Loss of function mutation in
mau-8, a maternal effect viable gene, results in abnormal cell division in early embryos suggesting that
mau-8 activity is essential for development. In addition, the genetic lesion generates general synaptic defects in animals that successfully develop as adult. We have cloned the
mau-8 gene and show that it encodes a protein highly related to Phosducin Like Protein (PhLP) in the nematode. In the developing embryos, MAU-8/PhLP localizes to the cortical region and concentrates to the centrosomes of mitotic cells. In adult animals, the MAU-8/PhLP protein is ubiquitously expressed in somatic tissues and germline cells. As in vertebrates, MAU-8/PhLP interacts with the PAR-5/14.3.3 protein. This interaction is not disturbed in
mau-8 mutants suggesting that either the mutation does not interfere with the binding and/or that MAU-8 acts downstream of PAR-5/14.3.3. We also show evidence that MAU-8/PhLP interacts with GPB-1, a ? subunit of heterotrimeric G proteins. In
mau-8 mutants, the disruption of MAU-8/PhLP induces GPB-1 sequestering and an exaggerated G? signalling accounting for the decreased locomotion and egg laying activity of adult hermaphrodites.