In a general screen for female mutants in C.briggsae, we found two alleles of a new gene required for spermatogenesis in both hermaphrodites and males. We named this gene cb-
fog-4 because of its Fog phenotype. Epistasis studies showed that
fog-4 acts downstream of
tra-2, and upstream of or in parallel to
tra-1. Genetic mapping located cb-
fog-4 on Chromosome II, and fine scale mapping placed it in a 160kb region between the SNPs
cb43333 and
cb43262. There are only 25 predicted genes in this region. One of these genes, cb-
trr-1, is
fog-4, since cb-
trr-1(RNAi) animals are Fog, and both mutants have lesions in cb-
trr-1. TRR-1 is a homolog of TRRAP in humans. Since both mutations are missense alleles, we set up a non-complementation screen using TMP/UV to isolate null alleles, and found 3 Fog alleles that have deletions in cb-
trr-1. TRRAP is highly conserved. It is a common subunit of several HAT complexes, including Tip60/NuA4 and PCAF/GCN5. RNAi against cb-
mys-1, the catalytic subunit of Tip60/NuA4, also causes a Fog phenotype, but RNAi against cb-
pcaf-1, the catalytic subunit of PCAF1/GCN5, does not. Furthermore, RNAi targeting four other components of the Tip60/NuA4 complex,
gfl-1, yl-1,
epc-1, and
ssl-1, also causes a Fog phenotype. Thus, we propose that the Tip60/NuA4 complex controls spermatogenesis in C. briggsae. In C. elegans,
trr-1 mutations cause a weakly penetrant vulval defect on their own, as well as slow growth and sterility, but do not create Fog animals. RNAi against either cb-
trr-1 or cb-
mys-1 in a
fem-2 mutant background caused embryonic lethality and L1 arrest. Moreover, RNAi showed that
epc-1 and
ssl-1 are also essential for the viability of embryos. By contrast, cb-
trr-1; cb-
fem-3 animals produce normal oocytes. These results suggest that the Tip60/NuA4 complex is essential for embryonic development and is redundant with FEM-2. We propose that cb-
trr-1 might provide a model for the recruitment of chromatin regulators into a development pathway.