FIG 5 .

A model describing the role of Sad1 protein in kinetochore clustering in C. neoformans. In a wild-type cell, the timely onset of kinetochore clustering allows proper kinetochore-microtubule attachment. The chromatin moves to the daughter cell in a microtubule-dependent manner followed by segregation of the sister chromatids. In the absence of Sad1, the kinetochore clustering is delayed, perturbing the critical timing of kinetochore-microtubule attachment. This leads to abnormal nuclear dynamics and mislocalization of the mitotic spindle, eventually resulting in chromosome missegregation in a population of cells. Remaining cells divide normally, giving rise to two separate nuclei, one each in the mother cell and the daughter cell. A zoomed view of the LINC complex localization at each cell cycle stage is shown for both wild-type and Sad1 mutant cells. LINC, linker of nucleoskeleton and cytoskeleton; MTs, microtubules; MTOC, microtubule-organizing center; NE, nuclear envelope.