Eye Formation Genes are Negatively Regulated by Proneural Genes atonal and daughterless During Drosophila Eye Development

碩士 === 國立陽明大學 === 神經科學研究所 === 89 === In the Drosophila eye development, eye formation genes eyeless, twin of eyeless, optix, eye gone, sine oculis, eyes absent, and dachshund specify the eye primordium, giving it the potential to form an eye disc. After eye disc formation, the proneural g...

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Bibliographic Details
Main Authors: Yu-Wen Chang, 張毓雯
Other Authors: Cheng-Ting Chien
Format: Others
Language:zh-TW
Published: 2001
Online Access:http://ndltd.ncl.edu.tw/handle/10139618118188262220
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Summary:碩士 === 國立陽明大學 === 神經科學研究所 === 89 === In the Drosophila eye development, eye formation genes eyeless, twin of eyeless, optix, eye gone, sine oculis, eyes absent, and dachshund specify the eye primordium, giving it the potential to form an eye disc. After eye disc formation, the proneural genes atonal (ato) and daughterless (da) encode subunits of heterodimeric basic helix-loop-helix proteins that promote the differentiation of photoreceptors. In the morphogenetic furrow (MF), where photoreceptor differentiation initiates, cells express Ato and higher levels of Da. Interestingly, eyeless, twin of eyeless and optix are downregulated in the MF. sine oculis and eyes absent are highly expressed both anterior and posterior to, but not in, the MF. Expression of dachshund (dac) is at a high level anterior to the MF and repressed to a basal level in the MF. I shown that misexpression of eyeless, or combination of eyes absent and sine oculis across the MF causes Ato repression in the MF, and consequently failure of photoreceptor differentiation in the eye disc. These results suggest that negative regulation of eye formation genes in the MF is necessary for cell differentiation in the compound eye. I observed that expression of Dac and Eyeless is upregulated in da or ato mutant clones in the MF. Co-misexpression of Da and Ato causes Dac and Eyeless being downregulated anterior to the MF, and misexpression of Da alone also causes a similar, but less effective, downregulation. The negative regulation of dac and ey is at least partly at the transcriptional level, which is also observed for other eye formation genes. The fusion protein of Da and VP16 activation domain that functions constitutively to promote sensory bristle development, also causes similar repressive effect on Dac. Therefore, Ato and Da may function as an activator to activate a repressor of the eye formation genes. Several other results will also be presented in this thesis.