Regulation of transcription termination by glucosylated hydroxymethyluracil, base J, in Leishmania major and Trypanosoma brucei.
Bottom Line: Reduction of J in Leishmania tarentolae via growth in BrdU resulted in cell death and indicated a role of J in the regulation of RNAP II termination.Reduction of J in L. major resulted in genome-wide defects in transcription termination at the end of polycistronic gene clusters and the generation of antisense RNAs, without cell death.In contrast, loss of J in T. brucei did not lead to genome-wide termination defects; however, the loss of J at specific sites within polycistronic gene clusters led to altered transcription termination and increased expression of downstream genes.
Affiliation: Department of Biochemistry and Molecular Biology, University of Georgia, Davison Life Sciences Building, 120 Green Street, Athens, GA 30602-7229, USA.Show MeSH
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Mentions: The termination defects observed in Leishmania spp. prompted us to examine T. brucei for similar transcription termination defects upon the loss of base J. Base J is not essential in T. brucei, as both JBP enzymes can be knocked out without obvious phenotypic effects (34). Consistent with this, wild-type T. brucei treated with 1-mM DMOG reduced global J levels beyond the limits of detection by anti-J dot blot (Figure 4A), with no significant growth defect (Supplementary Figure S4). Consistent with total J levels, all cSSRs examined had significantly reduced levels of J following DMOG treatment (Figure 4B).
Affiliation: Department of Biochemistry and Molecular Biology, University of Georgia, Davison Life Sciences Building, 120 Green Street, Athens, GA 30602-7229, USA.