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Erguvan, O.

Publications and source records attributed to Erguvan, O..

5 recordsLinked to original sources

Mechanical coordination of counter-gradient growth maintains organ curvature in apical hooks

How growing tissues convert mechanical tension into signals that stabilize form remains a central question in morphogenesis. Curved organ shapes in plants arise from differential growth, yet how such curvature is actively maintained while organs continuously grow remains poorly understood. In etiolated seedlings, the apical hook provides a tractable model to dissect this process, as its curvature is stably maintained over extended periods despite ongoing cell expansion. Using quantitative imaging and computational modeling, we show that antagonistic growth gradients at apical and basal regions are both necessary and sufficient to maintain hook curvature, with cuticle integrity being critical for establishing these counter-gradients. Mechanical cues linked to cuticle structure, coupled with apoplastic reactive oxygen species (ROS), coordinate cellular growth anisotropy, and disruptions in cuticle biosynthesis trigger defective hook development. These findings reveal that the apical hook curve maintenance is not a simple switch between growth promotion and repression, but a highly dynamic, tightly regulated process where mechanical and biochemical signals coordinate organ-scale morphogenesis, fundamentally reshaping how we understand developmental growth.

plant biology↗

Outer epidermal edges mediate cell-cell adhesion for tissue integrity in plants

Cell-cell adhesion in plants is generally thought to be primarily mediated by the middle lamella, a supposedly thin adhesive layer of the cell wall. Here, we challenge this view. Through computational simulation we found that outer edges of cellular interfaces of the epidermis are hotspot for cell separating tensile stress. Characterization of the ultrastructure of those edges in planta revealed that they are locally thickened regions that harbor cellulose lamellae and pectin-based structural continuity across adjacent cells. We confirmed their dominant role for adhesion by studying mutants where those edges are defective and through direct mechanical testing. This reveals the key role of outer epidermal cell edges, rather than the middle lamella, in mediating cell-cell adhesion for tissue integrity in plants.

plant biology↗

Rhamnogalacturonan-II dimerization deficiency impairs the coordination between growth and adhesion maintenance in plants

Cell adhesion is a fundamental feature of multicellular organisms. In plants, cell adhesion is mediated by the cell wall, but the control and maintenance of cell adhesion during growth and development remains poorly understood1. Here we uncover the role of a component of the cell wall, rhamnogalacturonan-II (RG-II) and its capacity to crosslink in the presence of Boron2, as a key regulator of plant cell adhesion maintenance. We show that RG-II dimerization deficiency leads to cell adhesion defects. Importantly, the analysis of mur1 mutants with RG-II dimerization defects uncovers a cell adhesion pathway that is distinct from that identified by the analysis of pectin deficient mutants3. We found that mutations in two cell wall integrity sensors, RESISTANCE TO FUSARIUM OXYSPORUM 1 and RECEPTOR-LIKE PROTEIN 44, as well as supplementation with the hormone brassinosteroid can partially rescue the adhesion defects associated with RG-II dimerization deficiency. We also show that adhesion defects associated with RG-II dimerization deficiency are related to increased epidermal tension as well as decreased homogalacturonan levels in the cell wall, which can also be rescued by supplementation with brassinosteroid. Overall, we propose that RG-II dimerization defects alter cell adhesion directly (reduced crosslinks) but also indirectly through cell wall integrity sensing, brassinosteroid signalling, cell wall remodelling and cell layer growth coordination. Thus, our results uncover the involvement of cell wall integrity sensors and hormonal signalling in the coordination between growth and adhesion maintenance in plants, which is a key feature for complex multicellularity. Highlights- RG-II dimerization is required for cell-cell adhesion in plants. - Cell wall integrity sensors and brassinosteroid signalling mediate cell adhesion downstream of RG-II dimerization. - Cell detachments due to defective RG-II dimerization are caused by weakened middle lamella and higher tissue tension.

plant biology↗

Cell wall integrity modulates a PHYTOCHROME-INTERACTING FACTOR (PIF) - HOOKLESS1 (HLS1) signalling module controlling apical hook formation in Arabidopsis.

Etiolated seedlings of dicots form an apical hook to protect the meristems during soil emergence. Hook formation is the result of differential growth on both sides of the hypocotyl apex and is tightly controlled by environmental cues and hormones, among which auxin and gibberellins (GAs) are the main contributors. Cell expansion is tightly regulated by the cell wall, but whether and how feedback from this structure contributes to hook development is still unclear. Here we show that etiolated seedlings of the Arabidopsis thaliana quasimodo2-1 (qua2) mutant, defective in pectin biosynthesis, display severe defects in apical hook formation and maintenance, accompanied by loss of asymmetric auxin maxima and differential cell expansion. Moreover, qua2 seedlings show reduced expression of HOOKLESS1 (HLS1) and PHYTOCHROME-INTERACTING FACTOR 4 and 5 (PIF4/5), positive regulators of hook formation, and accumulate reduced levels of the active gibberellin GA4. Treatment of wild-type seedlings with the cellulose inhibitor isoxaben (isx) also prevents hook development and represses HLS1 expression and PIF4 accumulation. Moreover, isx stabilizes the DELLA protein REPRESSOR OF ga1-3 (RGA), which inhibits HLS1 expression and hook formation. Exogenous GAs or HLS1 overexpression partially restore hook development in isx-treated seedlings. Notably, agar concentration in the medium restores, both in qua2 and isx-treated seedlings, hook development and WT-like levels of PIFs and HLS1. We propose that turgor-dependent signals link changes in cell wall integrity to the PIF4/5-HLS1 signalling module to repress differential cell elongation during hook formation. Significance statementCell wall integrity modulates apical hook development through poorly understood mechanisms. We show here that, in Arabidopsis, repression of hook formation by either mutations in pectin biosynthesis or by isoxaben treatment is at least partially mediated by the downregulation of a gibberellin-controlled signalling module that comprises PIF4/5 and HLS1. Our results indicate that the signals derived from changes in the cell wall can modulate hormone-mediated pathways to control asymmetric growth during plant development.

plant biology↗

Turning plants from passive to active material: FERONIA and microtubules independently contribute to mechanical feedback

To survive, cells must constantly resist mechanical stress. In plants, this involves the reinforcement of cell walls, notably through microtubule-dependent cellulose deposition, and thus wall sensing. Several receptor-like kinases have been proposed to act as mechanosensors. Here we tested whether the microtubule response to stress acts downstream of known wall sensors. Using a multi-step screen with eleven mutant lines, we identify FERONIA as the primary candidate for controlling the microtubule response to stress. However, when performing mechanical perturbations, we show that the microtubule response to stress can be independent from FER. We reveal that the feronia phenotype can be partially rescued by reducing tensile stress levels. Conversely, in the absence of both microtubules and FER, cells swell and burst like soap bubbles. Altogether, this shows that the microtubule response to stress acts as an independent pathway to resist stress, in parallel to FER. We propose that both pathways are key components to turn plant cells from passive to active material.

plant biology↗