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NICO-Webinar: "Dysregulation of FLVCR1-dependent mitochondrial calcium handling in neural stem cells causes congenital hydrocephalus." 5/4/2024 @ 2.00 pm

Published: Friday, March 29, 2024 by Giovanna Gambarotta

**Hybrid seminar: both in presence (max 25 people in Seminar room) and on webex


Friday 5/4/2024 h. 2.00 pm -  Hybrid seminar
Deborah Chiabrando, Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center “Guido Tarone”, University of Torino
Dysregulation of FLVCR1-dependent mitochondrial calcium handling in neural stem cells causes congenital hydrocephalus.

Congenital hydrocephalus (CH), occurring in approximately 1/1000 live births, represents an important clinical challenge due to the limited knowledge of underlying molecular mechanisms. The discovery of novel CH-genes is thus essential to shed light on the intricate processes responsible for ventricular dilatation in CH. Here, we identify FLVCR1 (Feline Leukemia Virus Subgroup C Receptor 1) as a novel gene responsible for a severe form of CH in humans and mice.

Mechanistically, our data reveal that FLVCR1a interacts with the IP3R3-VDAC complex located on mitochondria-associated membranes (MAMs) that controls mitochondrial calcium handling. Loss of Flvcr1a in mouse neural stem cells (NSCs) affects mitochondrial calcium levels and energy metabolism, leading to defective cortical neurogenesis and brain ventricle enlargement. These data point to defective NSC calcium handling and metabolic activity as one of the pathogenetic mechanisms driving CH.

Host: Enrica Boda | webex link

Last update: 29/03/2024 15:50
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