Plants have a remarkable ability to heal from various types of injuries. Though we don’t have a strong understanding of exactly how plants sense wounds and adjust their physiological processes to regenerate damaged tissues, the phytohormone auxin has been implicated in the process. Auxin is involved in nearly every aspect of plant development. Its long-distance transport within the plant, called polar flux, is key to defining body patterning because it maintains a gradient building toward growing tips that determines organ positions and maintains stem cell identity within the quiescent centre of the meristem.
In a new article published in PNAS, lead author Balkan Canher and colleagues treated plants with bleomycin, a DNA damaging drug, to induce vascular wounding in the roots. They then used cellular imaging and in silico modelling to investigate how auxin acts in plant recovery from wounding.
The researchers found that the death of vascular stem cells blocks the flow of auxin toward the meristem. The blockage leads to auxin accumulating in the endodermis, similar to, as the authors put it, “rocks in a stream,” diverting the flow. This auxin build-up in the tissues surrounding the wound causes the endodermal cells to take on stem cell identities, leading to cell division that replaces those that were damaged. Once the vascular tissue is repaired, auxin flow is reestablished, and the accumulation dissipates, leaving all as it was.
The authors also discovered that a gene in the plant ethylene response factor (ERF) transcription factor family is a key regulator of the process. The drug treatment used is known to trigger transcription of ERF115 in endodermal cells when vascular cells are destroyed. The new study takes this knowledge further, finding that the gene product acts in concert with auxin accumulation to enable regeneration. If ERF115 activity is suppressed in the endodermis, the plant’s recovery is impaired.
“These data suggest that ERF115 is a wound-inducible modulator of auxin signalling,” write the authors, “feeding wounding input into auxin-mediated developmental processes, such as tissue patterning and organ formation. Since our data also show that ERF115 expression is dependent on the presence of auxin, cell death-induced auxin accumulation by obstruction of polar transport simultaneously maintains ERF115 expression and induces regenerative divisions in a synergistic manner.”