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A genetic screen for dominant, temperature-sensitive, maternal-effect embryonic lethal mutations identified mel-43(sb41), a gene required for early embryonic viability (Mitenko et al., 1997). Linkage mapping placed mel-43 within a small region on chromosome IV. Genetic analyses suggested that mel-43(sb41) was a neomorphic mutation. While refining the genetic position of the mel-43 gene, data suggested that the genetic position of mel-43 was inconsistent with the published location. In light of this new location, previous conclusions regarding the genetic behaviour of mel-43(sb41) were re-examined. Deficiency analysis suggests that mel-43(sb41) is a haploinsufficient loss-of-function mutation. mel-43(sb41) embryos are significantly delayed in meiosis II independent of cyclin B1 degradation. Consequently, embryos fail to produce meiosis II polar bodies and do not establish proper polarity. Although the function of mel-43 remains unknown, the persistent meiotic spindle suggests that mel-43 acts upstream of the microtubule rearrangements necessary to promote the metaphase II to anaphase II transition. / Molecular Biology and Genetics