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Zou, Y.

Publications and source records attributed to Zou, Y..

At least 73 records · Page 4Linked to original sources

Cooperativity among clustered κB sites within promoters and enhancers dictates transcriptional specificity of NF-κB RelA along with specific cofactors

Non-consensus binding sites of transcription factors are often observed within the regulatory elements of genes; however, their effect on transcriptional strength is unclear. Within the promoters and enhancers of NF-{kappa}B-responsive genes, we identified clusters of non-consensus {kappa}B DNA sites, many exhibiting low affinity for NF-{kappa}B in vitro. Deletion of these sites demonstrated their collective critical role in transcription. We explored how these "weak" {kappa}B sites exert their influence, especially given the typically low nuclear concentrations of NF-{kappa}B. Using proteomics approaches, we identified additional nuclear factors, including other DNA-binding TFs, that could interact with {kappa}B site-bound NF-{kappa}B RelA. ChIP-seq and RNA-seq analyses suggest that these accessory TFs, referred to as the TF-cofactors of NF-{kappa}B, facilitate dynamic recruitment of NF-{kappa}B to the clustered weak {kappa}B sites. Overall, the occupancy of NF-{kappa}B at promoters and enhancers appears to be defined by a collective contribution from all {kappa}B sites, both weak and strong, in association with specific cofactors. This congregation of multiple factors within dynamic transcriptional complexes is likely a common feature of transcriptional programs. SIGNIFICANCEThe NF-{kappa}B RelA dimers undergo rapid activation by cytokines and pathogens, driving expeditious expression of target genes upon binding to DNA elements known as {kappa}B sites, located in the regulatory regions. We find that promoter and enhancer regions of RelA target genes harbor multiple {kappa}B sites, most being non-consensus with minimal affinity to NF-{kappa}B in vitro. Recruitment of RelA dimer in vivo depend on these {kappa}B sites, weak and strong, and appears to be regulated by various accessory factors, including other DNA-binding transcription factors. Overall, this study points to a coordinated network of factors communicating with both weak and strong {kappa}B sites to recruit RelA dimers, enabling rapid gene activation.

biochemistry↗

rarestR: An R package using rarefaction metrics to estimate α-diversity (species richness) and β-diversity (species shared) for incomplete samples

Species abundance data is commonly used to study biodiversity patterns. In this context, estimating - and {beta}-diversity based on incomplete samples can lead to undersampling biases. It is therefore essential to employ methods that enable accurate comparisons of - and {beta}-diversity across varying sample sizes. This involves relying on biodiversity measures that are focused on accurately estimating the total number of species within a community, as well as the total number of species shared by two communities. Rarefaction offers such a method, where -diversity is estimated for standardized sample sizes. Rarefaction methods can also be used as a basis for {beta}-diversity calculations for standardized sample sizes. In this application note, we introduce a new R package, rarestR, designed to estimate abundance-based - and {beta}-diversity measures for inconsistent samples using rarefaction metrics. Additionally, the package offers parametric extrapolations to estimate the total expected number of species within a single community and the total expected number of species shared between two communities. Furthermore, it provides visualization for the curve fitting associated with these estimators. Overall, the rarestR package is useful in estimating - and {beta}-diversity values for incomplete samples, for example in studies involving highly mobile or species-rich taxa. These species estimators offer a complementary approach to non-parametric methods, such as the Chao series of estimators.

ecology↗

Axo-axonic synaptic input drives homeostatic plasticity by tuning the axon initial segment structurally and functionally

The stability of functional brain network is maintained by homeostatic plasticity, which restores equilibrium following perturbation. As the initiation site of action potentials, the axon initial segment (AIS) of glutamatergic projection neurons (PyNs) undergoes dynamic adjustment that exerts powerful control over neuronal firing properties in response to changes in network states. Although AIS plasticity has been reported to be coupled with the changes of network activity, it is poorly understood whether it involves direct synaptic input to the AIS. Here we show that changes of GABAergic synaptic input to the AIS of cortical PyNs, specifically from chandelier cells (ChCs), are sufficient to drive homeostatic tuning of the AIS within 1-2 weeks, while those from parvalbumin-positive basket cells do not. This tuning is reflected in the morphology of the AIS, the expression level of voltage-gated sodium channels, and the intrinsic neuronal excitability of PyNs. Interestingly, the timing of AIS tuning in PyNs of the prefrontal cortex corresponds to the recovery of changes in social behavior caused by alterations of ChC synaptic transmission. Thus, homeostatic plasticity of the AIS at postsynaptic PyNs may counteract deficits elicited by imbalanced ChC presynaptic input. TeaserAxon initial segment dynamically responds to changes in local input from chandelier cells to prevent abnormal neuronal functions.

neuroscience↗

ATP13A1 engages GET3 to facilitate substrate-specific translocation

Proper localization of proteins to their final destinations is crucial for preserving cellular structure and functions. The interpretation and sorting of highly variable targeting sequences in secreted and membrane proteins, however, pose a challenge in achieving precise localization within specific secretory apparatus. In this study, we demonstrate that atypical signal sequences characterized by high hydrophobicity and/or the absence of characteristic charges undergo targeting to the endoplasmic reticulum (ER) in a reverse orientation, followed by partial cleavage. The P5A- ATPase ATP13A1 recognizes the cleaved signal sequence and dislocates it to the targeting factor GET3, subsequently engaging SEC61 for further translocation. Our findings unveil a comprehensive translocation pathway that operates in a substrate- specific manner, ensuring both high efficiency and fidelity in the protein subcellular localization.

biochemistry↗

Restoring O-glycosylation and expression of MUC2 limits progression of colorectal cancer

This study investigated the molecular mechanisms underlying the regulation of MUC2 expression and O-glycosylation modification in colorectal cancer. In addition, the potential of rosiglitazone to inhibit colorectal cancer by improving MUC2 glycosylation to protect intestinal barrier function was explored. In vitro, lectin staining combined with Co-IP assay was used to detect glycosyltransferases regulating MUC2 O-glycosylation. ChIP and Luciferase experiments were used to verify the transcription factors regulating MUC2 expression level. Samples from CRC patients were used to detect differences in multimolecular expression. The AOM/DSS mouse model was used to validate the effect of rosiglitazone on inhibiting colorectal cancer progression. Our results showed that B3GNT6 acts as a glycosyltransferase to enhance the O-glycosylation level of MUC2 and maintain protein stability to resist degradation by StcE secreting from pathogenic bacteria. Furthermore, KLF4 directly promotes the transcription of B3GNT6 and MUC2, which are regulated by PPARg. Rosiglitazone activated PPARg-KLF4-B3GNT6 axis which increased the expression level and glycosylation of MUC2 and further improved the intestinal mucosal barrier function to delay the development of colorectal cancer in mice. These data suggest that O-glycosylation and expression of MUC2 is key to the maintenance of functional intestinal mucosa and rosiglitazone is a potential colorectal cancer therapeutic agent.

cancer biology↗

Degenerative and regenerative peripheral processes are associated with persistent painful chemotherapy-induced neuropathies in males and females

This study aimed to investigate the time course of gene expression changes during the progression of persistent painful neuropathy caused by paclitaxel (PTX) in male and female mouse hind paws and dorsal root ganglia (DRG). Bulk RNA-seq was used to investigate the gene expression changes in the paw and DRG collected at 1, 16, and 31 days post-PTX. At these time points, differentially expressed DEGs were predominantly related to reduction or increase in epithelial, skin, bone, and muscle development and to angiogenesis, myelination, axonogenesis, and neurogenesis. These processes were accompanied by regulation of DEGs related to cytoskeleton, extracellular matrix organization and cellular energy production. This gene plasticity during persistent painful neuropathy progression likely represents biological processes linked to tissue regeneration and degeneration. Unlike regeneration/degeneration, gene plasticity related to immune processes was minimal at 1-31 days post-PTX. It was also noted that despite similarities in biological processes and pain chronicity in males and females, specific DEGs showed dramatic sex-dependency. The main conclusions of this study are that gene expression plasticity in paws and DRG during PTX neuropathy progression relates to tissue regeneration and degeneration, minimally affects the immune system processes, and is heavily sex-dependent at the individual gene level.

neuroscience↗

Legacy of warming and cover crops on the response of soil microbial function to repeated drying and rewetting cycles

The response of soils to extreme weather events will become increasingly important in the future as more frequent and severe floods and droughts are expected to subject soils to drying and rewetting cycles as a result of climate change. These extreme events will be experienced against a backdrop of overall warming. However, farmers are adopting cover cropping as a sustainable management practice to increase soil organic matter, benefit soil health, and to increase the resilience of soils to help mitigate the impacts of climate change. We examined the legacy of warming and cover crops on the response of soil microbial function to repeated drying and rewetting cycles. We introduced open top chambers to warm the soil surface of a field plot experiment in which cover crops (single species monocultures and 4-species polycultures) were grown over the summer after harvest and before planting of autumn sown cash crops in a cereal rotation. Soil samples were collected from warmed and ambient areas of the experimental plots in spring, before harvesting the cereal crop. We quantified respiration (a measure of soil microbial function) with high-frequency CO2 flux measurements after 0, 1, 2, 4, or 8 wet/dry cycles imposed in the laboratory and the addition of barley grass powder substrate at a ratio of 10 mg g-1 soil. Cover crop mixtures created a negative legacy effect in the soil which resulted in lower cumulative substrate induced respiration than expected from the average of the same species grown in monoculture. Repeated drying and rewetting cycles increased the cumulative substrate induced respiration rate observed, suggesting that repeated perturbations selected for a community adapted to processing the barley shoot powder more quickly. This adaptation may have resulted in a greater osmolyte production or reacquisition by microorganisms exposed to repeated drought events. Osmolytes are rapidly metabolised upon re-wetting and may have primed the decomposition of the barley shoot powder to a greater extent in soils previously exposed to drying and rewetting cycles. When we calculated the cumulative respiration after 8 wet/dry cycles, relative to cumulative respiration after 0 wet/dry cycles (which we infer represents the extent to which microbial communities adapted to repeated drying and rewetting cycles) our data revealed that the legacy of warming significantly reduced, but cover crops significantly increased, soil microbial community adaptation. This adaptation of the soil microbial community was positively correlated with the concentration of water extractable organic carbon in the soils prior to imposing the drying and rewetting cycles and/or adding the substrate. The availability of labile carbon may have mediated the ability of microorganisms to synthesise osmolytes in response to drought. We conclude that cover crops may enhance the ability of the soil microbial community to adapt to drought events and mitigate the impact of warming, possibly due to the provision of labile organic carbon for the synthesis of osmolytes.

microbiology↗

Site Effects in Multisite Fetal Brain MRI: Morphological Insights into Early Brain Development

BackgroundMultisite MRI studies have become prevalent given their advantage in revealing reliable biological or clinical findings. Adult and adolescent multisite studies have demonstrated inevitable site-related non-biological effects that introduce bias. However, the site effect on fetal brain MRI remains unknown. PurposeTo identify crucial acquisition factors affecting fetal brain structural measurements and developmental patterns, while assessing the effectiveness of existing harmonization methods in mitigating site effects. Materials and MethodsBetween May 2017 and March 2022, T2-weighted fast spin-echo sequences in-utero MRI were performed in healthy fetuses from prospectively recruited pregnant volunteers on four different scanners at four sites. A generalized additive model (GAM) was used to quantitatively assess site effects, including field strength (FS), manufacture (M), in-plane resolution (R), and slice thickness (ST), on subcortical volume and cortical morphological measurements, including cortical thickness, curvature, and sulcal depth. Growth models were selected to elucidate developmental trajectories of these morphological measurements. Welchs test was performed to evaluate the influence of site effects on developmental trajectories. ComBat-GAM harmonization method was applied to mitigate site-related biases. ResultsThe final analytic sample consisted of 340 MRI scans from 218 fetuses (mean gestational age, 30.1 weeks {+/-} 4.4 [range, 21.7-40 weeks]). GAM results showed that low FS and low spatial resolution led to overestimations in selected brain regions of subcortical volumes and cortical morphological measurements, and cortical measurements were more susceptible to site effects than subcortical volumes. Only the peak cortical thickness in developmental trajectories was significantly influenced by the effects of FS and R. Notably, ComBat-GAM harmonization effectively removed site effects while preserving developmental patterns. ConclusionOur findings pinpointed the key acquisition factors in in-utero fetal brain MRI and underscored the necessity of data harmonization when pooling multisite data for fetal brain morphology investigations.

bioengineering↗

Rapid and prolonged response of oligodendrocyte lineage cells in standard acute cuprizone demyelination model revealed by in situ hybridization

Dietary administration of a copper chelator, cuprizone (CPZ), has long been reported to induce intense and reproducible demyelination of several brain structures such as the corpus callosum (CC) in mice, followed by spontaneous remyelination after drug withdrawal. Despite the widespread use of CPZ as an animal model for demyelinating diseases such as multiple sclerosis (MS), the mechanism by which it induces demyelination and then allows robust remyelination is still unclear. An intensive mapping of the oligodendrocyte (OL) lineage cell dynamics during the de-and remyelination course would be of particular importance for a deeper understanding of this model. Here, using a panel of OL lineage cell markers as in situ hybridization (ISH) probes, including Pdgfra, Plp, Mbp, Mog, Enpp6, combined with immunofluorescence staining of CC1, SOX10, we provide a detailed dynamic profile of OL lineage cells during the entire course of the model from 3.5 days, 1, 2, 3, 4,5 weeks of CPZ treatment, i.e. the demyelination period, as well as after 1, 2, 3, 4 weeks of recovery (drug withdrawal) from 5 weeks of CPZ treatment, i.e. the remyelination period. The result showed an unexpected early death of mature OLs and response of OL progenitor cells (OPCs) in vivo upon CPZ challenge, and a prolonged upregulation of myelin-forming OLs compared to the intact control even 4 weeks after CPZ withdrawal. These data may point to the need to optimize the timing windows for the introduction of pro-remyelination therapies in demyelinating diseases such as MS, and may serve as a basic reference system for future studies of the effects of any intervention on demyelination and remyelination using the CPZ model.

neuroscience↗

ATG8 delipidation is dispensable for plant autophagy

Intracellular recycling via autophagy is governed by post-translational modifications of the autophagy-related (ATG) proteins. One notable example is ATG4-dependent delipidation of ATG8, a process that plays critical but distinct roles in autophagosome formation in yeast and mammals. Here, we aimed to elucidate the specific contribution of this process to autophagosome formation in species representative of evolutionary distant green plant lineages: unicellular green alga Chlamydomonas reinhardtii, with a relatively simple set of ATG genes, and a vascular plant Arabidopsis thaliana, harboring expanded ATG gene families. Remarkably, the more complex autophagy machinery of Arabidopsis rendered ATG8 delipidation entirely dispensable for the maturation of autophagosomes, autophagic flux and related stress tolerance; whereas autophagy in Chlamydomonas strictly depended on the ATG4-mediated delipidation of ATG8. Importantly, we uncovered the distinct impact of different Arabidopsis ATG8 orthologs on autophagosome formation, especially prevalent under nitrogen depletion, providing a new insight into potential drivers behind the expansion of the ATG8 family in higher plants. Our findings underscore the evolutionary diversification of the molecular mechanism governing the maturation of autophagosomes in eukaryotic lineages and highlight how this conserved pathway is tailored to diverse organisms.

plant biology↗

Transcriptional Profiles of Non-neuronal and Immune Cells in Mouse Trigeminal Ganglia

Non-neuronal cells constitute 90-95% of sensory ganglia. These cells play critical roles in modulation of nociceptive signal transmissions by sensory neurons. Accordingly, the aim of this review-study was to identify, profile and summarize TG non-neuronal cell types in naive male mice using published and our own data generated by single-cell RNA sequencing (scRNA-seq), flow cytometry (FC) and immunohistochemistry (IHC). TG contains 5 types of non-neuronal cells: glial, fibroblasts, smooth muscle, endothelial and immune cells. There is agreement among publications for glial, fibroblasts, smooth muscle and endothelial cells. Based on gene profiles, glial cells were classified as Schwann cells and satellite glial cells (SGC). Mpz had dominant expression in Schwann cells, and Fabp7 is specific for SCG. Two types of Col1a2+ fibroblasts located throughout TG were distinguished using gene profiles. TG smooth muscle and endothelial cells representing blood vessels were detected with well recognized markers. Our study split reported single TG immune cell group into 3 types of macrophages and 4 types of neutrophils. Macrophages were located among neuronal bodies and nerve fibers, and were sub-grouped by unique transcriptomic profiles and using Ccr2, Cx3cr1 and Iba1 as markers. S100a8+ neutrophils were located in dura surrounding TG and were sub-grouped by clustering and expressions of Csf3r, Ly6G, Ngp, Elane and Mpo. Overall, generated and summarized here dataset on non-neuronal TG cells could provide essential and fundamental information for studies on cell plasticity, interactomic network between neurons and non-neuronal cells and function during variety of pain conditions in the head and neck region.

neuroscience↗

Cell-type specific optogenetic fMRI on basal forebrain reveals functional network basis of behavioral preference

The basal forebrain (BF) is a complex structure that plays key roles in regulating various brain functions. However, it remains unclear how cholinergic and non-cholinergic BF neurons modulate large-scale functional networks and their relevance in intrinsic and extrinsic behaviors. With optimized awake mouse optogenetic fMRI approach, we revealed optogenetic stimulations of four BF neuron types evoked distinct cell-type specific whole-brain BOLD activations, which could attribute to BF-originated low dimensional structural networks. Additionally, optogenetic activation of VGLUT2, ChAT and PV neurons in BF modulated the preference of locomotion, exploration and grooming, respectively. Furthermore, we uncovered the functional network basis of the above BF-modulated behavioral preference, through a decoding model linking the BF-modulated BOLD activations, low dimensional structural networks, and behavioral preference. To summarize, we decoded functional network basis of differential behavioral preference with cell-type specific optogenetic fMRI on BF, and provided an avenue for investigating mouse behaviors from a whole-brain view.

neuroscience↗

Targeting Ribosome Biogenesis as a Novel Therapeutic Approach to Overcome EMT-related Chemoresistance in Breast Cancer.

Epithelial-to-mesenchymal transition (EMT) contributes significantly to chemotherapy resistance and remains a critical challenge in treating advanced breast cancer. The complexity of EMT, involving redundant pro-EMT signaling pathways and its paradox reversal process, mesenchymal-to-epithelial transition (MET), has hindered the development of effective treatments. In this study, we utilized a Tri-PyMT EMT lineage-tracing model and single-cell RNA sequencing (scRNA-seq) to comprehensively analyze the EMT status of tumor cells. Our findings revealed elevated ribosome biogenesis (RiBi) during the transitioning phases of both EMT and MET processes. RiBi and its subsequent nascent protein synthesis mediated by ERK and mTOR signalings are essential for EMT/MET completion. Importantly, inhibiting excessive RiBi genetically or pharmacologically impaired the EMT/MET capability of tumor cells. Combining RiBi inhibition with chemotherapy drugs synergistically reduced metastatic outgrowth of epithelial and mesenchymal tumor cells under chemotherapies. Our study suggests that targeting the RiBi pathway presents a promising strategy for treating patients with advanced breast cancer. SignificanceThis study uncovers the crucial involvement of ribosome biogenesis (RiBi) in the regulation of epithelial and mesenchymal state oscillations in breast cancer cells, which plays a major role in the development of chemoresistant metastasis. By proposing a novel therapeutic strategy targeting the RiBi pathway, the study offers significant potential to enhance treatment efficacy and outcomes for patients with advanced breast cancer. This approach could help overcome the limitations of current chemotherapy options and address the complex challenges posed by EMT-mediated chemoresistance.

cancer biology↗

Collagen type VI regulates TGFβ bioavailability in skeletal muscle

Collagen VI-related disorders (COL6-RDs) are a group of rare muscular dystrophies caused by pathogenic variants in collagen VI genes (COL6A1, COL6A2, and COL6A3). Collagen type VI is a heterotrimeric, microfibrillar component of the muscle extracellular matrix (ECM), predominantly secreted by resident fibroadipogenic precursor cells in skeletal muscle. The absence or mislocalizatoion of collagen VI in the ECM underlies the non-cell autonomous dysfunction and dystrophic changes in skeletal muscle with an as of yet elusive direct mechanistic link between the ECM and myofiber dysfunction. Here, we conduct a comprehensive natural history and outcome study in a novel mouse model of COL6-RDs (Col6a2-/-mice) using standardized (Treat-NMD) functional, histological, and physiologic parameter. Notably, we identify a conspicuous dysregulation of the TGF{beta} pathway early in the disease process and propose that the collagen VI deficient matrix is not capable of regulating the dynamic TGF{beta} bioavailability at baseline and also in response to muscle injury. Thus, we propose a new mechanism for pathogenesis of the disease that links the ECM regulation of TGF{beta} with downstream skeletal muscle abnormalities, paving the way for developing and validating therapeutics that target this pathway.

neuroscience↗

HiTE: An accurate dynamic boundary adjustment approach for full-length Transposable Elements detection and annotation in Genome Assemblies

Recent advancements in genome assembly have greatly improved the prospects for comprehensive annotation of Transposable Elements (TEs). However, existing methods for TE annotation using genome assemblies are less accurate and robust, requiring extensive manual editing. In addition, the currently available gold-standard TE databases are not comprehensive, even for extensively studied species, highlighting the critical need for an automated TE detection method to supplement existing repositories. In this study, we introduce HiTE, an accurate dynamic boundary adjustment approach designed to detect full-length TEs. The experimental results demonstrate that HiTE identified 932 perfect TE models with a precision of 0.971 on the rice reference genome, which are 142% and 4.42% higher than the state-of-the-art tool RepeatModeler2, respectively. Furthermore, HiTE discovers over 800 novel TIR elements with well-defined structures that are not included in known libraries, enabling the discovery of new insights. We have also implemented a Nextflow version of HiTE to enhance its parallelism reproducibility, and portability.

genomics↗

Evidence for a reproductive sharing continuum in cooperatively breeding mammals and birds: consequences for comparative research

Extreme reproductive skew occurs when a dominant female/male monopolises reproduction within a group of multiple sexually mature females/males. It is sometimes considered an additional, restrictive criterion in the definition of cooperative breeding (i.e., when conspecifics provide parental care to other group members offspring). However, datasets that use this restrictive definition to classify species as cooperative breeders have two critical shortcomings. First, reproductive skew is systematically overestimated by including groups with a single sexually mature female/male when calculating the reproductive output of "dominant" females/males. Second, a lack of reporting on which species are classified based on limited data prevents accounting for uncertainty in classification. Considering these shortcomings, we show that extreme reproductive skew in multi-female and multi-male groups only occurs rarely in species previously classified as cooperative breeders using restrictive definitions (11 mammal species, 12 bird species). We further provide updated datasets on reproductive sharing in multi-female/male groups of cooperatively breeding mammals and birds that allow accounting for classification uncertainty. Our results demonstrate a reproductive sharing continuum even among those cooperatively breeding species argued to exhibit extreme reproductive skew. At the practical level, these findings call for significant changes in datasets that classify species by social systems. At the conceptual level, we suggest that reproductive skew should not be a defining criterion of cooperative breeding.

animal behavior and cognition↗

Thermoprotection by a cell membrane-localized metacaspase in a green alga

Caspases are restricted to animals, while other organisms, including plants possess metacaspases (MCAs), a more ancient and broader class of structurally-related yet biochemically distinct proteases. Our current understanding of plant MCAs is derived from studies in streptophytes, and mostly in Arabidopsis expressing nine MCAs with partly redundant activities. In contrast to streptophytes, most chlorophytes contain only one or two hitherto uncharacterized MCAs, providing an excellent platform for MCA research. Here we investigate CrMCA-II, a single type II MCA from a model chlorophyte Chlamydomonas reinhardtii. Surprisingly, unlike other studied MCAs and similar to caspases, CrMCA-II dimerizes both in vitro and in vivo. Furthermore, activation of CrMCA-II in vivo correlates with the dimerization. Most of CrMCA-II in the cell is present as a zymogen attached to the plasma membrane (PM). Deletion of CrMCA-II by CRISPR/Cas9 compromises thermotolerance leading to increased cell death under heat stress. Adding back either wild-type or catalytically dead CrMCA-II restores thermoprotection, suggesting that its proteolytic activity is dispensable for this effect. Finally, we link the non-proteolytic role of CrMCA-II in thermotolerance to the ability to modulate PM fluidity. Our study reveals an ancient, MCA-dependent thermotolerance mechanism retained by Chlamydomonas and probably lost during the evolution of multicellularity.

plant biology↗

Root branching in salt requires auxin-independent modulation of LBD16 function

Salinity stress constrains lateral root (LR) growth and severely impacts plant growth. Auxin signaling is indispensable for the regulation of LR formation. Nevertheless, the molecular mechanism of how salinity affects root auxin signaling and whether salt would steer alternative pathway(s) to regulate LR development is unknown. Here we show that the auxin-regulated transcription factor LATERAL ORGAN BOUNDARY DOMAIN (LBD)16, known as an essential player for LR development under control conditions, is regulated by an alternative non-canonical pathway under salinity. Salt represses auxin signaling but in parallel activates an upstream transcriptional activator of LBD16, ZINC FINGER OF ARABIDOPSIS THALIANA 6 (ZAT6). ZAT6 modulates the activity of LBD16 to contribute to downstream cell wall remodeling, and promotes LR development under salinity stress. Our study thus shows that root developmental plasticity in response to salt stress is achieved by integration of auxin-dependent repressive and salt-activated auxin-independent pathways converging on LBD16 to modulate root branching modulation under salinity.

plant biology↗