During sexual reproduction, haploid gametes are generated by a specialized cell division program (meiosis) in which homologous chromosomes pair and their association is stabilized by a protein structure, the synaptonemal complex (SC). SC formation between homologous chromosomes is essential for reciprocal recombination that is required for faithful segregation of homologous chromosomes. In order to identify the genes responsible for proper homologous chromosome association during C. elegans meiosis, we have been conducting a genome-wide screen using: 1) a system for visualizing homologous pairing in live animals, and 2) a feeding RNAi library to knock-down gene function. This screen has allowed us to identify genes that were not previously known to function in pairing and/or synapsis. Here we report novel aspects of SC assembly discovered through the analyses of some of the newly identified genes. First, we found that pgl-1, a gene encoding a protein associated with P granules, was transiently required for the initiation of SC assembly after the shift to a high temperature. We found that the initiation of SC assembly was heat sensitive even in the wild type, which was further sensitized in pgl-1 mutant, suggesting that PGL-1 is regulating a factor(s) for the initiation of SC assembly. Second, we found that gld-2 and gld-3, components of a cytoplasmic poly(A) polymerase that is known to function in a mitosis-meiosis switch, were required for prompt SC assembly. In these mutants, SC formation was significantly delayed, and non-pairing center (PC) ends of chromosomes rarely showed homologous association. Interestingly, PCs showed stable homologous association during meiosis in these mutants, indicating SC was assembled at least at pairing centers. This observation suggests that initiation and progression of SC assembly are separable and gld-2 and gld-3 are involved in the latter process. Third, we found that mrg-1, a chromo-domain protein required for germ line development and X chromosome silencing in the germline, was required for proper synapsis establishment. The mrg-1 mutants showed partial synapsis and pairing defect at the non-PC ends (but not at the PC ends) of chromosomes. SC assembly initiated and progressed with the apparently normal timing and kinetics. This finding suggests that there is a mechanism to establish and/or maintain SC that is dedicated to non-PC region of chromosomes, possibly through chromatin modification. We are currently investigating how this mechanism is operating using cytological and genetic analyses.