Ashrafi, Kaveh
Bernstein, Harold S.
Black, Brian L
Blanc, Paul D
Botvinick, Elias H
Boushey, Homer A
Broaddus, V Courtney
Brodsky, Frances M
Brown, James K
Bruneau, Benoit G
Caughey, George H
Chapman, Harold A
Charo, Israel F
Chatterjee, Kanu
Chuang, Pao-Tien
Clyman, Ronald I
Conklin, Bruce R
Conte, Michael S
Coughlin, Shaun R
Derynck, Rik M
Dobbs, Leland G
Eisner, Mark D
Engel, Joanne N
Erle, David J
Fahy, John Vincent
Farese, Robert V
Fielding, Christopher J
Fineman, Jeffrey R
Gardner, David G
Gartner, Zev Jordan
Glantz, Stanton A
Gold, Warren M
Gropper, Michael
Grossman, William
Hawgood, Samuel
Hill, Arthur C
Hoffman, Julien I
Ingraham, Holly A
Jan, Lily Y
Julius, David J
Kan, Yuet W
Kane, John P
Karliner, Joel S
Kornberg, Thomas B
Kurtz, Theodore W
Kwok, Pui-Yan
Lazarus, Stephen C
Lee, Randall J
Lim, Wendell A
Mahley, Robert W
Malloy, Mary J.
Mann, Michael J
Martin, Gail R
Matthay, Michael A
Mcdonald, Donald M
Mikawa, Takashi
Minor, Daniel L
Mostov, Keith E
Nadel, Jay A
Olgin, Jeffrey E
Pearce, David
Pittet, Jean-Francois
Redberg, Rita F
Reiter, Jeremy F.
Rosen, Steven D
Rowitch, David H
Scheinman, Melvin M
Schiller, Nelson B
Shaw, Robin M.
Sheppard, Dean
Shokat, Kevan M
Simpson, Paul C
Springer, Matthew L
Srivastava, Deepak
Stainier, Didier Y. R.
Teitel, David F
Von Zastrow, Mark E
Wang, Rong
Weiner, Orion D
Weiss, Arthur
Weiss, Ethan J
Werb, Zena
Woodruff, Prescott G
Xu, Allison Wanting
Young, William L

CVRI Scientists

Gail R Martin, Ph.D.
Professor

Research Interests:
Function of the FGF family in early mammalian development; establishment of the vertebrate body plan during gastrulation

Summary:
The Martin lab is interested in understanding the mechanisms that control the early steps in organogenesis in the vertebrate embryo, and the subsequent outgrowth and patterning of the developing organs. We are particularly interested in the roles played by members of the Fibroblast Growth Factor (FGF) family of signaling molecules and their antagonists in these processes.

Our approach to elucidating a particular gene's function is to determine the consequences of perturbing its expression during mouse development. To accomplish this we produce loss- and gain-of-function alleles of the genes of interest and study the consequences of eliminating or increasing their expression in the embryo. Using this approach we have demonstrated that FGF signaling is essential for cell survival during the early development of the brain, kidney, limbs, and other organs. Recently, we have found that eliminating Sprouty gene expression, which essentially increases FGF signaling, has profound effects on the development of the heart and lungs.

CVRIHead