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Dr. Jody Rosenblatt

Education

Dr. Jody Rosenblatt received her BA in 1988 in Molecular Biology  and Transcription at the University of California at Berkeley. Her undergraduate project was titled “The role of puffing polytene chromosomes in transcription.” She then went on to earn her PhD in 1998 in Biophysics and Biochemistry at the University of California at San Francisco. Her project during this time was on the regulation of actin dynamics.

Below is an extensive list of all of her educational achievements:

Type	School	Degree
Postdoctoral Fellowship	University College London, MRC-LMCB	Postdoctoral Fellow
Postdoctoral Fellowship	University College London, American Cancer Society Cell Biology	Postdoctoral Fellow
Postdoctoral Fellowship	University College London, Department of Anatomy	Postdoctoral Fellow
Postdoctoral Fellowship	University College London, EMBO Cell Biology	Postdoctoral Fellow
Doctoral Training	University of California Biophysics & Biochemistry	Ph.D.
Fellowship	University of California San Francisco, National Science Foundation Cell Biology	Fellow
Fellowship	University of California Berkeley, Genetics Society of America Genetics	Fellow
Undergraduate	University of California Molecular Biology	B.A.

Honour's and Awards

Dr. Jody Rosenblatt has been awarded many honours and awards. These include:

-         Director's New Innovator Award. National Institute of Health, 07/2007

-         Fellow. Wellcome Trust, 04/2005

-         Postdoctoral Fellowship. American Cancer Society, 01/2000

-         Postdoctoral Fellowship. EMBO, 01/1999

-         Postdoctoral fellowship. HFSP, 01/1999

Current Occupation

Dr. Jody Rosenblatt is an Associate Professor at the Department of Oncological Sciences at the University Of Utah, School Of Medicine and a member of the Cell Response and Regulation Program. She is an Adjunct Assistant Professor of Biology and of Bioengineering as well. She also is an investigator at the Huntsman Cancer institute at her own Rosenblatt Lab. 

Area of Research

Cell Extrusion

Extrusion is a process that dying cells use to exit out of the epithelial layers. A dying cell will signal it’s live epithelial neighbouring cells to form an intercellular actin and myosin ring around the dying cell. This ring will then contract and squeeze the cell out of the layer of epithelium. At the same time the gap that is formed by the dying cell is quickly filled up to preserve epithelial barrier function. This process that Dr. Jody Rosenblatt has discovered plays an important role in maintaining epithelium barrier homeostasis and reducing crowding and has implication in cancer and asthma.

Cell Extrusion during Crowing of Cells

Dr. Rosenblatt’s work on cell crowding and homeostatic levels shows that the epithelium maintains a constant number of cells and excess epithelial cells are extruded out of the epithelial barrier. If there is a delay in the gap between the extrusion of cells and build up on cells, the excess will appear as tumors. This shows that that excess epithelial cells are shed by extrusion whether or not the cells are apoptotic. It was also shown that in worms, if the standard pathways of apoptosis are disrupted, cells still die. She has discovered that cells death still occurs by shedding and extrusion is not the only way dying cells are removed out of the epithelial barrier. 

Cell Extrusion during Apoptosis

Dr. Rosenblatt’s work on apoptosis shows that during the process of cell extrusion, an apoptotic cell signals it’s surrounding cells to form an actin and myosin ring. Subsequently the cell would be squeezed out the epithelium. Both intrinsic and extrinsic pathways activate these pathways. The signal produced by dying cells to initiate the process of forming and contracting a ring of actin and myosin to squeeze the dying cell out of the epithelium is sphingosine-1-phosphate (S1P). Decreases in S1P synthesis by inhibiting sphingosine kinase activity or by blocking extracellular S1P access to its receptor prevented apoptotic cell extrusion. Extracellular S1P activates the process of extrusion by binding to S1P₂ receptor in the cells neighbouring a dying cell.

S1P produced by apoptotic cells binds and activates S1P₂ in neighbouring cells to trigger contraction of an intercellular actin-myosin ring. This then activates Rho, presumably through p115 RhoGEF to trigger assembly and contraction of the actin-myosin extrusion ring at the live and dying cell interface.

S1P is known to help cells survive and the loss of S1P in the cell being extruded could help promote its death. They expect that defects in the S1P₂ signalling pathway may result in disease associated with compromised epithelial barriers. For example in mucosal barriers in asthma and metastasis of cancers. 

Tumour and Cancer Implications of Cell Extrusion

Dr. Jody Rosenblatt explores how basal cell extrusion could lead to tumors and cancers. Adenomatous polyposis coli (APC), a tumour suppressor protein, aids the actin and myosin ring contraction at the apex to cause basal cell extrusion or at the base causing apical extrusion. APC disruption causes more basal extrusion than wild type cells and typically disrupted APCs are found in colon and breast cancer. Furthermore, oncogenic K-Ras also predominantly extrudes basally by degrading the S1P and S1P2 receptor and is hypothesized to cause invasion that could lead to metastasis. Some cells with low amounts of S1P2 can survive basal extrusions and proliferate causing apoptotic-resistant masses and poor epidermal barriers. However, her research shows added S1P2 receptors as well as Focal Adhesion Kinase (FAK) inhibitors returns apical extrusion, causes cell death, reduces tumours, and metastases. Where FAK even reduces a less permeable barrier and does not affect surrounding cells.