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Papers In Press, published online ahead of print December 6, 2001
J. Biol. Chem, 10.1074/jbc.C100685200
Submitted on November 29, 2001
Revised on December 6, 2001
Accepted on December 6, 2001

MK2 targets AU-rich elements and regulates biosynthesis of TNF and IL-6 independently at different post transcriptional levels

Armin Neininger, Dimitris Kontoyiannis, Alexey Kotlyarov, Reinhard Winzen, Rolf Eckert, Hans-Dieter Volk, Helmut Holtmann, George Kollias, and Matthias Gaestel

Biochemistry, Medical School Hannover, Hannover 30625

Corresponding Author: gaestel.matthias{at}mh-hannover.de

We demonstrate that LPS-induced TNF biosynthesis becomes independent of MAPKAP kinase 2 (MK2) when the AU-rich element (ARE) of the TNF gene is deleted. In spleen cells and macrophages where TNF biosynthesis is restored as a result of this deletion, IL-6 biosynthesis is still dependent on MK2. In MK2 deficient macrophages the half life of IL-6 mRNA is reduced more than tenfold whereas half life of TNF mRNA is only weakly decreased. It is shown that the stability of a reporter mRNA carrying the AU-rich 3'UTR of IL-6 is increased by MK2. The data provide in vivo evidence that the AU-rich 3'UTRs of TNF and IL-6 are downstream to MK2 signaling and make MK2 an essential component of mechanisms that regulate biosynthesis of IL-6 at the levels of mRNA stability, and of TNF mainly through TNF-ARE-dependent translational control.


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