Abstract
Cell division involves the tightly coordinated rearrangement of actin and microtubules (MTs). We have previously shown that a member of the family of growth arrest-specific 2-like proteins, GAS2-like 1 (G2L1) regulates actin-MT crosstalk through its associations with plus-end microtubule tip-binding (EB) proteins. Here we show that G2L1 is involved in the regulation of cell division. We show that the depletion of G2L1 results in a reduction in the number of cells undergoing cell division and a significant proportion of those cells that do divide are either multinucleated, display deformed nuclei, or undergo cell division at a much slower rate. Exogenous expression of G2L1 mutants revealed that the association of G2L1 with EB1 is critical for regulated cell division and blocking this interaction inhibits cell division as observed in cells lacking G2L1. Taken together, our data suggest that G2L1 controls the precise regulation and successful progression of cell division through its binding to EB-proteins.
Highlights
Cell division is a vital process in the lifetime of a cell
Using GAS2-like 1 (G2L1) mutants we show that the binding of the C-terminus to end microtubule tip-binding (EB) proteins has a critical role in the observed processes
Results showing that the expression of a point mutant deficient in binding to EB proteins mimics in part the defects seen in G2L1 depleted cells show that the presence of G2L1, as well as its capability to bind EB proteins, is vital for coordinated regulation of cell division
Summary
Cell division is a vital process in the lifetime of a cell. Any aberrations during this process can lead to severe health problems, and uncontrolled division is a key hallmark of cancer. G2L1 and G2L2 contain a larger unstructured C-terminus domain with evolutionarily-conserved MT-tip localisation signals (MtLS) composed of the amino acid consensus sequence Ser/Thr-X-Ile/Leu-P (SxIP motifs) (Fig. 1A)[9] This motif is required for the interaction with MT plus-end (+end)-binding (EB) proteins[11] and regulate the crosstalk between MTs and F-actin[12,13]. EB3, on the other hand, has been shown to be responsible for stabilization of the midbody and focal adhesions (FA), which are required for coordinated spreading of daughter cells during cytokinesis[19]
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