SummarySequential modifications of the RNA polymerase II (Pol II) carboxyl-terminal domain (CTD) coordinate the stage-specific association and release of cellular machines during transcription. Here we examine the genome-wide distributions of the “early” (phospho-serine 5), “mid” (phospho-serine 7) and “late” (phospho-serine 2) CTD marks. We identify gene-class specific patterns and find widespread co-occurrence of the CTD marks. Contrary to its role in 3’ processing of non-coding RNA, the Ser7-P marks are placed early and retained until transcription termination at all Pol II-dependent genes. Chemical-genomic analysis reveals that the promoter-distal Ser7-P marks are not remnants of early phosphorylation, but are placed anew by the CTD kinase Bur1. Consistent with the ability of Bur1 to facilitate transcription elongation and suppress cryptic transcription, high levels of Ser7-P are observed at highly transcribed genes. We propose that Ser7-P could facilitate elongation and suppress cryptic transcription.

Phosphorylation of the carboxyl-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) governs stage-specific interactions with different cellular machines. The CTD consists of Y 1 S 2 P 3 T 4 S 5 P 6 S 7 heptad repeats, and sequential phosphorylations of Ser7, Ser5 and Ser2 occur universally across Pol II-transcribed genes. Phosphorylation of Thr4, however, appears to selectively modulate transcription of specific classes of genes. Here, we identify 10 new Thr4 kinases from different kinase structural groups. Irreversible chemical inhibition of the most active Thr4 kinase, Hrr25, reveals a novel role for this kinase in transcription termination of specific class of noncoding snoRNA genes. Genome-wide profiles of Hrr25 reveal a selective enrichment at 3ʹ regions of noncoding genes that display termination defects. Importantly, phospho-Thr4 marks placed by Hrr25 are recognized by Rtt103, a key component of the termination machinery. Our results suggest that these uncommon CTD kinases selectively place phospho-Thr4 marks to regulate expression of targeted genes.

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Khan, A. J., Akhtar, S., Singh, A. K., and Briddon, R. W. 2013. A distinct strain of Tomato leaf curl Sudan virus causes tomato leaf curl disease in Oman. Plant Dis. 97:1396-1402.Tomato leaf curl disease (ToLCD) is a significant constraint for tomato production in the Sultanate of Oman. The disease in the north of the country has previously been shown to be caused by the monopartite begomoviruses (family Geminiviridae) Tomato yellow leaf curl virus and Tomato leaf curl Oman virus. Many tomato plants infected with these two viruses were also found to harbor a symptom enhancing betasatellite. Here an analysis of a virus isolated from tomato exhibiting ToLCD symptoms originating from south and central Oman is reported. Three clones of a monopartite begomovirus were obtained. One of the clones was shown to be infectious to tomato and Nicotiana benthamiana and to induce symptoms typical of ToLCD. Analysis of the cloned sequences show them to correspond to isolates of Tomato leaf curl Sudan virus (ToLCSDV), a virus that occurs in Sudan and Yemen. However, the sequences showed less than 93% nucleotide sequence identity to previously characterized ToLCSDV isolates, indicating that the viruses represent a distinct strain of the species, for which we propose the name "Oman" strain (ToLCSDV-OM). Closer analysis of the sequences showed them to differ from their closest relative, the "Tobacco" strain of ToLCSDV originating from Yemen, in three regions of the genome. This suggests that the divergence of the "Oman" and "Tobacco" strains has occurred due to recombination. Surprisingly, ToLCSDV-OM was not found to be associated with a betasatellite, even though the isolates of the other ToLCSDV strains have been shown to be. The significance of these findings and the possible reasons for the distinct geographic distributions of the tomatoinfecting begomoviruses within Oman are discussed.