V-016 | Iron deficiency, through DMT1 (Malvolio) silencing, alters mitochondria dynamics

V-016 | Iron deficiency, through DMT1 (Malvolio) silencing, alters mitochondria dynamics 150 150 SAN 2024 Annual Meeting

Cellular and Molecular Neurobiology
Author: Maria Silvina Marcora | Email: silvinamarcora@gmail.com


Maria Silvina Marcora, Maximiliano Katz,Jorge Correale1°3°, Juana Maria Pasquini

Departamento de Química Biológica and Instituto de Química y Fisicoquímica Biológica (IQUIFIB)-, Facultad de Farmacia y Bioquímica. UBA- CONICET. Buenos Aires Argentina
Instituto de Fisiología y Biofísica Bernardo Houssay, (IFIBIO). Grupo de Neurociencias de Sistemas. Facultad de Medicina. UBA, CONICET. Buenos Aires, Argentina.
Instituto de Investigaciones Neurológicas Dr. Raúl Carrea, FLENI. Buenos Aires, Argentina

Iron is essential for several biological processes, including mitochondrial respiration and redox reactions, as it serves as a key cofactor of many catalytic enzymes. The Divalent Metal Transporter 1 (DMT1) participates in iron uptake in the cell.
In a previous work from aur lab, DMT1 was silenced by siRNA in astrocytes, and mitochondrial studies were performed. We found that siDMT1 astrocytes displayed an increased number and reduced size of mitochondria compared to control cells, in correlation with altered expression of fission and fusion genes, indicating disruption in mitochondrial dynamics.
Drosophila melanogaster has several genes related to iron metabolism, including Malvolio, the only ortholog of DMT1. In this study, we employed the fruit fly to evaluate the effect of silencing Malvolio on mitochondrial dynamics.
We found that, like in our previous observation in mammals, Malvolio mutants exhibited altered expression of fission and fusion genes, suggesting mitochondrial dysfunction. To further explore the role of Malvolio in glial cells, gene expression was specifically downregulated in these cells, and mitochondria morphology was assessed.
This in vivo model will complement our previous “in vitro” results and will be of great interest to uncover the effect of iron homeostasis on mitochondrial dynamics of glial cells.

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