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HOME > SEMINAR / EVENT > No.1312 How does HTLV-1 hide? Dynamics of HTLV-1 transcriptional latency and reactivation
Jan 27, 2020
No.1312 How does HTLV-1 hide? Dynamics of HTLV-1 transcriptional latency and reactivation
Date: January. 27, (Mon.) 2020 15:00~16:00
Room: Seminar Room,1st floor of Bldg. No.2 of Institute for Frontier Life and Medical Science, Kyoto University
Speaker: Dr. Charles R M Bangham
Imperial College London
Title: How does HTLV-1 hide? Dynamics of HTLV-1 transcriptional latency and reactivation

Abstract

It is now clear that the human leukaemia virus HTLV-1 is transcribed, like most human genes, in intermittent bursts.  Both the sense strand and the antisense strand of the HTLV-1 provirus are expressed in bursts, but the frequency and intensity of these bursts differs greatly between the two strands.  It is not yet fully understood what regulates the frequency, intensity and duration of these transcriptional bursts.  We have identified a number of factors that influence the burst frequency, including the genomic integration site of the provirus, the stress-responsive p38 MAP Kinase, polycomb repressive complex 1, cytosine methylation, hypoxia, and glycolysis.  Using single-molecule RNA fluorescence in situ hybridization and real-time imaging, we have developed a mathematical model of the transcriptional dynamics of HTLV-1.  We hypothesize that the chromatin architectural protein CTCF, which binds to the HTLV-1 provirus, confers a survival advantage on the virus by bringing the provirus near to actively transcribed regions of the host genome.  This hypothesis is now under test.
(Language: English)

 

Invitator Laboratory of Virus Control (Masao Matsuoka)Laboratory of Ultrastructural Virology(Takeshi Noda)

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