Biology subjects

Quintero, H.

Publications and source records attributed to Quintero, H..

5 recordsLinked to original sources

bioRxiv2025

Globally unified analysis of riverine eDNA reveals common associations of fish biodiversity with drainage characteristics

Freshwater biodiversity is declining at a pace that outstrips the capacity of existing monitoring approaches both in temporal and spatial dimensions, highlighting the urgent need for rapid and scalable assessment and attribution of biodiversity states and changes. Here, we present one of the first global assessments and unified analyses of riverine fish biodiversity using environmental DNA (eDNA) collected from 1818 sites across 113 river systems. We quantified species richness, functional redundancy, phylogenetic diversity, and genetic sequence diversity, and related them to drainage characteristics. Our results showed that eDNA effectively captured global patterns of multi-faceted riverine fish biodiversity and disentangled the roles of climate and human activities in shaping biodiversity-area relationships. Catchments in warmer climates consistently enhanced biodiversity accumulation with area, while higher human activity intensity weakened this scaling. Species richness, functional, and genetic sequence diversity exhibited stronger negative responses to human activities in larger catchments. In contrast, phylogenetic diversity showed the strongest negative effects in smaller catchments with these impacts diminishing as catchment area increased, highlighting the facet-dependent nature of biodiversity responses to environmental gradients. Our findings demonstrate the power of eDNA-based datasets for harmonized, multi-faceted biodiversity assessments, offering a scalable approach for detecting and attributing biodiversity change and informing conservation strategies under accelerating global change.

ecology↗

bioRxiv2025

Integrated reanalysis of global riverine fish eDNA datasets shows robustness and congruence of biodiversity conclusions

The analysis of environmental DNA (eDNA) has revolutionized biodiversity assessments in aquatic ecosystems, enabling non-invasive monitoring of fish communities across diverse regions. However, the global comparability of these eDNA datasets remains ambiguous due heterogeneous sampling protocols and bioinformatic workflows across studies, particularly regarding the robustness of their conclusions on biodiversity assessments. Here, we conducted a meta-analysis of 58 riverine fish eDNA metabarcoding datasets, covering 1,818 sampling sites worldwide, to evaluate the robustness of eDNA-derived biodiversity patterns. We found that species richness estimates and metrics of community structure derived under a common bioinformatic workflow were overall consistent with those of original analyses, despite the relatively high variability in bioinformatic analyses in the respective original studies. Contrastingly, congruence of species identity varied more extensively across datasets, mostly reflecting different completeness and regional relevance of reference databases. Restricting taxonomic assignment to basin-specific species pools improved species identification accuracy, while datasets lacking publicly accessible or well-curated reference data were more prone to mismatches. Year of sampling had a positive effect on taxonomic congruence, such that more recent studies showed increased robustness, also reflecting improved reference database coverage and enhanced species-level identification over time and overall method congruence in more recent years. Overall, the suitability and potential of eDNA for global biodiversity monitoring is corroborating overall robust biodiversity estimates, irrespective of the bioinformatic approaches. Our study underlines the effectiveness and need of further harmonization of bioinformatic workflows and strengthened region-specific reference databases for improved taxonomic resolution and comparability across studies.

ecology↗

bioRxiv2024

Stress-induced mitochondrial fragmentation in endothelial cells disrupts blood-retinal barrier integrity causing neurodegeneration.

Increased vascular leakage and endothelial cell (EC) dysfunction are major features of neurodegenerative diseases. Here, we investigated the mechanisms leading to EC dysregulation and asked whether altered mitochondrial dynamics in ECs impinge on vascular barrier integrity and neurodegeneration. We show that ocular hypertension, a major risk factor to develop glaucoma, induced mitochondrial fragmentation in retinal capillary ECs accompanied by increased oxidative stress and ultrastructural defects. Analysis of EC mitochondrial components revealed overactivation of dynamin-related protein 1 (DRP1), a central regulator of mitochondrial fission, during glaucomatous damage. Pharmacological inhibition or EC-specific in vivo gene delivery of a dominant negative DRP1 mutant was sufficient to rescue mitochondrial volume, reduce vascular leakage, and increase expression of the tight junction claudin-5 (CLDN5). We further demonstrate that EC-targeted CLDN5 gene augmentation restored blood-retinal-barrier integrity, promoted neuronal survival, and improved light-evoked visual behaviors in glaucomatous mice. Our findings reveal that preserving mitochondrial homeostasis and EC function are valuable strategies to enhance neuroprotection and improve vision in glaucoma.

neuroscience↗

bioRxiv2024

Dietary resilience of coral reef fishes to habitat degradation

The ability of consumers to adjust their diet in response to resource shifts is a key mechanism allowing the persistence of populations and underlying species adaptive capacity. Yet on coral reefs, one of the marine habitats most vulnerable to global change, the extent to which species alter their diet remains poorly understood. Here, we integrated DNA-based gut content analyses (metabarcoding), otolith analysis, body condition, and field surveys to test how diet can mediate effects of habitat degradation on two invertivorous fishes: Chaetodon capistratus, a browser, and Hypoplectrus puella, an active predator. Metabarcoding revealed significant dietary variation in both species across a habitat gradient. However, the response was more pronounced in the browser, whose diet was anthozoan-dominated on healthy reefs, whereas annelid-dominated on degraded reefs. We found reduced growth and body condition on degraded reefs in the browser but not the active predator. Our results reveal that dietary versatility can serve as a mechanism to cope with degraded environments, but that species differ as to whether these changes are sufficient to buffer from changes in habitat. We detected intraspecific dietary variation across sites that suggests food webs and energy flow differ at relatively small scales between healthy and degraded reefs.

ecology↗

bioRxiv2021

Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation through N-formyl peptide receptor 2 in a chronic murine model of Chagas disease

Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America and is widely distributed worldwide because of migration. After years of infection and in the absence of treatment, the disease progresses from an acute and asymptomatic phase to a chronic inflammatory cardiomyopathy, leading to heart failure and death. An inadequate balance in the inflammatory response is involved in the progression of chronic Chagas cardiomyopathy. Current therapeutic strategies cannot prevent or reverse the heart damage caused by the parasite. Aspirin-triggered resolvin D1 (AT-RvD1) is a pro-resolving mediator of inflammation that acts through N-formyl peptide receptor 2 (FPR2). AT-RvD1 participates in the modification of cytokine production, inhibition of leukocyte recruitment and efferocytosis, macrophage switching to a nonphlogistic phenotype, and the promotion of healing, thus restoring organ function. In the present study, AT-RvD1 is proposed as a potential therapy aid to regulate the pro-inflammatory state during the chronic phase of Chagas disease. C57BL/6 wild-type and FPR2 knock-out mice chronically infected with T. cruzi were treated for 20 days with 5 g/kg/day AT-RvD1, 30 mg/kg/day benznidazole, or the combination of 5 g/kg/day AT-RvD1 and 5 mg/kg/day benznidazole. At the end of treatment, changes in the immune response, cardiac tissue damage, and parasite load were evaluated. The administration of AT-RvD1 in the chronic phase of T. cruzi infection regulated the inflammatory response both at the systemic level and in the cardiac tissue, and it reduced cellular infiltrates, cardiomyocyte hypertrophy, fibrosis, and the parasite load in the heart tissue. Thus, AT-RvD1 was shown to be an attractive therapeutic due to its regulatory effect on the inflammatory response at the cardiac level and its ability to reduce the parasite load during chronic T. cruzi infection, thereby preventing the chronic cardiac damage induced by the parasite. Author SummaryChagas disease is prevalent in Latin America and is widely distributed worldwide due to migration. If the parasite is left untreated, the disease progresses from an acute symptomless phase to chronic myocardial inflammation, which can cause heart failure and death years after infection. Imbalances in the inflammatory response are related to this progression. Current treatments cannot prevent or reverse the cardiac damage produced by the parasite. Aspirin-triggered resolvin D1, also named AT-RvD1, can modify cellular and humoral inflammatory responses leading to the resolution of inflammation, thus promoting healing and restoring organ function. In this study, AT-RvD1, in an N-formyl peptide receptor 2 (FPR2)-dependent manner, was shown to regulate local and systemic inflammation and decrease cellular infiltration in the heart tissue of mice chronically infected with the parasite and reduce cardiac hypertrophy and fibrosis. Importantly, AT-RvD1 was able to decrease parasite load in the infected hearts. Thus, this research indicates that At-RvD1 treatment is a potential therapeutic strategy that offers an improvement on current drug therapies.

microbiology↗