Sensing the point of no return
When is it time to die, that is the question that lays behind the latest study of a group of Swedish researchers. They found that sensing depleted levels of the amino acid arginine tell the cell to throw in the towel.
Leaf senescence and subsequent dead are a normal part of a plant’s life. We see it in action every autumn when leaves turn red and yellow before they fall of the trees. It also happens during the normal development when older leaves die and during periods of stress like drought stress.
During leaf senescence cells degrade their proteins, nucleic acids, lipids, and cell structures to recycle the nutrients within. These they then transport out of the cell for use by younger organs or for storage. Although this doesn’t have to end in a cell’s death. If, like for example, in the case of drought stress the stress ends before the senescing cell has reached the point of no return the cell can recover.
Preventing to senescence
This begs the question: how does the cell know when it is time to die? Plant breeders see the answer to this question as a way to obtain more control over leaf senescence. This they hope will help reducing yield losses and allow the breeding of crops that are less sensitive to senescence inducing stress.
The first hint to the answer to this question the researchers got from a mutant that doesn’t initiate stress-induced senescence. The leaves of those plants accumulate large quantities of amino acids. To find out of any of these amino acids influence the senescence process the researchers exposed leaf discs to an extra amino acid. This showed that only in the case of extra arginine the leaf disc maintained more of its chlorophyll compared to discs treated with the other amino acids or the control ones. Suggesting that a reduction of arginine below threshold levels signals that it is time to senescence.
Restoring the ability to senescence
Next the researchers checked on genes that transport arginine out of the cytosol. Of two genes who did those jobs, AAP5 and BAC2, the researchers found that they were activated during senescence. Of these BAC2 was even activated directly by the senescence master regulator. Subsequently the researchers activated these arginine transporters in plants whose leaves don’t initiate senescence. Finding that this restored the ability to senescence.
Now the important question was, does this also work the other way around. That is if when arginine levels stay high the cell delays senescence during normal aging. So, they created plants without AAP5 or BAC2 or both. While plants who missed only one of these arginine transporters did not delay their developmental aging induced senescence, those who missed both did.
So, the levels cytosolic arginine likely functions as a way to tell the cell at what stage of senescence it is at. But like the researchers are saying more details are needed. Like if this does depend how cytosolic arginine is distributed. Or like how arginine is actually sensed. Nevertheless, breeders can already use this study by looking for variations of BAC2 and AAP5 that allow plants to senesce slower in response to stress.
Literature
Hussain, S., Boussardon, C. & Keech, O. The progression of leaf senescence is gated by the cytosolic arginine pool. Nat. Plants (2026). https://doi.org/10.1038/s41477-026-02328-2
Plant en Zo 