Differential Expression of the ARF GAP Genes GIT1 and GIT2 in Mouse Tissues

Robert Schmalzigaug ¹, Hyewon Phee ¹, Collin E. Davidson ¹, Arthur Weiss ¹ and Richard T. Premont ^1*

¹ Department of Medicine, Duke University Medical Center, Durham, North Carolina (RS,CED,RTP), and Department of Medicine, Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California (HP,AW)

^* To whom correspondence should be addressed. E-mail: richard.premont{at}duke.edu.

Submitted on February 2, 2007
Accepted on 1 June 2007

	Abstract

GIT1 and GIT2 belong to the family of ADP-ribosylation factor (Arf) GTPase-activating proteins and have been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation and aggregate formation in Huntington’s disease. Examination of endogenous GIT protein expression in tissues, however, has been hampered by the lack of GIT2-specific antibodies. To visualize GIT1 and GIT2 gene expression in mouse tissues, we created mice with -galactosidase (-Gal) reporters inserted into the two GIT genes. -Gal staining confirmed the broad tissue distribution of GIT1 and GIT2 in the mouse, but also revealed striking differences. GIT2 is expressed in most cells of the body, while GIT1 is restricted to only a subset of cells. For example, GIT2 is uniformly expressed throughout lung and liver, while GIT1 is restricted to cells lining blood vessels, bronchi and bile ducts. GIT1 and GIT2 expression is mutually exclusive in the testes, where a developmental expression shift occurs, with GIT2 present in spermatogonia but GIT1 in mature spermatids. In conclusion, analysis of endogenous GIT expression revealed a nearly ubiquitous distribution of GIT2, while GIT1 is restricted to specific cell types even in tissues with apparently high GIT1 expression, and is absent from some tissues entirely.

Key Words: GIT1, GIT2, ARF GAP, gene expression, -galactosidase, mice

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