charlatan, a gene encoding a Zn-finger factor involved in nervous system development. L.M. Escudero¹, E. Caminero¹, K.L. Schulze², H.J. Bellen², J. Modolell¹. 1) Centro de Biologia Molecular Severo Ochoa, CSIC and UAM. 28049 Madrid, Spain; 2) HHMI, Baylor College of Medicine, One Baylor Plaza, Houston TX 77030, USA.

   The charlatan (chn) gene was identified by Kania et al. (1995; Genetics 139: 1663-1678) as a P-element insertion allele that alters the morphology of the chordotonal organ clusters of the Drosophila embryonic PNS. We have found a new EP line (EPIL#6), inserted near the transcription origin of chn, that when overexpressed with several GAL4 drivers causes the appearance of ectopic macrochaetae. chn encodes a zinc-finger factor. In the wild-type, chn mRNA is detected in the embryonic and larval CNS and PNS. In the wing imaginal disc, chn is expressed in proneural clusters, and it is positively regulated by the proneural achaete (ac) and scute (sc) genes. We have obtained chn^ECJ1, a recesive null mutation, that removes and disorganizes elements from the embryonic PNS and, with low penetrance, suppresses notum bristles. These embryonic phenotypes are rescued by overexpression of chn. In the wing disc, misexpression of UAS-chn promotes ectopic expression of sc and formation of many extra bristles. UAS-chn appears to act on the proneural cluster-specific enhancers of ac/sc, as it activates in vivo constructs carrying different proneural enhancers of the AS-C. Cell clones homozygous for chn^ECJ1 show a decrease in the accumulation of Sc protein and in the expression of the isolated DC-lacZ and LIII-TSM-lacZ proneural enhancer constructs. Similar phenotypes have been observed by expressing a chn RNAi construct. Moreover, loss of function of chn by RNAi strongly potentiates the loss of bristles produced by the insuficiency of ac/sc. Our working hypothesis is that chn helps ac/sc to reach levels of expression in proneural clusters effective for the generation of sensory organ precursors.