Evidence map›Paper›PMID 37662191›Full record

ArticlebioRxiv : the preprint server for biology2023

Lineage tracing of newly accrued nuclei in skeletal myofibers uncovers distinct transcripts and interplay between nuclear populations.

Chengyi Sun, Casey O Swoboda, Michael J Petrany, Sreeja Parameswaran, Andrew VonHandorf, Matthew T Weirauch, Christoph Lepper, Douglas P Millay

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Chengyi SunDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Casey O SwobodaDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Michael J PetranyDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Sreeja ParameswaranDivision of Human Genetics, Center for Autoimmune Genetics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Andrew VonHandorfDivision of Human Genetics, Center for Autoimmune Genetics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Matthew T WeirauchDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Christoph LepperDepartment of Physiology & Cell Biology, College of Medicine, The Ohio State University, Columbus, OH, USA.
Douglas P MillayDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Cincinnati Children's Hospital Medical Center · USThe Ohio State University · US

Funding

Tissue Repository CoreP30AR070549 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI Leah Claire Kottyan · 2016 to 2026
$7.7M
Deciphering mechanisms of myoblast fusionR01AR068286 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2015 to 2024
$4.2M
Regulation of Muscle Stem Cell Number via Paracrine SignalingR01AR078231 · NIAMS · OHIO STATE UNIVERSITY · PI LEPPER, CHRISTOPH · 2021 to 2025
$1.9M
Role of skeletal muscle stem cell fusion and fibrosis during agingR01AG059605 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2018 to 2022
$1.7M
Myonuclear dynamics during skeletal muscle agingR01AG082697 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI Douglas Paul Millay · 2023 to 2026
$1.7M
Improving delivery of therapeutic material to skeletal muscleR61AR076771 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2019 to 2020
$795k
NIAMS NIH HHS P30 AR070549NIAMS NIH HHS R01 AR068286NIAMS NIH HHS R01 AR078231NIAMS NIH HHS R61 AR076771NIA NIH HHS R01 AG059605NIA NIH HHS R01 AG082697
6 · The paper itself

Abstract

Multinucleated skeletal muscle cells have an obligatory need to acquire additional nuclei through fusion with activated skeletal muscle stem cells when responding to both developmental and adaptive growth stimuli. A fundamental question in skeletal muscle biology has been the reason underlying this need for new nuclei in syncytial cells that already harbor hundreds of nuclei. To begin to answer this long-standing question, we utilized nuclear RNA-sequencing approaches and developed a lineage tracing strategy capable of defining the transcriptional state of recently fused nuclei and distinguishing this state from that of pre-existing nuclei. Our findings reveal the presence of conserved markers of newly fused nuclei both during development and after a hypertrophic stimulus in the adult. However, newly fused nuclei also exhibit divergent gene expression that is determined by the myogenic environment to which they fuse. Moreover, accrual of new nuclei through fusion is required for nuclei already resident in adult myofibers to mount a normal transcriptional response to a load-inducing stimulus. We propose a model of mutual regulation in the control of skeletal muscle development and adaptations, where newly fused and pre-existing myonuclear populations influence each other to maintain optimal functional growth.

Identifiers

PMID37662191
PMCPMC10473681
OpenAlexW4386157065

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.