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Fernandez-Gonzalez R.,University of Toronto | Fernandez-Gonzalez R.,Hubrecht Institute for Developmental Biology and Stem Cell Research | Zallen J.A.,Howard Hughes Medical Institute
Cell | Year: 2012

Tissues develop in confined volumes that can impose mechanical constraints on their growth, but it is unclear how cells respond to these limits to regulate tissue size and shape. Two papers show that overcrowding and cell deformation lead to the shedding of live cells to maintain homeostasis in epithelial cell sheets. © 2012 Elsevier Inc. Source

Deschamps J.,Hubrecht Institute for Developmental Biology and Stem Cell Research
Nature Genetics | Year: 2016

The recently discovered chromatin compartments called topologically associating domains (TADs) are essential for the three-dimensional organization of regulatory interactions driving gene expression. A new study documents the emergence of a TAD flanking the amphioxus Hox cluster, prefiguring the vertebrate anterior Hox TAD and preceding the appearance of the concurring posterior Hox TAD. © 2016 Nature America, Inc. Source

Mallo M.,Instituto Gulbenkian Of Ciencia | Mallo M.,University of Lisbon | Wellik D.M.,University of Michigan | Deschamps J.,Hubrecht Institute for Developmental Biology and Stem Cell Research
Developmental Biology | Year: 2010

Several decades have passed since the discovery of Hox genes in the fruit fly Drosophila melanogaster. Their unique ability to regulate morphologies along the anteroposterior (AP) axis (Lewis, 1978) earned them well-deserved attention as important regulators of embryonic development. Phenotypes due to loss- and gain-of-function mutations in mouse Hox genes have revealed that the spatio-temporally controlled expression of these genes is critical for the correct morphogenesis of embryonic axial structures. Here, we review recent novel insight into the modalities of Hox protein function in imparting specific identity to anatomical regions of the vertebral column, and in controlling the emergence of these tissues concomitantly with providing them with axial identity. The control of these functions must have been intimately linked to the shaping of the body plan during evolution. © 2010 Elsevier Inc. Source

van Es J.H.,Hubrecht Institute for Developmental Biology and Stem Cell Research
Nature communications | Year: 2010

Intestinal cells are constantly produced from a stem cell reservoir that gives rise to proliferating transient amplifying cells, which subsequently differentiate into one of the four principal cell types. Signalling pathways, including the Notch signalling pathway, coordinate these differentiation processes and their deregulation may cause cancer. Pharmacological inhibition through γ-secretase inhibitors or genetic inactivation of the Notch signalling pathway results in the complete loss of proliferating crypt progenitors due to their conversion into post-mitotic goblet cells. The basic helix-loop-helix transcription factor Math1 is essential for intestinal secretory cell differentiation. Because of the critical roles of both Math1 and Notch signalling in intestinal homeostasis and neoplastic transformation, we sought to determine the genetic hierarchy regulating the differentiation of intestinal stem cells into secretory cells. In this paper, we demonstrate that the conversion of intestinal stem cells into goblet cells upon inhibition of the Notch signalling pathway requires Math1. Source

Twiss F.,Hubrecht Institute for Developmental Biology and Stem Cell Research | De Rooij J.,Hubrecht Institute for Developmental Biology and Stem Cell Research
Cellular and Molecular Life Sciences | Year: 2013

Mechanical forces are increasingly recognized as central factors in the regulation of tissue morphogenesis and homeostasis. Central to the transduction of mechanical information into biochemical signaling is the contractile actomyosin cytoskeleton. Fluctuations in actomyosin contraction are sensed by tension sensitive systems at the interface between actomyosin and cell adhesion complexes. We review the current knowledge about the mechanical coupling of cell-cell junctions to the cytoskeleton and highlight the central role of α-catenin in this linkage. We assemble current knowledge about α-catenin's regulation by tension and about its interactions with a diversity of proteins. We present a model in which α-catenin is a force-regulated platform for a machinery of proteins that orchestrates local cortical remodeling in response to force. Finally, we highlight recently described fundamental processes in tissue morphogenesis and argue where and how this α-catenin-dependent cadherin mechanotransduction may be involved. © 2013 Springer Basel. Source

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