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Record W4417016281 · doi:10.1182/blood-2025-6765

The mitochondrial protease YME1L regulates type 1 interferon signaling via the cgas-sting pathway in AML

2025· article· en· W4417016281 on OpenAlexaff
Yihe Zhang, Geethu Emily Thomas, Rose Hurren, Yongran Yan, Dakai Ling, Marcela Gronda, Andrea Arruda, Mark Minden, Aaron D. Schimmer

Bibliographic record

VenueBlood · 2025
Typearticle
Languageen
FieldMedicine
TopicAcute Myeloid Leukemia Research
Canadian institutionsPrincess Margaret Cancer CentreUniversity of Toronto
Fundersnot available
KeywordsGene knockdownDownregulation and upregulationMyeloid leukemiaHaematopoiesisSignal transductionMyeloidInterferonCell growthRNA interference

Abstract

fetched live from OpenAlex

Abstract Yeast Mitochondrial Escape 1-Like 1 (YME1L) is an inner mitochondrial membrane–anchored ATP-dependent metalloprotease. Here, we investigated its expression and functional role in acute myeloid leukemia (AML). YME1L protein was upregulated in 6 out of 7 AML cell lines and 17 of 23 primary AML patient samples compared to normal hematopoietic stem cells. Analysis of the TCGA dataset revealed that high YME1L mRNA expression correlated with inferior 5-year overall survival in AML patients. To evaluate the essentiality of YME1L in AML, we knocked down the protease in AML cell lines (OCI-AML2, NB4, TEX, and THP-1) with shRNA. YME1L knockdown decreased cell proliferation and clonogenic growth in all tested cell lines. Moreover, YME1L depletion decreased the engraftment of TEX cells into the marrow of immune deficient mice. Interestingly, YME1L knockdown did not induce cell death as measured by Annexin V/PI staining. Rather, YME1L knockdown induced AML differentiation as evidenced by upregulation of CD14, a marker of monocytic differentiation. To understand how YME1L promoted differentiation and decreased proliferation, we performed RNA sequencing of AML cells after YME1L depletion. Knockdown of YME1L upregulated genes associated with type I interferon (IFN) signaling and viral mimicry pathways. By qPCR, we confirmed upregulation of IFN-β, IFN-γ, and interferon-stimulated genes, ISG15, IFI44, IFIT2 after YME1L knockdown. We demonstrated that activation of the IFN signaling was secondary to activation of the cGAS–STING pathway as pharmacologically inhibiting STING abolished the upregulation of IFN signaling after YME1L depletion. We also showed that YME1L knockdown promoted the release of mitochondrial double-stranded DNA into the cytoplasm, a known trigger of IFN signaling. Finally, we demonstrated that inhibiting the VDAC channel with VBIT-4 blocked the upregulation of IFN signaling after YME1L knockdown, thus supporting the functional importance of mtDNA efflux into the cytoplasm as the mechanism explaining increased IFN signaling after YME1L depletion. In summary, we demonstrated that YME1L is overexpressed in a subset of AML samples and is required for AML proliferation and clonogenic growth. YME1L regulates the leakage of mtDNA into the cytoplasm, activation of the cGAS–STING–IFN axis, and AML differentiation. Thus, we have uncovered novel functions for the mitochondrial protease YME1L in AML and new mechanisms for how a mitochondrial protease regulates nuclear gene expression and progenitor function.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.005

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.015
GPT teacher head0.278
Teacher spread0.263 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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