A MATERNAL PRODUCT OF THE PUNCH LOCUS OF DROSOPHILA-MELANOGASTER IS REQUIRED FOR PRECELLULAR BLASTODERM NUCLEAR DIVISIONS

The Punch locus of Drosophila melanogaster encodes the pteridine biosy nthesis enzyme guanosine triphosphate cyclohydrolase. One class of Pun ch mutants is defective for a maternal function that results in embryo nic death. We demonstrate here that the embryos exhibit nuclear divisi on defects during the precellular blastoderm stage of development. The se defects include abnormal nuclear distribution, mitotic asynchrony, and persisting chromatin bridges. Daughter nuclei that do not complete chromosome separation nevertheless initiate new interphase and mitoti c cycles. As a result, interconnected mitotic figures are observed. Mi totic spindles and nuclear envelopes appear essentially normal. A muta nt phenocopy was induced in wild-type embryos by treatment with the gu anosine triphosphate cyclohydrolase inhibitor, 2,4-diamino-6-hydroxypy rimidine, at a very early cleavage stage. Furthermore, an inhibitor of a terminal step in pteridine biosynthesis produced an identical pheno type. Immunolocalization experiments define expression of Punch protei n in nurse cells during oogenesis, The protein is packaged into granul es as it is transported into the oocyte cytoplasm. As syncytial blasto derm nuclear divisions proceed, Punch protein levels decrease and disa ppear by cellularization. Defects in the expression of the protein in Punch maternal effect mutants correlate well with the early phenotypes . These results show that a Punch product is directly involved in earl y nuclear divisions and suggest a possible role in chromosome separati on.