Evidence map›Paper›PMID 39508441›Full record

ArticleDevelopment (Cambridge, England)2024

The unique functions of Runx1 in skeletal muscle maintenance and regeneration are facilitated by an ETS interaction domain.

Meng Yu, Konrad Thorner, Sreeja Parameswaran, Wei Wei, Chuyue Yu, Xinhua Lin, Raphael Kopan, Matthew R Hass

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Development (Cambridge, England), 2024. 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. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Meng YuState Key Laboratory of Genetic Engineering, School of Life Sciences, Greater Bay Area Institute of Precision Medicine (Guangzhou), Zhongshan Hospital, Fudan University, Shanghai 200438, China.
Konrad ThornerDivision of Developmental Biology, Department of Pediatrics, University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Sreeja ParameswaranDivision of Human Genetics, Department of Pediatrics, University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Wei WeiState Key Laboratory of Genetic Engineering, School of Life Sciences, Greater Bay Area Institute of Precision Medicine (Guangzhou), Zhongshan Hospital, Fudan University, Shanghai 200438, China.
Chuyue YuState Key Laboratory of Genetic Engineering, School of Life Sciences, Greater Bay Area Institute of Precision Medicine (Guangzhou), Zhongshan Hospital, Fudan University, Shanghai 200438, China.
Xinhua LinState Key Laboratory of Genetic Engineering, School of Life Sciences, Greater Bay Area Institute of Precision Medicine (Guangzhou), Zhongshan Hospital, Fudan University, Shanghai 200438, China.
Raphael KopanDivision of Developmental Biology, Department of Pediatrics, University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Matthew R HassDivision of Developmental Biology, Department of Pediatrics, University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.ORCID 0000-0001-9507-4333

Funding

BIOCHEMICAL AND GENETIC ANALYSIS OF NOTCH SIGNALINGR01GM055479 · NIGMS · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL, WEIRAUCH, MATTHEW TYSON · 1996 to 2021
$6.4M
National Institutes of General Medical Sciences NIH GM55479National Natural Science Foundation of China 31730044NIGMS NIH HHS R01 GM055479NIH HHS GM55479Science and Technology Commission of Shanghai Municipality 20DZ2261200William K. Schubert Endowment
6 · The paper itself

Abstract

The conserved Runt-related (RUNX) transcription factor family are master regulators of developmental and regenerative processes. Runx1 and Runx2 are expressed in satellite cells (SCs) and in skeletal myotubes. Here, we examined the role of Runx1 in mouse satellite cells to determine the role of Runx1 during muscle differentiation. Conditional deletion of Runx1 in adult SCs negatively impacted self-renewal and impaired skeletal muscle maintenance even though Runx2 expression persisted. Runx1 deletion in C2C12 cells (which retain Runx2 expression) identified unique molecular functions of Runx1 that could not be compensated for by Runx2. The reduced myoblast fusion in vitro caused by Runx1 loss was due in part to ectopic expression of Mef2c, a target repressed by Runx1. Structure-function analysis demonstrated that the ETS-interacting MID/EID region of Runx1, absent from Runx2, is essential for Runx1 myoblast function and for Etv4 binding. Analysis of ChIP-seq datasets from Runx1 (T cells, muscle)- versus Runx2 (preosteoblasts)-dependent tissues identified a composite ETS:RUNX motif enriched in Runx1-dependent tissues. The ETS:RUNX composite motif was enriched in peaks open exclusively in ATAC-seq datasets from wild-type cells compared to ATAC peaks unique to Runx1 knockout cells. Thus, engagement of a set of targets by the RUNX1/ETS complex define the non-redundant functions of Runx1 in mouse muscle precursor cells.

Indexed as

Core Binding Factor Alpha 1 SubunitCore Binding Factor Alpha 2 SubunitMEF2 Transcription FactorsMuscle, SkeletalRegenerationSatellite Cells, Skeletal MuscleAnimalsCell DifferentiationCell FusionCell LineMiceMice, KnockoutMuscle DevelopmentMuscle Fibers, SkeletalMyoblastsProto-Oncogene Proteins c-etsCore Binding Factor Alpha 1 SubunitCore Binding Factor Alpha 2 SubunitMef2c protein, mouseMEF2 Transcription FactorsProto-Oncogene Proteins c-etsRunx1 protein, mouseRunx2 protein, mouseETSMuscleRunx1

Identifiers

PMID39508441
PMCPMC11664167

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.