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Updated: Jan 31, 2026

De Novo Generation of Somatic Stem Cells by YAP/TAZ
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Transient proliferation by reversible YAP and mitogen control of the cyclin D1/p27 ratio

Katherine R Ferrick1,2, Samsara W Upadhya1, Yilin Fan1,2,3

  • 1Department of Cell and Developmental Biology, Weill Cornell Medicine, New York, NY, USA.

Communications Biology
|January 29, 2026
PubMed

Insights

Hippo-YAP signaling controls cell proliferation during tissue repair. This study reveals YAP increases the cyclin D1/p27 ratio, promoting cell cycle entry, while contact inhibition later reverses this for safe regeneration.

Area of Science:

  • Cell Biology
  • Regenerative Medicine
  • Molecular Biology

Background:

  • Hippo-YAP signaling is crucial for tissue repair and regenerative medicine.
  • Understanding how YAP integrates signals to control cell proliferation is critical.

Purpose of the Study:

  • To elucidate the mechanism by which YAP integrates mitogenic and contact inhibition signals to regulate cell cycle entry and exit.
  • To identify key molecular players and ratios controlling proliferation during tissue repair.

Main Methods:

  • Investigated the role of YAP in regulating the nuclear cyclin D1/p27 protein ratio.
  • Examined the interplay between YAP, mitogen signaling (EGFR/ERK), and contact inhibition.
  • Analyzed the temporal dynamics of these factors during the cell cycle.

Main Results:

  • Reduced contact inhibition, increased mitogen signaling, and YAP-TEAD activation converge to raise the nuclear cyclin D1/p27 ratio in early G1 phase.
  • YAP induces mitogen signaling by upregulating receptors like EGFR, which signal via ERK.
  • Delayed contact inhibition suppresses YAP, downregulating mitogen signaling and the cyclin D1/p27 ratio, preventing uncontrolled proliferation.

Conclusions:

  • A YAP-induced, receptor-mediated, prolonged increase in the cyclin D1/p27 ratio is essential for robust proliferation in tissue regeneration.
  • Delayed suppression of receptor signaling following contact inhibition is critical for preventing cancer initiation during regeneration.

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