Fects in sog1 mutants have only been assessed at single time points following -irradiation (-IR) (two h) (13) or zeocin (1.5 h) (27) and, till recently (27), only a number of SOG1 targets had been identified (22, 25, 26, SignificanceDNA damage triggers a hugely conserved response that coordinates processes necessary to retain genome integrity, which includes cell cycle arrest, DNA repair, and cell death. In spite of the identification of key transcription components (TFs) that control these processes, understanding relating to the downstream genes and regulatory networks controlled by these TFs remains poorly understood. Working with Arabidopsis, we generated the initial model of the DNA damage response transcriptional network, revealing 11 coexpressed gene groups with distinct biological functions and cis-regulatory functions. Our characterization of this model demonstrates that SOG1 and 3 MYB3R TFs are, respectively, the important activator and repressors inside this network, coordinating the speedy induction of DNA Triallate Epigenetic Reader Domain repair genes and TF cascades as well as the subsequent repression of cell cycle genes.Author contributions: C.B., N.V., and J.A.L. designed analysis; C.B. and N.V. performed analysis; C.B. and J.A.L. analyzed information; and C.B. and J.A.L. wrote the paper. The authors declare no conflict of interest. This short article can be a PNAS Direct Submission. This open access post is distributed below Inventive Commons Attribution-NonCommercialNoDerivatives License four.0 (CC BY-NC-ND). Data deposition: The source information files and sequencing information reported within this paper happen to be deposited inside the Gene Expression Omnibus (GEO) database, https://ncbi.nlm. nih.gov/geo (accession no. GSE112773).| DREM | SOG1 | transcriptional networksThe genomes of all organisms incur different types of DNA damage resulting from both endogenous processes and exposure to exogenous stresses or toxic compounds (1, two). Of this harm, DNA double-strand breaks (DSBs) are especially hazardous, as no intact strand remains to guide the DNA repair, potentially major to chromosomal deletions and translocations (three, four). To cope with such harm, mechanisms are in location to sense DNA lesions and initiate a DNA damage response (1, five). This response involves the transcriptional and posttranscriptional regulation of diverse cellular pathways, ultimately major to DNA repair, via the expression and/or targeting of repair components to websites of harm, to cell cycle arrest, which delivers added time for DNA repair just before replication, or to cell death, when the damage is also extreme (5, six). Given the importance of maintaining genome stability for correct cellular function along with the faithful inheritance of genetic facts (1, 5), it is crucial to know how the DNA damage response is initiated, coordinated, and executed. Research in yeast, plants, and mammals have revealed numerous hugely conserved aspects in the DNA harm response (6). Inside the case of DSBs, conserved sensors, namely the MRN and Ku70/80 complexes, recognize the broken DNA and transducers, like the ATAXIA-TELANGIECTASIA MUTATED (ATM) and DPTIP In stock ATAXIATELANGIECTASIA MUTATED AND RAD3-RELATED (ATR) kinases, initiate signaling cascades by way of the posttranslational modification of target proteins (1, 80). These cascades modulate the activities of each shared and organism-specific effector proteins, culminating within the regulation of DSB repair, through homologous recombination and a variety of nonhomologous end joiningPresent address: Institut de biologie de l’Ecole standard.