Mol Omics. 2023 Feb 22. doi: 10.1039/d2mo00258b. Online ahead of print.

ABSTRACT

Zika virus (ZIKV) and dengue virus (DENV) are two closely related flaviviruses with similar symptoms. However, due to the implications of ZIKV infections for pregnancy outcomes, understanding differences in their molecular impact on the host is of high interest. Viral infections change the host proteome, including post-translational modifications. As modifications are diverse and of low abundance, they typically require additional sample processing which is not feasible for large cohort studies. Therefore, we tested the potential of next-generation proteomics data in its ability to prioritize specific modifications for later analysis. We re-mined published mass spectra from 122 serum samples from ZIKV and DENV patients for the presence of phosphorylated, methylated, oxidized, glycosylated/glycated, sulfated, and carboxylated peptides. We identified 246 modified peptides with significantly differential abundance in ZIKV and DENV patients. Amongst these, methionine-oxidized peptides from apolipoproteins and glycosylated peptides from immunoglobulin proteins were more abundant in ZIKV patient serum and generate hypotheses on the potential roles of the modification in the infection. The results demonstrate how data-independent acquisition techniques can help prioritize future analyses of peptide modifications.

PMID:36810580 | DOI:10.1039/d2mo00258b

Brief Bioinform. 2023 Feb 21:bbac624. doi: 10.1093/bib/bbac624. Online ahead of print.

ABSTRACT

Phosphorylation is an essential mechanism for regulating protein activities. Determining kinase-specific phosphorylation sites by experiments involves time-consuming and expensive analyzes. Although several studies proposed computational methods to model kinase-specific phosphorylation sites, they typically required abundant experimentally verified phosphorylation sites to yield reliable predictions. Nevertheless, the number of experimentally verified phosphorylation sites for most kinases is relatively small, and the targeting phosphorylation sites are still unidentified for some kinases. In fact, there is little research related to these understudied kinases in the literature. Thus, this study aims to create predictive models for these understudied kinases. A kinase-kinase similarity network was generated by merging the sequence-, functional-, protein-domain- and 'STRING'-related similarities. Thus, besides sequence data, protein-protein interactions and functional pathways were also considered to aid predictive modelling. This similarity network was then integrated with a classification of kinase groups to yield highly similar kinases to a specific understudied type of kinase. Their experimentally verified phosphorylation sites were leveraged as positive sites to train predictive models. The experimentally verified phosphorylation sites of the understudied kinase were used for validation. Results demonstrate that 82 out of 116 understudied kinases were predicted with adequate performance via the proposed modelling strategy, achieving a balanced accuracy of 0.81, 0.78, 0.84, 0.84, 0.85, 0.82, 0.90, 0.82 and 0.85, for the 'TK', 'Other', 'STE', 'CAMK', 'TKL', 'CMGC', 'AGC', 'CK1' and 'Atypical' groups, respectively. Therefore, this study demonstrates that web-like predictive networks can reliably capture the underlying patterns in such understudied kinases by harnessing relevant sources of similarities to predict their specific phosphorylation sites.

PMID:36810579 | DOI:10.1093/bib/bbac624

Sci Rep. 2023 Feb 21;13(1):2727. doi: 10.1038/s41598-023-29110-0.

ABSTRACT

Bacterial second messengers c-di-GMP and (p)ppGpp have broad functional repertoires ranging from growth and cell cycle control to the regulation of biofilm formation and virulence. The recent identification of SmbA, an effector protein from Caulobacter crescentus that is jointly targeted by both signaling molecules, has opened up studies on how these global bacterial networks interact. C-di-GMP and (p)ppGpp compete for the same SmbA binding site, with a dimer of c-di-GMP inducing a conformational change that involves loop 7 of the protein that leads to downstream signaling. Here, we report a crystal structure of a partial loop 7 deletion mutant, SmbA∆loop in complex with c-di-GMP determined at 1.4 Å resolution. SmbA∆loop binds monomeric c-di-GMP indicating that loop 7 is required for c-di-GMP dimerization. Thus the complex probably represents the first step of consecutive c-di-GMP binding to form an intercalated dimer as has been observed in wild-type SmbA. Considering the prevalence of intercalated c-di-GMP molecules observed bound to proteins, the proposed mechanism may be generally applicable to protein-mediated c-di-GMP dimerization. Notably, in the crystal, SmbA∆loop forms a 2-fold symmetric dimer via isologous interactions with the two symmetric halves of c-di-GMP. Structural comparisons of SmbA∆loop with wild-type SmbA in complex with dimeric c-di-GMP or ppGpp support the idea that loop 7 is critical for SmbA function by interacting with downstream partners. Our results also underscore the flexibility of c-di-GMP, to allow binding to the symmetric SmbA∆loop dimer interface. It is envisaged that such isologous interactions of c-di-GMP could be observed in hitherto unrecognized targets.

PMID:36810577 | DOI:10.1038/s41598-023-29110-0

JCI Insight. 2023 Feb 22;8(4):e154120. doi: 10.1172/jci.insight.154120.

ABSTRACT

SETD2, a H3K36 trimethyltransferase, is the most frequently mutated epigenetic modifier in lung adenocarcinoma, with a mutation frequency of approximately 9%. However, how SETD2 loss of function promotes tumorigenesis remains unclear. Using conditional Setd2-KO mice, we demonstrated that Setd2 deficiency accelerated the initiation of KrasG12D-driven lung tumorigenesis, increased tumor burden, and significantly reduced mouse survival. An integrated chromatin accessibility and transcriptome analysis revealed a potentially novel tumor suppressor model of SETD2 in which SETD2 loss activates intronic enhancers to drive oncogenic transcriptional output, including the KRAS transcriptional signature and PRC2-repressed targets, through regulation of chromatin accessibility and histone chaperone recruitment. Importantly, SETD2 loss sensitized KRAS-mutant lung cancer to inhibition of histone chaperones, the FACT complex, or transcriptional elongation both in vitro and in vivo. Overall, our studies not only provide insight into how SETD2 loss shapes the epigenetic and transcriptional landscape to promote tumorigenesis, but they also identify potential therapeutic strategies for SETD2 mutant cancers.

PMID:36810256 | DOI:10.1172/jci.insight.154120

Elife. 2023 Feb 22;12:e83662. doi: 10.7554/eLife.83662. Online ahead of print.

ABSTRACT

Background: In infertility treatment, blastocyst morphological grading is commonly used in clinical practice for blastocyst evaluation and selection, but has shown limited predictive power on live birth outcomes of blastocysts. To improve live birth prediction, a number of artificial intelligence (AI) models have been established. Most existing AI models for blastocyst evaluation only used images for live birth prediction, and the area under the receiver operating characteristic (ROC) curve (AUC) achieved by these models has plateaued at ~0.65.

Methods: This study proposed a multi-modal blastocyst evaluation method using both blastocyst images and patient couple's clinical features (e.g., maternal age, hormone profiles, endometrium thickness, and semen quality) to predict live birth outcomes of human blastocysts. To utilize the multi-modal data, we developed a new AI model consisting of a convolutional neural network (CNN) to process blastocyst images and a multi-layer perceptron to process patient couple's clinical features. The dataset used in this study consists of 17,580 blastocysts with known live birth outcomes, blastocyst images, and patient couple's clinical features.

Results: This study achieved an AUC of 0.77 for live birth prediction, which significantly outperforms related works in the literature. Sixteen out of 103 clinical features were identified to be predictors of live birth outcomes and helped improve live birth prediction. Among these features, maternal age, the day of blastocyst transfer, antral follicle count, retrieved oocyte number, and endometrium thickness measured before transfer are the top five features contributing to live birth prediction. Heatmaps showed that the CNN in the AI model mainly focuses on image regions of inner cell mass and trophectoderm (TE) for live birth prediction, and the contribution of TE-related features was greater in the CNN trained with the inclusion of patient couple's clinical features compared with the CNN trained with blastocyst images alone.

Conclusions: The results suggest that the inclusion of patient couple's clinical features along with blastocyst images increases live birth prediction accuracy.

Funding: Natural Sciences and Engineering Research Council of Canada and the Canada Research Chairs Program.

PMID:36810139 | DOI:10.7554/eLife.83662

FASEB J. 2023 Mar;37(3):e22823. doi: 10.1096/fj.202201511R.

ABSTRACT

The cell adhesion molecule L1 (L1CAM, L1 in short) plays crucial roles during neural development, regeneration after injury, synapse formation, synaptic plasticity and tumor cell migration. L1 belongs to the immunoglobulin superfamily and comprises in its extracellular part six immunoglobulin (Ig)-like domains and five fibronectin type III homologous repeats (FNs). The second Ig-like domain has been validated for self- (so-called homophilic) binding between cells. Antibodies against this domain inhibit neuronal migration in vitro and in vivo. The fibronectin type III homologous repeats FN2 and FN3 bind small molecule agonistic L1 mimetics and contribute to signal transduction. FN3 has a stretch of 25 amino acids that can be triggered with a monoclonal antibody, or the L1 mimetics, to enhance neurite outgrowth and neuronal cell migration in vitro and in vivo. To correlate the structural features of these FNs with function, we determined a high-resolution crystal structure of a FN2FN3 fragment, which is functionally active in cerebellar granule cells and binds several mimetics. The structure illustrates that both domains are connected by a short linker sequence allowing a flexible and largely independent organization of both domains. This becomes further evident by comparing the X-ray crystal structure with models derived from Small-Angle X-ray Scattering (SAXS) data for FN2FN3 in solution. Based on the X-ray crystal structure, we identified five glycosylation sites which we believe are crucial for folding and stability of these domains. Our study signifies an advance in the understanding of structure-functional relationships of L1.

PMID:36809668 | DOI:10.1096/fj.202201511R

Bioinformatics. 2023 Feb 21:btad095. doi: 10.1093/bioinformatics/btad095. Online ahead of print.

ABSTRACT

MOTIVATION: Characterizing all steady-state flux distributions in metabolic models remains limited to small models due to the explosion of possibilities. Often it is sufficient to look only at all possible overall conversions a cell can catalyze ignoring the details of intracellular metabolism. Such a characterization is achieved by elementary conversion modes (ECMs), which can be conveniently computed with ecmtool. However, currently, ecmtool is memory-intensive, and it cannot be aided appreciably by parallelization.

RESULTS: We integrate mplrs - a scalable parallel vertex enumeration method - into ecmtool. This speeds up computation, drastically reduces memory requirements, and enables ecmtool 's use in standard and high-performance computing environments. We show the new capabilities by enumerating all feasible ECMs of the near-complete metabolic model of the minimal cell JCVI-syn3.0. Despite the cell's minimal character the model gives rise to 4.2 × 109 ECMs and still contains several redundant sub-networks.

AVAILABILITY: ecmtool is available at https://github.com/SystemsBioinformatics/ecmtool.

SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

PMID:36808187 | DOI:10.1093/bioinformatics/btad095

Nat Commun. 2023 Feb 18;14(1):923. doi: 10.1038/s41467-023-36549-2.

ABSTRACT

The failure of metabolic tissues to appropriately respond to insulin ("insulin resistance") is an early marker in the pathogenesis of type 2 diabetes. Protein phosphorylation is central to the adipocyte insulin response, but how adipocyte signaling networks are dysregulated upon insulin resistance is unknown. Here we employ phosphoproteomics to delineate insulin signal transduction in adipocyte cells and adipose tissue. Across a range of insults causing insulin resistance, we observe a marked rewiring of the insulin signaling network. This includes both attenuated insulin-responsive phosphorylation, and the emergence of phosphorylation uniquely insulin-regulated in insulin resistance. Identifying dysregulated phosphosites common to multiple insults reveals subnetworks containing non-canonical regulators of insulin action, such as MARK2/3, and causal drivers of insulin resistance. The presence of several bona fide GSK3 substrates among these phosphosites led us to establish a pipeline for identifying context-specific kinase substrates, revealing widespread dysregulation of GSK3 signaling. Pharmacological inhibition of GSK3 partially reverses insulin resistance in cells and tissue explants. These data highlight that insulin resistance is a multi-nodal signaling defect that includes dysregulated MARK2/3 and GSK3 activity.

PMID:36808134 | DOI:10.1038/s41467-023-36549-2

Anal Sci. 2023 Feb 18. doi: 10.1007/s44211-023-00285-w. Online ahead of print.

ABSTRACT

High-frequency spectroscopy (HFS) is an analytical method that is sensitive to slight changes in the dielectric properties of materials. Since water has high permittivity, HFS can be used to detect changes in water content in materials. In this study, we employed HFS to measure human skin moisture during a water sorption-desorption test. Skin without any treatment showed a resonance peak at approximately 1150 MHz. Furthermore, the peak shifted to lower frequency immediately after the application of water to the skin and gradually returned to its original frequency as time progressed. The resonance frequency obtained via least-squares fitting showed that the applied water remained in the skin after 240 s from the beginning of the measurement. These results illustrated that HFS measurements can monitor the progression of decreasing moisture content in human skin during a water sorption-desorption test.

PMID:36807897 | DOI:10.1007/s44211-023-00285-w

J Integr Plant Biol. 2023 Feb 21. doi: 10.1111/jipb.13469. Online ahead of print.

ABSTRACT

Plants accumulate a vast array of secondary metabolites, which constitute a natural resource for pharmaceuticals. Oldenlandia corymbosa belongs to the Rubiaceae family, and has been used in traditional medicine to treat different diseases, including cancer. However, the active metabolites of the plant, their biosynthetic pathway and mode of action in cancer are unknown. To fill these gaps, we exposed this plant to eight different stress conditions and combined different omics data capturing gene expression, metabolic profiles and anti-cancer activity. Our results show that O. corymbosa extracts are active against breast cancer cell lines and that ursolic acid is responsible for this activity. Moreover, we assembled a high-quality genome and uncovered two genes involved in the biosynthesis of ursolic acid. Finally, we also revealed that ursolic acid causes mitotic catastrophe in cancer cells and identified three high-confidence protein binding targets by Cellular Thermal Shift Assay (CETSA) and reverse docking. Altogether, these results constitute a valuable resource to further characterize the biosynthesis of active metabolites in the Oldenlandia group, while the mode of action of ursolic acid will allow us to further develop this valuable compound. This article is protected by copyright. All rights reserved.

PMID:36807520 | DOI:10.1111/jipb.13469

Cell Rep. 2023 Feb 17;42(2):112131. doi: 10.1016/j.celrep.2023.112131. Online ahead of print.

ABSTRACT

Fibrosis represents the common end stage of chronic organ injury independent of the initial insult, destroying tissue architecture and driving organ failure. Here we discover a population of profibrotic macrophages marked by expression of Spp1, Fn1, and Arg1 (termed Spp1 macrophages), which expands after organ injury. Using an unbiased approach, we identify the chemokine (C-X-C motif) ligand 4 (CXCL4) to be among the top upregulated genes during profibrotic Spp1 macrophage differentiation. In vitro and in vivo studies show that loss of Cxcl4 abrogates profibrotic Spp1 macrophage differentiation and ameliorates fibrosis after both heart and kidney injury. Moreover, we find that platelets, the most abundant source of CXCL4 in vivo, drive profibrotic Spp1 macrophage differentiation. Single nuclear RNA sequencing with ligand-receptor interaction analysis reveals that macrophages orchestrate fibroblast activation via Spp1, Fn1, and Sema3 crosstalk. Finally, we confirm that Spp1 macrophages expand in both human chronic kidney disease and heart failure.

PMID:36807143 | DOI:10.1016/j.celrep.2023.112131

Methods Mol Biol. 2023;2611:269-282. doi: 10.1007/978-1-0716-2899-7_14.

ABSTRACT

Mitochondria are unique organelles of eukaryotic cells that carry their own multicopy number and circular genome. In most mammals, including humans and mice, the size of the chromosome is ~16,000 base pairs and unlike nuclear DNA, mitochondrial DNA (mtDNA) is not densely compacted. This results in mtDNA to be highly accessible for enzymes such as the Tn5 transposase, commonly used for accessible chromatin profiling of nuclear chromatinized DNA. Here, we describe a method for the concomitant sequencing of mtDNA and accessible chromatin in thousands of individual cells via the mitochondrial single-cell assay for transposase accessible chromatin by sequencing (mtscATAC-seq). Our approach extends the utility of existing scATAC-seq products and protocols as we (Nam et al, Nat Rev Genet 22:3-18, 2021) fix cells using formaldehyde to retain mitochondria and its mtDNA within its originating cell, (Buenrostro et al, Nat Methods 10:1213-1218, 2013) modify lysis conditions to permeabilize cells and mitochondria, and (Corces et al, Nat Methods 14:959-962, 2017) optimize bioinformatic processing protocols to collectively increase mitochondrial genome coverage for downstream analysis. Here, we discuss the essentials for the experimental and computational methodologies to generate and analyze thousands of multiomic profiles of single cells over the course of a few days, enabling the profiling of accessible chromatin and mtDNA genotypes to reconstruct clonal relationships and studies of mitochondrial genetics and disease.

PMID:36807073 | DOI:10.1007/978-1-0716-2899-7_14

Methods Mol Biol. 2023;2611:85-97. doi: 10.1007/978-1-0716-2899-7_7.

ABSTRACT

Spatial organization of the genome modulates pivotal biological processes. The emerging new technologies have provided novel insights into genome structure and its role in regulating cell activities. To examine the genome-wide chromatin interactions at accessible chromatin regions, we developed a DNA transposase-mediated analysis of chromatin looping (Trac-looping) method for simultaneously detecting chromatin interactions and chromatin accessibility. Here, we describe a detailed protocol of generating Trac-looping libraries.

PMID:36807066 | DOI:10.1007/978-1-0716-2899-7_7

Methods Mol Biol. 2023;2611:53-61. doi: 10.1007/978-1-0716-2899-7_4.

ABSTRACT

Chromatin accessibility has been an immensely powerful metric for identifying and understanding regulatory elements in the genome. Many important regulatory elements, such as enhancers and transcriptional start sites, are characterized by "open" or nucleosome-free regions. Understanding the areas of the genome that are not considered open chromatin has been more difficult. Protect-seq is a genomics technique that aims to identify inaccessible chromatin associated with the nuclear periphery. These regions are enriched for histone modifications associated with transcriptional repression and correlate with loci identified by other techniques measuring heterochromatin and peripheral localization. Here, we discuss the protocol and best practices to perform Protect-seq.

PMID:36807063 | DOI:10.1007/978-1-0716-2899-7_4

Methods Mol Biol. 2023;2611:39-52. doi: 10.1007/978-1-0716-2899-7_3.

ABSTRACT

Genome-wide accessible chromatin sequencing and identification has enabled deciphering the epigenetic information encoded in chromatin, revealing accessible promoters, enhancers, nucleosome positioning, transcription factor occupancy, and other chromosomal protein binding. The starting biological materials are often fixed using formaldehyde crosslinking. Here, we describe accessible chromatin library preparation from low numbers of formaldehyde-crosslinked cells using a modified nick translation method, where a nicking enzyme nicks one strand of DNA and DNA polymerase incorporates biotin-conjugated dATP, dCTP, and methyl-dCTP. Once the DNA is labeled, it can be isolated for NGS library preparation. We termed this method as universal NicE-seq (nicking enzyme-assisted sequencing). We also demonstrate a single tube method that enables direct NGS library preparation from low cell numbers without DNA purification. Furthermore, we demonstrated universal NicE-seq on FFPE tissue section sample.

PMID:36807062 | DOI:10.1007/978-1-0716-2899-7_3

Nanoscale. 2023 Feb 20. doi: 10.1039/d2nr05872c. Online ahead of print.

ABSTRACT

In the past four decades, a variety of self-assembly design frameworks have led to the construction of versatile DNA nanostructures with increasing complexity and controllability. The controllable dynamics of DNA nanostructures has garnered much interest and emerged as a powerful tool for conducting sophisticated tasks at the molecular level. In this minireview, we summarized the controllable reconfigurations of complex DNA nanostructures induced by nucleic acid strands, environmental stimuli and enzymatic treatments. We also envisioned that with the optimization of response time, sensitivity and specificity, dynamic DNA nanostructures have great promise in applications ranging from nanorobotics to life sciences.

PMID:36806876 | DOI:10.1039/d2nr05872c

Adv Sci (Weinh). 2023 Feb 19:e2206187. doi: 10.1002/advs.202206187. Online ahead of print.

ABSTRACT

Lipid nanoparticles (LNPs) are currently used to transport functional mRNAs, such as COVID-19 mRNA vaccines. The delivery of angiogenic molecules, such as therapeutic VEGF-A mRNA, to ischemic tissues for producing new blood vessels is an emerging strategy for the treatment of cardiovascular diseases. Here, the authors deliver VEGF-A mRNA via LNPs and study stoichiometric quantification of their uptake kinetics and how the transport of exogenous LNP-mRNAs between cells is functionally extended by cells' own vehicles called extracellular vesicles (EVs). The results show that cellular uptake of LNPs and their mRNA molecules occurs quickly, and that the translation of exogenously delivered mRNA begins immediately. Following the VEGF-A mRNA delivery to cells via LNPs, a fraction of internalized VEGF-A mRNA is secreted via EVs. The overexpressed VEGF-A mRNA is detected in EVs secreted from three different cell types. Additionally, RNA-Seq analysis reveals that as cells' response to LNP-VEGF-A mRNA treatment, several overexpressed proangiogenic transcripts are packaged into EVs. EVs are further deployed to deliver VEGF-A mRNA in vitro and in vivo. Upon equal amount of VEGF-A mRNA delivery via three EV types or LNPs in vitro, EVs from cardiac progenitor cells are the most efficient in promoting angiogenesis per amount of VEGF-A protein produced. Intravenous administration of luciferase mRNA shows that EVs could distribute translatable mRNA to different organs with the highest amounts of luciferase detected in the liver. Direct injections of VEGF-A mRNA (via EVs or LNPs) into mice heart result in locally produced VEGF-A protein without spillover to liver and circulation. In addition, EVs from cardiac progenitor cells cause minimal production of inflammatory cytokines in cardiac tissue compared with all other treatment types. Collectively, the data demonstrate that LNPs transform EVs as functional extensions to distribute therapeutic mRNA between cells, where EVs deliver this mRNA differently than LNPs.

PMID:36806740 | DOI:10.1002/advs.202206187

Mol Cell. 2023 Feb 14:S1097-2765(23)00075-8. doi: 10.1016/j.molcel.2023.01.023. Online ahead of print.

ABSTRACT

All species continuously evolve short open reading frames (sORFs) that can be templated for protein synthesis and may provide raw materials for evolutionary adaptation. We analyzed the evolutionary origins of 7,264 recently cataloged human sORFs and found that most were evolutionarily young and had emerged de novo. We additionally identified 221 previously missed sORFs potentially translated into peptides of up to 15 amino acids-all of which are smaller than the smallest human microprotein annotated to date. To investigate the bioactivity of sORF-encoded small peptides and young microproteins, we subjected 266 candidates to a mass-spectrometry-based interactome screen with motif resolution. Based on these interactomes and additional cellular assays, we can associate several candidates with mRNA splicing, translational regulation, and endocytosis. Our work provides insights into the evolutionary origins and interaction potential of young and small proteins, thereby helping to elucidate this underexplored territory of the human proteome.

PMID:36806354 | DOI:10.1016/j.molcel.2023.01.023

J Vis Exp. 2023 Feb 17;(192). doi: 10.3791/6531.

ABSTRACT

An erratum was issued for: Monitoring Protein-RNA Interaction Dynamics in vivo at High Temporal Resolution using χCRAC. The Authors section was updated from: Stuart W. McKellar1 Ivayla Ivanova1 Robert W. van Nues2 Ross A. Cordiner3 Will Worboys4 Andrew Langford4 Torben Heick Jensen3 Sander Granneman1 1Centre for Synthetic and Systems Biology, University of Edinburgh 2Institute of Cell Biology, University of Edinburgh 3Department of Molecular Biology and Genetics, Aarhus University, 4UVO3 Ltd. to: Stuart W. McKellar1 Ivayla Ivanova1 Robert W. van Nues2 Ross A. Cordiner3 Mehak Chauhan1 Niki Christopoulou1 Will Worboys4 Andrew Langford4 Torben Heick Jensen3 Sander Granneman1 1Centre for Engineering Biology, University of Edinburgh 2Institute of Cell Biology, University of Edinburgh 3Department of Molecular Biology and Genetics, Aarhus University, 4UVO3 Ltd.

PMID:36806121 | DOI:10.3791/6531

Hum Nat. 2023 Feb 21. doi: 10.1007/s12110-023-09443-5. Online ahead of print.

ABSTRACT

Humans are social animals that rely on different ways to interact with each other. The COVID-19 pandemic strongly changed our communication strategies. Because of the importance of direct contact for our species, we predict that immediately after the forced social isolation, people were more prone to engage in direct rather than in virtual interactions, thus showing a lower mimicry response in the use of smartphones. In a non-longitudinal study, we collected behavioral data under naturalistic contexts and directly compared the data of the mimicry response gathered immediately following the Italian lockdown (May-September 2020) with those gathered one year later (May-October 2021). Contrary to our expectations, the mimicry response in the use of smartphones was higher immediately after the lockdown than a year later. Probably the large use of these devices during the lockdown translated into a greater sensitivity to be affected by others' smartphone manipulation. Indeed, social isolation modified, at least in the short term, the ways we interact with others by making us more prone to engage in "virtual" social interactions. The bright side of the coin unveiled by our findings is that the effect seems to diminish over time. The large behavioral dataset analyzed here (1,608 events; 248 people) also revealed that the mimicry response in the use of smartphones was higher between familiar subjects than between strangers. In this view, mimicry in manipulating smartphones can be considered an example of joint action that fosters behavioral synchrony between individuals that, in the long-term, can translate into the formation of social bonding.

PMID:36806091 | DOI:10.1007/s12110-023-09443-5