The unique contributions of Rab11 and Rab35 to the completion of cell division
Rab11 and Rab35 were shown to be responsible for wide-scale intracellular membrane trafficking during the last phases of the cell cycle. Even though data suggests that Rab11 and Rab35 are abscission-related, each gives a different phenotype to dividing cells. Moreover, nobody has ever looked at both and systematically compared the two during the regulation of cancer cell division. Hence, the molecular interplay and compensatory mechanisms between Rab11 and Rab35 remain to be established. Our data shows that depletion of Rab11 or Rab35 inhibits cytokinetic abscission and is associated with aberrant levels of F-actin at the intercellular bridge. In contrast, overexpression of functionally similar Rab protein cannot rescue downregulation-associated cytokinetic defects in cancer cells. We also demonstrate that even though Rab11 and Rab35 function in the same molecular pathway, the input that each individual Rab11 and Rab35 carries out during a distinct mitotic M-phase stage differs. Thus, this research study is dedicated to getting a more in-depth understanding of molecular machinery behind Rab11- and Rab35-mediated cell progression from late anaphase to cytokinesis.