Evidence map›Paper›PMID 40067243›Full record

ArticleJournal of cell science2025

Miro1 expression alters global gene expression, ERK1/2 phosphorylation, oxidation and cell cycle progression.

Nathaniel Shannon, Cory Raymond, Chloe Palmer, Silver Homa, Marcelo Bonini, David Seward, Brian Cunniff

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cell science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Nathaniel ShannonDepartment of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.
Cory RaymondDepartment of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.
Chloe PalmerDepartment of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.
Silver HomaDepartment of Medicine and Biochemistry, Feinberg School of Medicine Northwestern University, Chicago, IL 60611, USA.
Marcelo BoniniDepartment of Medicine and Biochemistry, Feinberg School of Medicine Northwestern University, Chicago, IL 60611, USA.
David SewardDepartment of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.
Brian CunniffDepartment of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.ORCID 0000-0002-6035-2134

Funding

Mitochondrial positioning regulates redox-signaling during cell migrationR01GM143250 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI Brian Cunniff · 2023 to 2026
$1.3M
NIGMS NIH HHS 1R01 GM143250NIGMS NIH HHS GM143250NIGMS NIH HHS R01 GM143250University of Vermont
6 · The paper itself

Abstract

Mitochondrial positioning supports localized energy and signaling requirements. Miro1 is necessary for attachment of mitochondria to microtubule motor proteins for trafficking. When Miro1 is deleted (Miro1-/-) from mouse embryonic fibroblasts (MEFs), mitochondria become sequestered to the perinuclear space, disrupting subcellular signaling gradients. Here, we show that Miro1-/- MEFs grow slower than Miro1+/+ and Miro1-/- MEFs stably re-expressing a Myc-Miro1 plasmid. Miro1-/- MEFs have a decreased percentage of cells in G1 and increased percentage of cells in S phase. We conducted the first ever RNA sequencing experiment dependent upon Miro1 expression and found differentially expressed genes related to MAPK signaling, cell proliferation and migration. ERK1 and ERK2 (ERK1/2, also known as MAPK3 and MAPK1, respectively) phosphorylation is elevated both spatially and temporally following serum stimulation in Miro1-/- MEFs, whereas the expression levels and oxidation of the dual specificity phosphatases (DUSP1-DUSP6) is unchanged. Finally, we found the oxidation status of ERK1/2 is increased in Miro1-/- MEFs compared to that seen in Miro1+/+ and Myc-Miro1 MEFs. These results highlight transcriptional control based off Miro1 expression and demonstrate the dynamic regulation of ERK1/2 upon deletion of Miro1 which might support the observed cell cycle and proliferation defects.

Indexed as

Cell CycleMitochondrial ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3rho GTP-Binding ProteinsAnimalsCell ProliferationFibroblastsGene Expression RegulationMAP Kinase Signaling SystemMiceMitochondriaOxidation-ReductionPhosphorylationMiro-1 protein, mouseMitochondrial ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3rho GTP-Binding ProteinsCell cycleERK1/2Miro1MitochondriaRedox

Identifiers

PMID40067243
PMCPMC11993262

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.