Defects arising from whole-genome duplications in Saacharomyces cerevisiae

被引:65
作者
Andalis, AA
Storchova, Z
Styles, C
Galitski, T
Pellman, D
Fink, GR
机构
[1] MIT, Whitehead Inst Biomed Res, Cambridge, MA 02142 USA
[2] Childrens Hosp, Dept Pediat Oncol, Dana Farber Canc Inst, Dept Pediat Hematol Oncol, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Boston, MA 02115 USA
关键词
D O I
10.1534/genetics.104.029256
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Comparisons among closely related species have led to the proposal that the duplications found in many extant genomes are the remnants of an ancient polyploidization event, rather than a result of successive duplications of individual chromosomal segments. If this interpretation is correct, it would support Ohno's proposal that polyploidization drives evolution by generating the genetic material necessary for the creation of new genes. Paradoxically, analysis of contemporary polyploids suggests that increased ploidy is an inherently unstable state. To shed light on this apparent contradiction and to determine the effects of nascent duplications of the entire genome, we generated isogenic polyploid strains of the budding yeast Saccharomyces cerevisiae. Our data show that an increase in ploidy results in a marked decrease in a cell's ability to survive during stationary phase in growth medium. Tetraploid cells die rapidly, whereas isogenic haploids remain viable for weeks. Unlike haploid cells, which arrest growth as unbudded cells, tetraploid cells continue to bud and form mitotic spindles in stationary phase. The stationary-phase death of tetraploids can be prevented by mutations or conditions that result in growth arrest. These data show that whole-genome duplications are accompanied by defects that affect viability and subsequent survival of the new organism.
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收藏
页码:1109 / 1121
页数:13
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