Evidence map›Paper›PMID 39453814›Full record

ArticleCell reports2024

TASOR expression in naive embryonic stem cells safeguards their developmental potential.

Carlos A Pinzon-Arteaga, Ryan O'Hara, Alice Mazzagatti, Emily Ballard, Yingying Hu, Alex Pan, Daniel A Schmitz, Yulei Wei, Masahiro Sakurai, Peter Ly and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2024. 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

12 authors.

Carlos A Pinzon-ArteagaDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Howard Hughes Medical Institute, Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Ryan O'HaraCecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Alice MazzagattiDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Emily BallardDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Yingying HuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Alex PanDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; St. Mark's School of Texas, Dallas, TX 75230, USA.
Daniel A SchmitzDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Yulei WeiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; State Key Laboratory of Animal Biotech Breeding, College of Biological Sciences, China Agricultural University, Beijing 100193, China.
Masahiro SakuraiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Peter LyDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Cell Biology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Laura A BanaszynskiHamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Cecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: laura.banaszynski@utsouthwestern.edu.
Jun WuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Cecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: jun2.wu@utsouthwestern.edu.

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Kathryn Ann O'Donnell · 2010 to 2026
$53.7M
Chromatin Dynamics and Genome RegulationR35GM124958 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Laura Banaszynski · 2017 to 2026
$4.4M
Mechanisms of p300 Activation During Pluripotency and Differentiation.R01HD109239 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI Laura Banaszynski · 2022 to 2026
$2.1M
Dissect formative pluripotency using cultured pluripotent stem cellsR01GM138565 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI WU, JUN · 2021 to 2025
$1.7M
Spinning Disk Confocal for UT SouthwesternS10OD028630 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2020 to 2020
$600k
Derivation of chimera competent pig embryonic stem cells under a novel conditionR21OD028763 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI WU, JUN · 2020 to 2021
$452k
NCI NIH HHS P30 CA142543NICHD NIH HHS R01 HD109239NIGMS NIH HHS R01 GM138565NIGMS NIH HHS R35 GM124958NIH HHS R21 OD028763NIH HHS S10 OD028630
6 · The paper itself

Abstract

The seamless transition through stages of pluripotency relies on a balance between transcription factor networks and epigenetic mechanisms. Here, we reveal the crucial role of the transgene activation suppressor (TASOR), a component of the human silencing hub (HUSH) complex, in maintaining cell viability during the transition from naive to primed pluripotency. TASOR loss in naive pluripotent stem cells (PSCs) triggers replication stress, disrupts H3K9me3 heterochromatin, and impairs silencing of LINE-1 (L1) transposable elements, with more severe effects in primed PSCs. Notably, the survival of Tasor knockout PSCs during this transition can be restored by inhibiting caspase or deleting the mitochondrial antiviral signaling protein (MAVS). This suggests that unscheduled L1 expression activates an innate immune response, leading to cell death specifically in cells exiting naive pluripotency. Our findings highlight the importance of epigenetic programs established in naive pluripotency for normal development.

Indexed as

Embryonic Stem CellsAnimalsCell DifferentiationCell SurvivalEpigenesis, GeneticHumansLong Interspersed Nucleotide ElementsMicePluripotent Stem Cells5mCCP: Stem cell researchDNA methylationH3K9me3heterochromatinHUSH complexL1LINE-1naive pluripotencyprimed pluripotencyStem cellsTASOR

Identifiers

PMID39453814
PMCPMC11646706

What OpenQuestion 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 OpenQuestion graph.