X DNA damage network in ArabidopsisClara Spermine NONOate Technical Information Bourboussea,1, Neeraja Vegesnaa,b, and Julie A. Lawa,b,a Plant Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037; and bDivision of Biological Sciences, University of California, San Diego, La Jolla, CAEdited by Julia Bailey-Serres, University of California, Riverside, CA, and authorized November 14, 2018 (received for overview June 21, 2018)To combat DNA damage, organisms mount a DNA damage response (DDR) that benefits in cell cycle regulation, DNA repair and, in severe instances, cell death. Underscoring the significance of gene regulation in this response, research in Arabidopsis have demonstrated that all of the aforementioned processes rely on SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a NAC family transcription factor (TF) which has been functionally equated for the mammalian tumor suppressor, p53. Having said that, the expression networks connecting SOG1 to these processes remain largely unknown and, despite the fact that the DDR spans from minutes to hours, most transcriptomic information correspond to single timepoint snapshots. Right here, we generated transcriptional models of the DDR from GAMMA ()-irradiated wild-type and sog1 seedlings during a 24-hour time course applying DREM, the Dynamic Regulatory Events Miner, revealing 11 coexpressed gene groups with distinct biological functions and cis-regulatory functions. Inside these networks, further chromatin immunoprecipitation and transcriptomic experiments revealed that SOG1 will be the important activator, straight targeting probably the most strongly up-regulated genes, like TFs, repair things, and early cell cycle regulators, whilst three MYB3R TFs will be the major repressors, particularly targeting one of the most strongly down-regulated genes, which mainly correspond to G2/M cell cycle-regulated genes. Together these models reveal the temporal dynamics on the transcriptional events triggered by -irradiation and connects these events to TFs and biological processes over a time scale commensurate with important processes coordinated in response to DNA damage, tremendously expanding our understanding of your DDR.DNA damage responsepathways, at the same time as the regulation of gene expression, cell cycle arrest, cell death, and endoreduplication (1, six, 8, 11). To gain insight into the pathways and molecular interactions orchestrating these events, efforts in many organisms have focused on identifying and characterizing the important players, signaling cascades, and transcriptional programs that stem from the DBCO-PEG3-amine manufacturer recognition of DNA harm. In plants, the SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) transcription issue (TF) was identified from a DNA damage-suppressor screen (12) and was shown to be a major regulator in the DNA harm response (13). In the absence of SOG1, Arabidopsis plants exposed to DNA damaging agents show defects in gene regulation (13), cell cycle arrest (12), programmed cell death (14), endoreduplication (15), DNA repair, and genome stability (12, 13). These findings, in addition to these showing that SOG1 is regulated in an ATM-dependent manner by way of phosphorylation of conserved serine-glutamine motifs (16, 17), have led to SOG1 becoming functionally equated with p53 (eight, 18), a mammalian tumor suppressor that coordinates the DNA harm response and is also phosphorylated in an ATM/ATR-dependent manner (19, 20). Despite the central role of SOG1 in the DNA damage response, plus the numerous studies showing SOG1 is important for coping with DNA harm (125, 216), global expression de.
