Despite over 100 years of research, a clear picture of the centrosome's composition and its precise function in animal cells has not been determined. Furthermore, recent studies and the existence of cell types which lack the centriolar component of centrosomes have even raised questions on the necessity of the centrosome at all. We have identified a maternal-effect embyronic-lethal gene in Caenorhabditis elegans, called
spd-2 for spindle defective, which has a putative role in centrosome function as based on the behavior of two temperature- sensitive mutant alleles of the gene,
oj29 and
oj42. Analysis of the early embryonic mutant phenotypes by four-dimensional time-lapse microscopy and immunofluorescence microscopy have shown defects in microtubule dependent processes. Specifically, 4D-microscopy shows that pronuclear migration and rotation are defective, a pseudocleavage furrow is absent, and the first mitotic spindle is absent or small. Also,
oj29 embryos and the majority of
oj42 embryos fail to complete the first cytokinesis.
oj29 embyros then continue to cycle through periods of nuclear envelope breakdown and reformation; whereas,
oj42 embryos divide, albeit abnormally. These defects are most likely due to aberrant centrosome function. This is supported by immunofluorescence microscopy using an antibody to b-tubulin which shows that sperm associated microtubule asters are absent prior to the first mitosis in both
oj29 and
oj42 embryos. Furthermore, no foci of g-tubulin is seen in early
oj29 embryos. Together, these results indicate that the
spd-2 gene product has a role in centrosome function, and it is hoped that further analysis of this gene, including cloning, will help to yield a better view of centrosome function in C.elegans.