Fig. 8: Schematic representation of Leishmania kinetochore assembly and effect of CLK1/CKL2 inhibition by AB1, as inferred from XL-BioID proximity biotinylation data. | Communications Biology

Fig. 8: Schematic representation of Leishmania kinetochore assembly and effect of CLK1/CKL2 inhibition by AB1, as inferred from XL-BioID proximity biotinylation data.

From: CLK1/CLK2-driven signalling at the Leishmania kinetochore is captured by spatially referenced proximity phosphoproteomics

Fig. 8

MiniTurbo-tagged KKT3 (KKT3-mT, the bait) detects a core cohort of kinetochore subunits already present in the early S phase, which likely form part of the inner kinetochore bound to centromeric chromatin. Of these subunits, only KKT1 and KKT2 have detectable phosphorylation. Progression to S phase sees a large increase in phosphorylated kinetochore subunits and increasing enrichment of KKT4 and KKT20, but no detectable impact of CLK1/CLK2 inhibition by AB1. In mitosis, the kinetochore is fully formed and attached to microtubules of the mitotic spindle, possibly via KKT4, which has reached peak enrichment. At this stage, the consequences of inhibiting CLK1/CLK2 activity are detected as a reduction in phosphorylation of kinetochore subunits KKT1, KKT2, KKT3 and KKT4. Reduced phosphorylation of KKT7 is also observed, but we cannot exclude the possibility that this is due to reduced recruitment to the kinetochore. AB1-treated Leishmania can continue to complete nuclear division (karyokinesis) but are then arrested at cell division (cytokinesis).

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