Aurora T phosphorylation at intercellular canals doesn’t exclusively depend on its auto activation, since inhibition of Aurora B at this stage didn’t completely remove phospho T232 at intercellular canals. We ergo addressed its position in interphase cells with chromosome bridges. Using immunofluorescence o-n HeLa cells synchronized to 3 hr after mitotic shake off, we found Mklp1 localized to a thin ring at the channel connecting chromosome bridgecontaining brother cells, much like Aurora B. Using a phospho specific antibody, we found Mklp1 in these rings phosphorylated at a S911 deposit. Inhibition of Aurora B by ZM1 in chromosome link containing HeLa cells after c-omplete furrow ingression lowered phospho S911 levels in the ring to 3. 8 4. Four to six. Aurora supplier Lapatinib B inhibition also resulted in gradual loss of Mklp1 from the ring around chromosome bridges, which we quantitated with time lapse movies of cells coexpressing H2B mRFP and Mklp1 YFP. Together, these data identify Mklp1 like a excellent downstream effector candidate of Aurora B for stabilization of the ingressed furrow in chromosome bridgecontaining posttelophase cells. Our data support the view that chromatin stuck in the cleavage plane could be the main cause for spontaneous tetraploidization in cultured cells. But, we discovered that many cells with chromosome links suppressed furrow regression and continued to multiply normally. Our research provides a mechanistic explanation for this: these missegregating cells stabilized Cellular differentiation the ingressed furrow and overdue abscission to posttelophase phases. Elimination of chromosome bridges either by spontaneous resolution or by laser microsurgery resulted in rapid abscission. On the other hand, when abscission was mechanically blocked by asbestos fibers cells didn’t maintain an ingressed furrow during interphase. Together, this suggests a particular Afatinib solubility signal supplied by chromatin at the cleavage site to secure the ingressed furrow for overdue abscission. Our data lead us to suggest a model with as an important regulator of abscission time, which responds to unsegregated chromatin Aurora T. Aurora T inactivation probably involving dephosphorylation with a yet unknown mechanism normally encourages abscission about one hour after anaphase on-set. The clear presence of chromosome bridges prevents Aurora W inactivation, and leads to its re localization into a narrow ring at the intercellular tube upon midbody disassembly. This balances the intercellular canal for late abscission. Premature inactivation of Aurora B in cells with chromosome connections leads to furrow regression, probably due to premature destabilization of the intercellular channel in a level that is not yet compatible with abscission.