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Faculty
Jaquelin Dudley
Professor of Molecular Genetics & Microbiology

Email: jdudley@uts.cc.utexas.edu
Website
Main Office: NMS 2.122
Phone: 471-8415

Alternate Office: NMS 2.262
Alt. Phone: 471-5101

Mailing Address
The University of Texas at Austin
1 University Station A5000; NMS 2.104
Austin ,TX 78712-0162
Jaquelin Dudley

Research Summary

Mouse mammary tumor virus (MMTV) is a retrovirus that induces mammary carcinomas and T-cell lymphomas in mice by insertional mutagenesis. We have identified the Cux1 protein (also known as CCAAT-displacement protein, CDP, Cutl1 or Cux1) as a transcriptional repressor of MMTV expression. Developmentally programmed disappearance of the repressor, CDP, during lactation allows maximum virus expression during MMTV transmission from mothers to pups through the milk. We also have shown that Cux1 is important for expression of a number of mammary-specific genes. Most recently, Cux1 overexpression has been linked to poor prognosis for human breast cancer patients, and we have created Cux1-knockout mice to study mammary cancer progression in mouse models. These studies promise to increase our understanding of tissue-specific gene regulation and tumorigenesis. We also have been developing MMTV as a vector system for gene therapy of breast cancer. In this process, we discovered a new viral protein, Rem, which is involved in the nuclear export and expression of intron-containing viral mRNAs. These results are exciting because MMTV may be used as a mouse model for study of another retrovirus, human immunodeficiency virus (HIV), which causes AIDS. Finally, we are interested in studying the host response to viral and bacterial pathogens. We have developed a unique mouse strain called BALB/Mtv-null that is more than 99% identical to the inbred BALB/c mouse strain, but lack MMTV sequences in their germline. Unlike the parental BALB/c mice, Mtv-null mice are resistant to mammary tumors induced by MMTV, T-cell lymphomas induced by type B leukemogenic virus (TBLV), and death induced by infection with cholera-toxin producing strains of Vibrio cholera. Elucidation of the mechanism of this host resistance should allow us to develop novel methods for fighting different pathogenic organisms that might be used for bioterrorism.