Biology subjects

Gigli-Bisceglia, N.

Publications and source records attributed to Gigli-Bisceglia, N..

10 recordsLinked to original sources

bioRxiv2026

Phytosulfokine signaling modulates salt stress responses and cell wall remodeling in Arabidopsis

Salinity severely impairs plant growth and development. Increasing evidence suggests that the cell wall (CW) plays a central role in salt stress acclimation, not only as a structural barrier but also as a dynamic sensor that activates downstream stress signaling pathways. To identify extracellular factors involved in cell wall remodeling and integrity signaling during salt stress, we performed a comparative proteomic analysis of the Arabidopsis seedling apoplast. Among the proteins that accumulated under salt stress, we focused on three members of the Subtilisin-Like Protease family (SBT1.1, SBT1.6, and SBT5.3), which have previously been implicated in the processing of signaling peptides and CW-associated proteins. Functional analyses revealed that sbt1.1 and sbt5.3 mutants exhibit enhanced lignin deposition under salt stress, suggesting altered CW remodeling during stress application. Given the established role of SBT1.1 in processing PHYTOSULFOKINE (PSK) peptides, we investigated the involvement of PSK signaling in salt stress responses. Mutants lacking the two PSK RECEPTORS (pskr1 pskr2) displayed reduced growth and increased lignification under salt treatment. Exogenous application of PSK attenuated salt-induced responses, including MITOGEN ACTIVATED PROTEIN KINASE 6 (MPK6) phosphorylation, salt stress marker gene expression, and lignin accumulation, ultimately promoting root elongation under salt stress. Furthermore, PSK treatment mitigated salt-induced changes in CW composition. In cell wall integrity (CWI) mutants, PSK treatment failed to restore wild-type root growth under salt stress and induced a pronounced root bending phenotype in fer-4, indicating that CWI signaling influences PSK-mediated root growth responses. Together, these results support a role for PSK signaling in modulating CW-associated responses to salinity stress in Arabidopsis.

plant biology↗

bioRxiv2025

Cell wall integrity and elicitor peptide signaling modulate antimicrobial defense in Arabidopsis via jasmonic acid

Plant cell walls constitute dynamic barriers that are essential for defense against pathogens. The receptor kinase THESEUS1 (THE1) monitors cell wall integrity (CWI) and contributes to pathogen resistance in Arabidopsis, but the underlying mechanisms remain unclear. Here we show that THE1-dependent CWI signaling induces accumulation of the antimicrobial metabolite camalexin upon cell wall damage (CWD) caused by cellulose biosynthesis inhibition or fungal infection. CWD alters THE1 plasma membrane nanodomain organization and involves calcium signaling components that modulate camalexin production. Induction of camalexin requires jasmonic acid (JA)-dependent expression of the transcription factors MYB47 and MYB95. In line with its antagonistic function on CWI signaling, the plant elicitor peptide Pep3 suppresses camalexin biosynthesis downstream of THE1 by inhibiting JA-dependent pathways. Our findings reveal a regulatory network where CWI and Pep3 signaling modulate antimicrobial defense via JA-mediated camalexin production. This network requires independent CWD-induced pathways, providing insights into how plants balance defense activation and suppression in response to cell wall stress.

plant biology↗

bioRxiv2023

Antagonistic Regulation of Arabidopsis Leaf Senescence by SCOOP10 and SCOOP12 Peptides via MIK2 Receptor-Like Kinase

Leaf senescence plays a critical role in a plants overall reproductive success due to its involvement in nutrient remobilization and allocation. However, our current understanding of the molecular mechanisms controlling leaf senescence remains limited. In this study, we demonstrate that the receptor-like kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) functions as a negative regulator of leaf senescence. We report that the SERINE-RICH ENDOGENOUS PEPTIDES 10 and 12 (SCOOP10 and SCOOP12), previously known to physically interact with MIK2, compete with each other to control MIK2-dependent senescence mechanisms. We observed that increased expression of SCOOP10 or the application of exogenous SCOOP10 peptides accelerated leaf senescence in a MIK2-dependent manner. Conversely, SCOOP12 acted as a suppressor of MIK2-dependent senescence. Thus, the SCOOP10-MIK2 and the SCOOP12-MIK2 modules function antagonistically, allowing for fine-tuning the modulation of the leaf senescence process. Our research sheds light on the complex mechanisms underlying leaf senescence and provides valuable insights into the interplay between receptors, peptides, and the regulation of plant senescence.

plant biology↗

bioRxiv2023

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↗

bioRxiv2022

Cell wall extensin arabinosylation is required for root directional response to salinity

Soil salinity is a major contributor to crop yield losses. To improve our understanding of root responses to salinity, we developed and exploit here a real-time salt-induced tilting assay (SITA). This method follows root growth upon both gravitropic and salt challenges, revealing that root bending upon tilting is modulated by salinity, but not by osmotic stress. Next, this salt-specific response was measured in 345 natural Arabidopsis accessions and we discovered a genetic locus, encoding for the cell-wall modifying enzyme EXTENSIN ARABINOSE DEFICIENT TRANSFERASE (ExAD), to be associated with root bending in salt. Extensins are a class of structural cell wall glycoproteins [hydroxyproline-rich glycoproteins (HRGPs)] which are post-translationally modified by O-glycosylation mostly in the form of hydroxyproline (Hyp)-arabinosylation. We show that salt induces ExAD-dependent Hyp-arabinosylation, influencing root bending responses and cell wall thickness. We report that roots of exad mutants, which lack extensin Hyp-Araf4 modifications, display increased root epidermal cell wall thickness and porosity and altered gravitropic root bending in salt, as well as a reduced salt avoidance response. Our results suggest that extensin modification via Hyp-arabinosylation represents a novel salt-specific cellular process that is required for the directional response of roots exposed to salinity.

plant biology↗

bioRxiv2021

THESEUS1 modulates cell wall stiffness and abscisic acid production in Arabidopsis thaliana

Plant cells can be distinguished from animal cells by their cell walls and high turgor pressure. Although changes in turgor and stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. This mechanism monitors the functional integrity of the wall and maintains it through adaptive responses when cell wall damage occurs during growth, development, and interactions with the environment. The adaptive responses include osmo-sensitive-induction of phytohormone production, defence responses as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana. We show that the production of abscisic acid (ABA), the phytohormone modulating turgor pressure and responses to drought, depends on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point and ABA biosynthesis. We identify RECEPTOR-LIKE PROTEIN 12 as a new component of cell wall integrity maintenance controlling cell wall damage-induced jasmonic acid production. Based on the results we propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness. Significance statementPlants need to constantly adapt to a changing environment. This includes responses to biotic and abiotic stress. Key elements influencing the response to abiotic stress are the plant cell walls surrounding all cells and the phytohormone abscisic acid, which influences turgor pressure in plants. Turgor pressure in plant cells is much higher than in animal cells and a key driver of plant growth and development. Here we investigate the mechanism regulating cell wall stiffness and coordinating changes in stiffness and turgor. We characterize key elements of the mechanism and dissect its mode of action. This knowledge will enable us to pursue novel approaches to improve plant resistance to drought stress, which is crucial in a rapidly changing environment.

plant biology↗

bioRxiv2020

Salinity stress-induced modification of pectin activates stress signaling pathways and requires HERK/THE and FER to attenuate the response

Soil salinity is an increasing worldwide problem for agriculture, affecting plant growth and yield. To understand the molecular mechanisms activated in response to salt in plants, we investigated the Catharanthus roseus Receptor like Kinase 1 Like (CrRLK1L) family, which contains well described sensors previously shown to be involved in maintaining and sensing the structural integrity of the cell walls. We found that herk1the1-4 double mutants, lacking the function of the Arabidopsis thaliana Receptor like Kinase HERKULES1 combined with a gain-of-function allele of THESEUS1, phenocopied the phenotypes previously reported in plants lacking FERONIA (FER) function. We report that both fer-4 and herk1the1-4 mutants respond strongly to salt application, resulting in a more intense activation of early and late stress responses. We also show that salt triggers de-methyl esterification of loosely bound pectins, responsible for the activation of several salt response signaling pathways. Addition of calcium chloride or chemically inhibiting pectin methyl esterase (PME) activity reduced activation of the early signaling protein Mitogen Activated Protein Kinase 6 (MPK6) as well as amplitude of salt-induced marker gene induction. MPK6 is required for the full induction of the salt-induced gene expression markers we tested. The sodium specific root halotropism response on the other hand, appears independent of MPK6 or calcium application, and is only mildly influenced by the cell wall sensors FER/HERK1/THE1-4 or alteration of PME activity. We hypothesize a model where salt-triggered modification of pectin requires the functionality of FER alone or the HERK1/THE1 combination to attenuate salt responses. Collectively, our results show the complexity of salt stress responses and salt sensing mechanisms and their connection to cell wall modifications, responsible for several salt response pathways and ultimately plant resilience to salinity.

plant biology↗

bioRxiv2019

Functional characterization of genes mediating cell wall metabolism and responses to plant cell wall integrity impairment

Plant cell walls participate in all plant-environment interactions. Maintaining cell wall integrity (CWI) during these interactions is essential. This realization led to increased interest in CWI and resulted in knowledge regarding early perception and signalling mechanisms active during CWI maintenance. By contrast, knowledge regarding processes mediating changes in cell wall metabolism upon CWI impairment is very limited. To identify genes involved and to investigate their contributions to the processes we selected 23 genes with altered expression in response to CWI impairment and characterized the impact of T-DNA insertions in these genes on cell wall composition using Fourier-Transform Infrared Spectroscopy (FTIR) in Arabidopsis thaliana seedlings. Insertions in 14 genes led to cell wall phenotypes detectable by FTIR. A detailed analysis of four genes found that their altered expression upon CWI impairment is dependent on THE1 activity, a key component of CWI maintenance. Phenotypic characterizations of insertion lines suggest that the four genes are required for particular aspects of CWI maintenance, cell wall composition or resistance to Plectosphaerella cucumerina infection in adult plants. Taken together, the results implicate the genes in responses to CWI impairment, cell wall metabolism and/or pathogen defence, thus identifying new molecular components and processes relevant for CWI maintenance.

plant biology↗

bioRxiv2018

Cellulose biosynthesis inhibition reduces cell cycle activity in a nitrate reductase- and cytokinin-dependent manner

O_LIDuring growth, development and defense, cell wall integrity needs to be coordinated with cell cycle activity. In Saccharomyces cerevisiae, coordination is mediated by the cell wall integrity maintenance mechanism. In plants, little is known how coordination is achieved.\nC_LIO_LIHere we investigated coordination between plant cell wall and cell cycle activity in Arabidopsis thaliana seedlings by studying the impact of cell wall damage (CWD, caused by cellulose biosynthesis inhibition) on cell cycle gene expression, growth, phytohormone (jasmonic acid, salicylic acid, cytokinins) and lignin accumulation.\nC_LIO_LIWe found root growth and cell cycle gene expression are reduced by CWD in an osmo-sensitive manner. trans-zeatin application suppressed the CWD effect on gene expression. Quantification of cytokinins revealed CWD-induced, osmo-sensitive changes in several cytokinins. Expression of CYTOKININ OXIDASE2/DEHYDROGENASE (CKX2) and CKX3, encoding cytokinin-degrading enzymes, was elevated in CWD-exposed seedlings. Genetic studies implicated NITRATE REDUCTASE1/2 (NIA1/2) in the response to CWD. In nia1/2 seedlings CWD induced neither expression of CKX2/3 and cell cycle genes nor accumulation of jasmonic acid, salicylic acid and lignin.\nC_LIO_LIThis suggests that CWD causes increased CKX2/3 expression through a NIA1/2-mediated process. Increased CKX expression seems to cause changes in cytokinin levels, leading to reduced cell cycle gene expression.\nC_LI

plant biology↗

bioRxiv2017

Pattern-Triggered Immunity And Cell Wall Integrity Maintenance Jointly Modulate Plant Stress Responses

Plant cells are surrounded by walls, which must often meet opposing functional requirements during plant growth and defense. The cells meet them by modifying wall structure and composition in a tightly controlled and adaptive manner. The modifications seem to be mediated by a dedicated cell wall integrity (CWI) maintenance mechanism. Currently the mode of action of the mechanism is not understood and it is unclear how its activity is coordinated with established plant defense signaling. We investigated responses to induced cell wall damage (CWD) impairing CWI and the underlying mechanism in Arabidopsis thaliana. Interestingly inhibitor- and enzyme-derived CWD induced similar, turgor-sensitive stress responses. Genetic analysis showed that the receptor-like kinase (RLK) FEI2 and the mechano-sensitive, plasma membrane-localized Ca2+- channel MCA1 function downstream of the THE1 RLK in CWD perception. Phenotypic clustering with 27 genotypes identified a core group of RLKs and ion channels, required for activation of CWD responses. By contrast, the responses were repressed by pattern-triggered immune (PTI) signaling components including PEPR1 and 2, the receptors for the immune signaling peptide AtPep1. Interestingly AtPep1 application repressed CWD-induced phytohormone accumulation in a PEPR1/2-dependent manner. These results suggest that PTI suppresses CWD-induced defense responses through elicitor peptide-mediated signaling during defense response activation. If PTI is impaired, the suppression of CWD-induced responses is alleviated, thus compensating for defective PTI.\n\nSignificance statementStress resistance and plant growth determine food crop yield and efficiency of bioenergy production from ligno-cellulosic biomass. Plant cell walls are essential elements of the biological processes, therefore functional integrity of the cell walls must be maintained throughout. Here we investigate the plant cell wall integrity maintenance mechanism. We characterize its mode of action, identify essential signaling components and show that the AtPep1 signaling peptide apparently coordinates pattern triggered immunity (PTI) and cell wall integrity maintenance in plants. These results suggest how PTI and cell wall modification coordinately regulate biotic stress responses with plants possibly compensating for PTI impairment through enhanced activation of stress responses regulated by the CWI maintenance mechanism.

plant biology↗