The genetic activity of transposable elements is tightly controlled in many species. Transposons that are relatively quiescent under certain circumstances can excise or transpose at greatly increased rates under other circumstances. For example, 'genomic shock' can activate quiescent maize transposons, 'cytotype' and tissue-specific splicing regulate Drosophila P factors, copy number controls Tn5 transposition in bacteria, and developmental timing affects the production of transposon-like intracisternal A-particles in mouse embryos. The Caenorhabditis elegans transposable element Tc1 is subject to both strain-specific and tissue-specific control. Multiple copies of Tc1 are present in the genome of all C. elegans strains collected from nature. However, these elements are genetically active in only certain isolates. For example, in C. elegans variety Bristol transposition and excision of Tc1 are undetectable, but in variety Bergerac transposition and excision are frequent. Moreover, in variety Bergerac, Tc1 is about 1,000-fold more active in somatic cells than in germ cells. We have investigated the genetic basis for the germ/soma regulation of Tc1 activity. We have isolated mutants that exhibit increased frequencies of Tc1 excision in the germ line. The frequencies of Tc1 excision in the soma are unaltered in these mutants. These mutants also exhibit high frequencies of Tc1 germ-line transposition, and this results in a mutator phenotype. Nearly all mutator-induced mutations are caused by insertion of Tc1.