Scientists from the University of Gothenburg, Sweden say they have discovered how aged yeast cells manage to form new and undamaged daughter cells. In a study published in Cell, two collaborating research groups at the Department of Cell and Molecular Biology have been able to show how newly formed yeast cells transport damaged and aged proteins back to the mother cell, guaranteeing that the new cell is born young and healthy.

"Previously it was believed that these structures allowed only one-way traffic of proteins and organelles from mother cell to daughter cell," says professor Thomas Nyström from the Department of Cell and Molecular Biology. "We can now show that damaged proteins are transported in the opposite direction. In principle, this means that the daughter cell uses the mother cell as a dustbin for all the rubbish resulting from the aging process, ensuring that the newly formed cell is born without age-related damage."

Researchers demonstrated that this transportation is mechanical, using conveyor-like structures called actin cables. A special gene which controls the rate of ageing, called SIR2, is needed for these cables to form properly. Previous research has shown that changing the SIR2 gene can markedly extend the life-span of an organism.

"Increased SIR2 activity means a longer life, whereas a damaged SIR2 gene accelerates ageing," says Nyström. "This has been demonstrated in studies of yeast, worms, flies and fish, and may also be the case in mammals."

This knowledge of how age-damaged proteins are transported from daughter cell to mother cell could eventually be used in the treatment of age-related diseases caused by protein toxicity in humans.

"The first step is to study whether this transportation of damaged proteins also occurs in the cells of mammals, including humans, for example in the formation of sex sells and stem cells," says Nyström

Citation: Beidong Liu et al., 'The Polarisome Is Required for Segregation and Retrograde Transport of Protein Aggregates', Cell, January 2010, 140 (2), 257-267; doi: 10.1016/j.cell.2009.12.031