutants display an increased auxin response including shorter primary roots, longer root hairs, longer hypocotyls and altered lateral root formation while ectopic expression of CMI1 induces root growth arrest and reduced auxin responses at the root tip. When expressed alone, CMI1 is localized at the plasma membrane, the cytoplasm and in nuclei. Interaction of CMI1 and ICR1 results in exclusion of CMI1 from nuclei and suppression of the root growth arrest. CMI1 expression is directly upregulated by auxin while expression of auxin induced genes is enhanced in cmi1 concomitantly with repression of auxin induced Ca2+ increases in the lateral root cap and vasculature, indicating that CMI1 represses early auxin responses. Collectively, our findings identify a crucial function of Ca2+ signaling and CMI1 in root growth and suggest an auxin-Ca2+ regulatory feedback loop that fine tunes root development.

plant biology↗