Updated project metadata. The PKC-regulated genome protective pathway provides transformed cells a failsafe to successfully complete mitosis. Despite the necessary role for Aurora B in this programme, it is unclear whether its requirement is sufficient or if other PKC cell cycle targets are involved. To address this, we developed a trapping strategy using UV-photocrosslinkable amino acids encoded in the PKC kinase domain. The validation of the mRNA binding protein SERBP1 as a PKC substrate revealed a series of mitotic events controlled by the catalytic form of PKC. PKC represses protein translation, altering SERBP1 binding to the 40S ribosomal subunit and promoting the assembly of ribonucleoprotein granules containing SERBP1, termed M-bodies. Independent of Aurora B, SERBP1 is shown to be necessary for chromosome segregation and successful cell division, correlating with M-body formation. This requirement for SERBP1 demonstrates that Aurora B acts in concert with translational regulation in the PKC-controlled pathway exerting genome protection.