Abstract
Telomeres, which cap the ends of linear chromosomes, are maintained at a homeostatic length allowing for controlled division and cell survival in healthy human cells. However, cancer cells have mechanisms that subvert homeostatic telomere regulation, allowing for their uncontrolled growth. Several proteins that regulate telomere maintenance have been identified, but the majority remain unknown. We completed a CRISPR/Cas9-mediated genome screen to identify proteins with a presumed role in telomere maintenance. The screen marked KIF2A, an ATP-dependent microtubule depolymerizer, as a principal candidate essential for telomere lengthening. KIF2A has a well-established role in the separation of chromosomes during anaphase of mitosis and meiosis II. However, prior to this study, its role in telomere maintenance had not been studied nor suggested. We investigated KIF2A’s potential role in this capacity by infecting a KIF2A overexpression plasmid into colorectal carcinoma cells with critically shortened telomeres. Due to KIF2A’s assumed essentiality to telomere lengthening, it was expected that KIF2A overexpression would rescue telomere length in cells with shortened telomeres. Our findings did not confirm this hypothesis.