BEGIN:VCALENDAR
PRODID:-//Columba Systems Ltd//NONSGML CPNG/SpringViewer/ICal Output/3.3-
 M3//EN
VERSION:2.0
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTAMP:20160428T123747Z
DTSTART:20160510T120000Z
DTEND:20160510T130000Z
SUMMARY:Mechanics of leukocyte locomotion
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}p10i-ijo3oh
 ld-tzvfsk
DESCRIPTION:The organization principle of the immune system is based on h
 igh speed cell motility. Accordingly\, immune cells migrate up to 100 ti
 mes faster than mesenchymal and epithelial cell types. Although the biop
 hysical migration mode of such fast cells is still poorly investigated s
 ome principles are emerging and it is now well established that leukocyt
 es do not strictly rely on transmembrane adhesion receptors when they cr
 awl through the interstitial environment\, which is usually a 3D scaffol
 d of extracellular matrix molecules. Instead leukocytes are able to dire
 ctly transduce force by deformations of the cell body. Using in vitro an
 d ex vivo imaging approaches we demonstrate that deformation based migra
 tion is not the default strategy of leukocyte locomotion but rather part
  of a plasticity program that allows the cells to instantaneously switch
  between adhesion receptor dependent and independent migration. We find 
 that invasion of dense matrices and crawling over stiff surfaces relies 
 on adhesion while migration in the confined space of an interstitium doe
 s not and that leukocyte can shift back and forth between these modes wi
 thout altering their proteome. Apart from the geometry of the extracellu
 lar environment also the distribution of the guidance cue can dictate th
 e locomotion strategy and immobilized cues preferentially cause adhesive
  migration whereas soluble cues trigger adhesion independent movement. \
 nThe force generating module of leukocytes is exclusively based on actom
 yosin protrusions and contractions. But also here the cells show enormou
 s plasticity and we found that blocking contractility shifts the cells t
 owards a entirely protrusive lomomotion strategy\, while dampening protr
 usion activates the blebbing mode. When interfering with actin nucleator
 s we found that ablation of Arp2/3 activity at the leading edge abrogate
 d branching and shifted the cells towards a linearly elongated cell shap
 e. However\, this did not slow down locomotion\, but merely prevented th
 e cells from turning and responsing to directional cues\, while actual s
 peed was accelerated. \n
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:Michael Smith Lecture Theatre\, Michael Smith Building\, Manches
 ter
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