A supporting cell that never stopped being one — until the signal telling it what it was, stopped.
Published June 17, 2026, in Science Advances, a study led by Prof. Karen Avraham and Prof. David Sprinzak at Tel Aviv University, with lead researcher Lama Khalaily, identified a small, distinct subpopulation of supporting cells in the cochlea — transdifferentiating Deiters' cells — capable of converting into sound-sensing hair cells, a capacity not found in other supporting cells. Humans are born with roughly 15,000 hair cells per ear; once damaged by noise, age, or trauma, they do not regenerate in mammals. Researchers triggered the conversion by blocking Notch signaling, a pathway that runs continuously between cochlear cells, and documented the transformation in live tissue imaging for the first time.
A Deiters' cell holds a hair cell upright. That is its job, and it does that job completely — anchoring, cushioning, feeding the sensory cell beside it that actually catches the vibration and turns it into signal. There is nothing provisional about this arrangement. The supporting cell is not marking time until something better comes along. It is fully what the cochlea needs it to be, for as long as the cochlea needs it.
What keeps it that way is a pathway called Notch, running continuously, cell to cell, telling the cell what it is. A tissue where every cell held its shape loosely, ready to become something else at the first opportunity, would not be a functioning cochlea. It would be noise.
For years, the field tried to force the conversion directly — driving supporting cells toward a hair cell fate with genes switched on from outside, pushing them to become something they weren't yet built to be. The results were inconsistent, partial, cells that looked like hair cells without behaving like them. No one had spent much time watching what a supporting cell was doing while it stayed a supporting cell, because everyone was already looking past it, toward the transformation they expected to produce.
Under a microscope, before any of this began, these particular Deiters' cells looked exactly like every other Deiters' cell beside them — the same shape, the same shade of green, holding the same hair cell upright in the same way. Nothing about them stood out. It took sequencing run cell by cell to find that a small number carried a second set of instructions the others didn't have, instructions doing nothing, waiting on a signal that in a healthy, working ear never arrives. Among the thousands of Deiters' cells in a single cochlea, only this rare handful carry it. The rest hold their shape for a lifetime, whatever else happens around them, and none of what follows changes that.
Avraham's team stopped pushing and started watching. Blocking Notch took away the scaffolding holding this small handful of cells to their present shape. Destabilized, released from what had been holding them there, they began to become something else on their own terms. The imaging caught it live, for the first time: green turning to red, one identity giving way to another, in tissue no one had watched closely enough before.
It is a small number of cells, in a signal that almost never gets interrupted. Every other Deiters' cell in that same ear, at that same moment, kept doing exactly what it had always done — held its hair cell upright, asked nothing, changed nothing, and this too the imaging recorded, frame after frame of green that simply stayed green.
Avraham's team has spent years mapping the genetics of inherited hearing loss, and their work now provides a genetic diagnosis for roughly six in ten Israelis who carry it. There is still no treatment. Any future one would likely mean a surgeon injecting something into the inner ear of a person who cannot yet be told when. What Avraham gets, in the meantime, are letters from parents who have just been handed a genetic report, asking, in whatever words a person uses for this, whether there is anything left to hold onto.