Caspase 3 cleavage of the Ste20-related kinase SLK releases and activates an apoptosis-inducing kinase domain and an actin-disassembling region

Mol Cell Biol. 2000 Jan;20(2):684-96. doi: 10.1128/MCB.20.2.684-696.2000.

Abstract

We have demonstrated that a novel Ste20-related kinase, designated SLK, mediates apoptosis and actin stress fiber dissolution through distinct domains generated by caspase 3 cleavage. Overexpression of SLK in C2C12 myoblasts stimulated the disassembly of actin stress fibers and focal adhesions and induced apoptosis, as determined by annexin V binding and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling analysis. SLK was cleaved by caspase 3 in vitro and in vivo during c-Myc-, tumor necrosis factor alpha, and UV-induced apoptosis. Furthermore, cleavage of SLK released two domains with distinct activities: an activated N-terminal kinase domain that promoted apoptosis and cytoskeletal rearrangements and a C-terminus domain that disassembled actin stress fibers. Moreover, our analysis has identified a novel conserved region (termed the AT1-46 homology domain) that efficiently promotes stress fiber disassembly. Finally, transient transfection of SLK also activated the c-Jun N-terminal kinase signaling pathway. Our results suggest that caspase-activated SLK represents a novel effector of cytoskeletal remodeling and apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • Apoptosis* / drug effects
  • Apoptosis* / radiation effects
  • Caspase 3
  • Caspases / metabolism*
  • Cell Adhesion
  • Cell Line
  • Cloning, Molecular
  • Cytoskeleton / drug effects
  • Cytoskeleton / metabolism
  • Cytoskeleton / radiation effects
  • Enzyme Activation / drug effects
  • Enzyme Activation / radiation effects
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • MAP Kinase Signaling System
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism
  • Muscles / cytology
  • Muscles / enzymology
  • Muscles / metabolism
  • Mutation / genetics
  • Protein Processing, Post-Translational / drug effects
  • Protein Processing, Post-Translational / radiation effects
  • Protein Serine-Threonine Kinases / chemistry*
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Protein Structure, Tertiary / genetics
  • Protein Structure, Tertiary / physiology
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / physiology
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • Recombinant Fusion Proteins / chemistry
  • Recombinant Fusion Proteins / metabolism
  • Sequence Homology, Amino Acid
  • Tumor Necrosis Factor-alpha / pharmacology
  • Two-Hybrid System Techniques

Substances

  • Actins
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Recombinant Fusion Proteins
  • Tumor Necrosis Factor-alpha
  • SLK protein, human
  • Protein Serine-Threonine Kinases
  • SLK protein, mouse
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • CASP3 protein, human
  • Casp3 protein, mouse
  • Caspase 3
  • Caspases