DRP004882
The number of phosphorylated SOG1 sites regulates DNA damage response in A. thaliana
The A. thaliana transcription factor SOG1 regulates hundreds of genes in response to DNA damage, which results in the activation of cell-cycle arrest, DNA repair, endoreduplication, and programmed cell death. However, each pathway leads the cell to a different fate: cell-cycle arrest and DNA repair result in cell survival, endoreduplication leads to cell differentiation, and programmed cell death results in cell elimination. How this single transcription factor regulates each pathway is unknown. We previously reported that phosphorylation of five serine-glutamine (SQ) motifs in the C-terminal of SOG1 are required to activate downstream pathways. In this study, we introduced mutations in these five SQ motifs and examined the effects on DNA damage responses. We found that the expression level of most of genes gradually changed dependent on the number of SOG1 phosphorylation sites. Genes involved in DNA repair and cell-cycle progression undergo stepwise activation and inhibition, respectively, as the number of phosphorylated SQ sites increases. Furthermore, we showed that programmed cell death and cell differentiation are induced by fewer SOG1 phosphorylation sites than that needed for replication arrest. These results show that the number of SQ phosphorylation in SOG1 regulates gene expression and determines pathway activation in response to DNA damage.
The A. thaliana transcription factor SOG1 regulates hundreds of genes in response to DNA damage, which results in the activation of cell-cycle arrest, DNA repair, endoreduplication, and programmed cell death. However, each pathway leads the cell to a different fate: cell-cycle arrest and DNA repair result in cell survival, endoreduplication leads to cell differentiation, and programmed cell death results in cell elimination. How this single transcription factor regulates each pathway is unknown. We previously reported that phosphorylation of five serine-glutamine (SQ) motifs in the C-terminal of SOG1 are required to activate downstream pathways. In this study, we introduced mutations in these five SQ motifs and examined the effects on DNA damage responses. We found that the expression level of most of genes gradually changed dependent on the number of SOG1 phosphorylation sites. Genes involved in DNA repair and cell-cycle progression undergo stepwise activation and inhibition, respectively, as the number of phosphorylated SQ sites increases. Furthermore, we showed that programmed cell death and cell differentiation are induced by fewer SOG1 phosphorylation sites than that needed for replication arrest. These results show that the number of SQ phosphorylation in SOG1 regulates gene expression and determines pathway activation in response to DNA damage.