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Updated: Jan 7, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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DMTF1 up-regulation rescues proliferation defect of telomere dysfunctional neural stem cells via the SWI/SNF-E2F axis

Yajing Liang1,2, Oleg V Grinchuk1,3, Nadia Omega Cipta4

  • 1Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.

Science Advances
|January 2, 2026
PubMed

Insights

Neural stem cell (NSC) aging impairs brain function. We found DMTF1 down-regulation causes this defect by affecting SWI/SNF complexes, identifying DMTF1 as a therapeutic target for brain aging.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neural stem cell (NSC) proliferation declines with brain aging.
  • Mechanisms underlying NSC aging, particularly telomere dysfunction, are not fully understood.

Purpose of the Study:

  • Investigate the role of DMTF1 in NSC proliferation during aging.
  • Identify molecular pathways regulated by DMTF1 in NSCs.

Main Methods:

  • Utilized a telomerase-deficient premature aging model.
  • Assessed DMTF1 expression and function in NSCs.
  • Analyzed the impact of DMTF1 on SWI/SNF complex subunits (Arid2, Ss18) and H3K27ac levels.
  • Examined the regulation of E2F target genes.

Main Results:

  • DMTF1 is down-regulated in NSCs of premature aging models.
  • Upregulating DMTF1 rescued proliferation in telomere-dysfunctional NSCs.
  • DMTF1 transcriptionally regulates Arid2 and Ss18, SWI/SNF components.
  • DMTF1 controls H3K27ac at E2F promoters, promoting NSC proliferation.

Conclusions:

  • DMTF1 is a key regulator of NSC proliferation and a potential therapeutic target for brain aging.
  • DMTF1 orchestrates a distinct genetic program involving SWI/SNF complexes and H3K27ac for NSC maintenance.

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