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Bellegarde, F.

Publications and source records attributed to Bellegarde, F..

3 recordsLinked to original sources

LBD-type transcription factors suppress local and systemic nitrogen responses through distinct regulatory pathways

Nitrogen (N) is a major determinant of plant growth and productivity. Because soil N availability and internal N demand fluctuate, plants have evolved sophisticated mechanisms to coordinate N acquisition and utilization at the whole-plant level. However, how this coordination is achieved remains poorly understood. Here, we show that N-inducible LATERAL ORGAN BOUNDARIES DOMAIN transcription factors LBD37, LBD38, and LBD39 (LBDs) function as repressors of local N uptake and assimilation and systemic N-demand signaling in Arabidopsis. Triple mutants lacking these three LBDs displayed enhanced nitrate influx and increased accumulation of nitrate, amino acids, and total N. Transcriptome analysis identified an array of N-starvation- and nitrate-inducible genes derepressed in shoots and roots, including C-TERMINALLY ENCODED PEPTIDE (CEP) and CEP DOWNSTREAM (CEPD) genes, as well as genes involved in N uptake and assimilation. Grafting and genetic analyses revealed that LBDs gate the systemic N-demand signaling relay by repressing CEP and CEPD expression organ-autonomously. We also found that LBDs locally repress genes involved in N uptake and assimilation through a distinct regulatory mechanism. We propose that LBDs are key transcriptional repressors in a regulatory framework for optimizing N acquisition and utilization under fluctuating N conditions at the whole-plant level.

plant biology↗

NRT2.1 phosphorylation prevents root high affinity nitrate uptake activity in Arabidopsis thaliana

In Arabidopsis thaliana, NRT2.1 codes for a main component of the root nitrate high-affinity transport system. Previous studies revealed that post-translational regulation of NRT2.1 plays an important role in the control of root nitrate uptake and that one mechanism could correspond to NRT2.1 C-terminus processing. To further investigate this hypothesis, we produced transgenic plants with truncated forms of NRT2.1. It revealed an essential sequence for NRT2.1 activity, located between the residues 494-513. Using a phospho-proteomic approach, we found that this sequence contains one phosphorylation site, at serine 501, which can inactivate NRT2.1 function when mimicking the constitutive phosphorylation of this residue in transgenic plants. This phenotype could neither be explained by changes in abundance of NRT2.1 and NAR2.1, a partner protein of NRT2.1, nor by a lack of interaction between these two proteins. Finally, the relative level of serine 501 phosphorylation was found to be modulated by nitrate in wildtype plants. Altogether, these observations allowed us to propose a model for a new and essential mechanism for the regulation of NRT2.1 activity.

plant biology↗

HNI9 and HY5 maintain ROS homeostasis under high nitrogen provision in Arabidopsis

One sentence summaryExcessive N nutrition leads to ROS accumulation, and requires the function of major transcriptional regulators to maintain plants under physiological conditions.\n\nAuthor contributionsAn.M. and A.G. conceived research plans and supervised the experiments; F.B, Am.M., J.B., L.L., L.B. and An.M performed most of the experiments; F.B, Am.M., J.B., G.K., L.L., L.B. and An.M analyzed the data; An.M. wrote the article with contributions of all the authors.\n\nCompeting interestsThe authors declare no competing financial interests.\n\nSummaryReactive Oxygen Species (ROS) can accumulate in cells at excessive levels, leading to unbalanced redox status and to a potential oxidative stress, which can have damaging effects to the molecular components of plant cells. Several environmental conditions have been described as causing an elevation of ROS production in plants. Consequently, this requires the expression of detoxification responses in order to maintain ROS homeostasis at physiological levels. In case of mis-regulation of the detoxification systems, oxidative stress can lead ultimately to growth retardation and developmental defects. Here, we demonstrate that Arabidopsis plants growing under high nitrogen environment have to express a set of genes involved in detoxification of ROS in order to maintain ROS at physiological levels. We show that the chromatin factor HNI9 is an important actor of this response, required for the expression of these detoxification genes. Mutation in HNI9 leads to elevated ROS levels, and to ROS-dependent phenotypic defects under high but not low N provision. In addition, we identify HY5 as one of the major transcription factors also required for the expression of this detoxification program under high N condition. Our results demonstrate the requirement of a balance between N nutrition and ROS production, and identified the first major regulators required to control ROS homeostasis under excessive N nutrition.

plant biology↗