
Analysis of actin
dynamics at the cell edge of Ptk1 kidney
epithelial cells using fluorescent speckle microscopy (FSM). The presence of active RacQ61L causes a
widening of the lamellipodia and increased retrograde actin flow. This effect is blocked when the downstream
effector, p21-activated kinase 1 (PAK1) is inhibited by expressing of
the
(auto)inhibitory domain (PID). See
Delorme et al (2007) – in press.
(Movies prepared by
Violaine Delorme, Ph.D)
Normal HeLa cell
undergoing cell division. See Birkenfeld
et al Dev. Cell. May 8, 2007. Vol 12, Issue 5, pages
699-712.
(Movie prepared by
Joerg Birkenfeld, Ph.D.)
Movie 6:
Cells undergoing
division:
note the cell to the left fails to divide properly due to the
enhanced cofilin activity caused by overexrpression of the
cofilin
phosphatase Chronophin (CIN), discovered in our laboratory. See Gohla et al Nature Cell Biol. 7: 21, 2005.
(Movie prepared
by Céline DerMardirossian, Ph.D.)
A clonal HeLa cell ine stably expressing Cofilin1-GFP treated with Azide/2-deoxyglucose to deplete cellular ATP for 30 minutes. Cofilin-GFP is aggregated into large tapered rod inclusions by 30 minutes of ATP-depletion.
(Movie prepared by Timothy Huang, Ph.D.)
Cofilin1-GFP cells transfected with a CIN-targeting shRNA construct (simultaneously expressing mRFP, left field) are subjected to ATP depletion, and the rate of Cofilin1-GFP rod formation is compared between shRNA-expressing and non-expressing cells. CIN shRNA experssing reduces the rate of Cofilin1-GFP rod formation during ATP depletion.
(Movie prepared by Timothy Huang, Ph.D.)
Cofilin1-GFP cells have been ATP-depleted for 30 minutes, and subjected to glucose repletion in normal growth media for 30 minutes. Cofilin1-GFP images are acquired immediately after glucose repletion, and Cofilin1-GFP can be seen to rapidly disperse from rod-shaped inclusions to the cell periphery.
(Movie prepared by Timothy Huang, PhD.)