A tumor host range selection procedure identifies p150sal2 as a target of polyoma virus large T antigen

doi:10.1073/pnas.251447198

A tumor host range selection procedure identifies p150^sal2 as a target of polyoma virus large T antigen

Department of Pathology, Harvard Medical School, Boston, MA 02115

Edited by Peter K. Vogt, The Scripps Research Institute, La Jolla, CA, and approved October 10, 2001 (received for review August 23, 2001)

Abstract

Cancer cells may undergo loss or alterations in functions that certain viruses normally target to promote virus replication. Virus mutants that have lost the targeting function(s) should be able to grow in such cancer cells but not in normal cells. A “tumor host range” (t-hr) selection procedure has been devised and applied to polyoma virus based on this rationale. Studies of one t-hr mutant have led to the identification of the mSal2 gene product (p150^sal2) as a binding partner of the large T antigen. mSal2 encodes a multizinc finger protein and putative transcription factor homologous to the Drosophila homeotic gene Spalt. The t-hr mutant encodes an altered large T protein that fails to interact with p150^sal2 and is defective in replication and tumor induction in newborn mice.

Footnotes

↵ * To whom reprint requests should be addressed. E-mail: thomas_benjamin{at}hms.harvard.edu.
This paper was submitted directly (Track II) to the PNAS office.
Abbreviations:

GST,

glutathione S-transferase;

BMK,

primary baby mouse kidney epithelial cells