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ID 46878
本文ファイル
著者
Yamashita, Ichirou 自然科学研究支援開発センター 広大研究者総覧
キーワード
actin
cdc25
nim1
ploidy
scaling
wee1
抄録(英)
It has long been known that eukaryotic cells with more DNA content are larger in cell size. However, no molecular mechanisms for this universal rule have been given. Here I identify cell division genes that dose-dependently control cell growth or cell extension rate (CER) of diploid cells of the fission yeast Schizosaccharomyces pombe. Genetic analysis revealed a negative role of Cdc2, a conserved master regulator of eukaryotic cell cycle. Surprisingly, half dosage of cdc25+ or nim1+ (cdc25Δ/+ or nim1Δ/+), both activator for Cdc2, decreased CER. I discovered that these genes constitute three overlapping regulatory mechanisms for Cdc2: positive and negative feedback loops and a feedforward network. In the negative feedback loop, Cdc2-activating Cdc25 is required for nuclear accumulation of GFP-Wee1 that inhibits Cdc2. Actin monomers are associated with nuclear localization of GFP-Wee1 and accelerate CER, while actin polymers are related to nuclear accumulation of Cdc25-GFP. In the positive feedback loop, actin monomers are relevant to inhibition of Nim1 and subsequent activation of Cdc2 independently of Wee1, resulting in decrease in CER. Nim1 also plays a key role in the feedforward network for supplying sufficient amount of nuclear GFP-Wee1 and closely cooperates with Cdc25 in order to adjust CER to ploidy. Remarkably, doubling cell division genes in haploids reproduced CER of diploids. These findings establish that yeast cells control CER dependently upon dosage of cell division genes during G2 period in the cell division cycle, and provide a solid foundation for understanding the cell-size scaling with DNA content in other eukaryotes.
開始ページ
1
終了ページ
78
作成年月日
2019-01-28
言語
英語
NII資源タイプ
その他
広大資料タイプ
その他
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
author
権利情報
© Copyright by Ichiro Yamashita 2019
部局名
自然科学研究支援開発センター
備考
未発表原稿