Kimberly S Ponce, Lijun Meng, Longbiao Guo, Yujia Leng, Guoyou Ye

Int J Mol Science; 2021 Feb 24;22(5):2254.  doi: 10.3390/ijms22052254.

Review

Abstract

Soil salinity is one of the most significant abiotic stresses hampering plant growth and development, which ultimately translates to reduced crop yield. Soil salinization is exacerbated by excessive use of chemical fertilizers and soil amendments, improper drainage, and seawater ingress. It is estimated that over 6% of the world’s total land area is salt affected, of which over 12 million hectares are irrigated lands posing a serious threat to irrigated agriculture .

Salinity imposes two major stresses in rice, (i) osmotic stress, and (ii) ionic stress. Osmotic stress is characterized by hyperosmotic soil solution disrupting cell turgor, similar to drought’s effect. In contrast, ionic stress is characterized by altered Na⁺ and K⁺ concentrations inside the cell, disrupting many biological processes.

Soil salinity is a serious menace in rice production threatening global food security. Rice responses to salt stress involve a series of biological processes, including antioxidation, osmoregulation or osmoprotection, and ion homeostasis, which are regulated by different genes. Understanding these adaptive mechanisms and the key genes involved are crucial in developing highly salt-tolerant cultivars. In this review, we discuss the molecular mechanisms of salt tolerance in rice-from sensing to transcriptional regulation of key genes-based on the current knowledge. Furthermore, we highlight the functionally validated salt-responsive genes in rice.

See https://pubmed.ncbi.nlm.nih.gov/33668247/

Figure 1: Salt sensing and signaling involved in rice responses to salt stress. Under high salinity, salt-induced osmotic stress begins, which is sensed by putative osmosensor OsHK3b, activated by OsHpt2. SIT1 also acts as a sensor via elevated kinase activity and induces reactive oxygen species (ROS) production and mitogen-activated protein kinase (MAPK) signaling. The activity of SIT1 is deactivated by the B’κ-PP2A subunit. Later, ionic stress occurs and is sensed by an unknown Na⁺ sensor. The Na⁺ enters the mature epidermal cell through nonselective cation channel (NSCC), causing membrane depolarization, and is polarized by P-type ATPases. Excess salt triggers a spike in the concentration of cytosolic secondary messengers, including Ca²⁺, reactive oxygen species (ROS), and phosphatidic acid (PA). ROS triggers Ca²⁺ influx through the cyclic nucleotide-gated ion channel (CNGC), activated by an unknown molecule. Ca²⁺ not only decreases K⁺ efflux but also induces further ROS accumulation; thus, a positive feedback loop exists between Ca²⁺ and ROS. The cytosolic Ca²⁺ also induces vacuolar Ca²⁺ release and activates Ca²⁺-binding proteins, such as OsCIPK24-OsCBL4 complex. This complex, together with MAPK, activated by phosphatidic acid, upregulates the OsSOS1 to remove cytosolic Na⁺. The vacuolar OsNHX1 gene is activated by OsCPK21, whereas the V-type ATPase is activated by OsCIPK24, establishing a proton gradient and driving the activity of OsNHX1.