and have the ability to influence large-scale chromatin modifications. The implications of this spreading epigenetic regulation along the male X chromosome is thought to have implications for understanding the transfer of epigenetic activity along long genomic stretches. Decreased transcription of both hermaphroditic Xs by half Other species that do not follow the previously discussed conventions of XX females and XY males must find alternative ways to equalize X-linked gene expression among differing sexes. For example, in Caenorhabditis elegans (or C. elegans), sex is determined by the ratio of X chromosomes relative to autosomes; worms with two X chromosomes (XX worms) develop as hermaphrodites, whereas those with only one X chromosome (XO worms) develop as males. This system of sex determination is unique, because there is no male specific chromosome, as is the case in XX/XY sex determination systems. However, as is the case with the previously discussed mechanisms of dosage compensation, failure to express X-linked genes appropriately can still be lethal. In this XX/XO sex determination system, gene expression on the X chromosome is equalized by downregulating expression of genes on both X chromosomes of hermaphroditic XX organisms by half. In these XX organisms, the dosage compensation complex (DCC) is assembled on both X chromosomes to allow for this tightly regulated change in transcription levels. The DCC is often compared to the condensin complex, which is conserved across the mitotic and meiotic processes of many species. This complex is crucial to the condensation and segregation of chromosomes during both meiosis and mitosis. Because data substantiates the theory that dosage compensation in other species is caused by chromatin-wide modifications, many theorize that the DCC in particular functions similar to the condensin complex in its ability to condense or remodel the chromatin of the X chromosome. The role of the DCC in this form of dosage compensation was postulated by Barbara J. Meyer in the 1980s, and its individual components and their cooperative function were later parsed out by her lab. Notably, in 1999, data from Meyer's lab showed that SDC-2 is a particularly important transcriptional factor for targeting the DCC to the X chromosome and for assembling DCC components onto the X chromosomes in XX embryos. More recently, Meyer's lab has shown that proteins known as X-linked signal elements (XSEs) operate in concert with SDC-2 to differentially repress and activate other genes in the dosage compensation pathway. By selectively mutating a