Dysfunction of <i>Drosophila</i> mitochondrial carrier homolog (Mtch) alters apoptosis and disturbs development-Reference-Cited by-同舟云学术

Dysfunction of Drosophila mitochondrial carrier homolog (Mtch) alters apoptosis and disturbs development

Published:2023-12-19 Issue: Volume: Page:
ISSN:2211-5463
Container-title:FEBS Open Bio
language:en
Short-container-title:FEBS Open Bio

Author:

González Cristina¹,Martínez‐Sánchez Lidia¹,Clemente Paula¹,Toivonen Janne Markus²³⁴,Arredondo Juan José¹,Fernández‐Moreno Miguel Ángel⁵⁶,Carrodeguas José Alberto³⁷⁸^ORCID

Affiliation:

1. Departamento de Bioquímica & Instituto de Investigaciones Biomédicas “Alberto Sols” The Autonomous University of Madrid‐Consejo Superior de Investigaciones Científicas Spain

2. LAGENBIO, Departamento de Anatomía, Embriología y Genética Animal, Facultad de Veterinaria, Instituto Agroalimentario de Aragón (IA2) Universidad de Zaragoza Spain

3. IIS Aragón Zaragoza Spain

4. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED) Madrid Spain

5. Centro de Investigación Biomédica en Red en Enfermedades Raras (CIBERER) Facultad de Medicina, UAM Madrid Spain

6. Departamento de Bioquímica & Instituto de Investigaciones Biomédicas Sols‐Morreale The Autonomous University of Madrid‐Consejo Superior de Investigaciones Científicas Madrid Spain

7. Institute for Biocomputation and Physics of Complex Systems (BIFI) University of Zaragoza Spain

8. Department of Biochemistry and Molecular and Cellular Biology, School of Sciences University of Zaragoza Spain

Abstract

Mitochondrial carrier homologs 1 (MTCH1) and 2 (MTCH2) are orphan members of the mitochondrial transporter family SLC25. Human MTCH1 is also known as presenilin 1‐associated protein, PSAP. MTCH2 is a receptor for tBid and is related to lipid metabolism. Both proteins have been recently described as protein insertases of the outer mitochondrial membrane. We have depleted Mtch in Drosophila and show here that mutant flies are unable to complete development, showing an excess of apoptosis during pupation; this observation was confirmed by RNAi in Schneider cells. These findings are contrary to what has been described in humans. We discuss the implications in view of recent reports concerning the function of these proteins.

Funder

Ministerio de Ciencia e Innovación

Universidad de Zaragoza

Publisher

Wiley

Subject

General Biochemistry, Genetics and Molecular Biology

Link

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1002/2211-5463.13742

Reference55 articles.

1. Mitochondrial Regulation of Cell Death

2. Apoptosis: A Review of Programmed Cell Death

3. Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors

4. Structural Insights of tBid, the Caspase-8-activated Bid, and Its BH3 Domain

5. MTCH2/MIMP is a major facilitator of tBID recruitment to mitochondria

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