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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.
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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...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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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.
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Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Metabolic Control over mTOR-Dependent Diapause-like State.

Abdiasis M Hussein1, Yuliang Wang2, Julie Mathieu3

  • 1Department of Biochemistry, University of Washington, Seattle, WA 98195, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98109, USA.

Developmental Cell
|January 29, 2020
PubMed
Summary
This summary is machine-generated.

Embryonic diapause regulation involves activated lipolysis and glycolysis, driven by mTORC1/2 inhibition. This metabolic shift, influenced by amino acid levels, establishes a reversible dormant state essential for developmental arrest.

Keywords:
H4K16AcLKB1amino acidsdiapauseepigeneticsglutamine transporterlipolysismTORmetabolismpluripotent stem cells

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Area of Science:

  • Developmental Biology
  • Cellular Metabolism
  • Epigenetics

Background:

  • Embryonic diapause, a state of developmental arrest, is crucial for mammalian reproduction but its regulatory mechanisms remain unclear.
  • Understanding diapause is key to addressing infertility and reproductive challenges.

Purpose of the Study:

  • To elucidate the molecular and metabolic underpinnings of embryonic diapause in mice.
  • To identify key pathways and epigenetic modifications governing the dormant state.

Main Methods:

  • Transcriptional and metabolite profiling of mouse diapause embryos.
  • In vitro studies using mouse embryonic stem cells (ESCs) under starvation conditions.
  • Genetic manipulation and small molecule inhibition of key signaling pathways and transporters.

Main Results:

  • Diapause embryos exhibit activated lipolysis and glycolysis, regulated by AMPK and mTORC1/2 signaling.
  • Starvation induces a reversible, diapause-like dormant state in ESCs, characterized by specific metabolic and epigenetic changes (H4K16Ac-negative).
  • Glutamine transporters (SLC38A1/2) are essential for maintaining the diapause-associated epigenetic state.

Conclusions:

  • mTORC1/2 inhibition, triggered by amino acid availability, is a central regulator of diapause metabolism and epigenetics.
  • Lipolysis and glycolysis are critical metabolic adaptations supporting cell survival during diapause.
  • Targeting glutamine transporters offers a potential strategy to manipulate diapause states.