Biology subjects

Maia, T.

Publications and source records attributed to Maia, T..

5 recordsLinked to original sources

bioRxiv2026

AtNHR2A and AtNHR2B participate in unconventional protein secretion in response to environmental stress

The Arabidopsis thaliana nonhost resistance proteins 2A (AtNHR2A) and 2B (AtNHR2B) play crucial roles in plant immunity as the single mutants Atnhr2a and Atnhr2b and the double mutant Atnhr2bAtnhr2a are susceptible to the non-adapted pathogen Pseudomonas syringae pv. tabaci that is unable to infect wild-type Col-0 plants. The localization of fluorescent versions of AtNHR2A and AtNHR2B to compartments of the endomembrane system together with their interaction with secreted proteins suggested a function in endomembrane-mediated secretory processes participating in plant immunity. Comparative apoplastic proteomics analysis between wild type Col-0 and the double mutant Atnhr2bAtnhr2a after treatment P. syringae pv. tabaci, revealed that AtNHR2A and AtNHR2B are indeed required for the secretion of proteins containing N-terminal signal peptides that occurs through the conventional protein secretion pathway. In this work, we leveraged these apoplastic proteomics datasets to identify proteins lacking N-terminal signal peptide and expected to be secreted through unconventional secretion pathway(s). We discovered that AtNHR2A and AtNHR2B are also required for the secretion of proteins through an unconventional secretion pathway that, intriguingly, included proteins previously associated with abiotic stress. These findings led us to define the subcellular dynamics of AtNHR2A and AtNHR2B, and through co-localization analyses and the use of vesicle trafficking inhibitors, we uncovered their trafficking pathways transitioning through Golgi-dependent and Golgi-independent pathways to ultimately reach the central vacuole. Our findings suggest that AtNHR2A and AtNHR2B participate in a multivesicular bodies-vacuole-mediated unconventional secretion pathway that results in the release of proteins involved in plant responses to environmental stresses.

plant biology↗

bioRxiv2026

Organ identity shapes autophagy dynamics and selectivity in plants

Plants, with their unique evolutionary trajectory and complex physiological adaptations, have developed organ-specific mechanisms to cope with various environmental stresses. Autophagy, an essential catabolic process, plays an important role in maintaining plant growth, immunity, and overall fitness. In this study, we reveal the spatio-temporal dynamics of autophagic responses in Arabidopsis thaliana roots and shoots under different stress conditions, including AZD8055 treatment and carbon and nitrogen depletion. Our findings demonstrate that roots exhibit stronger autophagic activity than shoots under all three conditions, highlighting the unique adaptations of these two organs. Furthermore, we dissect the selectivity of autophagy in targeting organelles, revealing immediate, delayed, and no uptake categories. Additionally, we observe organelles coexisting within autophagic bodies, shedding light on the complexity of cargo selection. This study enhances our understanding of plant specific autophagy dynamics, emphasizing its role in sustaining the source-sink functions and offering insights into plant adaptation to diverse stressors.

plant biology↗

bioRxiv2025

Germination-stage transcriptomics of the grapevine rust fungus Neophysopella tropicalis reveals protein effectors with plant immunity-suppressing activity

Germination of urediniospores represents a critical early stage in the life cycle of Neophysopella tropicalis, the causal agent of Asian grapevine leaf rust in Brazil. Rust fungi deploy diverse effector proteins to manipulate host immunity and establish infection. This study identified and functionally characterized secreted proteins expressed during early fungal development using RNA-seq analysis of in-vitro-germinated urediniospores. Effectorome analysis revealed 386 putative secreted proteins with hallmarks of fungal effectors, designated as N. tropicalis effector candidates (NtECs). Fifteen highly expressed NtECs were selected for expression profiling by RT-qPCR across infection stages. Fluorescence microscopy with WGA-FITC staining defined key phases of pathogenesis. Although identified during germination, seven NtECs showed elevated transcript accumulation during the penetration and early biotrophic phases, suggesting roles in host entry and establishment. To evaluate immune-suppressing activity, nine NtECs were delivered into Nicotiana benthamiana using the Type III Secretion System of Pseudomonas fluorescens EtHAn. Three effectors (NtEC-05, -09, and -10) strongly suppressed AvrB-triggered cell death, and three others (NtEC-11, -12, and -13) showed moderate suppression. This work provides the first characterization of N. tropicalis effectors, offering insights into rust pathogenesis and supporting future effector-informed strategies for grapevine resistance. HighlightThe grapevine rust fungus Neophysopella tropicalis deploys effectors whose expression aligns with early infection and immune suppression, revealing key virulence mechanisms and guiding effector-informed strategies for grapevine rust resistance.

pathology↗

bioRxiv2025

Transcriptome Profiling of Resistance Genes Analogs in Soybean's Cross-Tolerance to Water Limitation and Rust Stress

Asian soybean rust (ASR), caused by Phakopsora pachyrhizi, is the most destructive foliar disease of soybean, with yield losses up to 90%. With climate change intensifying drought and expanding disease incidence, it is critical to understand how combined abiotic and biotic stresses influence plant defense. We investigated the transcriptomic response of a susceptible soybean cultivar to ASR infection under normal and water-limited conditions at four infection stages (12, 24, 72, and 192 hours after-inoculation). We observed a biphasic expression of defense-related genes, particularly resistance gene analogs (RGAs), with an early peak at 12 hours and a late resurgence at 192 hours. Combined stress induced a greater number of differentially expressed genes (DEGs) than rust alone, especially at early infection. Among the differentially expressed RGAs (RGADEs), over 64% belonged to the TM-LRR class, and NBS-LRR genes were the most enriched at known ASR resistance loci, particularly Rpp2. Water limitation strongly modulated gene expression at late stages, revealing stress-specific transcriptional reprogramming. These findings reveal cross-tolerance mechanisms in soybean, highlight the temporal dynamics of RGADEs under dual stress, and provide targets for developing cultivars with improved resilience to both rust and water scarcity.

plant biology↗

bioRxiv2019

Androgen-regulated transcription of ESRP2 drives alternative splicing patterns in prostate cancer

Prostate is the most frequent cancer in men. Prostate cancer progression is driven by androgen steroid hormones, and delayed by androgen deprivation therapy (ADT). Androgens control transcription by stimulating androgen receptor (AR) activity, yet also control pre-mRNA splicing through less clear mechanisms. Here we find androgens regulate splicing through AR-mediated transcriptional control of the epithelial-specific splicing regulator ESRP2. Both ESRP2 and its close paralog ESRP1 are highly expressed in primary prostate cancer. Androgen stimulation induces splicing switches in many endogenous ESRP2-controlled mRNA isoforms, including a key splicing switch in the metastatic regulator FLNB which is associated with disease relapse. ESRP2 expression in clinical prostate cancer is repressed by ADT, which may thus inadvertently dampen epithelial splice programmes. Supporting this, FLNB splicing was reciprocally switched by the AR antagonist bicalutamide (Casodex(R)). Our data reveal a new mechanism of splicing control in prostate cancer with important implications for metastatic disease progression.\n\nKey pointsO_LITranscriptional regulation of ESRP2 by the androgen receptor controls splice isoform patterns in prostate cancer cells.\nC_LIO_LISplicing switches regulated by the androgen-ESRP2 axis include a splice isoform in the FLNB gene that is a known metastatic driver.\nC_LIO_LIBoth ESRP1 and ESRP2 are highly expressed in prostate cancer tissue.\nC_LIO_LIEctopic expression of ESRP1 and 2 inhibits prostate cancer cell growth.\nC_LIO_LIBy repressing ESRP2 expression androgen deprivation therapy (ADT) may dampen epithelial splicing programmes to inadvertently prime disease progression towards metastasis.\nC_LI

molecular biology↗