Keywords: f. eye disc; p. transcriptional regulation
Many kinds of eye diseases, including those that result in blindness originate from genetic mutations of key genes involved in eye morphogenesis. Extradenticle (exd), is a TALE homeobox family transcription factor that is used in a variety of molecular processes such as embryogenesis and development of the central nervous system. However, it’s role in patterning the Drosophila eye has not been completely understood. The compound eye of Drosophila is composed of 800-unit eyes, called ommatidia, which are arranged in a stereotyped hexagonal array. This organization, down to the directional angle of the ommatidia, is key to proper vison in adult flies. This specific cell organization is achieved by a wave of cell differentiation called a morphogenic furrow. This furrow arises from a single point on the most posterior end of the eye-antennal imaginal disc and migrates anteriorly in a single wave of differentiation. This patterning event involves several signaling pathways to properly pattern the undifferentiated cells that composed the eye field. My preliminary findings have shown a role for exd in retina patterning, which revolves around the regulation of cell differentiation in the ventral side of the Drosophila eye. During a genetic screen I found that reductions in levels of Exd leads to the inappropriate release of a second wave of differentiation from the ventral margin of the eye field. This was accomplished by utilizing RNAi and a unique driver, c311-GAL4, that drives expression in a specific tissue layer of the imaginal disc known as the peripodial epithelium. This ectopic patterning results in a completely disorganized retina. A possible cause for the disorganized retina is that wingless (wg) expression is lost on the ventral margin when exd is knockdown. It has been well documented that wg signaling in the eye acts as a repressor to other key patterning genes. I hypothesize that the loss of exd leads to the loss of the ventral repression pathway of the eye field. Additionally, I conducted a genetic screen to identify potential binding partners of exd that functional in patterning the Drosophila eye. The results of my screen showed that the knockdown of hth in the peripodial epithelium phenocopies the loss of exd. This data shows that hth and exd maybe functioning as co-factors to properly spatially restrict the initiation and progression of cell differentiation in the Drosophila eye disc.