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Carvalho, J.

Publications and source records attributed to Carvalho, J..

At least 19 recordsLinked to original sources

Structural and evolutionary insights into DAF-12 interactions with transcriptional coactivators in parasitic nematodes

Parasitic nematodes infect billions of humans and livestock worldwide, causing major health and economic burdens, while the spread of anthelmintic resistance threatens current control strategies. A critical step in parasite infection is the resumption of development of infective third-stage larvae (iL3) upon host entry, a process controlled by the nuclear receptor DAF-12. Activation of DAF-12 by dafachronic acids promotes developmental progression and reproductive maturation, making this receptor an attractive therapeutic target. However, the molecular mechanisms governing DAF-12 activation, particularly transcriptional coactivator recruitment, remain poorly understood. Here, we combined biophysical, cellular, structural, and bioinformatic approaches to investigate coactivator recognition by DAF-12 from the parasitic nematodes Brugia malayi and Haemonchus contortus. Crystal structures of ligand-bound DAF-12 ligand-binding domains in complex with coactivator-derived peptides reveal conserved features of ligand-dependent coactivator recruitment shared with mammalian nuclear receptors. In addition, we uncover previously unrecognized interaction features, including motif-specific contacts that extend beyond the canonical LXXLL binding mode of coactivators and distinct patterns of DAF-12 conservation across nematode clades. Structure-guided analyses redefine the interaction motif of the only described parasite-specific coactivator DIP-1 and suggest novel candidate motifs for DAF-12-interacting proteins. Together, these findings establish the structural basis of coactivator binding to nematode DAF-12 and provide mechanistic insight into the transcriptional regulation underlying parasite development. These results expand current understanding of nuclear receptor signaling in parasitic nematodes and provide a framework for the future design of strategies aimed at disrupting DAF-12 activation as a potential antiparasitic approach. Author SummaryParasitic nematodes infect billions of people and livestock worldwide, causing major health and economic burdens, while increasing resistance threatens current treatments. These parasites rely on a developmental switch that allows infectious larvae to resume growth inside their host, a process controlled by the nuclear receptor DAF-12. Blocking this pathway could prevent parasites from establishing infection. However, the molecular mechanisms regulating DAF-12 activation remain poorly understood. Here, we investigate how DAF-12 from two parasitic nematodes, Brugia malayi and Haemonchus contortus, interacts with transcriptional coactivators that enable gene activation, using a combination of biophysical, cellular, structural, and bioinformatic approaches. We identified conserved features of ligand-dependent coactivator recruitment shared with mammalian nuclear receptors as well as nematode-specific interaction mechanisms that vary across evolutionary clades. These findings provide new insights into the structural basis of coactivator binding to DAF-12 and advance our understanding of a key pathway controlling parasitic nematode development.

biochemistry↗

Herbivore pressure modulates soil multifunctionality in a Mediterranean landscape

Ongoing global environmental changes demand cost-effective strategies to restore ecosystem functioning. Within this context, the reintroduction of large mammalian herbivores has emerged as a promising approach to recover ecological processes and foster self-sustaining, biodiverse ecosystems. However, the impacts of such initiatives remain poorly understood, particularly regarding their effects on soil functions and ecological processes. We tested whether large herbivore densities (wild horses (Garrano breed) and cattle (Maronesa breed, an ancient lineage close to aurochs) modulates soil multifunctionality (the simultaneous provision of multiple ecosystem functions) across habitats (grasslands, shrublands, and forests) and seasons (fall and spring) in a Mediterranean landscape. Using composite multivariate indices describing soil functions related to biogeochemical cycles (i.e., enzymatic activities) and physicochemical properties (pH, conductivity, organic matter, and nutrient loads), we found that soil enzymatic activities varied seasonally, being higher in spring, and interacted with habitat and herbivore pressure gradients. Habitat and herbivore pressure explained the variation in soil multifunctionality during spring, while in fall it was mainly driven by herbivore pressure. Enzymatic stoichiometry, particularly C:P ratios, strongly predicted soil fertility and multifunctionality, showing positive relationships in forest habitats and under herbivore pressure. A mechanistic approach confirmed that herbivore impacts on soil functioning operated primarily through changes in soil properties and nutrient cycling rather than direct effects. Mediterranean landscapes are rapidly changing, and our results highlight herbivore management as a key tool to sustain soil ecological processes under the rewilding framework. Highlights- Large herbivores impacted soil functions and properties in different habitats - Large herbivores significantly impacted soil nutrient cycling and multifunctionality. - The magnitude of the effects was dependent on season and habitat - Large herbivores indirectly impact soil ecosystem multifunctionality through changes in soil properties.

ecology↗

Bioelectric and Epigenetic Landscapes in Lateralized Breast Tumors Reveal Distinct Tumor Microenvironment Signatures.

Breast cancer heterogeneity is shaped not only by intrinsic tumor properties but by the surrounding microenvironment (TME). Here we report a left-right (L-R) asymmetry in the breast TME associated to tumor features. Bioinformatic analysis of TCGA RNA-seq and histological data revealed that R-sided tumors display higher stromal scores and are cancer-associated fibroblasts (CAFs) signatures. This difference was validated in paired L-R PDX and xenograft models, in which R-sided tumors showed increased -SMA expression. The asymmetry extended to tumor bioelectricity: across PDX and xenograft models, and in cells cultured with L- or R-conditioned media, L-sided tumors consistently displayed a more depolarized membrane potential than their R counterparts. In vitro, this bioelectric difference was methylation-dependent - abolished by the DNA methyltransferase inhibitor decitabine -and reversible when the laterality of the conditioned media was inverted. Methylome analysis of animal models identified the gap--unction gene GJA1 as significantly hypermethylated in L-sided tumors, accompanied by reduced expression of connexin genes. A computational model showed that membrane potential and methylation form two stable states, depending on gap-junction coupling strength. Together, these findings identify L-R asymmetry as an overlooked layer of breast tumor heterogeneity that integrates stromal, bioelectric, and epigenetic features. This framework may extend to other paired organs and suggests that tumor laterality could have biological and therapeutic relevance.

cancer biology↗

Urbanization drives genetic and plastic responses of the spotted jewelweed flower morphology

The spectacular diversity of flowers is largely driven by pollinator-mediated selection that favors attractive flowers and effective pollen transfer. Urbanization has the potential to affect floral trait evolution by altering pollinator communities through environmental changes. Additionally, abiotic changes in urban habitats can induce phenotypic plasticity, further shaping evolutionary trajectories. We investigated how urbanization affects the genetic and plastic components of flower morphology of Impatiens capensis across four Canadian cities. We found that urbanization influenced the pollinator community composition and the body size of bumblebees, the species main pollinator, although the magnitude of the size effect varied among cities. Using a combination of field surveys and a common garden experiment, our results suggest that urbanization affects sepal size - a tubular floral organ in which pollinators enter to access the nectar - through both genetic and plastic responses. While plasticity sometimes masked the genetic determination of sepal size in the field, we observed a positive correlation between the genetic component of the sepal size and bumblebee body size. These results suggest that urban habitats may drive evolutionary changes in floral traits by modifying pollinator communities.

evolutionary biology↗

Dating and quantifying past gene flow due to hybridization events in Iberian chubs

Hybridization - the successful reproductive cross between individuals from different species - is increasingly recognized as a relatively common phenomenon in nature, mostly due to the increasing availability of genomic data for many organisms and the development of sophisticated methods to detect past gene flow. As a result, evidence of past gene flow has been detected in the genomes of many species, allowing us to investigate the evolutionary forces that act upon hybrid genomes. Biological systems where multiple instances of hybridization have been detected at different time scales are especially useful for this, as they allow investigating the effects of selection and recombination at different time scales post-hybridization. The Iberian chubs (Squalius spp.) present an ideal study system for this. In this group of primary fish inhabiting the rivers of the Iberian Peninsula, multiple instances of past hybridization at different geographical and time scales were reported between different species. However, before we investigate the effects of selection and recombination, it is crucial that we date the hybridization events and quantify the contribution from each parental species. In this study, we infer the demographic history of two Iberian chub hybrid lineages, one resulting from a proposed ancient hybridization event (S. pyrenaicus) and another potentially much more recent (Sao Martinho). We generated whole genome resequencing data for 52 individuals from the two hybrid lineages and their putative parental populations. Our demographic modelling results confirm the hypothesis of ancient hybridization between S. carolitertii and S. tartessicus around 600,000-800,000 years ago, giving rise to the S. pyrenaicus lineage. We also confirm that S. carolitertii is the major parental, with S. tartessicus only contributing <10% to the S. pyrenaicus genome. Furthermore, we confirm the more recent hybridization between S. caetobrigus and S. pyrenaicus (around 4500 years ago) in the Sao Martinho population. We observe similar contributions from both parental species (around 50%) to the genome of the individuals of this population. Overall, our results give us a deeper understanding of how and when these past gene flow events happened and the contributions of each parental species to the genomes of the individuals of the hybrid lineages.

evolutionary biology↗

Give It Time: Green Anacondas Show Prolonged Behavioral Responses to Enclosure Enhancements

Information about green anacondas (Eunectes murinus) in human care is limited, especially concerning their behavior, welfare, and overall well-being. To help bridge this knowledge gap, this study evaluated how exhibit design enhancements influence E. murinus behavior. The aim was to assess immediate behavioral changes following enclosure modifications and investigate potential habituation over time, ultimately evaluating the effectiveness and longevity of the behavioral changes induced by the improved environment. Systematic observations were divided into three phases: before enclosure improvements, immediately after these modifications, and three weeks later. Enclosure modifications focused on areas less frequented by the anacondas during Phase 1. Results revealed decreased inactivity in Phase 2 and more balanced space use in Phase 3, with anacondas occupying previously underutilized areas, including the terrariums vertical dimension. Interaction with exhibit enhancement items increased in the studys final phase, where a decrease in engagement would be anticipated due to habituation. These results suggested the anacondas required additional time to acclimate to the modifications, even though environmental factors may have contributed to these changes. This study highlights how enclosure enhancements may benefit green anacondas welfare while underlining the importance of providing sufficient acclimation time to accurately evaluate the animals complete behavioral response. Simple SummaryGreen anacondas (Eunectes murinus) remain largely understudied, particularly in terms of their behavior and welfare in human care. To address this knowledge gap, improvements were made to the enclosure of green anacondas in captivity, and their behaviors were observed before and after the modifications. The observations were divided into three phases: before the changes (Phase 1), immediately after (Phase 2), and approximately three weeks later (Phase 3). The modifications focused on areas that were rarely utilized during Phase 1. After the improvements, the anacondas became more active and used their enclosure more evenly, including at varying heights. The anacondas interacted more with the new enclosure features after the three weeks, when increased disinterest would have been expected, although environmental conditions may have influenced these changes. These findings show how enclosure modifications may help enhance the welfare of green anacondas and emphasize the need for research that allows enough time for the animals to fully adjust, ensuring a complete understanding of their response.

animal behavior and cognition↗

Layer connective fields from ultrafast resting-state fMRI differentiate feedforward from feedback signaling

Deciphering the directionality of information flow in cortical circuits is essential for understanding brain dynamics, learning, and neuroplasticity after injury. However, current non-invasive methods cannot distinguish feedforward (FF) from feedback (FB) signals across entire networks, including deep brain regions. Here, we present a novel approach combining ultrafast fMRI with a Layer-based Connective Field (lCF) model to disentangle FF from FB signaling. Our findings reveal that lCF size, an indicator of spatial information integration, differentiates FF and FB activity through distinct layer-specific connectivity patterns during spontaneous activity, challenging the notion that FF signals are solely stimulus-driven. FF connectivity follows an inverted U-shape, peaking in layer IV, while FB exhibits a U-shaped pattern, with peaks in layers I and VI. These profiles generalize across sensory pathways (visual, somatosensory, and motor) and reveal injury-induced network reorganization, such as LGN bypassing V1 to provide direct FF input to higher visual areas.

neuroscience↗

Unveiling the Mechanisms to Bypass KRAS Inhibition: In Vitro Insights into the Influence of Fibroblast-Secretome

Novel KRAS-targeted therapies unlocked new treatment options for previously untreatable patients. However, in colorectal cancer (CRC), resistance to KRAS-targeted therapy develops rapidly, making it imperative to understand its underlying mechanisms. Cancer-associated fibroblasts (CAFs) induce therapy resistance by generating and maintaining cancer stem cells (CSCs). Additionally, CAFs secretome can modulate KRAS mutant CRC cells proteomic profile, independently of mutant KRAS. Hence, we investigated whether CAF-derived factors could induce resistance to KRAS inhibition by promoting a KRAS-independent stem-like phenotype. Evaluation of KRAS-mutant CRC cell lines (HCT15, HCT116, and SW480) revealed unique basal stem cell marker expression levels. Silencing KRAS lead to up-regulation of CD24, down- regulation of CD49f and CD104, and reduced stemness. However, CAF-secreted factors attenuated these effects, restoring stem cell markers expression and increasing stemness. RNA sequencing showed that CAF-secreted factors upregulate pro-tumorigenic pathways in KRAS-silenced cells, including cell cycle control, epithelial-mesenchymal transition (EMT), NOTCH, and immune regulation, leading to increased cell cycling and exit from quiescence. Overall, we provide mechanistic insights illuminating the role of fibroblasts in counteracting KRAS silencing-induced growth inhibition and enhancing stemness. Our results show that the limited success of KRAS-targeted therapies is not only derived from cell-intrinsic factors but also dependent on external factors derived from the tumor microenvironment, thus opening avenues to improve therapy responses in CRC.

cancer biology↗

Parallel evolution of local adaptation in Littorina saxatilis inferred with whole-genome pool-seq data

Parallel evolution of phenotypic divergence offers compelling evidence supporting the influence of natural selection on the divergence process. However, the existence of ecotypes adapted to different habitats in separate locations is not a definitive proof of parallel evolution. Here, we leverage a large pool-seq dataset of the rocky-shore gastropod, Littorina saxatilis to compare and contrast two explicit scenarios of ecotype formation. Populations of this species inhabit contrasting habitats, where the main selective pressure is either wave action or crab predation. Using approximate Bayesian computation to jointly infer demographic parameters and account for pool-seq specific sources of uncertainty, our analysis reveals that ecotype formation at a large geographical scale has occurred in parallel. Parameter estimates provide strong support for a demographic history marked by the spatial separation of the ancestral populations that later gave rise to parallel evolution of ecotypes in Spain and Sweden. Additionally, ecotype formation occurred in the face of continuous gene flow between the diverging ecotypes. These results shed new light on a important model of speciation driven by ecological factors and emphasize the effectiveness of combining pool-seq with ABC for studying parallel evolution across diverse geographical regions.

evolutionary biology↗

Purkinje-Enriched snRNA-seq in SCA7 Cerebellum Reveals Zebrin Identity Loss as a Central Feature of Polyglutamine Ataxias

Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disorder caused by a CAG-polyglutamine repeat expansion. SCA7 patients display a striking loss of Purkinje cell (PC) neurons with disease progression; however, PCs are rare, making them difficult to characterize. We developed a PC nuclei enrichment protocol and applied it to single-nucleus RNA-seq of a SCA7 knock-in mouse model. Our results unify prior observations into a central mechanism of cell identity loss, impacting both glia and PCs, driving accumulation of inhibitory synapses and altered PC spiking. Zebrin-II subtype dysregulation is the predominant signal in PCs, leading to complete loss of zebrin-II striping at motor symptom onset in SCA7 mice. We show this zebrin-II subtype degradation is shared across Polyglutamine Ataxia mouse models and SCA7 patients. It has been speculated that PC subtype organization is critical for cerebellar function, and our results suggest that a breakdown of zebrin-II parasagittal striping is pathological.

genomics↗

poolHelper: an R package to help in designing Pool-Seq studies

Next-generation sequencing of pooled samples (Pool-seq) is an important tool in population genomics and molecular ecology. In Pool-seq, the relative number of reads with an allele reflects the allele frequencies in the sample. However, unequal individual contributions to the pool and sequencing errors can lead to inaccurate allele frequency estimates. When designing Pool-seq studies, researchers need to decide the pool size (number of individuals) and average depth of coverage (sequencing effort). An efficient sampling design should maximize the accuracy of allele frequency estimates while minimizing the sequencing effort. We introduce an R package, poolHelper, enabling users to simulate Pool-seq data under different combinations of average depth of coverage, pool sizes and number of pools, accounting for unequal individual contribution and sequencing errors, modelled by parameters that users can modify. poolHelper can be used to assess how different combinations of those parameters influence the error of sample allele frequencies and expected heterozygosity. The mean absolute error is computed by comparing the sample allele frequencies obtained based on individual genotypes with the frequency estimates obtained with Pool-seq. Using simulations under a single population model, we illustrate that increasing the depth of coverage does not necessarily lead to more accurate estimates, reinforcing that finding the best Pool-seq study design is not straightforward. Moreover, we show that simulations can be used to identify different combinations of parameters with similarly low mean absolute errors. The poolHelper package provides tools for performing simulations with different combinations of parameters before sampling and generating data, allowing users to define sampling schemes that minimize the sequencing effort.

bioinformatics↗

Extensive topographic remapping and functional sharpening in the adult rat visual pathway upon first visual experience

Understanding the dynamics of stability/plasticity balances during adulthood is pivotal for learning, disease, and recovery from injury. However, the brain-wide topography of sensory remapping remains unknown. Here, using a first-of-its-kind setup for delivering patterned visual stimuli in a rodent Magnetic Resonance Imaging (MRI) scanner, coupled with biologically-inspired computational models, we noninvasively mapped brain-wide properties - receptive fields (RFs) and spatial frequency (SF) tuning curves - that were insofar only available from invasive electrophysiology or optical imaging. We then tracked the RF dynamics in the chronic Visual Deprivation Model (VDM) of plasticity, and found that light exposure progressively promoted a large-scale topographic remapping in adult rats. Upon light exposure, the initially unspecialized visual pathway progressively evidenced sharpened RFs (smaller and more spatially selective) and enhanced spatial frequency tuning curves. Our findings reveal that visual experience following VDM reshapes both structure and function of the visual system and shifts the stability/plasticity balance in adults.

neuroscience↗

Mutant KRAS-associated proteome is mainly controlled by exogenous factors

KRAS signaling has been extensively studied, yet the clarification between KRAS-autonomous and non-autonomous mechanisms are still less explored. Understanding how KRAS signaling and effects are affected by exogenous stimuli can provide valuable insights not only to understand resistance mechanisms that justify pathway inhibition failure, but also to uncover novel therapeutic targets for mutant KRAS patients. Hence, aiming at understanding KRAS-autonomous versus non autonomous mechanisms, we studied the response of two mutant KRAS colorectal cancer cell lines (HCT116 and LS174T) - control and KRAS silenced- to TGF{beta}1-activated fibroblasts secretome. By performing a total proteome analysis, we observed that TGF{beta}1-activated fibroblast-secreted factors triggered cell line-specific proteome alterations and that mutant KRAS governs approximately 1/3 of those alterations. Moreover, the analysis of the impact of exogenous factors on the modulation of KRAS proteome revealed that, in both cell lines, more than 2/3 of the KRAS-associated proteome is controlled in a KRAS-non-autonomous manner and dependent on the exogenous factors. This work highlights the context-dependency of KRAS-associated signaling and reinforces the importance of establishing more integrative models resembling the complexity of the tumor microenvironment to study KRAS-associated signals.

cancer biology↗

Mutant KRAS modulates colorectal cancer cells invasive response to fibroblast-secreted factors through the HGF/C-MET axis

Genetic alterations influence the malignant potential of cancer cells, and so does the tumor microenvironment. Herein, we combined the study of KRAS oncogenic effects in colorectal cancer cells with the influence of fibroblasts-derived factors. Results revealed that mutant KRAS regulates cell fate through both autonomous and non-autonomous signaling mechanisms. Specifically, processes such as proliferation and cell-cell aggregation were autonomously controlled by mutant KRAS independently of the stimulation with fibroblasts conditioned media. However, cancer cell invasion revealed to be a KRAS-dependent non-autonomous effect, resulting from the cooperation between fibroblasts-derived HGF and mutant KRAS regulation of C-MET expression. C-MET downregulation upon KRAS silencing rendered cells less responsive to HGF and thus less invasive. Yet, in one cell line, KRAS inhibition triggered invasion upon stimulation with fibroblasts conditioned media. Inhibition of PIK3CA oncogene did not promoted invasion, thus showing a KRAS-specific effect. Moreover, the invasive capacity also depended on the HGF-C-MET axis. Overall, our study awards oncogenic KRAS an important role in modulating the response to fibroblast-secreted factors either by promoting or impairing invasion, and depicts the HGF-C-MET axis as a putative therapeutic target to impair the invasive properties of mutant KRAS cancer cells. SignificanceTargeting mutant KRAS cancers is an urgent clinical need. HGF-C-MET axis inhibition arises as a possible strategy to target mutant KRAS CRC, both primary and metastatic tumors. Additional informationO_ST_ABSFinancial supportC_ST_ABSThis work was supported through FEDER funds through the Operational Programme for Competitiveness Factors (COMPETE 2020), Programa Operacional de Competitividade e Internacionalizacao (POCI), Programa Operacional Regional do Norte (Norte 2020), European Regional Development Fund (ERDF), and by National Funds through the Portuguese Foundation for Science and Technology (FCT) (PTDC/MED-ONC/31354/2017). PDC is a PhD student from Doctoral Program in Pathology and Molecular Genetics from the Institute of Biomedical Sciences Abel Salazar (ICBAS, University of Porto) and she is funded through a PhD fellowship (SFRH/BD/131156/2017) awarded by the FCT. FM is a PhD student from Doctoral Program in Biomedicine from the Faculty of Medicine of the University of Porto and she is funded through a PhD fellowship (SFRH/BD/143669/2019) awarded by the FCT. SM is a PhD student from Doctoral Program in Biomedicine from the Faculty of Medicine of the University of Porto and she is funded through a PhD fellowship (SFRH/BD/143642/2019) awarded by the FCT. AR is a junior researcher hired by IPATIMUP under the CaTCh project funded by FEDER and FCT (POCI-01-0145-FEDER-031354). ALM is a PhD student from Doctoral Program in Biomedicine from the Faculty of Medicine of the University of Porto and she is funded through a PhD fellowship (2020.08932.BD) awarded by the FCT. MJO is principal researcher at INEB. SV is hired by IPATIMUP under norma transitoria do DL n.{o} 57/2016 alterada pela lei n.{o} 57/2017.

cancer biology↗

Epithelial-mesenchymal plasticity induced by discontinuous exposure to TGFβ1 promotes tumour growth

Transitions between epithelial and mesenchymal cellular states (EMT/MET) contribute to cancer progression. We hypothesize that EMT followed by MET promotes cell population heterogeneity favouring tumour growth. We developed an EMT model by on/off exposure of epithelial EpH4 cells (E-cells) to TGF{beta}1 that mimics phenotypic EMT (M-cells) and MET. We aimed at understanding whether phenotypic MET is accompanied by molecular and functional reversion back to epithelia, by using RNA sequencing, Immunofluorescence (IF), proliferation, wound healing, focus formation and mamosphere formation assays, as well as cell-xenografts in nude mice. Phenotypic reverted-epithelial cells (RE-cells), obtained after MET induction, presented pure epithelial morphology and proliferation rate resembling E-cells. However, RE transcriptomic profile and IF staining of epithelial and mesenchymal markers revealed a unique and heterogeneous mixture of cell-subpopulations, with high self-renewal ability fed by oxidative phosporylation. RE-cells heterogeneity is stably maintained for long periods after TGF{beta}1 removal, both in vitro and in large derived tumours in nude mice. Overall, we show that phenotypic reverted-epithelial cells (RE-cells) do not return to the molecular and functional epithelial state, present mesenchymal features related with aggressiveness and cellular heterogeneity that favour tumour growth in vivo. This work strengthens epithelial cells reprogramming and cellular heterogeneity fostered by inflammatory cues as a tumour-growth promoting factor in vivo.

cell biology↗

Soma and Neurite Density MRI (SANDI) of the in-vivo mouse brain

Diffusion MRI (dMRI) provides unique insights into the neural tissue milieu by probing interaction of diffusing molecules and tissue microstructure. Most dMRI techniques focus on white matter tissues (WM) due to the relatively simpler modelling of diffusion in the more organized tracts; however, interest is growing in gray matter characterisations. The Soma and Neurite Density MRI (SANDI) methodology harnesses a model incorporating water diffusion in spherical objects (assumed to be associated with cell bodies) and in impermeable "sticks" (representing neurites), which potentially enables the characterisation of cellular and neurite densities. Recognising the importance of rodents in animal models of development, aging, plasticity, and disease, we here sought to develop SANDI for preclinical imaging and provide a validation of the methodology by comparing its metrics with the Allen mouse brain atlas. SANDI was implemented on a 9.4T scanner equipped with a cryogenic coil, and experiments were carried out on N=6 mice. Pixelwise, ROI-based, and atlas comparisons were performed, and results were also compared to more standard Diffusion Kurtosis MRI (DKI) metrics. We further investigated effects of different pre-processing pipelines, specifically the comparison of magnitude and real-valued data, as well as different acceleration factors. Our findings reveal excellent reproducibility of the SANDI parameters, including the sphere and stick fraction as well as sphere size. More strikingly, we find a very good rank correlation between SANDI-driven soma fraction and Allen brain atlas contrast (which represents the cellular density in the mouse brain). Although some DKI parameters (FA, MD) correlated with some SANDI parameters in some ROIs, they did not correlate nearly as well as SANDI parameters with the Allen atlas, suggesting a much more specific nature of the SANDI parameters. We conclude that SANDI is a viable preclinical MRI technique that can greatly contribute to research on brain tissue microstructure.

neuroscience↗

Binocular integrated visual field deficits are associated with changes in local network function in primary open-angle glaucoma: a resting-state fMRI study

Recent brain imaging studies have shown that the degenerative eye damage generally observed in the clinical setting, also extends intracranially. Both structural and functional brain changes have been observed in glaucoma participants, but we still lack an understanding of whether these changes also affect the integrity of cortical functional networks. This is relevant, as functional network integrity may affect the applicability of future treatments, as well as the options for rehabilitation or training. Here, we compare global and local functional connectivity between glaucoma and controls. Moreover, we study the relationship between functional connectivity and visual field (VF) loss. For our study, 20 subjects with primary open-angle glaucoma (POAG) and 24 age-similar healthy participants were recruited to undergo a complete ophthalmic assessment followed by two resting-state (RS) (f)MRI scans. For each scan and for each group, the ROIs with EC values higher than the 95th percentile were considered the most central brain regions ("hubs"). Hubs for which we found a significant difference in EC in both scans between glaucoma and healthy were considered to provide evidence for network changes. In addition, for each participant, behavioural scores were derived based on the notion that a brain regions hub function might relate to the: 1) sensitivity of the worse eye - indicating disease severity, 2) sensitivity of both eyes combined - with one eye potentially compensating for loss in the other, or 3) difference in eye sensitivity - requiring additional network interactions. By correlating each of these VF scores and the EC values, we assessed whether VF defects could be associated with centrality alterations in POAG. Our results show that no functional connectivity disruptions were found at the global brain level in POAG participants. This indicates that in glaucoma global brain network communication is preserved. Furthermore, a positive correlation was found between the EC value of the Lingual Gyrus, identified as a brain hub, and the behavioural score for the VF sensitivity of both eyes combined. The fact that reduced local network functioning is associated with reduced sensitivity of the binocular VF suggests the presence of local brain reorganisation that has a bearing on functional visual abilities.

neuroscience↗

A FGF2-mediated incoherent feedforward loop inducesErk inhibition and promotes naive pluripotency

Naive pluripotency is a transient state during mammalian development that can be recapitulated indefinitely in vitro by inhibition of the mitogen-activated protein kinase (MAPK/Erk) signalling and activation of STAT and Wnt pathways. How Erk is inhibited in vivo to promote naive pluripotency remains largely unknown. By combining live cell imaging and quantitative proteomics we found that FGF2, a known Erk activator and pro-differentiation cue, induces instead long-term Erk inhibition in both ES cells and mouse embryos. We show that Erk inhibition results from a FGF2-induced incoherent feedforward loop. Importantly, we see that FGF2 induces up-regulation of naive pluripotency factors, down-regulation of DNA methylation by suppression of de novo DNA methylases thereby helping maintain naive pluripotency. We show that FGF2 is expressed maternally and propose that integration of signals from the embryos niche may contribute to the generation of embryonic lineages with the right cell proportions. We suggest that feedforward regulation may play a role driving transient, reversible developmental transitions.

developmental biology↗