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Tak, S.

Publications and source records attributed to Tak, S..

2 recordsLinked to original sources

Dynamic Causal Modelling for Functional Near-Infrared Spectroscopy Using Spatial Priors Derived from Diffuse Optical Tomography

Functional near-infrared spectroscopy (fNIRS) is an optical neuroimaging technique that measures brain activity by detecting changes in oxygenated and deoxygenated hemoglobin concentrations. Although methods exist for estimating causal interactions among brain regions using fNIRS data, current approaches typically rely on node locations defined at the sensor measurement level near the cortical surface. To address this limitation, this study extends dynamic causal modeling (DCM) for fNIRS by incorporating source-level locations derived from diffuse optical tomography (DOT). The proposed method was applied to an experimental dataset comprising 104 participants recorded during a Go/No-Go response inhibition task. Bayesian model selection confirmed that DCM models using DOT-informed neuronal source locations outperformed models using sensor-level locations. Furthermore, posterior means of effective connectivity parameters validated the inhibitory influence of the right inferior frontal gyrus on regions within the motor network during response inhibition. By providing precise neuronal source localization informed by statistical parametric mapping of DOT-reconstructed data, the proposed DCM approach enables more accurate inference of directed connectivity at the neuronal level from optical density measurements. Given the compact and portable nature of fNIRS systems, this method can readily be applied in realistic, naturalistic environments to investigate network-level modulation of brain responses.

neuroscience↗

The C. elegans plectin homologue VAB-10 acts as a hemidesmosome mechanosensor

Mechanical forces control many cellular processes by eliciting a mechanotransduction response in target cells. The initial steps of mechanotransduction at hemidesmosomes remain undefined in contrast to focal adhesions and adherens junctions. Here, we focus on the C. elegans plectin homolog VAB-10A, the only evolutionary conserved hemidesmosome component. In C. elegans, muscle contractions induce a mechanotransduction pathway in the epidermis through hemidesmosomes. We used CRISPR to precisely remove spectrin repeats (SR) or a partially hidden Src-homology-3 (SH3) domain within the VAB-10 plakin domain. Deleting the SH3 or SR8 domains in combination with mutations affecting mechanotransduction, or just part of SR5 shielding the SH3 domain induced embryonic elongation arrest because hemidesmosomes collapse. Notably, recruitment of GIT-1, the first mechanotransduction player, requires the SR5 domain and the hemidesmosome transmembrane receptor LET-805. Furthermore, Molecular Dynamics simulations confirmed that forces acting on VAB-10 can render the central SH3 domain, otherwise in contact with SR4, available for interaction. Collectively, our data strongly argue that the plakin domain plays a central role in mechanotransduction and raise the possibility that VAB-10/plectin might act as a mechanosensor.\n\nSummary statementCRISPR-derived deletions reveal the roles of three spectrin repeats and an atypical SH3 domain from the plakin domain of the VAB-10 hemidesmosome component in mechanotransduction during C. elegans morphogenesis

developmental biology↗