Abstract

BackgroundDuring the development of the Drosophila eye, specific cell types differentiate from an initially equipotent group of uncommitted precursor cells. The lozenge (lz) gene, which is a member of the Runt family of transcriptional regulators, plays a pivotal role in mediating this process through regulating the expression of several fate-specifying transcription factors. However, the regulation of lz, and the control of lz expression levels in different cell types is not fully understood.ResultsHere, we show a genetic interaction between Tramtrack69 (Ttk69) a key transcriptional repressor and an inhibitor of neuronal fate specification, and lz, the master patterning gene of cells posterior to the morphogenetic furrow in the Drosophila eye disc. Loss of Ttk69 expression causes the development of ectopic R7 cells in the third instar eye disc, with these cells being dependent upon Lz for their development. Using the binary UAS Gal4 system, we show that overexpression of Ttk69 causes the loss of lz-dependent differentiating cells, and a down-regulation of Lz expression in the developing eye. The loss of lz-dependent cells can be rescued by overexpressing lz via a GMR-lz transgene. We provide additional data showing that factors functioning upstream of Ttk69 in eye development regulate lz in a Ttk69-dependent manner.ConclusionsOur results lead us to conclude that Ttk69 can either directly or indirectly repress lz gene expression to prevent the premature development of R7 precursor cells in the developing eye of Drosophila. We therefore define a mechanism for the tight regulatory control of the master pre-patterning gene, lz, in early Drosophila eye development and provide insight into how differential levels of lz expression can be achieved to effect specific cell fate outcomes.

Highlights

  • During the development of the Drosophila eye, specific cell types differentiate from an initially equipotent group of uncommitted precursor cells

  • We show that R7 development in third instar eye discs is dependent upon Lz function, and that Ttk69 may play a role in the direct or indirect repression of lz gene expression in cell types competent to develop as R7 cells

  • We found that 87.1% (N = 350) of ttk1e11 mutant ommatidia contained between 2-3 Runt-labelled presumptive R7 cells in the apical R7 focal plane approximately seven rows posterior to the furrow in the disc epithelium, while 89.8% of ttkrm730 mutant ommatidia exhibited this phenotype (N = 433). ttk1e11 and ttkrm730 clones were characterised by a lack of βgalactosidase staining in the early eye disc, and mutant clones constituted the majority of the eye disc, a result consistent with the large areas of w- clonal patches observed in the adult eye

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Summary

Introduction

During the development of the Drosophila eye, specific cell types differentiate from an initially equipotent group of uncommitted precursor cells. Eukaryotic cellular tissues are generally comprised of several cell types, many of which may be derived from a common pool of precursor cells. How such developmentally equivalent cells become distinct from one another remains a fundamental question in developmental biol-. The developing eye of Drosophila has been extensively used as a model system to determine how common signalling pathways can induce the generation of cellular diversity. Photoreceptor R8 is the first cell established in the eye, its recruitment mediated by signalling events coordinated by the furrow [3,4]. Addition of non-neuronal lens secreting cone cells, supporting pigment cells, and the generation of sensory bristle cells make up the full complement of ommatidial cells [4,9]

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