"In addition to affecting senescence, Spns1 impedes autophagy, the process whereby cells remove unwanted or destructive proteins and balance energy needs during various life stages."
New York, July 18 - In what could point towards the possibility of one day using therapeutics to combat ageing, researchers have found in animal models that a single gene plays a surprising role in ageing that can be detected early in development.

We believe that a previously uncharacterized developmental gene known as Spns1 may mediate the ageing process, said Shuji Kishi, an assistant professor at The Scripps Research Institute (TSRI) in the US.

Even a partial loss of Spns1 function can speed ageing, Kishi noted.

Using various genetic approaches to disturb Spns1 during the embryonic or larval stages of zebrafish, the scientists were able to produce some models with a shortened life span that lived long lives.

While most studies of senescence - declines in a cell's power of division and growth - have focused on later stages of life, the study is intriguing in exploring this phenomenon in early stages.

Mutations to Spns1 disturbs developmental senescence and badly affects the long-term bio-chronological ageing process, Kishi said.

The new study shows that Spns1, in conjunction with another pair of tumour suppressor genes, beclin 1 and p53 can, influences developmental senescence through two differential mechanisms: the Spns1 defect was enhanced by Beclin 1 but suppressed by 'basal' p53.

In addition to affecting senescence, Spns1 impedes autophagy, the process whereby cells remove unwanted or destructive proteins and balance energy needs during various life stages.

The study appeared in the journal PLOS Genetics.


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