Vimentin organization modulates the formation of lamellipodia

Author:

Helfand Brian T.1,Mendez Melissa G.2,Murthy S. N. Prasanna2,Shumaker Dale K.1,Grin Boris2,Mahammad Saleemulla2,Aebi Ueli3,Wedig Tatjana4,Wu Yi I.5,Hahn Klaus M.6,Inagaki Masaki7,Herrmann Harald4,Goldman Robert D.2

Affiliation:

1. Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611

2. Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611

3. M.E. Müller Institute for Structural Biology, Biozentrum, University of Basel, CH-4056 Basel, Switzerland

4. Department Molecular Genetics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany

5. University of Connecticut Health Center, Farmington, CT 06030

6. Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, NC 27599

7. Division of Biochemistry, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya, Aichi 464-8681, Japan

Abstract

Vimentin intermediate filaments (VIF) extend throughout the rear and perinuclear regions of migrating fibroblasts, but only nonfilamentous vimentin particles are present in lamellipodial regions. In contrast, VIF networks extend to the entire cell periphery in serum-starved or nonmotile fibroblasts. Upon serum addition or activation of Rac1, VIF are rapidly phosphorylated at Ser-38, a p21-activated kinase phosphorylation site. This phosphorylation of vimentin is coincident with VIF disassembly at and retraction from the cell surface where lamellipodia form. Furthermore, local induction of photoactivatable Rac1 or the microinjection of a vimentin mimetic peptide (2B2) disassemble VIF at sites where lamellipodia subsequently form. When vimentin organization is disrupted by a dominant-negative mutant or by silencing, there is a loss of polarity, as evidenced by the formation of lamellipodia encircling the entire cell, as well as reduced cell motility. These findings demonstrate an antagonistic relationship between VIF and the formation of lamellipodia.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

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