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Genome editing delays ageing in mice

25 January 2021
Appeared in BioNews 1080

A novel driver of cellular senescence has been identified which, when targeted, slows ageing in mice.

Old age is a risk factor for many diseases, such as cancer and dementia. Cellular senescence, a process in which cells stop dividing, promotes ageing. Therefore, slowing this senescence is an attractive prospect and an increasing research focus. Recently, scientists at the Chinese Academy of Sciences in Beijing, China, investigated novel drivers of senescence to try and delay ageing in mice.

'These mice show after six to eight months overall improved appearance and grip strength and, most importantly, they have extended lifespan for about 25 percent,' Professor Qu Jing, co-lead author of the study said.

The team first generated human mesenchymal stem cells (hMPCs) that carried mutations causative of either Werner syndrome or Hutchinson-Gilford progeria syndrome – both accelerated ageing disorders. The team employed a genome-wide CRISPR/Cas9-based screen in the mutated hMPCs, whereby they reduced the expression of thousands of genes to observe the effects of their deficiency.

Deficiency of the KAT7 gene made the cells more youthful in appearance and improved their survival rate, thus reducing cellular senescence. Furthermore, KAT7 overexpression accelerated cellular senescence. Overall, the research has demonstrated that KAT7 is a senescence gene.

The researchers then investigated the effect of KAT7 deficiency in mice and discovered that in both naturally aged mice and mice with premature ageing mutations, targeted genome editing of KAT7 improved their liver function and extended their lifespans.

'We just tested the function of the gene in different kinds of cell types, in the human stem cell, the mesenchymal progenitor cells, in the human liver cell and the mouse liver cell and for all of these cells we didn't see any detectable cellular toxicity,' Professor Jing told the Daily Mail. 'And for the mice, we also didn't see any side effect yet.'

Although a long way off, inactivation of KAT7 could potentially slow ageing in humans. Professor Jing added, 'It's still definitely necessary to test the function of KAT7 in other cell types of humans and other organs of mice and in the other pre-clinical animals before we use the strategy for human ageing or other health conditions.'

This research was published in the journal Science Translational Medicine.

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