Figure 2.

Interactions between stress/response signaling cascades and cell cycle regulation. Plant growth depends on cell division and expansion. Upon biotic stress, cell surface pattern recognition receptors (PRRs) recognize conserved microbe-associated molecular patterns (MAMPs) or damage-associated molecular patterns (DAMPs) or resistant (R) proteins and then transduce primary signal to secondary signal molecules including Ca²⁺ flux, ROS, jasmonates (JA) and MAPK and eventually initiate immunity. Immune response induces prolonged cell cycle progression or programmed cell death. Overexpression of CDKs or cyclins could enhance immune responses. Besides, G1-S phase checkpoint proteins Rb and E2F engaged in immune-related programmed cell death. Similarly, under abiotic stress conditions, plant cells sense and percept the signals and transmit them to downstream signal molecules, such as Ca²⁺, Na⁺, ABA, and ROS. These signaling cascades halt cell cycle progression through inhibiting the transcription of CDK/cyclins-related genes. Manipulating the level of CDK or cyclins could change the defense response abilities. Severe abiotic stresses trigger programmed cell death.