Sere, D. | Search bioRxiv

bioRxiv2024

A RALF-Brassinosteroid morpho-signaling circuit regulates Arabidopsis hypocotyl cell shape

Plant cells survey and modulate their cell wall to control their shape and anisotropic growth. Signaling mediated by the plant steroid hormones brassinosteroids (BR) plays a central role in coordinating cell wall status and cell growth, and alterations in the cell wall - BR feedback loop leads to life-threatening defects in tissue and cellular integrity. How the status of the cell wall is relayed to BR signaling remains largely unclear. Increasing evidence shows that RAPID ALKALANIZATION FACTORs (RALFs), a class of secreted peptides, play structural and signaling roles at the cell surface. Here we show that perception of RALF23 promotes the formation and signaling of the main BR receptor complex formed by BRASSINOSTEROID INSENSITIVE 1 (BRI1) and BRI1-BRASSINOSTEROID INSENSITIVE1-BRASSINOSTEROID-ASSOCIATED KINASE 1 (BAK1). The loss of the plasma membrane-localized RALF receptor complex FERONIA (FER)-LORELEI LIKE GPI-anchor protein 1 (LLG1) leads to defects in cell expansion and anisotropy, as well as uncontrolled BRI1-BAK1 complex formation and signaling. RALF23 bioactivity relies on pectin status and its perception induces changes in pectin composition and the activity of pectin-modifying enzymes. Our observations suggest a model in which RALF23 functions as a cell wall-informed signaling cue initiating a feedback loop that solicits BR signaling, modifies the cell wall, and coordinates cell morphogenesis. Highlights-The RALF receptor complex FER-LLG1 regulates cell anisotropic growth -RALF23 promotes BRI1-BAK1 complex formation and signaling -RALF23 functions as a cell wall-informed and wall-modifying signaling cue

plant biology↗

bioRxiv2022

Signaling pathways involved in the repression of root nitrate uptake by nitrate in Arabidopsis thaliana

In Arabidopsis thaliana, root high-affinity nitrate (NO3-) uptake depends mainly on NRT2.1, 2.4 and 2.5, which are repressed by high NO3- supply at the transcript level. For NRT2.1, this regulation is due to the action of (i) feedback downregulation by N metabolites and (ii) repression by NO3- itself mediated by the transceptor NRT1.1(NPF6.3). However, for NRT2.4 and NRT2.5 the signaling pathway(s) remain unknown along with the molecular elements involved. Here we show that unlike NRT2.1, NRT2.4 and NRT2.5 are not induced in a NO3- reductase mutant but are strongly upregulated following replacement of NO3- by ammonium (NH4+) as the N source. Moreover, increasing NO3- concentration in a mixed nutrient solution with constant NH4+ concentration results in a gradual repression of NRT2.4 and NRT2.5, which is suppressed in a nrt1.1 mutant. This indicates that NRT2.4 and NRT2.5 are subjected to repression by NRT1.1-mediated NO3- sensing, and not to feedback repression by reduced N metabolites. We further show that key regulators of NRT2s transporters, such as HHO1, HRS1, PP2C, LBD39, BT1 and BT2, are also regulated by NRT1.1-mediated NO3- sensing, and that several are involved in NO3- repression of NRT2.1, 2.4 and 2.5. Finally, we provide evidence that it is the phosphorylated form of NRT1.1 at the T101 residue, which is most active in triggering the NRT1.1-mediated NO3- regulation of all these genes. Altogether, these data led to propose a regulatory model for high-affinity NO3- uptake in Arabidopsis, highlighting several NO3- transduction cascades downstream the phosphorylated form of the NRT1.1 transceptor. One sentence summaryCharacterisation and identification of molecular elements involved in the signaling pathways repressing NRT2s transporters and root nitrate uptake in response to nitrate.

plant biology↗