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Phosphorylation of cytokeratin fibers alters their response to mechanical extension
Author(s) -
Fois Giorgio,
Weimer Michael,
Felder Erika T,
Zheng Xing,
Tobias Busch,
Seufferlein Thomas,
Dietl Paul,
Felder Edward
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.656.12
Subject(s) - phosphorylation , dephosphorylation , microbiology and biotechnology , chemistry , myosin , strain (injury) , myosin light chain kinase , biophysics , phosphatase , biochemistry , anatomy , biology
Cytokeratin (CK) fibers protect epithelia from mechanical stress. High loads of mechanical strain lead to overextension of the CK‐fibers, discernible by wavy CK‐fibers in living cells after the strain is released. As mechanical properties of CK‐fibers are modulated by phosphorylation, we investigated the effect of phosphorylation on the waviness of overextended CK‐fibers. Using FP‐labeled CK8/18 constructs and a cell stretching device, we found that wavy CK‐fibers were prevented by treatment with Staurosporin (unspecific kinase inhibitor), by depleting the cells of ATP and with CK‐mutants that abrogate phosphorylation at specific sites. Interfering with actin/myosin had a similar effect. The time that it took the CK‐fibers to regain their taut structure was not affected by phosphorylation but clearly depended on intact microtubuli. Further experiments will identify the signaling pathway for CK‐fiber dephosphorylation and will demonstrate if the mechanical stimulation itself triggers this pathway ‐ possibly as an adaptive mechanism to protect the CK‐fibers from mechanical damage. This work was supported by the DFG, grant DI 1402/1‐1 and DI1402/3‐1, and the Baden‐Württemberg Stiftung, grant P‐LS‐Biomat/03.