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Published online
doi:10.1083/jcb.200902119
The Journal of Cell Biology, Vol. 186, No. 2, 243-254
The Rockefeller University Press, 0021-9525 $30.00
© Landeira et al.
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Article

Cohesin regulates VSG monoallelic expression in trypanosomes



David Landeira, Jean-Mathieu Bart, Daria Van Tyne, and Miguel Navarro

Instituto de Parasitología y Biomedicina López-Neyra, Consejo Superior de Investigaciones Cientificas, 18100 Granada, Spain

Correspondence to Miguel Navarro: miguel.navarro{at}ipb.csic.es

Antigenic variation allows Trypanosoma brucei to evade the host immune response by switching the expression of 1 out of ~15 telomeric variant surface glycoprotein (VSG) expression sites (ESs). VSG ES transcription is mediated by RNA polymerase I in a discrete nuclear site named the ES body (ESB). However, nothing is known about how the monoallelic VSG ES transcriptional state is maintained over generations. In this study, we show that during S and G2 phases and early mitosis, the active VSG ES locus remains associated with the single ESB and exhibits a delay in the separation of sister chromatids relative to control loci. This delay is dependent on the cohesin complex, as partial knockdown of cohesin subunits resulted in premature separation of sister chromatids of the active VSG ES. Cohesin depletion also prompted transcriptional switching from the active to previously inactive VSG ESs. Thus, in addition to maintaining sister chromatid cohesion during mitosis, the cohesin complex plays an essential role in the correct epigenetic inheritance of the active transcriptional VSG ES state.

Abbreviations used in this paper: BB, basal body; BC, basic copy; ES, expression site; ESB, ES body; IF, immunofluorescence; LUT, look up table; MITat, Molteno Institute Trypanozoon antigenic type; qRT-PCR, quantitative RT-PCR; rDNA, ribosomal DNA; VSG, variant surface glycoprotein.

© 2009 Landeira et al.
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