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Related Concept Videos

Nucleosome Remodeling02:54

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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The perpendicular-axis theorem states that the moment of inertia of a planar object about an axis perpendicular to its plane is equal to the sum of the moments of inertia about two mutually perpendicular concurrent axes lying in the plane of the body.
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The parallel-axis theorem provides a convenient and quick method of finding the moment of inertia of an object about an axis parallel to the axis passing through its center of mass. Consider a thin rod as an example. There is a striking similarity between the process of finding the moment of inertia of a thin rod about an axis through its middle, where the center of mass lies, and about an axis through its end using the conventional method. In the conventional method, the concept of linear mass...
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Related Experiment Video

Updated: Jan 21, 2026

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
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Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases

Published on: May 2, 2025

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mTORC1-PGC1 axis regulates mitochondrial remodeling during reprogramming.

Lulu Wang1,2,3,4,5, Xueting Xu1,2,3,4,6, Che Jiang1,2,3,4,5

  • 1Key Laboratory of Regenerative Biology and Guangdong Provincial Key Laboratory of Stem Cells and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health (GIBH), Chinese Academy of Sciences (CAS), Guangzhou, China.

The FEBS Journal
|July 31, 2019
PubMed
Summary
This summary is machine-generated.

Somatic cell reprogramming involves metabolic changes, but the role of mitophagy is debated. This study found no evidence for mitophagy, instead confirming mTORC1-PGC1 pathway suppression drives mitochondrial remodeling during reprogramming.

Keywords:
PGC1mTORC1mitochondrial remodelingmitophagyreprogramming

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Area of Science:

  • Cellular reprogramming
  • Metabolic pathways
  • Mitochondrial dynamics

Background:

  • Metabolic reprogramming, characterized by increased glycolysis and decreased mitochondrial activity, is crucial for early somatic cell reprogramming.
  • Existing research presents conflicting theories on the mechanisms of mitochondrial remodeling, including canonical and noncanonical mitophagy, mitochondrial fission, and reduced biogenesis via mTORC1 suppression.

Purpose of the Study:

  • To systematically investigate mitochondrial remodeling during somatic cell reprogramming.
  • To clarify the discrepancies regarding the role of mitophagy and other mechanisms in metabolic changes during reprogramming.
  • To elucidate the interplay between metabolic alterations and nutrient sensing pathways in cellular reprogramming.

Main Methods:

  • Systematic exploration of mitochondrial remodeling across diverse culture media and reprogramming factor combinations.
  • Application of rigorous quantification methods and statistical analysis.
  • Comparative analysis of different cellular reprogramming conditions and mitophagy detection techniques.

Main Results:

  • No evidence supporting a role for mitophagy in mitochondrial remodeling during somatic cell reprogramming was found.
  • The study confirmed that suppression of the mTORC1-PGC1 pathway is the primary driver of mitochondrial remodeling in this context.
  • Established clear distinctions from previous studies by employing standardized methodologies and comprehensive statistical validation.

Conclusions:

  • Mitophagy is not a significant contributor to mitochondrial remodeling in somatic cell reprogramming.
  • The mTORC1-PGC1 pathway's suppression is a key mechanism regulating metabolic shifts during reprogramming.
  • Findings provide a clearer understanding of metabolic reprogramming, with implications for development, aging, and cancer research.