Non-homologous end joining (NHEJ) is a highly conserved mechanism of DNA double-stranded break (DSB) repair. Here we utilize a computational protein-protein interaction method to identify human PRKACB as a potential candidate interacting with NHEJ proteins. We show that the deletion of its yeast homolog, TPK1 that codes for the protein kinase A catalytic subunit reduces the efficiency of NHEJ repair of breaks with overhangs and blunt ends in plasmid-based repair assays. Additionally, tpk1Δ mutants showed defects in the repair of chromosomal breaks induced by HO-site specific endonuclease. Our double deletion mutant analyses suggest that TPK1 and YKU80, a key player in NHEJ could function in parallel pathways. Altogether, here we report a novel involvement for TPK1 in NHEJ.

非同源末端连接（NHEJ）是DNA双链断裂（DSB）修复的高度保守的机制。在这里，我们利用计算蛋白质-蛋白质相互作用的方法来鉴定人PRKACB作为与NHEJ蛋白质相互作用的潜在候选者。我们表明删除其酵母同源物，编码蛋白激酶A催化亚基的TPK1降低了NHEJ修复断裂的效率，在基于质粒的修复方法中具有突出端和平末端。此外，tpk1Δ突变体在修复HO位特异性核酸内切酶诱导的染色体断裂中显示出缺陷。我们的双缺失突变体分析表明，TPK1和YKU80，NHEJ的关键参与者可以在平行途径中发挥作用。总而言之，我们在这里报告了NHEJ中TPK1的一种新型参与。