When drought, salinity, extreme temperatures and other adversities strike, plants—rooted in place—cannot escape. Instead, they deploy tiny molecular messengers—signaling peptides—to orchestrate a precise defense network. A recent review in Frontiers in Plant Science shows that these small peptides act like “commanders”, transmitting signals cell-to-cell to regulate the plant’s stress responses. In this article, we unpack how signal peptides execute their “battle strategies” under drought, salinity, oxidative stress and nutrient hunger—revealing the molecular code of plant resilience.
Drought Stress: The “Water-Saving Fortress” Built by Signal Peptides
CLE25 – The “Drought Alarm” from Root to Leaf
CLE9 – The “Guard Cell Intelligent Valve”
IDA and PSK – Multi-line Strategists in Action

High Salinity Stress: The “Ion-Shield Fortress” Built by Peptides
RALF22-FER Module – The “Cell-Wall Reinforcement Engineer”
In salt stress, the RALF22 peptide binds the FERONIA (FER) receptor; via LRX3/4/5 proteins it senses cell-wall changes and triggers calcium signaling to maintain pectin cross-links. This prevents root cells from rupturing under osmotic imbalance. Plants lacking FER detach cell walls more easily under salt stress, while RALF22 treatment rescues them.
CAPE1 – The “Tolerance Brake”
Unlike most peptides that promote stress resistance, CAPE1 acts as a negative regulator under salt stress: it suppresses osmotic-adjustment gene expression, decreasing salt tolerance. In CAPE1-deficient mutants, plants grow better under high salt; adding CAPE1 peptide restores sensitivity. This suggests CAPE1 is a key molecular switch limiting tolerance.
AtPEP3 – The “Dual Hub” of Immunity and Salt Tolerance
The AtPEP3 peptide, via the PEPR1 receptor, links innate immunity with salt-stress response. Overexpression of AtPEP3 improves survival under salt; plants lacking PEPR1 lose this benefit. This highlights how signaling peptides can cross-regulate multiple stress pathways.
Oxidative & Heat Stress: The “Cellular Emergency Response Team”
IDL6/7 – The “Fire-Extinguishers of ROS Storms”
When reactive oxygen species (ROS) surge under stress, the IDL6 and IDL7 peptides down-regulate WRKY-type stress genes, mitigating oxidative damage. In idl7 mutants, ROS bursts under pathogen or abiotic stress worsen dramatically; applying IDL7 peptide alleviates damage.
CLE45 – The “Reproductive Escort under Heat”
Under high temperatures (~30 °C), CLE45 peptide via SKM1/2 receptor maintains pollen-tube growth and fertility. skm1/2 double mutants show drastically reduced fruit set under heat, while CLE45 over-expression retains high fertility—offering a blueprint for heat-resilient crops.
Nutrient Hunger: The “Resource-Acquisition Campaign” Led by Peptides
CEP1-CEPD Circuit: Nitrogen Deficit Command
Under nitrogen deficiency, root-derived CEP1 peptide moves to shoots, triggers CEPD1/2 signals back to roots and activates nitrate transporter NRT2.1, enhancing nitrogen uptake.
CLE14-CLV2 Pathway: Phosphorus Starvation Strategy
When phosphorus is scarce, CLE14 peptide binds CLV2 receptor in roots, suppresses meristem activity, activates iron mobilization and reshapes root architecture to improve phosphorus acquisition efficiency.
Future Outlook: A “Peptide-Driven Stress-Tolerance Revolution”?
- Gene-editing of drought‐alert peptides (e.g., CLE25) to create more resilient crops.
- Enhancing root growth pathways (e.g., PSK signaling) to adapt to marginal soils.
- Suppressing negative regulators (e.g., CAPE1) to lift the bounds on salt tolerance.
