<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kamps D</submitter><funding>Natural Sciences and Engineering Research Council of Canada</funding><funding>Bundesministerium für Bildung und Forschung</funding><funding>Leverhulme Trust</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>European Research Council</funding><funding>Wolfson Foundation</funding><funding>Horizon 2020 Framework Programme</funding><funding>Isaac Newton Institute for Mathematical Sciences</funding><funding>Stiftung Mercator</funding><funding>Knut och Alice Wallenbergs Stiftelse</funding><funding>Engineering and Physical Sciences Research Council</funding><pagination>108467</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7710677</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(9)</volume><pubmed_abstract>Local cell contraction pulses play important roles in tissue and cell morphogenesis. Here, we improve a chemo-optogenetic approach and apply it to investigate the signal network that generates these pulses. We use these measurements to derive and parameterize a system of ordinary differential equations describing temporal signal network dynamics. Bifurcation analysis and numerical simulations predict a strong dependence of oscillatory system dynamics on the concentration of GEF-H1, an Lbc-type RhoGEF, which mediates the positive feedback amplification of Rho activity. This prediction is confirmed experimentally via optogenetic tuning of the effective GEF-H1 concentration in individual living cells. Numerical simulations show that pulse amplitude is most sensitive to external inputs into the myosin component at low GEF-H1 concentrations and that the spatial pulse width is dependent on GEF-H1 diffusion. Our study offers a theoretical framework to explain the emergence of local cell contraction pulses and their modulation by biochemical and mechanical signals.</pubmed_abstract><journal>Cell reports</journal><pubmed_title>Optogenetic Tuning Reveals Rho Amplification-Dependent Dynamics of a Cell Contraction Signal Network.</pubmed_title><pmcid>PMC7710677</pmcid><funding_grant_id>EP/T00410X/1</funding_grant_id><funding_grant_id>EP/J016780/1</funding_grant_id><pubmed_authors>Banerjee S</pubmed_authors><pubmed_authors>Madzvamuse A</pubmed_authors><pubmed_authors>Graessl M</pubmed_authors><pubmed_authors>Mazel T</pubmed_authors><pubmed_authors>Portet S</pubmed_authors><pubmed_authors>Kamps D</pubmed_authors><pubmed_authors>Koch J</pubmed_authors><pubmed_authors>Juma VO</pubmed_authors><pubmed_authors>Campillo-Funollet E</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Nalbant P</pubmed_authors><pubmed_authors>Dehmelt L</pubmed_authors><pubmed_authors>Wu YW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Optogenetic Tuning Reveals Rho Amplification-Dependent Dynamics of a Cell Contraction Signal Network.</name><description>Local cell contraction pulses play important roles in tissue and cell morphogenesis. Here, we improve a chemo-optogenetic approach and apply it to investigate the signal network that generates these pulses. We use these measurements to derive and parameterize a system of ordinary differential equations describing temporal signal network dynamics. Bifurcation analysis and numerical simulations predict a strong dependence of oscillatory system dynamics on the concentration of GEF-H1, an Lbc-type RhoGEF, which mediates the positive feedback amplification of Rho activity. This prediction is confirmed experimentally via optogenetic tuning of the effective GEF-H1 concentration in individual living cells. Numerical simulations show that pulse amplitude is most sensitive to external inputs into the myosin component at low GEF-H1 concentrations and that the spatial pulse width is dependent on GEF-H1 diffusion. Our study offers a theoretical framework to explain the emergence of local cell contraction pulses and their modulation by biochemical and mechanical signals.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Dec</publication><modification>2024-11-20T11:36:42.866Z</modification><creation>2021-02-20T09:59:00Z</creation></dates><accession>S-EPMC7710677</accession><cross_references><pubmed>33264629</pubmed><doi>10.1016/j.celrep.2020.108467</doi></cross_references></HashMap>