Probable serine/threonine kinase. Plays a central role in cell-cycle regulation by transmitting DNA damage signals to downstream effectors of cell-cycle progression. May recognize the substrate consensus sequence [ST]-Q and phosphorylate histone variant H2AX to form H2AXS139ph at sites of DNA damage, thereby regulating DNA damage response mechanism. Seems to be required for the G2-phase checkpoint in response to replication blocks but not absolutely required in the G2-arrest response to double-strand breaks. May also be involved in the meiosis process. Required for the basal expression of RNR1 (ribonucleotide reductase large subunit). Acts in concert with telomerase to maintain telomeric DNA tracts. Not required for telomere length homeostasis. Required for effective immune responses that involve activation of DNA damage responses (PubMed:24207055). ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Strongly induced by replication blocking agents (UVB, aphidicolin and hydroxyurea) but only mildly induced by DNA damaging agents (gamma-radiation) (PubMed:15075397). Negatively regulated by the key immune regulator SNI1 (PubMed:24207055). Suppressor of sni1 mutation symptoms including the accumulation of DNA damage leading to a constitutively activated DNA damage responses (DDR) and increased basal expression of pathogenesis-related (PR) genes. Loss-of-function mutations (T-DNA insertion) are hypersensitive to replication antagonists, including UV light, aphidicolin, and hydroxyurea, and are defective in G2 checkpoints induced by these agents. Belongs to the PI3/PI4-kinase family. ATM subfamily.