Evidence map›Paper›PMID 39910760›Full record

ArticleAging cell2025

Novel TORC1 inhibitor Ecl1 is regulated by phosphorylation in fission yeast.

Hokuto Ohtsuka, Sawa Kawai, Yurika Ito, Yuka Kato, Takafumi Shimasaki, Kazuki Imada, Yoko Otsubo, Akira Yamashita, Emi Mishiro-Sato, Keiko Kuwata and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2025. 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

11 authors.

Hokuto OhtsukaDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.ORCID 0000-0001-7843-2602
Sawa KawaiDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.
Yurika ItoDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.
Yuka KatoDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.
Takafumi ShimasakiDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.ORCID 0000-0003-2558-9395
Kazuki ImadaDepartment of Chemistry and Biochemistry, Suzuka College, National Institute of Technology (KOSEN), Suzuka, Japan.ORCID 0000-0002-9894-6579
Yoko OtsuboDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-2401-4808
Akira YamashitaDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-1805-1434
Emi Mishiro-SatoInstitute of Transformative bio-Molecules, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.ORCID 0000-0001-5528-4440
Keiko KuwataInstitute of Transformative bio-Molecules, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.
Hirofumi AibaDepartment of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Laboratory of Molecular Microbiology, Tokai National Higher Education and Research System, Nagoya University, Nagoya, Japan.ORCID 0000-0002-7775-0446

Funding

JSPS KAKENHI JP21K05363JSPS KAKENHI JP23H02125
6 · The paper itself

Abstract

Extender of chronological lifespan 1 (Ecl1) inhibits target of rapamycin complex 1 (TORC1) and is necessary for appropriate cellular responses to various stressors, such as starvation, in fission yeast. However, little is known about the effect of posttranslational modifications on Ecl1 regulation. Thus, we investigated the phosphorylation levels of Ecl1 extracted from yeast under conditions of sulfur or metal starvation. Mass spectrometry analysis revealed that Ecl1 was phosphorylated at Thr7, and the level was decreased by starvation. The phosphorylation-mimetic mutation of Thr7 significantly reduced the effects of Ecl1-induced cellular responses to starvation, suggesting that Ecl1 function was suppressed by Thr7 phosphorylation. By contrast, regardless of starvation exposure, TORC1 was significantly suppressed, even when Thr7 phosphorylation-mimetic Ecl1 was overexpressed. This indicated that Ecl1 suppressed TORC1 regardless of Thr7 phosphorylation. We newly identified that Ecl1 physically interacted with TORC1 subunit RAPTOR (Mip1). Based on these evidences, we propose that, Ecl1 has dual functional modes: quantity-dependent TORC1 inhibition and Thr7 phosphorylation-dependent control of cellular function.

Indexed as

Mechanistic Target of Rapamycin Complex 1SchizosaccharomycesSchizosaccharomyces pombe ProteinsNuclear ProteinsPhosphorylationEcl1 protein, S pombeMechanistic Target of Rapamycin Complex 1Nuclear ProteinsSchizosaccharomyces pombe ProteinsEcl1fission yeasphosphorylationstarvationTORC1

Identifiers

PMID39910760
PMCPMC11984688

What Socratic holds

Textmetadata
LicenceCC BY
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.