Also known as DNA endonuclease ctp1 (Double-strand break repair protein ctp1) (Meiotically up-regulated gene 38 protein) (Nbs1-interacting protein 1) (Sporulation in the absence of SPO11 protein 2 homolog) (SAE2).
Endonuclease that cooperates with the MRN complex in processing meiotic and mitotic double-strand breaks by allowing the endonucleolytic removal of rec12 from the break sites and ensuring both resection and intrachromosomal association of the broken ends. Required for the formation of RPA-coated single strand DNA adjacent to the DSBs where it functions together with the MRN complex in 5'- 3' resection. Required for the repair of programmed meiotic DSBs. Involved also in an rhp51 recombinase-dependent recombinational repair pathway.

Endonuclease that cooperates with the MRE11-RAD50-NBN (MRN) complex in processing meiotic and mitotic double-strand breaks (DSBs) by ensuring both resection and intrachromosomal association of the broken ends.

Also known as DNA endonuclease SAE2 (Completion of meiotic recombination protein 1) (Sporulation in the absence of SPO11 protein 2).
Endonuclease that cooperates with the MRX complex in processing meiotic and mitotic double-strand breaks by allowing the endonucleolytic removal of SPO11 from the break sites and ensuring both resection and intrachromosomal association of the broken ends. Required for proper recovery from checkpoint-mediated cell cycle arrest after DNA damage. MRX complex and SAE2 remove a small oligonucleotide(s) from the DNA ends to form an early intermediate which is rapidly processed by EXO1 and/or SGS1 to generate extensive tracts of single-stranded DNA that serve as substrate for RAD51. Plays a transitional role in the dissociation of MRE11 from, and the recruitment of RAD52 to, repair foci. Ensures that both ends of a DSB participate in a recombination event and impairs the formation of palindromic structures in the genome. With TEL1, promotes microhomology-mediated end joining (MMEJ) but inhibits non-homologous end joining (NHEJ), likely by regulating MRE11-dependent ssDNA accumulation at DNA break. SAE2 and MRX are particularly important for removal of hairpins, bulky adducts and other irregular end structures. Facilitates telomere length reequilibration and subsequent checkpoint switch off. Involved in homing efficiency of VMA1 intein VDE and in repair of transposon excision sites.