Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.9K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

4.1K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.1K
Maintenance of the ES Cell State01:14

Maintenance of the ES Cell State

2.3K
The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
2.3K
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

2.3K
Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
2.3K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

5.7K
Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.7K
Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

1.9K
Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
1.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Adult attachment profiles, death attitudes, and intention to remain in nursing among Chinese intern nursing students.

Frontiers in medicine·2026
Same author

Latent profiles of ethical sensitivity and correlates in nursing interns.

Nursing ethics·2026
Same author

A Rras2-BMPR2 feedback loop sustains osteogenesis and represents a therapeutic target for osteoporosis.

Nature communications·2026
Same author

Mitochondrial NADH-redox inflexibility constrains genomic and epigenetic stability in pluripotent stem cells.

The EMBO journal·2026
Same author

CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

HuR coordinates systemic aging through platelet infiltration.

Nature communications·2026

Related Experiment Video

Updated: Oct 11, 2025

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening
07:18

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening

Published on: May 12, 2017

6.6K

The mTORC1-eIF4F axis controls paused pluripotency.

Xueting Xu1,2,3, Tanveer Ahmed2,3, Lulu Wang2,3

  • 1School of Life Sciences, University of Science and Technology of China, Hefei, China.

EMBO Reports
|December 6, 2021
PubMed
Summary

Mechanistic target of rapamycin complex 1 (mTORC1) inhibition induces paused pluripotency in mouse embryonic stem cells (mESCs) by regulating translation initiation. This process impacts both cytosolic and mitochondrial ribosome subunit production, revealing context-dependent pluripotency regulation.

Keywords:
eIF4FmTORC1mitochondrial translationpluripotencyself-renewal

More Related Videos

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
08:47

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

3.2K
A Two-Step Strategy that Combines Epigenetic Modification and Biomechanical Cues to Generate Mammalian Pluripotent Cells
08:01

A Two-Step Strategy that Combines Epigenetic Modification and Biomechanical Cues to Generate Mammalian Pluripotent Cells

Published on: August 29, 2020

2.4K

Related Experiment Videos

Last Updated: Oct 11, 2025

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening
07:18

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening

Published on: May 12, 2017

6.6K
Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
08:47

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

3.2K
A Two-Step Strategy that Combines Epigenetic Modification and Biomechanical Cues to Generate Mammalian Pluripotent Cells
08:01

A Two-Step Strategy that Combines Epigenetic Modification and Biomechanical Cues to Generate Mammalian Pluripotent Cells

Published on: August 29, 2020

2.4K

Area of Science:

  • Stem cell biology
  • Molecular and Cell Biology
  • Biochemistry

Background:

  • Mouse embryonic stem cells (mESCs) possess indefinite self-renewal and pluripotency.
  • Understanding the mechanisms of pluripotency regulation is crucial for stem cell applications.
  • The role of mechanistic target of rapamycin (mTOR) in mESC self-renewal is complex and context-dependent.

Purpose of the Study:

  • To elucidate the specific mTOR complex involved in mTOR inhibition-induced paused pluripotency in mESCs.
  • To investigate the downstream targets and mechanisms by which mTOR regulates self-renewal and pluripotency.
  • To compare the regulation of translation and pluripotency under different culture conditions (Serum/LIF vs. 2iL).

Main Methods:

  • Pharmacological inhibition of mTOR using INK128.
  • Culture of mESCs in Serum/LIF (SL) and 2iL media.
  • Analysis of protein translation initiation factors (eIF4F).
  • Assessment of cytosolic and mitochondrial ribosome subunit mRNA translation.
  • Evaluation of pluripotency gene expression and cell cycle status.

Main Results:

  • mTOR complex 1 (mTORC1), not mTOR complex 2 (mTORC2), mediates paused pluripotency induced by mTOR inhibition in both SL and 2iL media.
  • mTORC1 regulates mESC self-renewal primarily via eIF4F-mediated translation initiation, affecting mRNAs for both cytosolic and mitochondrial ribosome subunits.
  • Inhibition of mitochondrial translation alone is sufficient to induce paused pluripotency.
  • eIF4F also regulates pluripotency independently of mTORC1 but dependent on MEK/ERK signaling in SL medium, highlighting differential regulation in SL versus 2iL.

Conclusions:

  • mTORC1 is the key mediator of mTOR inhibition-induced paused pluripotency in mESCs across different culture conditions.
  • Regulation of translation initiation, particularly for ribosome subunits, is a critical mechanism by which mTORC1 controls mESC self-renewal.
  • The study uncovers a context-dependent role for eIF4F in maintaining pluripotency, with distinct regulatory pathways in SL and 2iL media.