The nuclear division takes place in the daughter cell in the basidiomycetous budding yeast
Cryptococcus neoformans
. Unclustered kinetochores gradually cluster and the nucleus moves to the daughter bud as cells enter mitosis. Here, we show that the evolutionarily conserved Aurora B kinase Ipl1 localizes to the nucleus upon the breakdown of the nuclear envelope during mitosis in
C
.
neoformans
. Ipl1 is shown to be required for timely breakdown of the nuclear envelope as well. Ipl1 is essential for viability and regulates structural integrity of microtubules. The compromised stability of cytoplasmic microtubules upon Ipl1 depletion results in a significant delay in kinetochore clustering and nuclear migration. By generating an
in silico
model of mitosis, we previously proposed that cytoplasmic microtubules and cortical dyneins promote atypical nuclear division in
C
.
neoformans
. Improving the previous
in silico
model by introducing additional parameters, here we predict that an effective cortical bias generated by cytosolic Bim1 and dynein regulates dynamics of kinetochore clustering and nuclear migration. Indeed,
in vivo
alterations of Bim1 or dynein cellular levels delay nuclear migration. Results from
in silico
model and localization dynamics by live cell imaging suggests that Ipl1 spatio-temporally influences Bim1 or/and dynein activity along with microtubule stability to ensure timely onset of nuclear division. Together, we propose that the timely breakdown of the nuclear envelope by Ipl1 allows its own nuclear entry that helps in spatio-temporal regulation of nuclear division during semi-open mitosis in
C
.
neoformans
.
The mitotic spindle formation in pathogenic budding yeast, Cryptococcus neoformans, depends on multitudes of intertwined interactions primarily between kinetochores, microtubules (MT), spindle pole bodies (SPBs) and various molecular motors. Prior to spindle formation microtubule organizing centers (MTOCs), embedded on the outer nuclear envelope (NE), coalesce into a single SPB.We propose a 'grow-and-catch' model, in which cytoplasmic MTs (cMTs) nucleated by MTOCs grow and catch each other, to facilitate MTOC clustering. Our quantitative modeling analysis supported by experiments, for the first time, identifies multiple redundant mechanisms mediated by cMT-cell cortex interactions via dynein and Bim1, act in synchrony for timely clustering of MTOCs. Implementing a similar stochastic model of 'grow-and-catch' kinetochores, here we demonstrate that pre-clustered kinetochores and highly biased MTs are a pre-requisite for timely capture of duplicated kinetochores. Further, in the absence of an error correction mechanism, the mitotic division culminates in a biased and asymmetric distribution of the nuclear mass. The model predicts that either a marginal delay in MT nucleation from the daughter SPB or an enhanced MT nucleation from the mother SPB can independently account for the asymmetry as observed in the experiment.
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