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Gabriel, R.

Publications and source records attributed to Gabriel, R..

6 recordsLinked to original sources

Global failure to track international biodiversity targets on islands

Islands harbour exceptional biodiversity but face severe threats, making their conservation crucial to achieving the goals and targets of the Kunming-Montreal Global Biodiversity Framework. We therefore evaluated whether existing indicators can track progress toward the Framework's 23 targets across islands worldwide. We screened 504 biodiversity and socioeconomic indicators from the official framework and other global initiatives, retaining 47 indicators. Historical time series from 1950 onward were modelled and projected to 2030. Indicators were also classified using the Driver-Pressure-State-Impact-Response (DPSIR) and Theory of Change (ToC). Results showed uneven progress: eight targets improved across all available indicators, while ten displayed conflicting trends. Nearly half of the indicators focused on policy and management responses showed improvement, whereas trends in biodiversity pressures and states were mixed. Critically, 15 of 23 targets (65%) lacked a suitable headline indicator, and five targets had no indicator at all. Notably, Targets 2 and 8, addressing ecosystem restoration and climate change impacts, respectively, lacked island indicators entirely. Over half of the available indicators (29 of 47; 62%) were reported at the national level, limiting their applicability to subnational island jurisdictions and potentially obscuring differences between mainland and island conditions. Most targets also lacked quantitative objectives, limiting evaluation of whether the rate of change is sufficient to meet the targets by 2030. We recommend island-level reporting, island-specific indicators, and quantitative benchmarks tailored to island needs.

ecology↗

SELF-PRUNING 5G interplays with age and gibberellin pathways downstream of SlCOL1 to orchestrate photoperiodic tomato flowering

Tomato (Solanum lycopersicum) is classified as a day-neutral plant, whereas its wild relatives exhibit delayed flowering under long day (LD) conditions due to higher activity of the SELF-PRUNING 5G (SP5G). In Arabidopsis thaliana, CONSTANS (CO) activates FLOWERING LOCUS T (FT), a homolog of SP5G, but whether and how CO integrates with SP5G in tomato flowering was unclear. Here, we demonstrate that SlCOL1 (the tomato CO homolog) delays flowering by directly activating SP5G in a PHYTOCHROME B1 (PHYB1)-dependent manner. Importantly, genetic and molecular analyses combining a photoperiod-responsive tomato line carrying the wild SP5G allele from S. pennellii, together with SlCOL1 and flowering-pathway mutants, revealed synergistic crosstalk among the photoperiodic SlCOL1-SP5G module, age-dependent pathway (mediated mainly by the microRNA156-SlSBP module), gibberellin (GA) pathway, and SINGLE FLOWER TRUSS (SFT) pathway. Mechanistically, we show that SP5G forms a complex with miR156-targeted SlSBP13 to directly regulate SFT expression, and that GA may interfere with SP5G activity. Together, these findings revealed a coordinated network that integrates multiple flowering signals to modulate both shared and pathway-specific targets. Our findings provide a significant advance in understanding the molecular regulation of tomato flowering and offer promising avenues for breeding strategies optimized for diverse environmental conditions and latitudes.

plant biology↗

Single cell transcriptomic profiling of human brain organoids reveals developmental timing- and cell-type-specific vulnerabilities induced by NRXN1 CNVs in schizophrenia

De novo mutations and copy number deletions in NRXN1 (2p16.3) pose a significant risk for schizophrenia (SCZ). It is unclear how NRXN1 deletions impact cortical development in a cell type-specific manner and disease background modulates these phenotypes. Here, we leveraged human pluripotent stem cell-derived forebrain organoid models carrying NRXN1 heterozygous deletions in isogenic and SCZ patient genetic backgrounds and conducted single-cell transcriptomic analysis over the course of brain organoid development from 3 weeks to 3.5 months. Intriguingly, while both deletions similarly impacted molecular pathways associated with ubiquitin-proteasome system, alternative splicing, and synaptic signaling in maturing glutamatergic and GABAergic neurons, SCZ-NRXN1 deletions specifically perturbed developmental trajectories of early neural progenitors and accumulated disease-specific transcriptomic signatures. Using calcium imaging, we found that both deletions led to long-lasting changes in spontaneous and synchronous neuronal networks, implicating synaptic dysfunction. Our study reveals developmental-timing- and cell-type-dependent actions of NRXN1 deletions in unique genetic contexts.

neuroscience↗

The influence of biotic and abiotic drivers on arthropod co-occurrence network topology in native forest remnants in the Azores

Island biota are in imminent threat from anthropogenic impacts. Of these impacts the negative effects of exotic species on the taxonomic and functional diversity of the local fauna are of particularly major concern. Aside from their impact on the diversity of native fauna, exotics may also have a detrimental effect on native interactions which, in turn, can destabilise ecological networks. Species co-occurrence networks are used to predict ecological interaction networks and utilised as tools to assess environmental impacts on community structure. Here, we investigate the topological differences of the arthropod co-occurrence networks among native forest fragments from seven Azorean islands and reveal the influence of the abiotic environment and exotic species on these networks. We found that co-occurrence networks were sensitive to environmental and community dissimilarities, showing a clear separation between islands and pinpointed differences between indigenous and exotic networks. Most exotics are little connected and exotic networks have a large proportion of unconnected species. The resulting decreased connectance and the increased modularity with the increase of the proportions of exotics in the networks suggests that most exotics have too low prevalence to show associations with other species, and only a few dominants drive co-occurrences. Moreover, the proportion of negative links, as indicators of competition, did not increase with the increase of exotics in the habitats, suggesting that exotics occupied empty niches when they colonised native forest remnants. However, when the theoretical networks consisting of only indigenous species were investigated both the number of negative associations and modularity increased with the increase of exotics, suggesting obscure competition and processes of network degradation. Since our study provides ample evidence for the usefulness of co-occurrence network analysis in studying island ecosystems, we recommend the use of this tool for ecosystem assessments, early warning systems and decision making in island biodiversity conservation. Significance statementGlobal anthropogenic biodiversity decline affects islands to a disproportionately greater extent than other ecosystems. One major cause of declining island biodiversity is the spread of exotic species which may overcompete and replace native biota. In this study, we show, by using arthropod species co-occurrence networks from the Azorean archipelago, that species association patterns reflect both abiotic and biotic impacts and that the increasing proportion of exotics in an ecosystem seemingly has little impact on association networks at large. However, when the effects on the association network of solely indigenous species were scrutinised, signs of network degradation were observed, suggesting an obscure, and most likely slow, negative impact of exotics on native arthropod assemblages. This disintegration of the co-occurrence networks can be the first sign of disappearing interaction links which, in turn, may jeopardise ecosystem function and can lead to regime shifts. In this work, we used a unique long-term dataset collected across the islands of the Azorean archipelago with standardised methodology. We built on the deep knowledge gathered over two decades on the ecology of species, as well as on the ongoing processes shaping the islands arthropod fauna, yet took a novel methodological approach and disentangled hidden ecological processes of great ecological and conservation concern.

ecology↗

Loss of Neurodevelopmental Gene CASK Disrupts Neural Connectivity in Human Cortical Excitatory Neurons

Loss-of-function (LOF) mutations in CASK cause severe developmental phenotypes, including microcephaly with pontine and cerebellar hypoplasia, X-linked intellectual disability, and autism. Unraveling the pathogenesis of CASK-related disorders has been challenging due to limited human cellular models to study the dynamic roles of this molecule during neuronal and synapse development. Here, we generated CASK knockout (KO) isogenic cell lines from human embryonic stem cells (hESCs) using CRISPR/Cas9 and examined gene expression, morphometrics, and synaptic function of induced neuronal cells during development. While young (immature) CASK KO neurons show robust neuronal outgrowth, mature CASK KO neurons displayed severe defects in synaptic transmission and synchronized burst activity without compromising neuronal morphology and synapse numbers. In developing human cortical neurons, CASK functioned to promote both structural integrity and establishment of cortical excitatory neuronal networks. These results lay the foundation for future studies to identify suppressors of such phenotypes relevant to human patients. HighlightsO_LICASK LOF mutations increase neuronal complexity in immature developing neurons C_LIO_LICASK LOF does not alter synapse formation and neurite complexity in mature neurons C_LIO_LISynaptic transmission and network synchronicity are compromised in CASK KO neurons C_LIO_LIDifferential gene expression analysis reveals enrichment of synaptic gene networks in mature CASK KO neurons C_LI

neuroscience↗

Development of genetic tools for the thermophilic filamentous fungus Thermoascus aurantiacus

BackgroundFungal enzymes are vital for industrial biotechnology, including the conversion of plant biomass to biofuels and bio-based chemicals. In recent years, there is increasing interest in using enzymes from thermophilic fungi, which often have higher reaction rates and thermal tolerance compared to currently used fungal enzymes. The thermophilic filamentous fungus Thermoascus aurantiacus produces large amounts of highly thermostable plant cell wall degrading enzymes. However, no genetic tools have yet been developed for this fungus, which prevents strain engineering efforts. The goal of this study was to develop strain engineering tools such as a transformation system, a CRISPR/Cas9 gene editing system and a sexual crossing protocol to improve enzyme production. ResultsHere we report Agrobacterium tumefaciens-mediated transformation (ATMT) of T. aurantiacus using the hph marker gene, conferring resistance to hygromycin B. The newly developed transformation protocol was optimized and used to integrate an expression cassette of the transcriptional xylanase regulator xlnR, which led to up to 500% increased xylanase activity. Furthermore, a CRISPR/Cas9 gene editing system was established in this fungus, and two different gRNAs were tested to delete the pyrG orthologue with 10% and 35% deletion efficiency, respectively. Lastly, a sexual crossing protocol was established using a hygromycin B- and a 5-fluororotic acid-resistant parent strain. Crossing and isolation of progeny on selective media was completed in a week. ConclusionThe genetic tools developed for T. aurantiacus can now be used individually or in combination to further improve thermostable enzyme production by this fungus.

microbiology↗