Iva

Greenwald

Dr. Iva Greenwald is pictured.
Professor
804A Fairchild, 1212 Amsterdam Avenue. MC2421
New York
NY
10027
Office Phone: 
(212) 853-6928
Fax: 
(212) 865-8246
Short Research Description: 

Cell-cell interactions, signal transduction, and cell fate specification in C. elegans http://greenwaldlab.org/

Full Research Description: 

We study cell-cell interactions, signal transduction, and cell fate specification during C. elegans development.  Much of our work is centered on LIN-12/Notch, the receptor component of a major signaling system for specifying cell fate during animal development.  In addition, mutations in core components and modulators of the LIN-12/Notch pathway have been implicated in cancer, Alzheimer's disease, and other diseases and syndromes. Using C. elegans, we study how LIN-12/Notch signaling is modulated during normal development and identify potential ways it may be modulated to combat disease.

In our developmental studies, we aim to understand the fundamental logic and molecular events that govern cell fate decision-making. We mainly study two simple cell fate decision paradigms in which LIN-12/Notch signaling is essential: the “AC/VU decision” and “VPC fate specification.” These simple paradigms offer the opportunity to apply powerful methods of genetic analysis to fundamental mechanisms of cell fate specification that operate in all animals.  During these events, different modulatory mechanisms regulate LIN-12/Notch activity and different signaling inputs are integrated so that correct cell fate decisions are made.   

We also use sensitive and specific suppressor and enhancer screens in C. elegans for “gene discovery”, with the aim of identifying new, conserved modulators of LIN-12/Notch and other signaling pathways. 

Representative Publications: 
  • de la Cova, C. and Greenwald, I. (2012) SEL-10/Fbw7-dependent negative feedback regulation of LIN-45/Braf signaling in C. elegans via a conserved phosphodegron   Genes Dev 26, 2524-2535. 
  • Karp, X. and Greenwald, I.  (2013) Control of cell fate plasticity and maintenance of multipotency by DAF-16/FoxO in quiescent C. elegans. Proc Natl Acad Sci (USA) 110, 2181-2186.
  • Sallee, M.D. and Greenwald, I. (2015) Dimerization-driven degradation of C. elegans and human E proteins.  Genes Dev 29, 1356-1361.   

Business Office

Department of Biological Sciences
500 Fairchild Center
Mail Code 2401
Columbia University
1212 Amsterdam Avenue
New York, NY 10027

Academic Office

Department of Biological Sciences
600 Fairchild Center
Mail Code 2402
Columbia University
1212 Amsterdam Avenue
New York, NY 10027
biology@columbia.edu
212 854-4581