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Adroher, B.

Publications and source records attributed to Adroher, B..

4 recordsLinked to original sources

Developmental rewiring of the NGAL/CUC/KLU network associated with pleiotropic roles of NGAL genes

Gene Regulatory Networks (GRNs) play prominent roles in regulating developmental processes, and their modulation across species is a major source for evolutionary innovation. However, it remains poorly understood how GRNs are rewired between different organs within a single species. This question is particularly relevant for pleiotropic genes, which may exhibit organ-specific GRN modulations potentially reflecting their diverse functions. To address this, we investigated the NGATHA-like (NGAL) genes, as a model for pleiotropic genes that regulate growth or patterning in multiple Arabidopsis organs via two distinct pathways involving the CUP-SHAPED COTYLEDON (CUC) and KLUH (KLU) genes. By combining genetic analysis with gene expression characterization, we uncovered significant organ-specific rewiring of the NGAL/CUC/KLU regulatory module. Our findings highlight that changes in gene expression patterns, potentially arising from developmental constraints, play a pivotal role in the organ-specific modulation of GRNs. Furthermore, GRNs at the molecular and functional levels do not always align perfectly, potentially due to the influence of additional regulatory mechanisms. Altogether, our findings reveal significant modulation of the GRNs associated with pleiotropic genes. We propose that this flexibility in GRNs facilitates gene pleiotropy.

plant biology↗

Compensation of compromised PRC2 regulation by a miRNA ensures robustness of Arabidopsis leaf development

Robustness is pervasive throughout biological systems, enabling them to maintain persistent outputs despite perturbations in their components. Here, we reveal a novel mechanism contributing to leaf morphology robustness in the face of genetic perturbations. In Arabidopsis, leaf shape is established during early development through the quantitative action of the CUP-SHAPED COTYLEDON2 (CUC2) gene that is negatively regulated by the co-expressed MICRORNA164A (MIR164A) gene. Compromised epigenetic regulation due to defective Polycomb Repressive Complex 2 (PRC2) function results in the transcriptional derepression of CUC2 but has no impact on CUC2 protein dynamics or early morphogenesis. We solve this apparent paradox by showing that compromised PRC2 function simultaneously activates a compensatory mechanism involving another member of the MIR164 gene family, the MIR164B gene. This mechanism dampens CUC2 protein levels, thereby compensating for compromised PRC2 function and canalizing early leaf morphogenesis. Furthermore, we show that this compensation mechanism is active under different environmental conditions. Our findings shed light on how the interplay between different types of transcriptional regulation can contribute to developmental robustness.

plant biology↗

De novo stem cell establishment in meristems requires repression of organ boundary cell fate

Stem cells play important roles in animal and plant biology as they sustain morphogenesis and tissue replenishment following aging or injuries. In plants, stem cells are embedded in multicellular structures called meristems and the formation of new meristems is essential for the plastic expansion of the highly branched shoot and root systems. In particular, axillary meristems that produce lateral shoots arise from the division of boundary domain cells at the leaf base. The CUP-SHAPED COTYLEDON (CUC) genes are major determinants of the boundary domain and are required for axillary meristem initiation. However, how axillary meristems get structured and how stem cells become established de novo remains elusive. Here, we show that two NGATHA-LIKE transcription factors, DPA4 and SOD7, redundantly repress CUC expression in the initiating axillary meristem. Ectopic boundary fate leads to abnormal growth and organisation of the axillary meristem and prevents de novo stem cell establishment. Floral meristems of the dpa4 sod7 double mutant show a similar delay in stem cell de novo establishment. Altogether, while boundary fate is required for the initiation of axillary meristems, our work reveals how it is later repressed to allow proper meristem establishment and de novo stem cell niche formation.

plant biology↗

A cell wall-associated gene network shapes leaf boundary domains

Boundary domains delimit and organize organ growth throughout plant development almost relentlessly building plant architecture and morphogenesis. Boundary domains display reduced growth and orchestrate development of adjacent tissues in a non-cell autonomous manner. How these two functions are achieved remains elusive despite the identification of several boundary-specific genes. Here, we show using morphometrics at the organ and cellular levels that leaf boundary domain development requires SPINDLY (SPY), an O-fucosyltransferase, to act as cell growth repressor. Further we show that SPY acts redundantly with the CUP-SHAPED COTYLEDON transcription factors (CUC2 and CUC3), which are major determinants of boundaries development. Accordingly at the molecular level, CUC2 and SPY repress a common set of genes involved in cell wall loosening providing a molecular framework for the growth repression associated with boundary domains. Atomic force microscopy (AFM) confirmed that young leaf boundary domain cells have stiffer cell walls than marginal outgrowth. This differential cell wall stiffness was reduced in spy mutant. Taken together our data reveal a concealed CUC2 cell wall associated gene network linking tissue patterning with cell growth and mechanics. Summary statementDecreased cell-wall loosening gene expression contributes to the coordination of cell growth and mechanics with tissue patterning thus driving boundary development.

plant biology↗