Biomedical subjects

Javier Cabrera

Publications and source records attributed to Javier Cabrera.

6 recordsLinked to original sources

PubMed2026

Penicillium melinii promotes root growth through subtle host reprogramming across model and crop species.

Root development is highly responsive to microbial interactions, yet the mechanisms by which beneficial fungi promote root growth remain incompletely understood. Here, we identified Penicillium melinii 'isolate 2' through a screen of endophytic fungi isolated from Arabidopsis and characterized it as a promoter of root development in both Arabidopsis and crop species. We combined phenotyping in vitro, rhizotron, greenhouse and field assays with reporter and mutant analyses, transcriptomics, phytohormone profiling and sequencing and annotation of the fungal genome to investigate the basis of this interaction. P. melinii consistently stimulated root growth and modified root architecture across experimental systems and host species. These effects were associated with subtle but reproducible host transcriptional reprogramming, supporting a model in which the fungus fine-tunes endogenous developmental programmes rather than broadly perturbing stress or growth pathways. Genetic and reporter analyses further suggested that this interaction modulates root branching through localized developmental reprogramming. Genomic analysis provided a framework for understanding the fungal traits associated with this beneficial interaction. The conservation of the response across model and crop species supports the relevance of P. melinii as both a useful experimental system to study beneficial plant-fungus interactions and a promising candidate for improving root traits and crop performance.

Penicillium melinii↗

PubMed2025

Root growth promotion by Penicillium melinii : mechanistic insights and agricultural applications.

This study characterizes Penicillium melinii , an endophytic fungus isolated from Arabidopsis thaliana roots, as a plant growth-promoting fungus with potential use as a model to study root development and as a biostimulant for sustainable agriculture. Although endophytes are known to promote plant growth, the underlying molecular mechanisms often remain poorly understood. Here, we aimed to elucidate how P. melinii enhances root system development and to assess its applicability across different crops. Phenotypic assays were conducted in Arabidopsis, quinoa and tomato under in vitro , greenhouse and field conditions. Root architecture and biomass were quantified using image-based phenotyping. Transcriptomic and phytohormone profiling assessed plant responses, and fungal genome sequencing coupled with secretome analysis was used to identify candidate effectors and metabolic traits. P. melinii consistently promoted root growth and increased plant biomass across species and environments, both in vitro and in the greenhouse. In tomato field trials, this translated into a significant increase in yield. The fungus colonized root surfaces without vascular penetration and triggered a mild transcriptomic response: early activation of stress-response genes followed by their attenuation and sustained upregulation of auxin-related pathways. Notably, the interaction modulates the SLR-ARF-LBD pathway and the number of pre-branch sites probably through increased auxin signalling in the oscillation zone. Additional hormonal changes were limited and mainly associated with the attenuation of the plant response to microorganisms. P. melinii enhances lateral root formation through a subtle molecular and metabolic dialogue with the host plant, underscoring its relevance as a model for studying root developmental plasticity. Its strong and reproducible growth-promoting effect, demonstrated with different fungal strains and under controlled and field conditions, supports its potential as a biostimulant for sustainable crop production.

Journal Article↗

PubMed2005

Double bootstrapping a tolerance limit.

We consider the problem of constructing tolerance limits in the context of a one-way random effects model The usual parametric method for calculating tolerance intervals is based on the normality assumption. However, in practice, we frequently observe nonnormally distributed data. We propose the use of the double bootstrap (or nested bootstrap) method to estimate tolerance limits, which allows us to relax the normality assumption.

Confidence Intervals↗

PubMed2003

Melatonin prevents apoptosis and enhances HSP27 mRNA expression induced by heat shock in HL-60 cells: possible involvement of the MT2 receptor.

Previous studies have reported that melatonin protects cells and tissues against stressful stimuli. In the present study using HL-60 cells, we show that cells acquire increased resistance to apoptosis normally induced by heat shock when they are incubated with melatonin. This effect of melatonin is saturable at nanomolar concentrations and appears to be mediated by the MT2 subtype melatonin receptor. The high affinity melatonin receptor agonist, 2-iodomelatonin, reproduced the melatonin effect while it was fully blocked by the selective MT2 antagonist 4-phenyl-2-propionamidotetraline. The melatonin response to heat shock-induced apoptosis was pertussis toxin sensitive and, interestingly, the non-selective MT1/MT2 melatonin receptor ligand luzindole was found to display agonistic activity. Furthermore, we provide evidence that melatonin enhanced HSP27 mRNA expression as a result of heat shock - HSP27, is known to play an important role in the defense of cells against apoptosis induced by stressful agents. Together, these results demonstrate that melatonin, likely via receptor mechanisms, interferes with the apoptotic pathway activated by heat shock.

Apoptosis↗

PubMed2000

Melatonin suppresses autoxidation and hydrogen peroxide-induced lipid peroxidation in monkey brain homogenate.

OBJECTIVES: Melatonin, the major secretory product of the pineal gland, is known as an effective antioxidant and neuroprotector. Its neuroprotective actions and mechanisms have been documented in a variety of rodent brain models. However, little is known of melatonin's antioxidative capacity in the brain of primates. Herein, we investigated whether melatonin would suppress autoxidation and exogenous hydrogen peroxide-induced lipid peroxidation in monkey cerebral cortical homogenates. MATERIALS AND METHODS: The monkey brain was dissected during routine autopsy and immediately frozen at -80 degrees C until the experiment. A sample of cerebral cortex (50 mg) was homogenized in 1 ml ice cold phosphate buffer (20 mM, pH 7.4) at 0-4 degrees C. Four different treatments of cerebral cortical homogenates were performed: 1) homogenates incubated in a water bath at different temperatures (4 degrees C, 25 degrees C or 37 degrees C, respectively) for two hours to induce autoxidation; 2) homogenates co-incubated with different concentrations of melatonin at 37 degrees C for 2 hours; 3) homogenates co-incubated with 1 mM vitamin C and different concentrations of hydrogen peroxide at 37 degrees C for 1 hour to induce membrane lipid peroxidation; 4) homogenates incubated with different concentrations of melatonin and 1 mM H2O2 plus 1 mM vitamin C. After incubation, homogenates were analyzed for products of lipid peroxidation (malondialdehyde and 4-hydroxy-alkenals). RESULTS: The levels of lipid peroxidation products significantly increased in monkey cerebral cortical homogenates as a consequence of autoxidation or after the addition of H2O2 plus vitamin C. Melatonin not only suppressed the increase in lipid peroxidation induced by H2O2 plus vitamin C but also inhibited lipid breakdown resulting from autoxidation. The concentrations of melatonin required to suppress lipid peroxidation resulting from autoxidation or induced by exogenous oxidants in monkey cerebral cortical homogenates were in the same dose range. CONCLUSION: The results show for the first time that melatonin functions as an antioxidant and neuroprotector in primate brain tissue as was observed previously in rodent brain. The data provide information supporting the use of melatonin in the treatment of neurodegenerative disorders that involve oxidative damage to brain lipids.

Journal Article↗

PubMed2000

Melatonin prevents oxidative damage to protein and lipid induced by ascorbate-Fe(3+)-EDTA: Comparison with glutathione and alpha-tocopherol.

OBJECTIVES: The ability of melatonin to protect protein and lipid against oxidative damage induced by an ascorbate-Fe(3+)-EDTA (AFE) system which generates the hydroxyl radical was investigated using bovine serum albumin (BSA) and phosphatidylcholine (PC) liposomes, respectively, and compared with the protective effects of reduced glutathione and alpha-tocopherol. The comparison study was also performed using PC liposomes containing BSA. METHODS: BSA, PC liposomes or their mixtures were exposed to the HO.-generating system of AFE composed of 0.1 mM EDTA-Fe(3+) and 0.5 mM ascorbate in 0.1 M phosphate buffer, pH 7.4, at 37 degrees C for 1 h. Oxidative damage of BSA was determined by measuring the carbonyl content and the fragmentation of protein by the reaction with dinitrophenylhydrazine (DNPH) and electrophoresis, respectively. Lipid peroxidation of PC liposomes was indicated by the quantity of malondialdehyde and 4hydroxyalkenals. RESULTS: Melatonin inhibited protein damage as indicated by the reduced formation of carbonyl groups and fragmentation of BSA by AFE as effectively as did glutathione while alpha-tocopherol was ineffective. Melatonin also prevented lipid peroxidation to the same extent as did alpha-tocopherol in PC liposomes. CONCLUSION: Both BSA and PC lipid exposed to AFE are effectively protected by melatonin while hydrophilic glutathione and hydrophobic alpha-tocopherol are as effective as melatonin only in one target, i.e., BSA or PC lipid, respectively.

Journal Article↗