Open AccessBTat, a trans ‐acting regulatory protein, contributes to bovine immunodeficiency virus‐induced apoptosis
Author(s) -
Xuan Chenghao,
Qiao Wentao,
Li Jian,
Peng Guoyuan,
Liu Min,
Chen Qimin,
Zhou Jun,
Geng Yunqi
Publication year - 2008
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.01011.x
Subject(s) - biology , apoptosis , terminal deoxynucleotidyl transferase , programmed cell death , flow cytometry , microbiology and biotechnology , caspase , poly adp ribose polymerase , virus , virology , polymerase , gene , genetics , tunel assay
Summary Bovine immunodeficiency virus (BIV) is a member of the lentivirus subfamily of retroviruses highly related to human immunodeficiency virus in morphologic, antigenic and genomic features. BIV is known to induce chronic pathological changes in infected hosts, which are often associated with the development of immune‐mediated lesions. However, the molecular events underlying the cytopathic effect of BIV remain poorly understood. In this study, BIV was found to induce apoptotic cell death, and a small trans ‐acting regulatory protein encoded by BIV, BTat, was found to participate in the pro‐apoptotic action of BIV. Introduction of exogenous BTat to cells triggered apoptosis dramatically, as revealed by assays such as terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labelling, nuclear morphology analysis, flow cytometry, and cleavages of caspases and poly(ADP‐ribose)polymerase. Interestingly, the pro‐apoptotic effect of BTat was found to be mediated through its interaction with cellular microtubules and its interference with microtubule dynamics. These results provide the first evidence that induction of apoptosis may contribute to the cytopathic effect of BIV. In addition, these results uncover a novel role for BTat in regulating microtubule dynamics in addition to its conventional role in regulating gene transcription.