Salt and drought stress signal transduction in plants

Abstract

Salt and drought stress signal transduction consists of ionic and osmotic homeostasis signaling pathways, detoxification (i.e., damage control and repair) response pathways, and pathways for growth regulation. The ionic aspect of salt stress is signaled via the SOS pathway where a calcium-responsive SOS3-SOS2 protein kinase complex controls the expression and activity of ion transporters such as SOS1. Osmotic stress activates several protein kinases including mitogen-activated kinases, which may mediate osmotic homeostasis and/or detoxification responses. A number of phospholipid systems are activated by osmotic stress, generating a diverse array of messenger molecules, some of which may function upstream of the osmotic stress-activated protein kinases. Abscisic acid biosynthesis is regulated by osmotic stress at multiple steps. Both ABA-dependent and -independent osmotic stress signaling first modify constitutively expressed transcription factors, leading to the expression of early response transcriptional activators, which then activate downstream stress tolerance effector genes.

Figure 1

Functional demarcation of salt and drought stress signaling pathways. The inputs for ionic and osmotic signaling pathways are ionic (excess Na⁺) and osmotic (e.g., turgor) changes. The output of ionic and osmotic signaling is cellular and plant homeostasis. Direct input signals for detoxification signaling are derived stresses (i.e., injury), and the signaling output is damage control and repair (e.g., activation of dehydration tolerance genes). Interactions between the homeostasis, growth regulation, and detoxification pathways are indicated.

Figure 2

Regulation of ion (e.g., Na⁺ and K⁺) homeostasis by the SOS pathway. High Na⁺ stress initiates a calcium signal that activates the SOS3-SOS2 protein kinase complex, which then stimulates the Na⁺/H⁺ exchange activity of SOS1 and regulates transcriptionally and posttranscriptionally the expression of some genes. SOS3-SOS2 may also stimulate or suppress the activities of other transporters involved in ion homeostasis under salt stress, such as vacuolar H⁺-ATPases and pyrophosphatases (PPase), vacuolar Na⁺/H⁺ exchanger (NHX), and plasma membrane K⁺ and Na⁺ transporters.

Figure 3

Activation of protein kinases by hyperosmotic stress. The MAP kinase cascade shown is also activated by other stresses. Currently, the functional significance of the kinase activation is unclear (hence the “unknown output”). SIPK, SIMK, and ATMPK6 are homologous MAP kinases from tobacco, alfalfa, and Arabidopsis, respectively.

Figure 4

Phospholipid signaling under salt stress, drought, cold, or ABA. Osmotic stress, cold, and ABA activate several types of phospholipases that cleave phospholipids to generate lipid messengers (e.g., PA, DAG, and IP₃), which regulate stress tolerance partly through modulation of stress-responsive gene expression. FRY1 (a 1-phosphatase) and 5-phosphatase-mediated IP₃ degradation attenuates the stress gene regulation by helping to control cellular IP₃ levels. PLC, phospholipase C; PLD, phospholipase D; PLA₂, phospholipase A₂; PA, phosphatidic acid; DAG, diacyglycerol.

Figure 5

ABA metabolism is regulated by osmotic stress at multiple steps. The ABA biosynthesis genes ZEP, NCED, LOS5/ABA3, and AAO are upregulated by salt and drought stresses. ABA degradation is also important in controlling cellular ABA content, and biochemical evidence suggests osmotic stress inhibition of the first step of catabolism.

Figure 6

Model showing osmotic stress regulation of early-response and delayed-response genes. (A) Model integrating stress sensing, activation of phospholipid signaling and MAP kinase cascade, and transcription cascade leading to the expression of delayed-response genes. (B) Examples of early-response genes encoding inducible transcription activators and their downstream delayed-response genes encoding stress tolerance effector proteins. Question marks denote unknown transcription factors that activate the early-response genes.