Biology subjects

Basso, G.

Publications and source records attributed to Basso, G..

6 recordsLinked to original sources

bioRxiv2026

Brain signatures of semantic activation for words that do not exist.

The experience of making sense of novel words is ubiquitous in human communication. Still, novel words have traditionally been considered as meaningless by cognitive research. Here we combined behavioral, univariate and multivariate fMRI techniques, and computational modelling to explore whether and how novel words activate the neurocognitive hallmarks of semantic processing triggered by existing words, and whether this process is influenced by the presence of familiar functional linguistic elements, i.e., morphemes. We observed that semantic activation for novel words is comparable to that of existing words, provided that novel words contain a concatenation of identifiable morphemes. In addition, representational similarity analysis highlighted that existing words and novel words containing morphemes (but not novel words not containing morphemes) can activate fine-grained semantic representations. These results suggest that the difference in the neurocognitive underpinnings of semantic processing for existing and novel words might be quantitative rather than qualitative and based on how reliably linguistic form points to meaning.

neuroscience↗

bioRxiv2026

How artists experience their own art

Humanity has always admired and created artwork, but the neurocognitive mechanisms behind artistic experience are still elusive. Professional artists and their intimate relationship with their artworks provide a unique opportunity to study the nature of art experience due to their expertise in both art making and art appreciation. During two fMRI tasks, professional artists (N=20) made aesthetic judgments on their own and other artists paintings (aesthetic appreciation task); they also mentally reconstructed the moments when they conceived their artworks or, as a control condition, when they visited now-familiar places for the first time (reconstruction by imagery task). During art appreciation of their own (as compared to other artists) paintings, participants showed stronger recruitment of bilateral posterior parietal cortices, the left lateral occipitotemporal cortex, and the dorso-central sector of the right insula, that is, action-related brain regions also involved in encoding the emotional components of movements. The reconstruction of their own artistic creation (as compared to episodic memory retrieval) involved the left fronto-parietal network associated with motor cognition. Altogether, these results suggest that the mental representations of the actions involved in creating art are integral to the overall artistic experience of painters, supporting an embodied view of the artists experience of art.

neuroscience↗

bioRxiv2025

Neural mechanisms for visuomotor co-regulation in social synchronization

During social activities, people coordinate their movements by exchanging visuomotor information. Interpersonal coordination occurs from two complementary processes entailing voluntary (planned) and spontaneous (emergent) synchronization, of which neurofunctional underpinnings are unknown. We investigated the brain correlates of these two synchronization processes during an fMRI finger-tapping task. Dyads formed by IN and OUT scanner participants were instructed to reproduce a target tempo and concurrently try to synchronize to (Joint Action, JA) or resist synchronization with (Non-interactive, NI) the partners tapping, whose hand was always visible to the IN participant. Faster, slower, or equal tempi were used to induce within-dyad co-regulation. Results revealed the emergence of tempo contagion: participants tapped faster in response to the partners faster taps and vice versa for slower taps. The magnitude of such an interpersonal contagion effect was similar across conditions but associated with the activity of different neural structures. Tempo contagion correlated positively with lateral occipitotemporal cortex (LOTc) activations in the JA condition but negatively with cerebellar activations in the NI condition. This suggests visuomotor information is exploited in opposite ways depending on the task instructions: the LOTc promotes co-regulation to achieve synchronization in JA, whereas the cerebellum prevents tempo contagion to preserve individual stability in NI. This latter result is supported by a negative functional connectivity between the cerebellum and LOTc. These findings have implications for understating the interplay between planned and emergent synchronization during motor interactions.

neuroscience↗

bioRxiv2021

A SIMPLI (Single-cell Identification from MultiPLexed Images) approach for spatially resolved tissue phenotypingat single-cell resolution.

Multiplexed imaging technologies enable the study of biological tissues at single-cell resolution while preserving spatial information. Currently, high-dimension imaging data analysis is technology-specific and requires multiple tools, restricting analytical scalability and result reproducibility. Here we present SIMPLI (Single-cell Identification from MultiPlexed Images), a novel, flexible and technology-agnostic software that unifies all steps of multiplexed imaging data analysis. After raw image processing, SIMPLI performs a spatially resolved, single-cell analysis of the tissue slide as wells as cell-independent quantifications of marker expression to investigate features undetectable at the cell level. SIMPLI is highly customisable and can run on desktop computers as well as high-performance computing environments, enabling workflow parallelisation for large datasets. SIMPLI produces multiple tabular and graphical outputs at each step of the analysis. Its containerised implementation and minimum configuration requirements make SIMPLI a portable and reproducible solution for multiplexed imaging data analysis. SIMPLI is available at: https://github.com/ciccalab/SIMPLI.

bioinformatics↗

bioRxiv2020

RAS activation via CRLF2 signaling is a widespread mechanism in Down syndrome acute lymphoblastic leukemia regardless of RAS mutations

BackgroundDown syndrome acute lymphoblastic leukemia (DS-ALL) is characterized by the high frequency of CRLF2-rearrangements, JAK2-mutations, or RAS-pathway mutations. Intriguingly, JAK2 and RAS mutations are mutually exclusive in leukemic sub-clones, causing dichotomy in therapeutic target choices. ResultsHere we show that in primary leukemic cells from DS-ALL, in the absence of RAS-mutations, wild-type (wt)RAS is active, and/or can be induced by the physiological ligand TSLP of the transmembrane-receptor CRLF2. We show active/inducible RAS in 14/20 (70%) of primary DS-ALL samples analyzed, 8 of which had no RAS-mutations, but 75% of those had either mutated or hyperphosphorylated JAK2. No wtRAS cases with mutated/hyperphosphorylated JAK2 were observed that lacked activated RAS protein. We prove in a cell model that elevated CRLF2 in combination with constitutionally active JAK2 is sufficient to activate wtRAS. We show that TSLP boosts the direct binding of active PTPN11 to wtRAS. Pre-inhibition of RAS or PTPN11, but not of PI3K or JAK signaling, prevented TSLP-induced RAS-GTP boost. Using multivariate-clustering based on RAS-activity/inducibility we show significant separation between standard-risk and high-risk DS-ALL groups. Cox proportional-hazards model showed protein-activity (but not mutation status) as independently predictive of outcome. ConclusionsOur data indicate that RAS protein activity levels (and not JAK2/RAS mutation profiles), are predictive of outcome. Importantly, our data suggest that inhibition of RAS and direct RAS-pathway components should be combined with PI3K/mTOR and/or JAK2 inhibitors for high-risk cases. Therapeutically this is relevant for >75% of DS-ALL and our additional data suggest that it warrants further investigation in high-risk non-DS-ALL.

cancer biology↗

bioRxiv2018

USP7 cooperates with NOTCH1 to drive the oncogenic transcriptionalprogram in T cell leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease, affecting children and adults. Treatments1-6 show high response rates but have debilitating effects and carry risk of relapse5,7,8. Previous work implicated NOTCH1 and other oncogenes1,2,9-20. However, direct inhibition of these pathways affects healthy tissues and cancer alike. Here, we demonstrate that ubiquitin-specific protease 7 (USP7)21-32 controls leukemia growth by stabilizing the levels of the NOTCH1 and JMJD3 demethylase. USP7 is overexpressed T-ALL and is transcriptionally regulated by NOTCH1. In turn, USP7 controls NOTCH1 through deubiquitination. USP7 is bound to oncogenic targets and controls gene expression through H2B ubiquitination and H3K27me3 changes via stabilization of NOTCH1 and JMJD3. We also show that USP7 and NOTCH1 bind T-ALL superenhancers, and USP7 inhibition alters associated gene activity. These results provide a new model for deubiquitinase activity through recruitment to oncogenic chromatin loci and regulation of both oncogenic transcription factors and chromatin marks to promote leukemia. USP7 inhibition33 significantly blocked T-ALL cell growth in vitro and in vivo. Our studies also show that USP7 is upregulated in the aggressive high-risk cases of T-ALL and suggest that USP7 expression might be a prognostic marker in ALL and its inhibition could be a therapeutic tool against aggressive leukemia.

cancer biology↗