The Wiskott-Aldrich Syndrome protein (WASP) binds both Cdc42 and actin, and mutation of the human WASP gene leads to actin disorganization and defects in immune cell chemotaxis and antigen recognition. But it has proven difficult to define other members of the WASP pathway by biochemistry, as WASP overexpression results in a mess of aggregated filamentous actin.
Bear et al. (page ) have tackled this problem with genetics. They started with Dictyostelium cells mutant in cAR2, one of four cyclic AMP receptors. These G protein–coupled receptors transduce chemotactic and morphogenetic signals. Loss of cAR2 function arrests the cells after they have aggregated but before the aggregate has formed a single tip, the precursor to the slug form. Deletion of the gene for SCAR (suppressor of cAR2) allowed cAR2 mutant cells to form a single tip; the same deletion caused each aggregate of otherwise wild-type cells to form multiple tips and...
