PROGRESSIVE CELL FATE DETERMINATION OF SENSORY NEURONS IN
DROSOPHILA
Cheng-Ting Chien
1,2,3
, Ming-Lang Hunag
1,2
, Tzu Liu
1,3
, Shao-Kuei Huang
1,2
Haiwei Pi
1
1
Institute of Molecular Biology, Academia Sinica,
2
Institute of Neuroscience, National
Yang-Ming University, and
3
Institute of Molecular Medicine, National Taiwan University,
Taipei, Taiwan
Development of the Drosophila sensory organs is a multi-step process, initiated with expression of the proneural genes that confers naïve cells competence to adopt neural fate. The proneural genes are expressed in patches of ectodermal cells. However, only one or a few cells are selected to become the sensory organ precursors (SOP). This step is mediated by the mechanism of lateral inhibition that prevents neighboring cells from adopting the same neural fate. Once the SOP cells are selected, they divide asymmetrically to generate daughter cells of distinct fates, including the sensory neurons. These daughter cells of a single SOP cell thus constitute a sensory organ.
We show that amos is a novel proneural gene that promotes multiple dendritic (MD) neuron formation. amos encodes a basic-helix-loop-helix (bHLH) protein of the Atonal family.
During embryonic development, amos is expressed in patches of ectodermal cells, and the expression is quickly restricted to SOP cells. Loss of amos function eliminates MD neurons that remain in ASC;atonal double mutants. Misexpression of amos generates ectopic MD and other types of neurons. Amos interacts with the ubiquitously expressed Daughterless protein in vivo and in vitro. Our misexpression experiments suggest that a domain located outside the
DNA-binding domain of Amos determines the MD neuronal specificity.
phyllopod ( phyl ), previously identified to be essential for R7 photoreceptor differentiation, is required in two processes of external sensory organ development. phyl mutations cause failure in SOP formation, and cell fate transformation of the SOP progeny. Conversely, misexpression of phyl promotes ectopic SOP formation, and opposite cell fate transformation of SOP daughter cells to the phyl mutants. Genetic interactions are consistent with the model that Phyl and Sina, a component of E3 ligase, function by targeting the transcriptional repressor
Ttk for protein degradation. We further demonstrated that phyl acts epistatically to Notch in
SOP lineage. In embryos, phyl is expressed specifically in neural precursors and a subset of
SOP progeny, and phyl mRNA levels are negatively regulated by Notch signaling. All these analyses suggest that Notch signaling represses neural fate by removing phyl activity, thus allowing Ttk to exert its repression function.
連 絡 人：簡正鼎 地 址：中央研究院分子生物研究所

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