According to research published in the journal Science, genetically identical yeast cells placed in the same environment can still age in strikingly different ways, a finding that may eventually lead to therapies that will slow the ageing process.
Early in life, yeast cells appear to go down one of two ‘ageing paths’. Around half of the yeast cells aged because of a decline in their nucleolus – a region of the nucleus responsible for producing ribosomes (structures that build proteins for the cell). The other half of the yeast cells instead suffered a decline in their mitochondria, which serve as the cell’s energy factories.
The above video depicts the two pathways followed by the cells, as measured by fluorescent imaging of nuclear DNA (red) and ribosomal DNA (green). Both of these ageing pathways have already been studied, but researchers wanted to see if they could understand and manipulate the underlying systems that determine which ageing path the cell ‘chooses’.
“To understand how cells make these decisions, we identified the molecular processes underlying each aging route and the connections among them, revealing a molecular circuit that controls cell aging, analogous to electric circuits that control home appliances,” said Nan Hao, senior author of the study and an associate professor in UCSD’s division of biological sciences’ molecular biology section.
Researchers found they could manipulate and optimize the process of aging, using computer simulations to reprogram the master circuit and modify its DNA. Following this, they were then able to create a “novel aging route” with a dramatically extended lifespan, possibly leading to the possibility of delaying human aging.
A programmable fate decision landscape underlies single-cell aging in yeast: DOI: 10.1126/science.aax9552
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