Evidence map›Paper›PMID 41368786›Full record

ArticleBiology open2026

Retrograde signaling is required for Slm35-mediated negative regulation of mitophagy in yeast.

Hilario Ruelas-Ramírez, Ariann E Mendoza-Martínez, P Abril Medina-Flores, Soledad Funes

Abstract read
In one paragraph

Article in Biology open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Hilario Ruelas-RamírezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, Mexico.ORCID 0009-0004-8644-627X
Ariann E Mendoza-MartínezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, Mexico.ORCID 0000-0001-7195-1004
P Abril Medina-FloresDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, Mexico.ORCID 0009-0008-9716-0807
Soledad FunesDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, Mexico.ORCID 0000-0003-1815-1977

Funding

Direccion General de Asuntos del Personal Academico, Universidad Nacional Autonoma de Mexico IN208921Direccion General de Asuntos del Personal Academico, Universidad Nacional Autonoma de Mexico IN218424Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN208921Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN218424Secretaria de Ciencia, Humanidades, Tecnologia e Innovacion 925455Secretaria de Ciencia, Humanidades, Tecnologia e Innovacion CF-2019-MG-58550Secretaria de Ciencia, Humanidades, Tecnologia e Innovacion CF-2023-I-1545Secretaría de Ciencia, Humanidades, Tecnología e Innovación 925455Secretaría de Ciencia, Humanidades, Tecnología e Innovación CF-2019-MG-58550Secretaría de Ciencia, Humanidades, Tecnología e Innovación CF-2023-I-1545Universidad Nacional Autónoma de México
6 · The paper itself

Abstract

Mitophagy is essential for mitochondrial quality control, selectively removing damaged or superfluous mitochondria to maintain cellular health and metabolic homeostasis. While positive regulators of mitophagy are relatively well characterized, the mechanisms governing its downregulation remain less understood. In this study, we investigate the role of Saccharomyces cerevisiae Slm35 - a protein previously involved in oxidative stress response - in the regulation of mitophagy. We discovered that Slm35 is a soluble mitochondrial matrix protein and functions as a novel negative regulator of mitophagy and the mitochondrial retrograde (RTG) signaling pathway. Our results show that Slm35 modulates mitophagy through the RTG pathway, independently of Atg32 proteolytic processing by Yme1 or mitochondrial membrane potential dissipation. Notably, Slm35 is crucial for the dynamic regulation of the RTG pathway in mitophagy-inducing conditions. These findings highlight the importance of Slm35 in fine-tuning mitochondrial quality control in response to metabolic cues and suggest a critical role for dynamic RTG pathway regulation in mitophagy control.

Indexed as

Mitochondrial ProteinsMitophagySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionMitochondriaMitochondrial ProteinsSaccharomyces cerevisiae ProteinsAtg32MitochondriaMitochondrial retrograde signalingMitophagyYeast

Identifiers

PMID41368786
PMCPMC12817334

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.