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Pravata, M. V.

Publications and source records attributed to Pravata, M. V..

2 recordsLinked to original sources

DCHS1 Modulates Forebrain Proportions in Modern Humans via a Glycosylation Change

Comparative anatomical studies of primates and extinct hominins, including Neanderthals, show that the modern human brain is characterised by a disproportionately enlarged neocortex relative to the striatum. To explore the molecular basis of this difference, we screened for missense mutations that are unique to modern humans and occur at high frequency and that alter post-translational sites. One such mutation was identified in DCHS1, a protocadherin family gene, and it was found to disrupt an N-glycosylation site in modern humans. Using CRISPR/Cas9-editing we introduced into human-induced pluripotent stem cells (hiPSCs) this ancestral DCHS1 variant present in Neanderthals and other primates, representing the ancestral state before the modern human-specific substitution. Leveraging hiPSCs-derived neural organoids, we observed an expansion of striatal progenitors at the expense of the neocortex, mirroring the anatomical distribution seen in non-human primates. We further identify the ephrin receptor EPHA4 as a binding partner of DCHS1 and show that modern human-specific alterations in DCHS1 modulate EPHA4-ephrin signalling, contributing to a gradual shift in the neocortex-to-striatum ratio - a hallmark of brain organisation in our species.

neuroscience↗

Intrinsic and extrinsic mechanisms alter neural cell fate specification in EPM1 Epilepsy

The extracellular milieu, including extracellular vesicles (EVs), plays a pivotal role in brain development by regulating neural processes such as proliferation, differentiation, and migration. In this study, we sought to elucidate the pathogenesis of progressive myoclonus epilepsy type 1 (EPM1), a disease caused by mutations in the CSTB gene, using cerebral organoids (COs) derived from EPM1 patient cells. The results demonstrate that EPM1 COs display increased electrophysiological activity and a disrupted excitatory/inhibitory balance. Single-cell RNA sequencing (scRNA-seq) analysis of ventral EPM1-Cos revealed an abnormal specification of progenitor fate, with a shift toward dorsal neuron identities at the expense of inhibitory interneurons. In addition, pathological alterations in EV biogenesis and cargo were identified, including aberrant Sonic Hedgehog (SHH) signaling, which may disrupt cortical patterning. These findings suggest that both intrinsic progenitor identity shifts and extrinsic EV-mediated signaling contribute to EPM1 pathology. Our study highlights potential therapeutic strategies mediated by EVs as a novel approach to mitigate disease progression.

neuroscience↗