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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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YAP mediates apoptosis through failed integrin adhesion reinforcement.

Lidan Shi1, Elisabeth Nadjar-Boger1, Hamidreza Jafarinia2

  • 1Department of Genetics and Developmental Biology, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 31096, Israel.

Cell Reports
|February 23, 2024
PubMed
Summary

Cellular apoptosis on soft matrices is driven by Yes-associated protein (YAP) signaling. YAP translocation to the nucleus, triggered by soft matrix interactions, induces programmed cell death, revealing a new role for YAP in cell fate.

Keywords:
CP: Cell biologySrcYAPactomyosinanchorage-independenceapoptosisc-AblmechanosensingpYAP-Y357rigidity sensing

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Area of Science:

  • Cell Biology
  • Biophysics
  • Biochemistry

Background:

  • Extracellular matrix (ECM) rigidity significantly influences cell fate decisions, impacting processes like proliferation.
  • While the role of Yes-associated protein (YAP) in cell proliferation on stiff matrices is established, its function in apoptosis induction on soft matrices remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which YAP regulates apoptosis in response to varying extracellular matrix rigidity.
  • To investigate the role of YAP phosphorylation and localization in mediating cell fate decisions on soft versus stiff matrices.

Main Methods:

  • Analysis of YAP localization and phosphorylation at the Y357 residue in cells cultured on matrices of differing rigidities.
  • Investigation of the impact of actomyosin contractility modulation on YAP signaling and cell fate.
  • Microscopy and biochemical assays to assess cell adhesion dynamics and nuclear translocation of YAP.

Main Results:

  • On soft matrices, YAP is recruited to small adhesions, phosphorylated at Y357, and translocates to the nucleus, promoting apoptosis.
  • Conversely, stiff matrices exhibit low Y357 phosphorylation levels in large adhesions, correlating with cell proliferation.
  • Reduced actomyosin contractility on soft matrices facilitates adhesion growth, decreases Y357 phosphorylation, and promotes cell growth.

Conclusions:

  • Failed adhesion reinforcement on soft matrices drives YAP-mediated, rigidity-dependent apoptosis.
  • Cell fate decisions are determined not solely by ECM rigidity but by the interplay between cellular forces and matrix stiffness.
  • YAP plays a dual role in cell fate, regulating both proliferation on stiff matrices and apoptosis on soft matrices.