Abstract
Preventing transcription-replication head-on conflict (HO-TRC)-triggered R-loop formation is essential for maintaining genome integrity in bacteria, plants, andmammals. The R-loop eraser RNase H can efficiently relax HO-TRCs. However, it is not clear how organisms resist HO-TRC-triggered R-loops whenRNase H proteins are deficient. By screening factors that may relieve R-loop accumulation in the Arabidopsis atrnh1c mutant, we find that overexpression of theR-loop helicase RHON1 can rescue the defects ofaberrantly accumulated HO-TRC-triggered R-loops co-transcriptionally. In addition, we find that RHON1 interacts with and orchestrates thetranscriptional activity of plastid-encoded RNA polymerases to release the conflicts between transcription and replication. Our study illustrates that organisms employ multiple mechanisms to escape HO-TRC-triggered R-loop accumulation and thus maintain genome integrity.
Highlights
DNA replication and RNA transcription processes use the same genome as a template in all organisms, which could be problematic when replication and transcription are concurrent
We found that RHON1 formed a complex with plastid-encoded RNA polymerase (PEP) and coordinated PEP activity to suppress co-transcriptional R-loop formation and relax HO-transcription-replication conflicts (TRCs), maintaining the chloroplast genome
RHON1 Is a Potential R-Loop Regulator in Chloroplasts Highly conserved HO-TRC formation and regulation have been found in bacteria, plants, and mammals (Hamperl et al, 2017; Lang et al, 2017; Yang et al, 2017)
Summary
DNA replication and RNA transcription processes use the same genome as a template in all organisms, which could be problematic when replication and transcription are concurrent. Transcription-replication conflicts (TRCs) are a major source of genome instability (Gaillard and Aguilera, 2016; Hamperl and Cimprich, 2016). TRCs can be either co-directional (CD) or head-on (HO), depending on the respective orientations of transcription and replication (Hamperl and Cimprich, 2016). Recent analysis demonstrated that HO-TRCs, but not CD-TRCs, are the primary source of genome instability. HO-TRCs promote the accumulation of R-loops (DNA:RNA hybrids) and lead to the genome being more fragile. HO-TRCs, but not CD-TRCs, cause R-loop accumulation and DNA replication stress and induce a dramatic increase in DNA damage responses (Hamperl et al, 2017)
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