Open AccessThe role of gene dosage in budding yeast centrosome scaling and spontaneous diploidization
Author(s) -
Jingjing Chen,
Zhiyong Xiong,
Danny E. Miller,
Zulin Yu,
Scott McCroskey,
W. David Bradford,
Ann M. Cavanaugh,
Sue L. Jaspersen
Publication year - 2020
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1008911
Subject(s) - biology , ploidy , centrosome , gene duplication , gene dosage , genetics , spindle pole body , saccharomyces cerevisiae , mitotic crossover , mutation , mutant , gene , genetic fitness , microbiology and biotechnology , genetic screen , spindle apparatus , cell division , cell cycle , cell , gene expression
Ploidy is the number of whole sets of chromosomes in a species. Ploidy is typically a stable cellular feature that is critical for survival. Polyploidization is a route recognized to increase gene dosage, improve fitness under stressful conditions and promote evolutionary diversity. However, the mechanism of regulation and maintenance of ploidy is not well characterized. Here, we examine the spontaneous diploidization associated with mutations in components of the Saccharomyces cerevisiae centrosome, known as the spindle pole body (SPB). Although SPB mutants are associated with defects in spindle formation, we show that two copies of the mutant in a haploid yeast favors diploidization in some cases, leading us to speculate that the increased gene dosage in diploids ‘rescues’ SPB duplication defects, allowing cells to successfully propagate with a stable diploid karyotype. This copy number-based rescue is linked to SPB scaling: certain SPB subcomplexes do not scale or only minimally scale with ploidy. We hypothesize that lesions in structures with incompatible allometries such as the centrosome may drive changes such as whole genome duplication, which have shaped the evolutionary landscape of many eukaryotes.