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@ARTICLE{Ramalingam:255856,
      author       = {Ramalingam, Nagendran and Franke, Christof and Jaschinski,
                      Evelin and Winterhoff, Moritz and Lu, Yao and Brühmann,
                      Stefan and Junemann, Alexander and Meier, Helena and Noegel,
                      Angelika A. and Weber, Igor and Zhao, Hongxia and Merkel,
                      Rudolf and Schleicher, Michael and Faix, Jan},
      title        = {{A} resilient formin-derived cortical actin meshwork in the
                      rear drives actomyosin-based motility in 2{D} confinement},
      journal      = {Nature Communications},
      volume       = {6},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {FZJ-2015-05962},
      pages        = {8496 -},
      year         = {2015},
      abstract     = {Cell migration is driven by the establishment of disparity
                      between the cortical properties of the softer front and the
                      more rigid rear allowing front extension and
                      actomyosin-based rear contraction. However, how the cortical
                      actin meshwork in the rear is generated remains elusive.
                      Here we identify the mDia1-like formin A (ForA) from
                      Dictyostelium discoideum that generates a subset of
                      filaments as the basis of a resilient cortical actin sheath
                      in the rear. Mechanical resistance of this actin compartment
                      is accomplished by actin crosslinkers and IQGAP-related
                      proteins, and is mandatory to withstand the increased
                      contractile forces in response to mechanical stress by
                      impeding unproductive blebbing in the rear, allowing
                      efficient cell migration in two-dimensional-confined
                      environments. Consistently, ForA supresses the formation of
                      lateral protrusions, rapidly relocalizes to new prospective
                      ends in repolarizing cells and is required for cortical
                      integrity. Finally, we show that ForA utilizes the
                      phosphoinositide gradients in polarized cells for
                      subcellular targeting.},
      cin          = {ICS-7},
      ddc          = {500},
      cid          = {I:(DE-Juel1)ICS-7-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000363148700001},
      pubmed       = {pmid:26415699},
      doi          = {10.1038/ncomms9496},
      url          = {https://juser.fz-juelich.de/record/255856},
}