Institut für Genetik, Universität Mainz, Saarstraße 21, D-55122 Mainz, Germany,
The matzerath (maz) mutation was obtained after imprecise P-element excision of the Gal4 P-element insertion line Mz1580. This enhancer trap line expresses Gal4 in most of the CNS glial cells, in the MP2 neurons and in macrophages from early stage on. The P-element was mapped to the region 5C by in situ hybridization. The excision mutagenesis resulted in 10 mutants, all belonging to one complementation group. Four of these are homozygous viable showing ectopic wing vein material near vein 2. The other 6 mutants are homozygous lethal before the adult stage. One of these 6 mutant strains (maz6) has the same ectopic wing vein phenotype as the viable excisions but dominant. The lethality of the excission mutants maz1 to maz5was rescued in the presence of the duplication Dp(1;2)rb71g (duplicated region = 3F3 to 5E8) placing the mutated gene in the same region the P-element was mapped. Stainings with antibodies against the glia-specific antigen Repo as well as with BP102 and 22C10 showed no detectable phenotype in the nervous system of the homozygous mutant embryos of all lethal excisions. However, a closer inspection of the phenotype of maz1 to maz5 revealed, that they show a developmental arrest at first instar larva (L1). Moreover, it is possible to keep them up to three weeks at this developmental stage. To study the reasons for the developmental arrest, we looked at the proliferation pattern in the brain of first instar larvae. A continuous BrdU feeding over two weeks showed the same pattern of incorporated BrdU as in wildtype after 20 hours. On the other hand, a posthatching BrdU pulse of 20 hours in the mutants gave the same results as the continuous BrdU incorporation over two weeks, showing that they stop proliferation in the CNS at the end of L1. Molecular investigations are on the way to identify the gene responsible for this phenotype. (Supported by the EEC (grant SCI-CT92-0790 to J.U. and G.M.T.))