PhD 1986 MRC Laboratory of Molecular Biology, Cambridge UK
Postdoc HHMI & Department of Molecular Cell Biology, UC Berkeley
Albert Einstein College of Medicine 1991-present
Fundamental mechanisms of growth and development
Dr. Baker’s laboratory studies the communication between cells that creates and maintains the organization of the body during development. They use the fruitfly Drosophila melanogaster in order to study these processes in vivo. Dr isolated the wingless gene from Drosophila which gives its name to the Wnt family of developmental signals and helped define the roles of wingless in the Drosophila embryo and adult limbs. Dr. Baker then characterized Drosophila eye development as a simple model for the determination and patterning of neural cells. Only a single bHLH transcription factor controls neurogenesis in the Drosophila retina in place of families of such proteins that function in most mammalian neural tissues. Dr. Baker’s research contributed to understanding the mechanisms of Notch signaling and Receptor Tyrosine Kinase signaling in the patterning or neural development, and in the coordination of neural development with cell proliferation and cell death.
Since the main mechanisms of cell fate determination and patterning during development are now understood, at least in general terms, the Baker laboratory increasingly investigates mechanisms that control and maintain the size and shape of organs. Much less is known about this important issue than about the determination of tissue and cell type. How do different organs develop and maintain particular morphologies? Growth and morphogenesis are regulated in many ways. Growth stops with terminal cell cycle exit and must be up-regulated for regeneration, tissue regulation, or response to damage. Dr. Baker’s laboratory defined the ways that neural differentiation uses developmental signals to control proliferation and survival of progenitor cells to achieve a precise number of cells in the Drosophila retina. They are currently interested in the ways bHLH transcription factors, which control neuronal differentiation and contribute to many diseases, both influence progenitor cell growth and also maintain the integrity of progenitor cell populations.
One emerging aspect of organ growth is the ‘cell competition’ occurring between cells growing at different speeds, for example because of mutations affecting ribosome assembly. Cell competition causes selective apoptosis of the out-competed cells only when they are close to the competing cell type. Even normal cells can be out-competed, for example if they are exposed to cells with an extra copy of the myc proto-oncogene, which grow faster, although not all differences in cell growth rate lead to cell competition. Dr. Baker’s lab showed that cells that loss of the Salvador-Warts-Hippo pathway of tumor suppressors also makes cells super-competitors that eliminate wild type cells, and that the protocadherin Fat is a cell surface regulator of the SWH pathway. Cell competition is hypothesized to represent a surveillance mechanism for the fittest progenitor cells during organ growth and might plausibly play several roles in cancer development. Cell competition may be a factor in the success of stem cell transplantation and regenerative therapies. Current research addresses the role of new components of cell competition uncovered during forward genetic screens that implicate regulatory signals from the ribosome in both cell competition and the control of cellular growth rate, and their potential conservation in mammals.
For more details, and complete list of publications, please see our website at
Selected recent publications
Baker, N.E. and Kale, A. (2016). Mutations in ribosomal proteins: apoptosis, cell competition and cancer. Mol Cell Oncol advance online publication: DOI:10.1080/23723556.2015.1029065.
Wang, L. H. and Baker, N.E. (2015). E-proteins and ID-proteins: Helix-loop-helix partners in development and disease. Dev Cell 35: 269-80.
Wang, L.-H. and Baker, N.E. (2015). Salvador-Warts-Hippo pathway in a developmental checkpoint monitoring Helix-Loop-Helix proteins. Dev Cell 32: 191-202.
Kale, A., Li, W., Lee, C.-H. and Baker, N.E. (2015). Apoptotic mechanisms during competition of ribosomal protein mutant cells: roles of the initiator caspases Dronc and Dream/Strica. Cell Death Differen 2: 1300-1312.
Fullard, J.F. and Baker, N.E. (2015). Signaling by the engulfment receptor Draper: a screen in Drosophila melanogaster implicates cytoskeletal regulators, Jun N-terminal Kinase, and Yorkie. Genetics 199: 117-134.
Baker, N.E. and Jenny, A. (2014). Metabolism and the other fat: a protocadherin in mitochondria. Cell 158: 1240-1.
Ruggiero, R., Kale, A., Thomas, B. and Baker, N.E. (2012) Mitosis in neurons: Roughex and Anaphase Promoting Complex maintain cell cycle exit to prevent cytokinetic and axonal defects in Drosophila photoreceptor neurons. PLoS Genetics 8:e1003049.
Bhattacharya, A. and Baker, N.E. (2011). A network of broadly-expressed HLH genes regulates tissue-specific cell fates. Cell 147, 881-892.
Lubensky, D.K., Pennington, M.W., Shraiman, B., and Baker, N.E. (2011). A dynamical model of ommatidial crystal formation. Proc Natl Acad Sci 108: 11145-11150.
Baker, N.E., and Firth, L.C. (2011). Retinal Determination Genes function along with cell-cell
signals to regulate Drosophila eye development: examples of multi-layered regulation by Master
Regulators. Bioessays 33: 538-546.
Baker, N.E. (2011). Cell competition. Curr Biol 21: R11-15.
More Information About Dr. Nicholas Baker
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Albert Einstein College of Medicine
Jack and Pearl Resnick Campus
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Ullmann Building, Room 805
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