Evolutionarily conserved transcription factor Apontic controls the G1/S progression by inducing cyclin e during eye development
Type
ArticleKAUST Department
Biological and Environmental Sciences and Engineering (BESE) DivisionComputational Bioscience Research Center (CBRC)
Environmental Science and Engineering Program
Bioscience Program
Date
2014-06-16Online Publication Date
2014-06-16Print Publication Date
2014-07-01Permanent link to this record
http://hdl.handle.net/10754/563598
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Show full item recordAbstract
During Drosophila eye development, differentiation initiates in the posterior region of the eye disk and progresses anteriorly as a wave marked by the morphogenetic furrow (MF), which demarcates the boundary between anterior undifferentiated cells and posterior differentiated photoreceptors. However, the mechanism underlying the regulation of gene expression immediately before the onset of differentiation remains unclear. Here, we show that Apontic (Apt), which is an evolutionarily conserved transcription factor, is expressed in the differentiating cells posterior to the MF. Moreover, it directly induces the expression of cyclin E and is also required for the G1-to-S phase transition, which is known to be essential for the initiation of cell differentiation at the MF. These observations identify a pathway crucial for eye development, governed by a mechanism in which Cyclin E promotes the G1-to-S phase transition when regulated by Apt.Citation
Liu, Q.-X., Wang, X.-F., Ikeo, K., Hirose, S., Gehring, W. J., & Gojobori, T. (2014). Evolutionarily conserved transcription factor Apontic controls the G1/S progression by inducingcyclin Eduring eye development. Proceedings of the National Academy of Sciences, 111(26), 9497–9502. doi:10.1073/pnas.1407145111Sponsors
We thank Helena Richardson for Cyclin E antibody and Yash Hiromi for valuable suggestions. This work was supported by National Basic Research Program of China Grant 2012CB114600 (to Q.-X. L. and X.-F.W.), a Grant in Aid for Scientific Research (to S. H.), and a Research Grant for the Cell Innovation Project from the Ministry of Education, Culture, Sports, Science and Technology of Japan (to K.I. and T.G.).PubMed ID
24979795PubMed Central ID
PMC4084451Additional Links
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084451ae974a485f413a2113503eed53cd6c53
10.1073/pnas.1407145111
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