Most eukaryotes rely on crossing over between homologs to direct meiotic chromosome segregation, yet make very few crossovers per chromosome pair. Despite a physical size range that varies almost 2-fold, each of the six C. elegans chromosomes has a genetic length of roughly 50 cM, indicating an average of one crossover per meiosis. Our previous results demonstrated that this process is subject to chromosome-wide regulation: end-to-end fusions of two and three whole chromosomes still enjoy an average of approximately one crossover per chromosome pair. These results indicated that the fused chromosomes are being perceived as a single chromosome unit by the organism, and implied that meiotic crossovers in C. elegans are limited by a robust chromosome-wide interference mechanism by which a (nascent) crossover discourages additional crossovers. Further experiments suggested that the functional unit upon which chromosome-wide interference operates may correspond to chromosome regions with contiguous chromosome axes and/or contiguous homologous synapsis. To test the hypothesis that integrity of meiotic chromosome axis structures is important for crossover interference, we examined the effects of the
him-3(
me80) mutation. HIM-3 is a component of meiotic chromosome axes, and is required for loading of central region components (e.g. SYP-1) of the synaptonemal complex (SC), a structure that assembles between homologous chromosomes during meiotic prophase. In the absence of HIM-3, SYP-1 does not load and no crossovers form. The
me80 mutant has a reduced level of HIM-3 protein, at least some of which loads onto chromosomes; the subset of chromosomes that load most HIM-3
(me80) protein also load some SYP-1. We asked whether impaired integrity of meiotic structures would affect chromosome-wide crossover control by assessing the frequency of non-crossover, single crossover and double crossover meiotic products produced by the
me80 mutant. For chromosome I, we found an increased frequency of non-crossover products, presumably reflecting the subset of chromosomes that failed to recruit sufficient SYP-1 protein. Among crossover products, however, double crossover products (which are rare in wild-type meiosis) were substantially elevated compared to single crossover products, indicating that the
him-3(
me80) mutant is indeed defective in inhibiting multiple crossovers on chromosome I. All chromosomes are likely affected; preliminary results suggest that interference on the X chromosome is also disrupted in
me80. Our results strongly support the hypothesis that integrity of chromosome axes, and/or the SC structures that assemble between them, is required to confer crossover interference.