Abstract
Cytokinesis failure leads to the emergence of tetraploid cells and multiple centrosomes. Chronic lymphocytic leukaemia (CLL) is the most common haematological malignancy in adults and is characterized by clonal B cell expansion. Here, we show that a significant number of peripheral blood CLL cells are arrested in cytokinesis and that this event occurred after nuclear envelope reformation and before cytoplasmic abscission. mRNA expression data showed that several genes known to be crucial for cell cycle regulation, checkpoint and centromere function, such as ING4, ING5, CDKN1A and CDK4, were significantly dysregulated in CLL samples. Our results demonstrate that CLL cells exhibit difficulties in completing mitosis, which is different from but may, at least in part, explain the previously reported accumulation of CLL cells in G0/1.
Highlights
Chronic lymphocytic leukaemia (CLL) is characterized by clonal expansion of mature CD5+CD19+CD23+ B lymphocytes that accumulate in the bone marrow and lymphoid tissue, such as spleen and lymph nodes
When we performed immunofluorescence staining for Plk[1] and Aurora B, proteins known to regulate cytokinesis,[11,12] we found that Plk[1] localized at the cytokinesis contractile ring in CLL doublets (Figure 1C), which is a hallmark of cytokinesis.[11]
We report for the first time that a significant number of CLL cells are arrested in cytokinesis
Summary
Chronic lymphocytic leukaemia (CLL) is characterized by clonal expansion of mature CD5+CD19+CD23+ B lymphocytes that accumulate in the bone marrow and lymphoid tissue, such as spleen and lymph nodes. Cytokinesis is the final step of cell division ending with the physical separation into 2 daughter cells It starts after chromosome segregation in anaphase during mitosis, with the cleavage furrow formation at the equatorial cortex ingressing inwards to divide the mother cell, and ending with the physical detachment of the 2 daughter cells. This process involves a series of spatio-temporal regulated events ensuring an equal distribution of genomic and cytoplasmic material between the 2 nascent daughter cells.[5]. The described cytokinesis defect is distinct from the previously reported accumulation of cells in G0/1
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