Magdy S. Alabady, PhD, MSc

Faculty, Scientist, and Director



Department of Plant Biology

University of Georgia Athens

Address 1:
Department of Plant Biology
2502 Miller Plant Sciences
University of Georgia
Athens, GA 30602

Address 2:
Georgia Genomics and Bioinformatics Lab
110 Riverbend Rd., Room 161
Athens, GA 30602



Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of siRNA Loci in Trypanosoma brucei


Journal article


D. Reynolds, Brigitte T. Hofmeister, L. Cliffe, Magdy S. Alabady, T. Siegel, R. Schmitz, R. Sabatini
PLoS Genetics, 2016

Semantic Scholar DOI PubMedCentral PubMed
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APA   Click to copy
Reynolds, D., Hofmeister, B. T., Cliffe, L., Alabady, M. S., Siegel, T., Schmitz, R., & Sabatini, R. (2016). Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of siRNA Loci in Trypanosoma brucei. PLoS Genetics.


Chicago/Turabian   Click to copy
Reynolds, D., Brigitte T. Hofmeister, L. Cliffe, Magdy S. Alabady, T. Siegel, R. Schmitz, and R. Sabatini. “Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of SiRNA Loci in Trypanosoma Brucei.” PLoS Genetics (2016).


MLA   Click to copy
Reynolds, D., et al. “Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of SiRNA Loci in Trypanosoma Brucei.” PLoS Genetics, 2016.


BibTeX   Click to copy

@article{d2016a,
  title = {Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of siRNA Loci in Trypanosoma brucei},
  year = {2016},
  journal = {PLoS Genetics},
  author = {Reynolds, D. and Hofmeister, Brigitte T. and Cliffe, L. and Alabady, Magdy S. and Siegel, T. and Schmitz, R. and Sabatini, R.}
}

Abstract

Base J, β-D-glucosyl-hydroxymethyluracil, is a chromatin modification of thymine in the nuclear DNA of flagellated protozoa of the order Kinetoplastida. In Trypanosoma brucei, J is enriched, along with histone H3 variant (H3.V), at sites involved in RNA Polymerase (RNAP) II termination and telomeric sites involved in regulating variant surface glycoprotein gene (VSG) transcription by RNAP I. Reduction of J in T. brucei indicated a role of J in the regulation of RNAP II termination, where the loss of J at specific sites within polycistronic gene clusters led to read-through transcription and increased expression of downstream genes. We now demonstrate that the loss of H3.V leads to similar defects in RNAP II termination within gene clusters and increased expression of downstream genes. Gene derepression is intensified upon the subsequent loss of J in the H3.V knockout. mRNA-seq indicates gene derepression includes VSG genes within the silent RNAP I transcribed telomeric gene clusters, suggesting an important role for H3.V in telomeric gene repression and antigenic variation. Furthermore, the loss of H3.V at regions of overlapping transcription at the end of convergent gene clusters leads to increased nascent RNA and siRNA production. Our results suggest base J and H3.V can act independently as well as synergistically to regulate transcription termination and expression of coding and non-coding RNAs in T. brucei, depending on chromatin context (and transcribing polymerase). As such these studies provide the first direct evidence for histone H3.V negatively influencing transcription elongation to promote termination.





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