@article{7c9b20fe7339409fa40008a1b8f0f18c,
title = "Regulation of the Drosophila ID protein extra macrochaetae by proneural dimerization partners",
abstract = "Proneural bHLH proteins are transcriptional regulators of neural fate specification. Extra macrochaetae (Emc) forms inactive heterodimers with both proneural bHLH proteins and their bHLH partners (represented in Drosophila by Daughterless). It is generally thought that varying levels of Emc define a prepattern that determines where proneural bHLH genes can be effective. We report that instead it is the bHLH proteins that determine the pattern of Emc levels. Daughterless level sets Emc protein levels in most cells, apparently by stabilizing Emc in heterodimers. Emc is destabilized in proneural regions by local competition for heterodimer formation by proneural bHLH proteins including Atonal or AS-C proteins. Reflecting this post-translational control through protein stability, uniform emc transcription is sufficient for almost normal patterns of neurogenesis. Protein stability regulated by exchanges between bHLH protein dimers could be a feature of bHLH-mediated developmental events.",
author = "Ke Li and Baker, {Nicholas E.}",
note = "Funding Information: We thank Drs. Abhishek Bhattacharya, Jorge Blanco, Jean Hebert, Andreas Jenny, Marianthi Kiparaki, Ertugrul Ozbudak, Francesca Pignoni and Lan-Hsin Wang for comments on the manuscript, Dr. Abhishek Bhattacharya for initial contributions to the project, and Dr. Marianthi Kiparaki for DNA constructs. Drosophila stocks were obtained from the Flytrap Project, the Zurich ORFeome Project (FlyORF) and the Bloomington Drosophila Stock Center (supported by NIH P40OD018537). S2 cells were obtained from the Drosophila Genomics Resource Center (supported by NIH 2P40OD010949-10A1). Confocal microscopy was performed in the Analytical Imaging Facility of the Albert Einstein College of Medicine (supported by the NCI P30CA013330). DNA sequencing was performed by the Genomics Core of Albert Einstein College of Medicine. This work was supported by the NIH grant GM047892. Data in this paper are from a thesis submitted in partial fulfillment of the requirement for the degree of Doctor of Philosophy in the Graduate Division of Biomedical Sciences, Albert Einstein College of Medicine, Yeshiva University, USA. National Institute of General Medical Sciences GM047892 Nicholas E Baker. Funding Information: We thank Drs. Abhishek Bhattacharya, Jorge Blanco, Jean Hebert, Andreas Jenny, Marianthi Kipar-aki, Ertugrul Ozbudak, Francesca Pignoni and Lan-Hsin Wang for comments on the manuscript, Dr. Abhishek Bhattacharya for initial contributions to the project, and Dr. Marianthi Kiparaki for DNA constructs. Drosophila stocks were obtained from the Flytrap Project, the Zurich ORFeome Project (FlyORF) and the Bloomington Drosophila Stock Center (supported by NIH P40OD018537). S2 cells were obtained from the Drosophila Genomics Resource Center (supported by NIH 2P40OD010949-10A1). Confocal microscopy was performed in the Analytical Imaging Facility of the Albert Einstein College of Medicine (supported by the NCI P30CA013330). DNA sequencing was performed by the Genomics Core of Albert Einstein College of Medicine. This work was supported by the NIH grant GM047892. Data in this paper are from a thesis submitted in partial fulfillment of the requirement for the degree of Doctor of Philosophy in the Graduate Division of Biomedical Sciences, Albert Einstein College of Medicine, Yeshiva University, USA. Publisher Copyright: {\textcopyright} Li and Baker.",
year = "2018",
month = apr,
day = "24",
doi = "10.7554/eLife.33967",
language = "English (US)",
volume = "7",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",
}