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
.
High fidelity chromosome segregation is essential for efficient transfer of the genetic material from the mother to daughter cells. The kinetochore (KT), which connects the centromere DNA to the spindle apparatus, plays a pivotal role in this process. In spite of considerable divergence in the centromere DNA sequence, basic architecture of a KT is evolutionarily conserved from yeast to humans. However, the identification of a large number of KT proteins paved the way of understanding conserved and diverged regulatory steps that lead to the formation of a multiprotein KT super-complex on the centromere DNA in different organisms. Because it is a daunting task to summarize the entire spectrum of information in a minireview, we focus here on the recent understanding in the process of KT assembly in three yeasts: Saccharomyces cerevisiae, Schizosaccharomyces pombe and Candida albicans. Studies in these unicellular organisms suggest that although the basic process of KT assembly remains the same, the dependence of a conserved protein for its KT localization may vary in these organisms.
The AGC kinase Sch9 regulates filamentation in Candida albicans. Here, we show that Sch9 binding is most enriched at the centromeres in C. albicans, but not in Saccharomyces cerevisiae. Deletion of CaSch9 leads to a 150-to 750-fold increase in chromosome loss. Thus, we report a previously unknown role of Sch9 in chromosome segregation.
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