How cells handle physical stress depends on their nucleus
Cells constantly sense and respond to mechanical forces from their surroundings. A new study maps how those signals travel inside the cell with unprecedented precision, and finds the cell nucleus plays a more nuanced role than expected.
The process of converting mechanical forces into biochemical signals is called mechanotransduction. Disruptions in this process have been linked to age-related conditions including tissue stiffening and impaired repair. Understanding the molecular players involved could point toward new therapeutic targets.
Two types of lamins, two types of response
A study published in eLife combined two precision techniques to measure tension dynamics inside living cells following mechanical stimulation. The researchers focused on lamins, proteins that form the network surrounding the cell nucleus and give it shape and rigidity. There are two main types: A-type lamins and B-type lamins.
The measurements revealed that the two types respond differently to mechanical force. A-type lamins contribute to nuclear elasticity, enabling the nucleus to spring back. B-type lamins influence the viscous response, the way the nucleus absorbs energy and recovers more slowly. Together, these two properties determine how well a cell tolerates mechanical stress.
Microtubules compensate when lamins are absent
In cells where A-type lamin was removed (a knockout model), the microtubules, part of the cell’s internal scaffold, took over and redistributed mechanical tension across the cell. In healthy cells, the microtubules behaved differently: they kept tension localised rather than spreading it.
This distinction matters for aging research. The composition of lamins changes as cells age. This may alter how cells process mechanical signals. Whether and how this contributes to tissue aging or disease is a question for future work. The study provides a mechanistic framework for examining cells with disrupted lamin composition more precisely.