SnapShot: Mechanical Forces in Development I

Pasakarnis, Laurynas; Dreher, David; Brunner, Damian

doi:10.1016/j.cell.2016.03.044

Cited by 14 publications

(10 citation statements)

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“…During the last decade there has been a renewed interest in the study of the role of mechanical forces and their interplay with molecular signaling during development ( Hernández-Hernández et al, 2014 ; Hamada, 2015 ; Pasakarnis et al, 2016 ; Dreher et al, 2016 ). Our work constitutes a new example of such interactions and raises the possibility that the elusive mechanism that triggers supporting-cell proliferation after the loss of hair cells in nonmammalian species is mechanical in nature.…”

Section: Discussionmentioning

confidence: 99%

Elastic force restricts growth of the murine utricle

Gnedeva

Jacobo

Salvi

et al. 2017

eLife

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Dysfunctions of hearing and balance are often irreversible in mammals owing to the inability of cells in the inner ear to proliferate and replace lost sensory receptors. To determine the molecular basis of this deficiency we have investigated the dynamics of growth and cellular proliferation in a murine vestibular organ, the utricle. Based on this analysis, we have created a theoretical model that captures the key features of the organ’s morphogenesis. Our experimental data and model demonstrate that an elastic force opposes growth of the utricular sensory epithelium during development, confines cellular proliferation to the organ’s periphery, and eventually arrests its growth. We find that an increase in cellular density and the subsequent degradation of the transcriptional cofactor Yap underlie this process. A reduction in mechanical constraints results in accumulation and nuclear translocation of Yap, which triggers proliferation and restores the utricle’s growth; interfering with Yap’s activity reverses this effect.DOI: http://dx.doi.org/10.7554/eLife.25681.001

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Section: Discussionmentioning

confidence: 99%

Elastic force restricts growth of the murine utricle

Gnedeva

Jacobo

Salvi

et al. 2017

eLife

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“…The generation of form in living organisms is one of the most fascinating unsolved problems in biology ( Dreher et al., 2016 , Pasakarnis et al., 2016 ). Genetic analysis of epithelial tissue morphogenesis in model organisms has revealed that epithelia can elongate by either polarized cell intercalation ( Pare et al., 2014 , Blankenship et al., 2006 , Bertet et al., 2004 , Zallen and Wieschaus, 2004 , Heisenberg et al., 2000 , Irvine and Wieschaus, 1994 , Keller, 1980 ) or oriented cell division ( Campinho et al., 2013 , Gibson et al., 2011 , Mao et al., 2011 , da Silva and Vincent, 2007 , Baena-Lopez et al., 2005 , Gong et al., 2004 , Wei and Mikawa, 2000 , Concha and Adams, 1998 ).…”

Section: Introductionmentioning

confidence: 99%

“…A third general mechanism of epithelial morphogenesis is cell shape change. Recent research has been focused mainly on forces acting to shape the apical domain in two dimensions ( Dreher et al., 2016 , Pasakarnis et al., 2016 , Paluch and Heisenberg, 2009 ). However, epithelial cells can also undergo three-dimensional shape changes to drive morphogenesis.…”

Section: Introductionmentioning

confidence: 99%

Apical and Basal Matrix Remodeling Control Epithelial Morphogenesis

et al. 2018

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SummaryEpithelial tissues can elongate in two dimensions by polarized cell intercalation, oriented cell division, or cell shape change, owing to local or global actomyosin contractile forces acting in the plane of the tissue. In addition, epithelia can undergo morphogenetic change in three dimensions. We show that elongation of the wings and legs of Drosophila involves a columnar-to-cuboidal cell shape change that reduces cell height and expands cell width. Remodeling of the apical extracellular matrix by the Stubble protease and basal matrix by MMP1/2 proteases induces wing and leg elongation. Matrix remodeling does not occur in the haltere, a limb that fails to elongate. Limb elongation is made anisotropic by planar polarized Myosin-II, which drives convergent extension along the proximal-distal axis. Subsequently, Myosin-II relocalizes to lateral membranes to accelerate columnar-to-cuboidal transition and isotropic tissue expansion. Thus, matrix remodeling induces dynamic changes in actomyosin contractility to drive epithelial morphogenesis in three dimensions.

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“…Plants perceive and respond to mechanical forces, including those resulting from extracellular stimuli such as wind and rain, as well as stimuli manifested during cell proliferation and the differential growth of neighboring cells [1][2][3][4][5][6][7] . Plants respond to mechanostimulation throughout growth and development 2,8 , and these responses are thought to play essential roles in pattern formation 9 .…”

Section: Introductionmentioning

confidence: 99%

Quantitative and functional posttranslational modification proteomics reveals that TREPH1 plays a role in plant touch-delayed bolting

Wang

Yang

Qing

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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Plants can sense both intracellular and extracellular mechanical forces and can respond through morphological changes. The signaling components responsible for mechanotransduction of the touch response are largely unknown. Here, we performed a high-throughput SILIA (stable isotope labeling in Arabidopsis)-based quantitative phosphoproteomics analysis to profile changes in protein phosphorylation resulting from 40 seconds of force stimulation in Arabidopsis thaliana. Of the 24 touch-responsive phosphopeptides identified, many were derived from kinases, phosphatases, cytoskeleton proteins, membrane proteins and ion transporters. TOUCH-REGULATED PHOSPHOPROTEIN1 (TREPH1) and MAP KINASE KINASE 2 (MKK2) and/or MKK1 became rapidly phosphorylated in touch-stimulated plants. Both TREPH1 and MKK2 are required for touch-induced delayed flowering, a major component of thigmomorphogenesis. The treph1-1 and mkk2 mutants also exhibited defects in touch-inducible gene expression. A nonphosphorylatable site-specific isoform of TREPH1 (S625A) failed to restore touch-induced flowering delay of treph1-1, indicating the necessity of S625 for TREPH1 function and providing evidence consistent with the possible functional relevance of the touch-regulated TREPH1 phosphorylation. Bioinformatic analysis and biochemical subcellular fractionation of TREPH1 protein indicate that it is a soluble protein. Altogether, these findings identify new protein players in Arabidopsis thigmomorphogenesis regulation, suggesting that protein phosphorylation may play a critical role in plant force responses.Like neural systems in animals, plants respond to a delicate force signal, such as a light touch, with extreme sensitivity, being it thigmotropism, thigmonastic movement, and thigmomorphogenesis. To understand the complex force signaling networks in plants, we applied SILIA-based quantitative PTM proteomics to measure 40 seconds of protein phosphorylation changes in Arabidopsis in response to cotton and human hair touches, and identified 4895 repeatable and non-redundant phosphopeptides, 579 of which are novel phosphosites derived from the 509 phosphoprotein groups, and finally identified 24 TOUCH-REGUALTED PHOSPHOPROTEIN (TREPHs) groups. Consequent molecular biological and bioinformatic studies revealed that both TREPH1 and MKK2 proteins are required for Arabidopsis touch response. These studies suggest that protein phosphorylation is involved in mechanotransduction of plant thigmomorphogenesis.

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SnapShot: Mechanical Forces in Development I

Cited by 14 publications

References 0 publications

Elastic force restricts growth of the murine utricle

Elastic force restricts growth of the murine utricle

Apical and Basal Matrix Remodeling Control Epithelial Morphogenesis

Quantitative and functional posttranslational modification proteomics reveals that TREPH1 plays a role in plant touch-delayed bolting

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