Biology subjects

Hosseini, K.

Publications and source records attributed to Hosseini, K..

9 recordsLinked to original sources

bioRxiv2026

Age and Social Observation Effects on Theta Synchrony and Its Role in Adolescent Post-Error Control: A Computational Approach

Error monitoring allows for detecting mistakes and adapting behavior. Error monitoring is associated with increased theta (4-7 Hz) EEG activity recorded at midfrontal electrode sites located over the medial frontal cortex. Increases in theta synchrony after errors between midfrontal and lateral electrode sites, located over lateral prefrontal, motor, and sensory/parietal brain regions, are associated with post-error behavioral adaptations. However, there is a lack of research into whether such error-related theta inter-regional synchrony dynamics exhibit age-related changes across adolescence and whether such changes differ as a function of social observation. Moreover, there are discrepancies across studies in terms of how error-related theta synchrony between different electrode sites relates to specific forms of post-error adjustments. In this study, we used behavioral and EEG data from 262 adolescents aged 10-14 years who performed a flanker task twice: alone and while observed by a peer. Regardless of social observation, we found age-related increases in error-related midfrontal-frontolateral and midfrontal-midlateral theta synchrony. Additionally, we found that error-related theta synchrony between midfrontal and posterolateral regions increased only in the alone condition. Leveraging the shrinking spotlight drift diffusion model (SSP-DDM), we identified a positive association between error-related midfrontal-posterolateral theta synchrony and post-error attentional control but found no effects of social observation. These results are the first to demonstrate that error-related theta synchrony increases from early to mid-adolescence. Additionally, this work specifically links error-related midfrontal-posterolateral theta synchrony to post-error attentional control using computational modeling.

neuroscience↗

bioRxiv2025

Error-Related Memory Biases Are Specific to Social Stimuli for Socially Anxious Individuals

Social anxiety (SA) is associated with enhanced error monitoring, yet underlying mechanisms remain unclear. Consistent with cognitive models of SA, we propose that stronger error monitoring contributes to SA by strengthening memory encoding of errors (including relevant social cues), negatively biasing what is remembered. Supporting this hypothesis, our prior work demonstrated that high SA individuals exhibit better memory for faces presented during error (vs. correct) trials. To test whether this Memory Bias for Error Events is specific to social stimuli, 140 participants completed a Flanker task with trial-unique faces (social) or objects (non-social) as background images, followed by a surprise memory test. Results revealed that higher SA symptoms were associated with enhanced memory for faces on error (vs. correct) trials, but not for objects. These findings replicate and extend our prior work, demonstrating that SA-related memory biases for errors are specific to social stimuli, rather than reflecting general encoding biases.

neuroscience↗

bioRxiv2025

Social observation influences the trajectory of performance monitoring across trials: evidence from single-trial estimates of the ERN and CRN

The error-related negativity (ERN) and correct-related negativity (CRN) are event-related potentials (ERPs) that reflect performance monitoring following error and correct responses, respectively. Prior work demonstrates the ERN is sensitive to the motivational significance of errors, which increases under social observation. However, most studies testing how social observation impacts performance monitoring rely on trial-averaged ERPs, potentially obscuring meaningful fluctuations in ERN/CRN over time. Here, we had participants complete a Flanker task twice (social observation vs. alone) and employed mixed-effects modeling of single-trial ERPs to test if social observation impacts ERN/CRN trajectories over short (within blocks) or long (between blocks) timescales. We found that social observation selectively influenced ERN/CRN trajectories over short timescales: for blocks performed under social observation (but not alone), ERN magnitudes increased across trials and CRN magnitudes decreased. At longer timescales, ERN/CRN significantly decreased across all blocks, regardless of social observation and consistent with a vigilance decrement. To our knowledge, this is the first demonstration that social observation influences performance monitoring trajectories over short timescales. Results highlight the importance of analyzing ERN/CRN trajectories over relatively short timescales to fully characterize the impact of social observation on performance monitoring dynamics. These findings lay the groundwork for future investigation into whether social observation interacts with individual differences in motivation/affect to differentially impact performance monitoring dynamics.

neuroscience↗

bioRxiv2023

Towards a mechanistic understanding of the role of error monitoring and memory in social anxiety

Cognitive models state social anxiety (SA) involves biased cognitive processing that impacts what is learned and remembered within social situations, leading to the maintenance of SA. Neuroscience work links SA to enhanced error monitoring, reflected in error-related neural responses arising from mediofrontal cortex (MFC). Yet, the role of error monitoring in SA remains unclear, as it is unknown whether error monitoring can drive changes in memory, biasing what is learned or remembered about social situations. Thus, we developed a novel paradigm to investigate the role of error-related MFC theta oscillations (associated with error monitoring) and memory biases in SA. EEG was collected while participants completed a novel Face-Flanker task, involving presentation of task-unrelated, trial-unique faces behind target/flanker arrows on each trial. A subsequent incidental memory assessment evaluated memory biases for error events. Severity of SA symptoms were associated with greater error-related theta synchrony over MFC, as well as between MFC and sensory cortex. SA was positively associated with memory biases for error events. Consistent with a mechanistic role in biased cognitive processing, greater error-related MFC-sensory theta synchrony during the Face-Flanker predicted subsequent memory biases for error events. Our findings suggest high SA individuals exhibit memory biases for error events, and that this behavioral phenomenon may be driven by error-related MFC-sensory theta synchrony associated with error monitoring. Moreover, results demonstrate the potential of a novel paradigm to elucidate mechanisms underlying relations between error monitoring and SA.

neuroscience↗

bioRxiv2023

Epithelial-mesenchymal transition induces cell-cycle-dependent changes of cortical signalling

Epithelial-mesenchymal transition (EMT) is a key cellular transformation for many physiological and pathological processes ranging from cancer over wound healing to embryogenesis. Changes in cell migration, cell morphology and cellular contractility were identified as hallmarks of EMT. These cellular properties are known to be tightly regulated by the actin cytoskeleton. EMT-induced changes of actin-cytoskeletal regulation were demonstrated by previous reports of cell-cycle-dependent changes of actin cortex mechanics in conjunction with characteristic modifications of cortex-associated f-actin and myosin. However, at the current state, the changes of upstream actomyosin signalling that lead to corresponding mechanical and compositional changes of the cortex are not well understood. In this work, we show in breast epithelial cancer cells MCF-7 that EMT results in characteristic changes of the cortical signalling of Rho-GTPases Rac1, RhoA and RhoC and downstream actin regulators cofilin, mDia1 and Arp2/3. In the light of our findings, we propose that cell-cycle-dependent EMT-induced changes in cortical mechanics rely on two hitherto unappreciated signalling paths - i) a cell-cycle-dependent interaction between Rac1 and RhoC and ii) an inhibitory effect of Arp2/3 activity on cortical association of myosin II.

cell biology↗

bioRxiv2022

Skin epithelial cells change their mechanics and proliferation upon Snail-mediated EMT signalling

Skin cancer is the most commonly occurring cancer in the USA and Germany, and the fourth most common cancer worldwide. Snail-dependent epithelial-mesenchymal transition (EMT) was shown to initiate and promote skin cancer. Previous studies could show that EMT changes actin cortex regulation and cellular mechanics in epithelial cells of diverse tissue origin. However, in spite of its potentially high significance in the context of skin cancer, the effect of EMT on cellular mechanics, mitotic rounding and proliferation has not been studied in skin epithelial cells so far. In this work we show that TGF-{beta}-induced partial EMT results in a transformation of the mechanical phenotype of skin epithelial cells in a cell-cycle dependent manner. Concomitantly, we looked at EMT-induced changes of cell proliferation. While EMT decreases proliferation in 2D culture, we observed an EMT-induced boost of cellular proliferation when culturing cells as mechanically confined aggregates of skin epithelial cells. This proliferation boost was accompanied by enhanced mitotic rounding and composition changes of the actin cortex. We give evidence that observed EMT-induced changes depend on the EMT-upregulated transcription factor Snail. Overall, our findings indicate that EMT-induced changes of cellular mechanics might play a currently unappreciated role in EMT-induced promotion of skin tumor proliferation. Significance statementThis study describes how epithelial-mesenchymal transition (EMT) alters the actin cytoskeleton, cellular mechanics and proliferation in a benign tumor model of skin epithelial cells. We show that corresponding EMT-induced phenotypes depend on the signalling of the transcription factor Snail. Our findings suggest that EMT-induced changes of cellular mechanics and proliferation might play a currently under-appreciated role in EMT-induced promotion of skin tumors.

biophysics↗

bioRxiv2020

EMT changes actin cortex rheology in a cell-cycle dependent manner

The actin cortex is a key structure for cellular mechanics and cellular migration. Accordingly, cancer cells were shown to change their actin cytoskeleton and their mechanical properties in correlation with different degrees of malignancy and metastatic potential. Epithelial-Mesenchymal transition (EMT) is a cellular transformation associated with cancer progression and malignancy. To date, a detailed study of the effects of EMT on the frequency-dependent viscoelastic mechanics of the actin cortex is still lacking. In this work, we have used an established AFM-based method of cell confinement to quantify the rheology of the actin cortex of human breast, lung and prostate epithelial cells before and after EMT in a frequency range of 0.02 - 2 Hz. Interestingly, we find for all cell lines opposite EMT-induced changes in interphase and mitosis; while the actin cortex softens upon EMT in interphase, the cortex stiffens in mitosis. Our rheological data can be accounted for by a rheological model with a characteristic time scale of slowest relaxation. In conclusion, our study discloses a consistent rheological trend induced by EMT in human cells of diverse tissue origin reflecting major structural changes of the actin cytoskeleton upon EMT. Significance statementThe actin cortex is a key structure for cellular mechanics and cellular migration. Correspondingly, migratory cancer cells were shown to change their mechanical properties to a softer phenotype. EMT is a cellular transformation associated with cancer progression and malignancy. To date, a detailed study of the effects of EMT on the mechanics of the actin cortex is still lacking. In this work, we provide such a study for human breast, lung and prostate epithelial cells in dependence of the cell cycle stage. We observe a softening of the actin cortex in interphase but stiffening in mitosis upon EMT. In conclusion, our study discloses a consistent mechanical trend induced by EMT in human cells of diverse tissue origin.

biophysics↗

bioRxiv2020

Binding dynamics of α-actinin-4 in dependence of actin cortex tension

Mechano-sensation of cells is an important prerequisite for cellular function, e.g. in the context of cell migration, tissue organisation and morphogenesis. An important mechano-chemical-transducer is the actin cytoskeleton. In fact, previous studies have shown that actin cross-linkers, such as -actinin-4, exhibit mechanosensitive properties in its binding dynamics to actin polymers. However, to date, a quantitative analysis of tension-dependent binding dynamics in live cells is lacking. Here, we present a new technique that allows to quantitatively characterize the dependence of cross-linking lifetime of actin cross-linkers on mechanical tension in the actin cortex of live cells. We use an approach that combines parallel plate confinement of round cells, fluorescence recovery after photo-bleaching, and a mathematical mean-field model of cross-linker binding. We apply our approach to the actin cross-linker -actinin-4 and show that the cross-linking time of -actinin-4 homodimers increases approximately twofold within the cellular range of cortical mechanical tension rendering -actinin-4 a catch bond in physiological tension ranges.

biophysics↗

bioRxiv2019

EMT-induced cell mechanical changes enhance mitotic rounding strength

To undergo mitosis successfully, most animal cells need to acquire a round shape to provide space for the mitotic spindle. This mitotic rounding relies on mechanical deformation of surrounding tissue and is driven by forces emanating from actomyosin contractility. Cancer cells are able to maintain successful mitosis in mechanically challenging environments such as the increasingly crowded environment of a growing tumor, thus, suggesting an enhanced ability of mitotic rounding in cancer. Here, we show that epithelial mesenchymal transition (EMT), a hallmark of cancer progression and metastasis, gives rise to cell-mechanical changes in breast epithelial cells. These changes are opposite in interphase and mitosis and correspond to an enhanced mitotic rounding strength. Furthermore, we show that cell-mechanical changes correlate with a strong EMT-induced change in the activity of Rho GTPases RhoA and Rac1. Accordingly, we find that Rac1 inhibition rescues the EMT-induced cortex-mechanical phenotype. Our findings hint at a new role of EMT in successful mitotic rounding and division in mechanically confined environments such as a growing tumor.

biophysics↗