@article{22956,
  abstract     = {Tissue regeneration requires de novo patterning, which has been proposed to be facilitated by cellular heterogeneity. Yet how such heterogeneities are integrated with the mechanochemical state of the tissue and stabilized at the chromatin level into stable, spatially organized fates remains poorly understood. Using in vivo mouse intestinal regeneration models and organoids, we identify a critical density regime that produces a permissive window for heterogeneity in the mechanosensor Yes-associated protein 1 (YAP1). We show that YAP1 heterogeneity is coupled to lineage-biased chromatin accessibility and is decoded through FOXA1, which integrates the permissive chromatin state to Delta-Notch supracellular feedback and lineage commitment. This circuit generates fate bistability and preserves a memory of transient YAP1 activity, thereby maintaining spatial patterning as tissues return to homeostasis after injury. Together, our findings establish a multiscale framework in which tissue-scale mechanics tune single-cell competence and, through FOXA1-mediated bistability, convert transient heterogeneity into stable and self-organized tissue architecture.},
  author       = {Schwayer, Cornelia and Barbiero, Silvia and Brückner, David and Oost, Koen C. and Baader, Clara and Repina, Nicole A. and Kim, Jinse and Diaz, Oscar E. and Uccelli, Isa and Capolupo, Laura and Meylan, Ludivine Challet and Kalck, Veronique and Moos, Franziska and Suppinger, Simon and Yang, Qiutan and Schnabl, Jakob and Kilik, Umut and Bourdon, Matthieu and Camp, J. Gray and Stockinger, Brigitta and Ferrari, Alessandra and Bühler, Marc and Stadler, Michael B. and Hannezo, Edouard B and Liberali, Prisca},
  issn         = {1097-4172},
  journal      = {Cell},
  keywords     = {tissue patterning, heterogeneity, mechanics, intestinal regeneration, epigenetic competence, multiscale integration, modeling, organoids, image-based phenotyping, Yap1},
  number       = {17},
  pages        = {5266--5282.e17},
  publisher    = {Cell Press},
  title        = {{Multiscale integration of tissue and chromatin context converts cell heterogeneity into stable intestinal patterning}},
  doi          = {10.1016/j.cell.2026.06.009},
  volume       = {189},
  year         = {2026},
}

@article{7128,
  abstract     = {Loss of functional cardiomyocytes is a major determinant of heart failure after myocardial infarction. Previous high throughput screening studies have identified a few microRNAs (miRNAs) that can induce cardiomyocyte proliferation and stimulate cardiac regeneration in mice. Here, we show that all of the most effective of these miRNAs activate nuclear localization of the master transcriptional cofactor Yes-associated protein (YAP) and induce expression of YAP-responsive genes. In particular, miR-199a-3p directly targets two mRNAs coding for proteins impinging on the Hippo pathway, the upstream YAP inhibitory kinase TAOK1, and the E3 ubiquitin ligase β-TrCP, which leads to YAP degradation. Several of the pro-proliferative miRNAs (including miR-199a-3p) also inhibit filamentous actin depolymerization by targeting Cofilin2, a process that by itself activates YAP nuclear translocation. Thus, activation of YAP and modulation of the actin cytoskeleton are major components of the pro-proliferative action of miR-199a-3p and other miRNAs that induce cardiomyocyte proliferation.},
  author       = {Torrini, Consuelo and Cubero, Ryan J and Dirkx, Ellen and Braga, Luca and Ali, Hashim and Prosdocimo, Giulia and Gutierrez, Maria Ines and Collesi, Chiara and Licastro, Danilo and Zentilin, Lorena and Mano, Miguel and Zacchigna, Serena and Vendruscolo, Michele and Marsili, Matteo and Samal, Areejit and Giacca, Mauro},
  issn         = {2211-1247},
  journal      = {Cell Reports},
  keywords     = {cardiomyocyte, cell cycle, Cofilin2, cytoskeleton, Hippo, microRNA, regeneration, YAP},
  number       = {9},
  pages        = {2759--2771.e5},
  publisher    = {Elsevier},
  title        = {{Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation}},
  doi          = {10.1016/j.celrep.2019.05.005},
  volume       = {27},
  year         = {2019},
}