Disruptions affecting either the structural or regulatory functions of the protein:DNA complex referred to as chromatin can lead to dramatic effects on cellular homeostasis, for example by affecting global transcriptional processes. One way cells regulate the local chromatin environment is by post-translational modifications of the DNA-packaging histone proteins, including lysine methylation. The recent discovery of a lysine-specific histone demethylase (LSD1) confirmed that regulation of histone methylation involves the active removal of methyl groups. These newly discovered enzymes provide novel opportunities to understand how histone modifications function in chromatin-related processes, with model organisms providing a valuable in vivo approach. We are therefore using the nematode C. elegans to study the biological roles of the LSD1 homolog SPR-5. The mammalian LSD1 is a H3 lysine 4 demethylase, and SPR-5 shows in vitro activity against H3K4me2 as well, indicating conservation of enzymatic activity between worms and mammals. spr-5 mutant germlines show an increase in H3K4me2, indicating SPR-5 acts in vivo in the germline to modulate H3K4me2. Further studies uncovered an unexpected role for SPR-5 in meiotic DNA double strand break repair (DSBR). spr-5 mutants experience increased levels of p53-dependent germline apoptosis, indicating that a DNA damage checkpoint is triggered in the germline. Immunolocalization of RAD-51, a marker of DSBR, shows increased number of foci in spr-5 mutants, suggesting either an increase in the levels of DSB formation or a delay in DSBR. spr-5 mutants are also sensitive to DSB-inducing radiation, and in wild-type animals SPR-5 relocalizes within the nucleus upon radiation, suggesting SPR-5 may play an active role in responding to DNA damage in the germline. Perturbations of meiotic DSBR may be associated with alterations in chromatin state, so we are further evaluating whether additional histone modification patterns and progression of DNA damage repair are affected in the germline in spr-5 mutants. An alternate (but not mutually exclusive) explanation is that loss of SPR-5 may lead to misregulation of DNA damage repair processes through the deregulation of target genes. We have therefore performed germline-specific microarrays to identify potential SPR-5 targets that are important for normal meiotic processes including DSBR.