Biology subjects

Oliveira, M. M.

Publications and source records attributed to Oliveira, M. M..

At least 19 recordsLinked to original sources

bioRxiv2026

Astrocytes instructively regulate neuronal translation

Neuronal protein synthesis is essential for synaptic plasticity and long-term memory, yet whether its regulation is shaped by other cell types remains poorly understood. Here, we show that astrocyte-secreted proteins regulate global neuronal translation depending on astrocytic state. Astrocyte-conditioned medium (ACM) increased neuronal translation under basal conditions, an effect enhanced by astrocyte stimulation with the activity-dependent factor BDNF, whereas ACM from neurotoxic reactive astrocytes, a state linked to neuroinflammation and Alzheimers disease, suppressed neuronal translation. Across these conditions, neuronal mTORC1 activity consistently tracked with translational output, whereas the integrated stress response (ISR) acted through distinct, state-specific mechanisms that did not always track with neuronal translation. Furthermore, we identified astrocyte-secreted apolipoprotein E (APOE) and its associated cargo as a negative regulator of neuronal translation that contributed to the decreased translation induced by neurotoxic reactive astrocytes. We also found that astrocyte-secreted signals required neuronal endocytosis to influence translation and drove synaptic remodeling dependent on glutamatergic signaling and neuronal mTORC1 activity. Together, these findings identify astrocytes as active, instructive regulators of neuronal translation and synaptic structure, with implications for understanding how astrocyte dysfunction may disrupt the translational mechanisms underlying impairments in synaptic plasticity and long-term memory in neurodegenerative disease. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=142 SRC="FIGDIR/small/741020v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@74ecborg.highwire.dtl.DTLVardef@1c620a0org.highwire.dtl.DTLVardef@881b8corg.highwire.dtl.DTLVardef@1c8b7e4_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2026

Evolutionary and functional diversification of cork oak NLRs reveals RNL expansion and dual roles in biotic and abiotic stress

The Nucleotide-Binding Domain Leucine-Rich Repeat (NLR) gene family is a central component of plant immune systems, yet its diversity and evolutionary dynamics remain poorly characterized in long-lived tree species. Here, we performed a genome-wide analysis of the NLR gene family in Quercus suber (cork oak) using InterNLR, a new annotation tool, and explored their expression regulation in response to biotic and abiotic stresses. A total of 918 NLR and NLR-like genes were identified, encompassing both canonical and non-canonical members. Phylogenetic analyses based on the NB-ARC domain highlighted the distinct evolutionary trajectory of RNL proteins, which function as helper NLRs and show evidence of clade-specific gene duplication. Transcriptomic analyses revealed pronounced tissue-specific expression patterns, with RNLs exhibiting significantly elevated expression in xylem, suggesting a specialized role in this tissue. Under drought stress, seven NLR genes were differentially expressed and shared orthology with known abiotic stress-responsive genes. Notably, a CNL gene (LOC111996439) responded to both biotic and abiotic stresses, indicating a potential role as an integrative regulator of early defence responses, while an ADR1 orthologue (LOC112022539) suggests molecular crosstalk between stress signaling pathways. Population genetic analyses further revealed signatures of both positive and balancing selection acting on NLR genes. Together, these results provide new insights into the evolution, expression, and functional diversification of NLRs in cork oak. This work advances our understanding of immune gene architecture in an ecologically and economically important forest tree species.

plant biology↗

bioRxiv2025

Microglia coordinate activity-dependent protein synthesis in neurons through metabolic coupling

De novo protein synthesis is required for long-lasting synaptic plasticity and memory, but it comes with a great metabolic cost. In the mammalian brain, it remains unclear which cell types and biological mechanisms are critical for sensing and responding to increased metabolic demand. Here we demonstrate that microglia, resident macrophages of the brain, coordinate metabolic coupling between endothelial cells, astrocytes, and neurons to fuel protein synthesis in active neurons. Increasing metabolic demand via a motor task stimulates microglia to secrete the hypoxia-responsive protein CYR61, increasing glucose transporter expression in brain vasculature. Depleting microglia reduces training-induced metabolic fluxes and neuronal protein synthesis, which can be reproduced by blocking CYR61 signaling. Thus, we define a neuroimmune metabolic circuit required for on-demand protein synthesis in mouse motor cortex.

neuroscience↗

bioRxiv2025

CRISPR-engineered deletion of POGZ alters transcription factor binding at promoters of genes involved in synaptic signaling

One of the seminal discoveries from genetic studies of autism spectrum disorder and related neurodevelopmental disorders (NDD) has been that loss-of-function (LoF) mutations in many genes that impact chromatin and transcriptional regulation confer substantial liability to NDD. Haploinsufficiency of the epigenetic regulator POGZ represents one of the strongest such associations; however, little is known about the direct or indirect regulatory targets of POGZ, or the mechanisms by which loss of this chromatin modifier alters early neuronal development and synaptic functions. Here, we created an allelic series of CRISPR-engineered human induced pluripotent stem cell (hiPSC) clones harboring mono- and biallelic POGZ deletions. In hiPSC-derived neural stem cells (NSC) and Neurogenin 2-induced neurons (iN), POGZ LoF altered the expression of genes associated with critical cellular processes and neuronal functions, including synaptic and intracellular signaling and extracellular matrix organization. Our multiomics profiling also showed altered footprinting of critical transcription factors (e.g., activator protein 1 complexes) that were enriched at promoters of differentially expressed genes associated with synaptic function. To further interrogate the shared molecular changes in neuronal development associated with NDD and POGZ regulation, we compared our results to deletions of the transcription factor MEF2C and the sodium channel gene SCN2A that we generated in these same isogenic iN. These analyses revealed strong enrichment of extracellular matrix and intracellular signaling disruption associated with POGZ and MEF2C deletion, whereas POGZ and SCN2A haploinsufficiency exhibited shared transcriptional effects on gene modules enriched for NDD-associated genes with opposing regulatory effects. Notably, we also observed alterations to synaptic firing rate and neurite extension with biallelic deletions, but not heterozygous lines, suggesting subtle effects in neuronal development associated with haploinsufficiency. Overall, these shared molecular consequences suggest key points of convergence that connect epigenetic regulation to neuronal function in the etiology of neurodevelopmental pathologies.

genomics↗

bioRxiv2025

Aberrant recursive splicing in a human disease locus

Recursive splice sites are rare motifs postulated to facilitate splicing across massive introns and shape isoform diversity, especially for long, brain-expressed genes. The necessity of this unique mechanism remains unsubstantiated, as does the role of recursive splicing (RS) in human disease. From analyses of rare copy number variants (CNVs) from almost one million individuals, we previously identified large, heterozygous deletions eliminating an RS site (RS1) in the first intron of CADM2 that conferred substantial risk for attention deficit hyperactivity disorder (ADHD) and other neurobehavioral traits. CADM2 encodes a neuronally expressed cell adhesion molecule that has repeatedly been associated with ADHD and numerous similar traits. To explore the molecular impact of RS ablation in CADM2, we used CRISPR to model patient deletions and to target a smaller region ([~]500 base pairs) containing RS1 in both human induced neurons (iNs) and rats. Transcriptome analyses in unedited iNs provided a catalog of CADM2 transcripts, including novel transcripts that retained RS exons. Intriguingly, ablating RS1 altered the gradient of RNA abundance across the first intron of CADM2, decreased the level of CADM2 expression, and impacted transcript usage. Decreased CADM2 expression was reflected in reduced exon usage downstream of the RS1 site and global alteration to genes involved in neuronal processes including synapse and axon development. Given the scale of our analyses and the widespread association of CADM2 with neurobehavioral traits, we sought to validate these findings using in vivo models and found that rodent models harboring Cadm2 RS1 deletions exhibited significant changes in relevant behaviors and functional brain connectivity. In summary, our analyses demonstrate a functional role for RS as a noncoding regulatory mechanism in a gene associated with a spectrum of neuropsychiatric and behavioral traits. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=140 SRC="FIGDIR/small/666599v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@171156borg.highwire.dtl.DTLVardef@13553baorg.highwire.dtl.DTLVardef@bee7forg.highwire.dtl.DTLVardef@156f19e_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG

genomics↗

bioRxiv2025

Whole-genome polymorphisms and relatedness of rice varieties circulating in the Mediterranean market

Rice cultivation in Europe is declining as consumers increasingly prefer imported exotic varieties, such as aromatic and basmati rice, which are prone to fraudulent varietal claims due to their higher market value. To address this issue, we sequenced 20 high-value rice cultivars circulating in the Mediterranean market, analyzing their phylogeny and whole-genome polymorphisms. Our results revealed that two basmati varieties are genetically closer to two Mediterranean varieties, and that no direct link exists between genome-wide single nucleotide polymorphism (SNP) patterns and the rice commercial category. We further discuss genes located in previously described quantitative trait loci (QTLs) related to eating quality and seed properties. A variant in the WX1 gene, associated with higher amylose content, was found in both the Basmati group and Mediterranean varieties. Additionally, a SNP that could disrupt the drought tolerance gene OsbHLH148 was identified in five European varieties, while a variant affecting splicing of OsPol lambda, related to drought response, was present in four of those. This data could assist certification offices in reducing fraud in the rice market and provide valuable insights for researchers and breeders, particularly regarding the production, consumption, and adaptation of these cultivars to the Mediterranean region.

genomics↗

bioRxiv2025

Neuron type-specific mRNA translation programs provide a gateway for memory consolidation.

Long-term memory consolidation is a dynamic process that requires a heterogeneous ensemble of neurons, each with a highly specialized molecular signature. Considerable effort has been devoted to identifying molecular changes that accompany the process of consolidation, but mostly hours or days after training, when memory consolidation is already complete. Studies have shown that protein synthesis is elevated during the early stages of consolidation, but how this increase impacts neuronal function remains unclear. We hypothesize that mRNAs translated during the early stages of consolidation could provide information on how diverse neurons involved in memory formation restructure their molecular signatures to support memory. Here, we generate a landscape of the translatome of three neuron types in the dorsal hippocampus during the first hour of contextual memory consolidation. Our results reveal that translation programs associated with consolidation are different among neurons, fueling the reconfiguration of specific biological processes. We further demonstrate the patterned translation of mRNAs in different neuron types during consolidation is explained by features hard-coded in the mRNA sequence, suggesting ubiquitous mechanisms controlling activity-induced neuronal translation. Altogether, our work uncovers previously unknown mechanisms controlling activity-induced translation in neurons and provides a large, readily available resource for scientists interested in the role of memory formation in health and disease.

neuroscience↗

bioRxiv2024

Aberrant TSC-Rheb axis in Oxytocin receptor+ cells mediate stress-induced anxiety

Stress is a major risk for the onset of several maladaptive processes including pathological anxiety, a diffuse state of heightened apprehension over anticipated threats1. Pathological anxiety is prevalent in up to 59% of patients with Tuberous Sclerosis complex (TSC)2, a neurodevelopmental disorder (NDD) caused by loss-of-function mutations in genes for Tuberin (Tsc2) and/or Hamartin (Tsc1) that together comprise the eponymous protein complex. Here, we generated cell type-specific heterozygous knockout of Tsc2 in cells expressing oxytocin receptor (OTRCs) to model pathological anxiety-like behaviors observed in TSC patient population. The stress of prolonged social isolation induces a sustained negative affective state that precipitates behavioral avoidance, often by aberrant oxytocin signaling in the limbic forebrain3,4. In response to social isolation, there were striking sex differences in stress susceptibility in conditional heterozygote mice when encountering situations of approach-avoidance conflict. Socially isolated male mutants exhibited behavioral avoidance in anxiogenic environments and sought more social interaction for buffering of stress. In contrast, female mutants developed resilience during social isolation and approached anxiogenic environments, while devaluing social interaction. Systemic and medial prefrontal cortex (mPFC)-specific inhibition of downstream effector of TSC, the integrated stress response (ISR), rescued behavioral approach toward anxiogenic environments and conspecifics in male and female mutant mice respectively. Further, we found that Tsc2 deletion in OTRCs leads to OTR-signaling elicited network suppression, i.e., hypofrontality, in male mPFC, which is relieved by inhibiting the ISR. Our findings present evidence in support of a sexually dimorphic role of prefrontal OTRCs in regulating emotional responses in anxiogenic environments, which goes awry in TSC. Our work has broader implications for developing effective treatments for subtypes of anxiety disorders that are characterized by cell-autonomous ISR and prefrontal network suppression.

neuroscience↗

bioRxiv2024

CloVarS: a simulation of single-cell clonal variability

High-throughput time-lapse microscopy has allowed researchers to monitor individual cells as they grow into colonies and react to treatments, but a deeper understanding of the data obtained after image analysis is still lacking. This is partly due to the biological and computational challenges related to long-running experiments and single-cell tracking. In this work, we present the Clonal Variability Simulator (CloVarS), a Python tool for generating synthetic data of single-cell lineage trees to model time-lapse microscopy experiments. After colony initialization, each individual cell is simulated for a given number of simulation frames. Over the course of the simulation, cells are able to migrate, enter mitosis (divide), and enter apoptosis (die). These events are determined by distributions of cell division and death times, which can be inferred from and fit to experimental data. Colonies have an adjustable fitness memory, meaning cells are able to inherit their parent cells fitness (i.e. their parents time to division/death) to a higher or lesser degree. Arbitrary treatments are able to be delivered to colonies at any time point, modifying their division and death distributions, and fitness memory. CloVarS is an important asset for quickly exploring colony fitness dynamics, testing biological hypotheses, bench-marking cell tracking algorithms, and ultimately improving our understanding of single-cell lineage data.

bioinformatics↗

bioRxiv2023

Drought impact on phellem development: identification of novel gene regulators and evidence of photosynthetic activity

Quercus suber (cork oak) is a sustainably exploited forest resource, producing a unique renewable raw material known as cork. With drought events imposing a negative impact on tree vitality, we need more knowledge on the genetic and environmental regulation of cork development to protect the cork sector. We focused on characterizing long-term drought-induced molecular adaptations occurring in stems, and identifying key genetic pathways regulating phellem development. One-year-old cork oak plants were grown for 6 months under well-watered, or water-deficit (WD) conditions and main stems were targeted for histological characterization and transcriptomic analysis. WD treatment impaired secondary growth, by reducing meristem activity at both vascular cambium and phellogen. We analyzed the transcriptional changes imposed by WD in phellem, inner bark, and xylem, and found a global downregulation of genes related to cell division, differentiation, and cell wall biogenesis. Phellem and inner bark showed upregulation of photosynthesis-related genes, highlighting a determinant role of stem photosynthesis in the adaptation to long-term drought. We show that developing phellem cells contain chloroplasts and their abundance increases under WD. Finally, we propose new candidate regulatory genes involved in the regulation of phellogen activity and demonstrate the involvement of phellem in drought-induced bark photosynthesis in young plants. HighlightPhellem development in cork oak is impaired in drought adaptation, by negative regulation of cell division and differentiation programs, while photosynthesis is induced to contributing to CO2 recycling in the stem.

plant biology↗

bioRxiv2023

Opto4E-BP, an optogenetic tool for inducible, reversible, and cell type-specific inhibition of translation initiation

The protein kinase mechanistic target of rapamycin complex 1 (mTORC1) is one of the primary triggers for initiating cap-dependent translation. Amongst its functions, mTORC1 phosphorylates eIF4E-binding proteins (4E-BPs), which prevents them from binding to eIF4E and thereby enables translation initiation. mTORC1 signaling is required for multiple forms of protein synthesis-dependent synaptic plasticity and various forms of long-term memory (LTM), including associative threat memory. However, the approaches used thus far to target mTORC1 and its effectors, such as pharmacological inhibitors or genetic knockouts, lack fine spatial and temporal control. The development of a conditional and inducible eIF4E knockdown mouse line partially solved the issue of spatial control, but still lacked optimal temporal control to study memory consolidation. Here, we have designed a novel optogenetic tool (Opto4E-BP) for cell type-specific, light-dependent regulation of eIF4E in the brain. We show that light-activation of Opto4E-BP decreases protein synthesis in HEK cells and primary mouse neurons. In situ, light-activation of Opto4E-BP in excitatory neurons decreased protein synthesis in acute amygdala slices. Finally, light activation of Opto4E-BP in principal excitatory neurons in the lateral amygdala (LA) of mice after training blocked the consolidation of LTM. The development of this novel optogenetic tool to modulate eIF4E-dependent translation with spatiotemporal precision will permit future studies to unravel the complex relationship between protein synthesis and the consolidation of LTM.

neuroscience↗

bioRxiv2023

The Integrated Stress Response effector GADD34 is repurposed by neurons to promote stimulus-induced translation

Neuronal protein synthesis is required for long-lasting plasticity and long-term memory consolidation. Dephosphorylation of eukaryotic initiation factor 2 is one of the key translational control events that is required to increase de novo protein synthesis that underlies long-lasting plasticity and memory consolidation. Here, we interrogate the molecular pathways of translational control that are triggered by stimulation of neurons with brain-derived neurotrophic factor (BDNF), which results in eIF2 dephosphorylation and de novo protein synthesis. Primary rodent neurons exposed to BDNF displayed elevated translation, but not transcription, of GADD34, which facilitates eIF2 dephosphorylation and subsequent de novo protein synthesis. Furthermore, GADD34 requires G-actin generated by cofilin to dephosphorylate eIF2 and enhance protein synthesis. Finally, GADD34 is required for the BDNF-induced translation of synaptic plasticity-related proteins. Overall, we provide evidence that neurons repurpose GADD34, an effector of the Integrated Stress Response, as an orchestrator of rapid increases in eIF2-dependent translation in response to plasticity-inducing stimuli.

neuroscience↗

bioRxiv2022

Cell type-specific disruption of cortico-striatal circuitry drive repetitive patterns of behaviour in fragile X syndrome model mice

Individuals with fragile X syndrome (FXS) are frequently diagnosed with autism spectrum disorder (ASD), including increased risk for restricted and repetitive behaviours (RRBs). Consistent with observations in humans, FXS model mice display distinct RRBs and hyperactivity that are consistent with dysfunctional cortico-striatal circuits, an area relatively unexplored in FXS. Using a multidisciplinary approach, we dissected the contribution of two populations of striatal medium spiny neurons (SPNs) in the expression of RRBs in FXS model mice. We found that dysregulated protein synthesis at cortico-striatal synapses is a molecular culprit of the synaptic and ASD-associated motor phenotypes displayed by FXS model mice. Cell-type-specific translational profiling of the FXS mouse striatum revealed differentially translated mRNAs, providing critical information concerning potential therapeutic targets. Our findings represent the first evidence of a cell-type specific impact of the loss of FMRP on translation and the sequence of neuronal events in the striatum that drive RRBs in FXS. HighlightsDysregulated striatal protein synthesis underlies altered synaptic plasticity and RRBs displayed by FXS model mice FXS model mice exhibit cell type-specific molecular, morphological, and synaptic changes in the dorsolateral striatum Selective deletion of Fmr1 from dSNPs in mice alters translation and causes repetitive behavior TRAP-Seq indicates that there is altered binding of >120 mRNAs to ribosomes in dSNPs of Fmr1 KO mice G-protein signaling (RGS) 4 translation is significantly reduced in dSPNs in FXS model mice Treatment of FXS model mice with VU0152100, a positive allosteric modulator of the M4 muscarinic receptor that is upstream of RGS4, can reverse RRBs

neuroscience↗

bioRxiv2021

Phellem translational landscape throughout secondary development in Arabidopsis roots

O_LIThe phellem is a specialized boundary tissue providing the first line of defense against abiotic and biotic stresses in organs undergoing secondary growth. Phellem cells undergo several differentiation steps, which include cell wall suberization, cell expansion and programmed cell death. Yet, the molecular players acting particularly in phellem cell differentiation remain poorly described, particularly in the widely used model plant Arabidopsis thaliana. C_LIO_LIUsing specific marker lines we followed the onset and progression of phellem differentiation in A. thaliana roots, and further targeted the translatome of new developed phellem cells using Translating Ribosome Affinity Purification followed by mRNA sequencing (TRAP-SEQ). C_LIO_LIWe showed that phellem suberization is initiated early after phellogen (cork cambium) division. The specific translational landscape was organized in three main domains related to energy production, synthesis and transport of cell wall components, and response to stimulus. Novel players in phellem differentiation, related to suberin monomer transport and assembly, as well as novel transcription regulators were identified. C_LIO_LIThis strategy provided an unprecedented resolution of the transcriptome of developing phellem cells, giving a detailed and specific view on the molecular mechanisms controlling cell differentiation in periderm tissues of the model plant Arabidopsis. C_LI Significance statementTo improve the understanding of phellem differentiation into a suberized protective layer, we followed the establishment of periderm in Arabidopsis roots and sequenced the phellem-specific translatome. We found that phellem suberization occurs shortly after pericycle cell divisions with the induction of pivotal suberin biosynthesis genes. In parallel, we detected the activation of three central genetic modules acting throughout the phellem differentiation. This study provides a unique and targeted genetic resource for further functional studies of phellem tissues.

plant biology↗

bioRxiv2020

Ecdysone coordinates plastic growth with robust pattern in the developing wing

Animals develop in unpredictable, variable environments. In response to environmental change some aspects of development adjust to generate plastic phenotypes. Other aspects of development, however, are buffered against environmental change to produce robust phenotypes. How organ development is coordinated to accommodate both plastic and robust developmental responses is poorly understood. Here, we demonstrate that the steroid hormone ecdysone coordinates both plasticity of organ size and robustness of organ pattern in the developing wings of the fruit fly Drosophila melanogaster. Using fed and starved larvae that lack prothoracic glands, which synthesise ecdysone, we show that nutrition regulates growth both via ecdysone and via an ecdysone-independent mechanism, while nutrition regulates patterning only via ecdysone. We then demonstrate that growth shows a graded response to ecdysone concentration, while patterning shows a threshold response. Collectively, these data support a model where nutritionally-regulated ecdysone fluctuations confer plasticity by regulating disc growth in response to basal ecdysone levels, and confers robustness by initiating patterning only once ecdysone peaks exceeds a threshold concentration. This could represent a generalizable mechanism through which hormones coordinate plastic growth with robust patterning in the face of environmental change.

developmental biology↗

bioRxiv2020

Correction of eIF2-dependent defects in brain protein synthesis, synaptic plasticity, and memory in mouse models of Alzheimer's disease

Neuronal protein synthesis is essential for long-term memory consolidation. Conversely, dysregulation of protein synthesis has been implicated in a number of neurodegenerative disorders, including Alzheimers disease (AD). Several types of cellular stress trigger the activation of protein kinases that converge on the phosphorylation of eukaryotic translation initiation factor 2 (eIF2-P). This leads to attenuation of cap-dependent mRNA translation, a component of the integrated stress response (ISR). We show that AD brains exhibit increased eIF2-P and reduced eIF2B, key components of the eIF2 translation initiation complex. We further demonstrate that attenuating the ISR with the small molecule compound ISRIB (ISR Inhibitor) rescues hippocampal protein synthesis and corrects impaired synaptic plasticity and memory in mouse models of AD. Our findings suggest that attenuating eIF2-P-mediated translational inhibition may comprise an effective approach to alleviate cognitive decline in AD.

neuroscience↗

bioRxiv2020

Dysregulation of the de novo proteome accompanies pathology progression in the APP/PS1 mouse model of Alzheimer's disease

Alzheimers disease (AD) is an age-related neurodegenerative disorder, but neuropathological changes in AD begin years before memory impairment. Investigation of the early molecular abnormalities in AD might offer innovative opportunities to target memory impairment prior to its onset. Decreased protein synthesis plays a fundamental role in AD, yet the consequences for cellular function remain unknown. We hypothesize that alterations in the de novo proteome drive early metabolic changes in the hippocampus that persist throughout AD progression. Using a combinatorial amino acid tagging approach to selectively label newly synthesized proteins, we found that the de novo proteome is disturbed in APP/PS1 mice prior to pathology development, affecting the synthesis of multiple components of synaptic, lysosomal and mitochondrial pathways. Furthermore, the synthesis of large clusters of ribosomal subunits were affected throughout neuropathology development in these mice. Our data suggest that large-scale changes in protein synthesis could underlie cellular dysfunction in AD.

neuroscience↗

bioRxiv2020

SUMOylation of rice DELLA SLR1 modulates transcriptional responses and improves yield under salt stress

DELLA proteins modulate GA signalling and are major regulators of plant plasticity to endure stress. DELLAs are mostly regulated at the post-translational level, and their activity relies on the interaction with upstream regulators and transcription factors (TFs). SUMOylation is a post-translational modification (PTM) capable of changing protein interaction and found to influence DELLA activity in Arabidopsis. We determined that SUMOylation of the single rice DELLA SLENDER RICE1 (SLR1) occurs in a lysine residue different from the one previously identified in Arabidopsis REPRESSOR OF GA (RGA). Remarkably, artificially increasing SUMOylated SLR1 (SUMO1SLR1) levels attenuated the penalty of salt stress on plant yield. Gene expression analysis revealed that the overexpression of SUMOylated SLR1 regulates key dioxygenases that modulate active GA levels, namely GA20ox2 and GA2ox3, which could partially explain the sustained productivity upon salt stress imposition. Besides, SLR1 SUMOylation blocked the interaction with the growth regulator YAB4, which may fine-tune GA20ox2 expression. Mechanistically, we propose that SLR1 SUMOylation disrupts the interaction with members of several transcription factor families to modulate gene expression. We found that SLR1 SUMOylation represents a novel mechanism modulating DELLA activity, which attenuates the impact of stress on plant performance. One sentence summaryRice plants show increased yield under salt stress when its gibberellin transcriptional regulator DELLA protein is artificially SUMOylated.

plant biology↗