Research press release


Nature Cell Biology

Cellular senescence and ageing


細胞分裂タンパク質BubR1の発現レベルが低い変異体マウスでは、短寿命、筋肉萎縮や脂肪減少などの特徴をもつ早期老化が起こることが明らかにされている。影響が現れる組織のうちで、骨格筋と脂肪にはp16Ink4aとp19Arfというタンパク質が高濃度で集積する。J van Deursenたちはp16Ink4aとp19Arf遺伝子の加齢における役割を調べるために、BubR1欠失マウスでこれらの遺伝子を不活性化してその影響を検討した。p16Ink4aを除去すると細胞の老化とマウスの早期加齢の両方が軽減されたが、p19Arfの不活性化ではこうした影響が増大した。


Two tumour suppressor genes with crucial effects on the ability of cells to divide and replicate have been found to affect the ageing process in mice. A report online this week in Nature Cell Biology demonstrates for the first time a direct link between the mechanisms of cellular senescence ? the irreversible ceasing of cell replication ? and ageing of the whole organism.

Mutant mice expressing low levels of the cell division protein BubR1 have been shown to undergo premature ageing characterized by a shorter lifespan, muscle atrophy and loss of fat. Of the tissues affected, skeletal muscle and fat accumulate high levels of the proteins p16Ink4a and p19Arf. Jan van Deursen and colleagues investigated the role of p16Ink4a and p19Arf genes in ageing by studying the consequences of their inactivation in BubR1-deficient mice. They found that elimination of p16Ink4a reduces both cellular senescence and premature ageing, whereas, in contrast, inactivation of p19Arf exacerbates these effects.

A role for the tumour suppressor genes p16Ink4a and p19Arf in ageing was previously suspected on the basis of findings that their expression increases with age; however, a direct involvement in the ageing process was never proven because mice lacking these genes die early of tumours.

doi: 10.1038/ncb1744


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