@article{6412,
  abstract     = {Polycomb group (PcG) proteins play critical roles in the epigenetic inheritance of cell fate. The Polycomb Repressive Complexes PRC1 and PRC2 catalyse distinct chromatin modifications to enforce gene silencing, but how transcriptional repression is propagated through mitotic cell divisions remains a key unresolved question. Using reversible tethering of PcG proteins to ectopic sites in mouse embryonic stem cells, here we show that PRC1 can trigger transcriptional repression and Polycomb-dependent chromatin modifications. We find that canonical PRC1 (cPRC1), but not variant PRC1, maintains gene silencing through cell division upon reversal of tethering. Propagation of gene repression is sustained by cis-acting histone modifications, PRC2-mediated H3K27me3 and cPRC1-mediated H2AK119ub1, promoting a sequence-independent feedback mechanism for PcG protein recruitment. Thus, the distinct PRC1 complexes present in vertebrates can differentially regulate epigenetic maintenance of gene silencing, potentially enabling dynamic heritable responses to complex stimuli. Our findings reveal how PcG repression is potentially inherited in vertebrates.},
  author       = {Moussa, Hagar F. and Bsteh, Daniel and Yelagandula, Ramesh and Pribitzer, Carina and Stecher, Karin and Bartalska, Katarina and Michetti, Luca and Wang, Jingkui and Zepeda-Martinez, Jorge A. and Elling, Ulrich and Stuckey, Jacob I. and James, Lindsey I. and Frye, Stephen V. and Bell, Oliver},
  issn         = {20411723},
  journal      = {Nature Communications},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing}},
  doi          = {10.1038/s41467-019-09628-6},
  volume       = {10},
  year         = {2019},
}

@article{6465,
  abstract     = {Tight control over protein degradation is a fundamental requirement for cells to respond rapidly to various stimuli and adapt to a fluctuating environment. Here we develop a versatile, easy-to-handle library of destabilizing tags (degrons) for the precise regulation of protein expression profiles in mammalian cells by modulating target protein half-lives in a predictable manner. Using the well-established tetracycline gene-regulation system as a model, we show that the dynamics of protein expression can be tuned by fusing appropriate degron tags to gene regulators. Next, we apply this degron library to tune a synthetic pulse-generating circuit in mammalian cells. With this toolbox we establish a set of pulse generators with tailored pulse lengths and magnitudes of protein expression. This methodology will prove useful in the functional roles of essential proteins, fine-tuning of gene-expression systems, and enabling a higher complexity in the design of synthetic biological systems in mammalian cells.},
  author       = {Chassin, Hélène and Müller, Marius and Tigges, Marcel and Scheller, Leo and Lang, Moritz and Fussenegger, Martin},
  issn         = {20411723},
  journal      = {Nature Communications},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{A modular degron library for synthetic circuits in mammalian cells}},
  doi          = {10.1038/s41467-019-09974-5},
  volume       = {10},
  year         = {2019},
}

@article{6899,
  abstract     = {Intra-organ communication guides morphogenetic processes that are essential for an organ to carry out complex physiological functions. In the heart, the growth of the myocardium is tightly coupled to that of the endocardium, a specialized endothelial tissue that lines its interior. Several molecular pathways have been implicated in the communication between these tissues including secreted factors, components of the extracellular matrix, or proteins involved in cell-cell communication. Yet, it is unknown how the growth of the endocardium is coordinated with that of the myocardium. Here, we show that an increased expansion of the myocardial atrial chamber volume generates higher junctional forces within endocardial cells. This leads to biomechanical signaling involving VE-cadherin, triggering nuclear localization of the Hippo pathway transcriptional regulator Yap1 and endocardial proliferation. Our work suggests that the growth of the endocardium results from myocardial chamber volume expansion and ends when the tension on the tissue is relaxed.},
  author       = {Bornhorst, Dorothee and Xia, Peng and Nakajima, Hiroyuki and Dingare, Chaitanya and Herzog, Wiebke and Lecaudey, Virginie and Mochizuki, Naoki and Heisenberg, Carl-Philipp J and Yelon, Deborah and Abdelilah-Seyfried, Salim},
  issn         = {20411723},
  journal      = {Nature communications},
  number       = {1},
  pages        = {4113},
  publisher    = {Nature Publishing Group},
  title        = {{Biomechanical signaling within the developing zebrafish heart attunes endocardial growth to myocardial chamber dimensions}},
  doi          = {10.1038/s41467-019-12068-x},
  volume       = {10},
  year         = {2019},
}