El CRAI romandrà tancat del 24 de desembre de 2025 al 6 de gener de 2026. La validació de documents es reprendrà a partir del 7 de gener de 2026.
El CRAI permanecerá cerrado del 24 de diciembre de 2025 al 6 de enero de 2026. La validación de documentos se reanudará a partir del 7 de enero de 2026.
From 2025-12-24 to 2026-01-06, the CRAI remain closed and the documents will be validated from 2026-01-07.
 
Carregant...
Miniatura

Tipus de document

Article

Versió

Versió publicada

Data de publicació

Llicència de publicació

cc-by (c) Pérez Rius, Carla et al., 2019
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/168234

Comparison of zebrafish and mice knockouts for Megalencephalic Leukoencephalopathy proteins indicates that GlialCAM/MLC1 forms a functional unit

Títol de la revista

Director/Tutor

ISSN de la revista

Títol del volum

Resum

Background: Megalencephalic Leukoencephalopathy with subcortical Cysts (MLC) is a rare type of leukodystrophy characterized by astrocyte and myelin vacuolization, epilepsy and early-onset macrocephaly. MLC is caused by mutations in MLC1 or GLIALCAM, coding for two membrane proteins with an unknown function that form a complex specifically expressed in astrocytes at cell-cell junctions. Recent studies in Mlc1-/- or Glialcam-/- mice and mlc1-/- zebrafish have shown that MLC1 regulates glial surface levels of GlialCAM in vivo and that GlialCAM is also required for MLC1 expression and localization at cell-cell junctions. Methods: we have generated and analysed glialcama-/- zebrafish. We also generated zebrafish glialcama-/- mlc1-/- and mice double KO for both genes and performed magnetic resonance imaging, histological studies and biochemical analyses. Results: glialcama-/- shows megalencephaly and increased fluid accumulation. In both zebrafish and mice, this phenotype is not aggravated by additional elimination of mlc1. Unlike mice, mlc1 protein expression and localization are unaltered in glialcama-/- zebrafish, possibly because there is an up-regulation of mlc1 mRNA. In line with these results, MLC1 overexpressed in Glialcam-/- mouse primary astrocytes is located at cell-cell junctions. Conclusions: this work indicates that the two proteins involved in the pathogenesis of MLC, GlialCAM and MLC1, form a functional unit, and thus, that loss-of-function mutations in these genes cause leukodystrophy through a common pathway.

Citació

Citació

PÉREZ RIUS, Carla, FOLGUEIRA, Mónica, ELORZA VIDAL, Xabier, ALIA, Alia, HOEGG-BEILER, Maja b., EEZA, Muhamed n.h., DÍAZ, María luz, NUNES MARTÍNEZ, Virginia, BARRALLO GIMENO, Alejandro, ESTÉVEZ POVEDANO, Raúl. Comparison of zebrafish and mice knockouts for Megalencephalic Leukoencephalopathy proteins indicates that GlialCAM/MLC1 forms a functional unit. _Orphanet Journal of Rare Diseases_. 2019. Vol. 14, núm. 1, pàgs. 268. [consulta: 8 de gener de 2026]. ISSN: 1750-1172. [Disponible a: https://hdl.handle.net/2445/168234]

Exportar metadades

JSON - METS

Compartir registre