Evidence map›Paper›PMID 30979898›Full record

ArticleNature communications2019

MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation.

Xiao Hu, Zongzhi Z Liu, Xinyue Chen, Vincent P Schulz, Abhishek Kumar, Amaleah A Hartman, Jason Weinstein, Jessica F Johnston, Elisa C Rodriguez, Anna E Eastman and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
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

37 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
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  8. Review
  9. Review
  10. Review
  11. Plasticity in leukocyte migration during haematopoiesis and inflammation.Journal of muscle research and cell motility · 2025
    Review
  12. Article
  13. Don't be so naïve.eLife · 2024
    Article
  14. Emerin deficiency drives MCF7 cells to an invasive phenotype.bioRxiv : the preprint server for biology · 2024
    Article
  15. Article
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  17. Article
  18. Article
  19. Article
  20. Review
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

20 authors at 2 institutions in 1 country.

Xiao HuDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Zongzhi Z LiuDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Xinyue ChenDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Vincent P SchulzDepartment of Pediatrics, Yale University, New Haven, CT, 06520, USA.
Abhishek KumarDepartment of Medicine (Cardiology), Yale University, New Haven, CT, 06520, USA.ORCID http://orcid.org/0000-0003-3235-1916
Amaleah A HartmanDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Jason WeinsteinDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Jessica F JohnstonDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.ORCID http://orcid.org/0000-0001-6696-7909
Elisa C RodriguezDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Anna E EastmanDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Jijun ChengYale Stem Cell Center, Yale University, New Haven, CT, 06520, USA.
Liz MinDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Mei ZhongDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Christopher CarrollDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Patrick G GallagherDepartment of Pathology, Yale Cancer Center, Yale University, New Haven, CT, 06520, USA.
Jun LuYale Stem Cell Center, Yale University, New Haven, CT, 06520, USA.
Martin SchwartzDepartment of Medicine (Cardiology), Yale University, New Haven, CT, 06520, USA.ORCID http://orcid.org/0000-0002-2071-1243
Megan C KingDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Diane S KrauseDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA.
Shangqin GuoDepartment of Cell Biology, Yale University, New Haven, CT, 06520, USA. shangqin.guo@yale.edu.
Yale Cancer Center · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
YEAST MEMBRANE CYTOSKELETONP01DK032094 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI GALLAGHER, PATRICK G · 1987 to 2021
$26.7M
Yale Cooperative Hematology Specialized Core CenterU54DK106857 · NIDDK · YALE UNIVERSITY · PI JOHN HWA, Diane S Krause · 2015 to 2026
$9.7M
Mechanisms of megakaryocyte maturationR01DK094934 · NIDDK · YALE UNIVERSITY · PI KRAUSE, DIANE S · 2012 to 2016
$2.7M
Molecular definition of cancer cell-of-originDP2GM123507 · NIGMS · YALE UNIVERSITY · PI GUO, SHANGQIN · 2016 to 2016
$2.5M
Remodeling of the structure and function of the nuclear lamina by LINC complex-dependent tensionR01GM129308 · NIGMS · YALE UNIVERSITY · PI KING, MEGAN C · 2018 to 2021
$1.3M
NCATS NIH HHS UL1 TR001863NIDDK NIH HHS P01 DK032094NIDDK NIH HHS R01 DK094934NIDDK NIH HHS U54 DK106857NIGMS NIH HHS DP2 GM123507NIGMS NIH HHS R01 GM129308
6 · The paper itself

Abstract

Actin cytoskeleton is well-known for providing structural/mechanical support, but whether and how it regulates chromatin and cell fate reprogramming is far less clear. Here, we report that MKL1, the key transcriptional co-activator of many actin cytoskeletal genes, regulates genomic accessibility and cell fate reprogramming. The MKL1-actin pathway weakens during somatic cell reprogramming by pluripotency transcription factors. Cells that reprogram efficiently display low endogenous MKL1 and inhibition of actin polymerization promotes mature pluripotency activation. Sustained MKL1 expression at a level seen in typical fibroblasts yields excessive actin cytoskeleton, decreases nuclear volume and reduces global chromatin accessibility, stalling cells on their trajectory toward mature pluripotency. In addition, the MKL1-actin imposed block of pluripotency can be bypassed, at least partially, when the Sun2-containing linker of the nucleoskeleton and cytoskeleton (LINC) complex is inhibited. Thus, we unveil a previously unappreciated aspect of control on chromatin and cell fate reprogramming exerted by the MKL1-actin pathway.

Indexed as

Cellular ReprogrammingActin CytoskeletonAnimalsCell DifferentiationCell NucleusChromatinCytoskeletonFemaleFibroblastsFluorescence Resonance Energy TransferGenotypeGreen Fluorescent ProteinsMaleMiceOncogene Proteins, FusionPluripotent Stem CellsChromatinGreen Fluorescent ProteinsMrtfa protein, mouseOncogene Proteins, FusionTrans-Activators

Identifiers

PMID30979898
PMCPMC6461646
OpenAlexW2940283586

What OpenQuestion holds

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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.