Genetic evidence suggests that the product of the
mei-1 gene of Caenorhabditis elegans is specifically required for meiosis in the female germline. Loss-of-function
mei-1 mutations block meiotic spindle formation while a gain-of-function allele instead results in spindle defects during the early mitotic cleavages. In this report, we use immunocytochemistry to examine the localization of the
mei-1 product in wild-type and mutant embryos. During metaphase of meiosis I in wild-type embryos,
mei-1 protein was found throughout the spindle but was more concentrated toward the poles. At telophase I,
mei-1 product colocalized with the chromatin at the spindle poles. The pattern was repeated during meiosis II but no
mei-1 product was visible during the subsequent mitotic cleavages. The
mei-1 gain-of-function allele resulted in ectopic
mei-1 staining in the centers of the microtubule-organizing centers during interphase and in the spindles during the early cleavages. This aberrant localization is probably responsible for the poorly formed and misoriented cleavage spindles characteristic of the mutation. We also examined the localization of
mei-1(+) product in the presence of mutations of genes that genetically interact with
mei-1 alleles.
mei-2 is apparently required to localize
mei-1 product to the spindle during meiosis while
mel-26 acts as a postmeiotic inhibitor. We conclude that
mei-1 encodes a novel spindle component, one that is specialized for the acentriolar meiotic spindles unique to female meiosis. The genes
mei-2 and
mel-26 are part of a regulatory network that confines
mei-1 activity to meiosis.