The maternal-effect sterile (mes) genes are crucial for the survival of the C. elegans germ line. MES-2, MES-3, and MES-6 form a complex, and MES-4 functions independently from the other MES proteins. MES-2 and MES-4 each contain a SET domain and are histone methyltransferases. MES-2 performs all detectable H3K27 methylation, a repressive mark, in most regions of the germ line and early embryos. MES-4 is responsible for dimethylating H3K36 in the germ line and early embryos, and is located on autosomes and excluded from the X chromosomes. I investigated the roles that the MES proteins serve in regulating gene expression in the adult germ line. In collaboration with Valerie Reinke and Andreas Rechtsteiner, I performed microarray analysis on gonad arms dissected from mes-2, mes-3, mes-4, and mes-6 M+Z-mutant hermaphrodites utilizing amplicon and oligo arrays as the platforms. The results indicate that although MES-4 is dramatically concentrated on the autosomes, its major targets of regulation are genes on the X chromosome; many X-linked genes are up-regulated in mes-4 mutants compared to wild type. Microarray results also suggest MES-4 is involved in regulating the expression of some autosomal genes. The MES-2/3/6 complex also participates in repressing gene expression from the X chromosome. Significantly, MES-4 and the MES-2/3/6 complex target many of the same genes on the X. In agreement with the latter finding, worms lacking both MES-4 and MES-2/3/6 display a more severe phenotype than worms lacking either MES alone. My results indicate that the MES proteins work together to silence the X chromosomes in the germ line and to maintain germline viability. In an attempt to better understand the state of the germ line prior to the onset of sterility in the M-Z- generation, I performed germ cell counts in M-Z- larvae and observed that germ cell proliferation in mes-4 mutants is dramatically reduced compared to wild type and the other mes mutants. Finally, I performed quantitative PCR on M-Z- mes L1s to assess transcript levels of essential germline-expressed genes, and observed that the mes genes are not needed to turn on those essential genes in the earliest larval stages.