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Jonsson, K.

Publications and source records attributed to Jonsson, K..

3 recordsLinked to original sources

Robust Organ Shape During Growth Requires Local Morphogen Signaling and Global Curvature Feedback

Precise organ shape during development requires feedback between organ-scale geometry and cell-level growth dynamics. Here, we use the apical hook of dicotyledonous plants as a model to study this multiscale control. This protective structure forms a [~]180{degrees} bend that is stably maintained despite rapid elongation. Combining quantitative growth mapping, multiscale modeling, and hormone analysis, we identify the cellular dynamics underlying hook maintenance. Contrary to the prevailing model, hook stability does not arise from sustained inner-outer growth asymmetry. Instead, stable curvature emerges from a biphasic, self-similar growth pattern that remains spatially fixed despite continuous cell flux. Auxin-driven growth asymmetry induces bending but is spatially restricted and insufficient to maintain shape. By contrast, a graded, auxin-independent autotropic response provides curvature-dependent growth regulation that counteracts bending and stabilizes shape against perturbations. Together, these findings establish a general principle in which local morphogen-driven bending and global geometry-dependent feedback jointly maintain robust organ shape during growth. HighlightsO_LISelf-similar growth maintains apical hook curvature despite continuous cell flux C_LIO_LICurvature stability emerges from coordinated axial and differential growth C_LIO_LIAuxin asymmetry is spatially restricted and insufficient for shape maintenance C_LIO_LICurvature-dependent feedback ensures robust and optimized hook shape C_LI

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↗

External mechanical cues reveal core molecular pathway behind tissue bending in plants

Tissue folding is a central building block of plant and animal morphogenesis. In dicotyledonous plants, hypocotyl folds to form hook after seedling germination that protects their aerial stem cell niche during emergence from soil. Auxin response factors and auxin transport are classically thought to play a key role in this process. Here we show that the microtubule-severing enzyme katanin contributes to hook formation. However, by exposing hypocotyls to external mechanical cues mimicking the natural soil environment, we reveal that auxin response factors ARF7/ARF19, auxin influx carriers, and katanin are dispensable for apical hook formation, indicating that these factors primarily play the role of catalyzers of tissue bending in the absence of external mechanical cues. Instead, our results reveal the key roles of the non-canonical TMK-mediated auxin pathway, PIN efflux carriers and cellulose microfibrils as components of the core pathway behind hook formation in presence or absence of external mechanical cues.

plant biology↗