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Jobert, F.

Publications and source records attributed to Jobert, F..

4 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↗

Pectin remodeling belongs to a homeostatic system and triggers transcriptomic and hormonal modulations

O_LIHere, we focused on the biological modifications arisen from a strong and transient variation of the pectin methylesterification status during the seed-to-seedling transition. C_LIO_LIA reverse genetic approach was used to trigger specific reduction of pectin de-methylesterification during the seed maturation stage and the related physiological effects were assessed using a combination of biochemical, transcriptomic and microscopic analyses. C_LIO_LIArabidopsis PME36 is required to implement the characteristic pattern of de-methylesterified pectin in the mature seed. While this pattern is strongly impaired in pme36-1 and pme36-2 mature seed, no phenotypical effect is observed in the knockout mutant during seed germination. By analyzing hormone homeostasis and gene expression regulation, we show a strong and dynamic physiological disorder in the mutant, which reveals the existence of a complex compensatory mechanism overcoming the defect in pectin de-methylesterification. C_LIO_LIOur results reveal that pectin methylesterification status acts as upstream modulator involved in an undescribed homeostatic system in which pectin remodeling, hormone signaling and transcriptomic regulations interact to ensure the maintenance of a normal seed-to-seedling developmental program. C_LI

plant biology↗

Auxin and pectin remodeling interplay during rootlet emergence in white lupin

Secondary root emergence is a crucial trait that shapes the plants underground system. Virtually every developmental step of root primordium morphogenesis is controlled by auxin. However, how the hormone controls cell separation in primordium-overlaying tissues through wall loosening is poorly understood. Here, we took advantage of white lupin and its spectacular cluster root development to assess the contribution of auxin to this process. We show that auxins positive role on rootlet emergence is associated with an upregulation of cell wall pectin modifying and degrading genes. Downregulation of a pectinolytic enzyme gene expressed in cells surrounding the primordium resulted in delayed emergence. Pectins were demethylesterified in the emergence zone and auxin treatment further enhanced this effect. Additionally, we report specific rhamnogalacturonan-I modifications during cortical cell separation. In conclusion, we propose a model in which auxin has a dual role during rootlet emergence: Firstly, through active pectin demethylesterification and secondly by regulating the expression of cell wall remodeling enzymes.

plant biology↗

Molecular framework for TIR1/AFB-Aux/IAA-dependent auxin sensing controlling adventitious rooting in Arabidopsis

In Arabidopsis thaliana, canonical auxin-dependent gene regulation is mediated by 23 transcription factors from the AUXIN RESPONSE FACTOR (ARF) family, most of which interact with 29 auxin/indole acetic acid (Aux/IAA) repressors, themselves forming, in the presence of auxin, coreceptor complexes with one of six TRANSPORT INHIBITOR1/AUXIN-SIGNALLING F-BOX PROTEINS (TIR1/AFB). Different combinations of co-receptors drive specific sensing outputs, allowing auxin to control a myriad of processes. Considerable efforts have been made to discern the temporal and spatial specificity of auxin action. However, owing to a lack of obvious phenotype in single loss-of-function mutants in Aux/IAA genes, most genetic studies have relied on gain-of-function mutants, which are highly pleiotropic. In this article, we describe a molecular framework for the role of several members of the auxin sensing machinery. Using loss-of-function mutants, we demonstrate that TIR1 and AFB2 are positive regulators, whereas IAA6, IAA9 and IAA17 are negative regulators of adventitious root (AR) formation. The three Aux/IAA proteins interact with ARF6 and/or ARF8, which we have previously shown to be positive regulators of AR formation upstream of jasmonate, and likely repress their activity. Our data also suggest a dual role for TIR1 in the control of JA biosynthesis and conjugation, as revealed by upregulation of several JA biosynthesis genes in the tir1-1 mutant. In conclusion, we propose that in the presence of auxin, TIR1 and AFB2 form specific sensing complexes with IAA6, IAA9 and/or IAA17 that modulate JA homeostasis to control AR initiation.\n\nSignificanceAdventitious root (AR) formation is a quantitative trait with high phenotypic plasticity and auxin plays a major role in its control. In previous studies, we have shown that, in Arabidopsis hypocotyls, AR formation is negatively regulated by jasmonate, whose homeostasis is controlled by a regulatory module composed of three AUXIN RESPONSE FACTORS (ARF), two of which are positive regulators of three auxin inducible Gretchen Hagen3 (GH3) genes. The present work demonstrates that the two F-box proteins, i.e., TIR1 and AFB2, together with at least three Aux/IAA proteins are likely to interact in a combinatorial manner to control the activity of the two activator ARFs upstream of JA biosynthesis and/or homeostasis, thereby controlling AR initiation in Arabidopsis hypocotyls.

plant biology↗