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All Good Things Must Come to an End: How Is Notch Signaling Turned off?
Raphael Kopan (23 November 1999)
Sci. STKE 1999 (9), pe1-pe1. [DOI: 10.1126/stke.1999.9.pe1]
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Is it all about Tramtrack?

A potential target for proteasome degradation in the sensory organ precursor (SOP) may have been inadvertently described elsewhere. Dong et al. (1) identified the protein tramtrack (Ttk) as a target for proteasome mediated degradation. Like Enhancer of Split (Espl), ttk is a transcriptional target of Notch signaling (2-4) and it mediates the antineurogenic activity of Notch in the support cells of the SOP. Ttk is negatively regulated by Numb, which is inherited asymmetrically by neuro-competent cells in the SOP lineage(5). Ttk stabilization in DTS5 expressing flies could lead to the outcome described by Schweisguth in his recent paper (6). If this were true, then Notch would promote Ttk accumulation while Numb and the proteasome would reduce it. The ultimate fate of sister cells in the SOP lineage might then be determined by the amounts of Ttk in individual nuclei.

1. Dong, X. Z., Tsuda, L., Zavitz, K. H., Lin, M., Li, S. H., Carthew, R. W., and Zipursky, S. L. (1999). ebi regulates epidermal growth factor receptor signaling pathways in Drosophila. Genes & Development 13:954-965.

2. Campos-Ortega, J. A. (1996). Numb diverts notch pathway off the tramtrack. Neuron 17:1-4.

3. Guo, M., Bier, E., Y., J. L., and Jan, Y. N. (1995) Tramtrack acts downstream of numb to specify distinct daughter cell fates during asymmetric cell divisions in the Drosophila PNS. Neuron 14:913-925.

4. Guo, M., Jan, L. Y., and Jan, Y. N. (1996). Control of daughter cell fates during asymmetric division - interaction of numb and notch. Neuron 17:27-41.

5. Posakony, J. W. (1994). Nature versus nurture: asymmetric cell divisions in Drosophila bristle development. Cell 76: 415-418.

6. Schweisguth, F. (1999). Dominant negative mutation in the b2 and b6 proteasome subunit genes affect alternative cell fate decisions in the Drosophila sense organ lineage. Proc. Natl. Acad. Sci. U.S.A. 96:11382-11386.

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