Genetic Research Progress: Heat Tolerance in Rice

Huaqing Liu, Bohong Zeng, Jialiang Zhao, Song Yan, Jianlin Wan, Zhibin Cao

Int J Mol Sci.; 2023 Apr 12; 24(8):7140. doi: 10.3390/ijms24087140.

Abstract

Heat stress (HS) caused by high-temperature weather seriously threatens international food security. Indeed, as an important food crop in the world, the yield and quality of rice are frequently affected by HS. Therefore, clarifying the molecular mechanism of heat tolerance and cultivating heat-tolerant rice varieties is urgent. Here, we summarized the identified quantitative trait loci (Quantitative Trait Loci, QTL) and cloned rice heat tolerance genes in recent years. We described the plasma membrane (PM) response mechanisms, protein homeostasis, reactive oxygen species (ROS) accumulation, and photosynthesis under HS in rice. We also explained some regulatory mechanisms related to heat tolerance genes. Taken together, we put forward ways to improve heat tolerance in rice, thereby providing new ideas and insights for future research.

See https://pubmed.ncbi.nlm.nih.gov/37108303/

Figure 1

Molecular mechanism mediated by heat-tolerant genes in rice. HS mainly caused four major hazards to rice: the stability and fluidity of PM were affected, a large number of toxic proteins were produced, the level of ROS was significantly increased, and photosynthesis was damaged. Indeed, excessive ROS could also destroy the structure and function of the PM. ER, OsCNGC14, and OsNGC16 improve the heat tolerance of rice through the signal transduction pathway. HTS1 enhances heat tolerance by regulating fatty acid biosynthesis and stress signal transduction. HTS1, TT3, OsFBN1, and OsNSUN2 improve heat tolerance by maintaining chloroplast stability. OsNSUN2, TOGR1, and SLG1 improve heat tolerance by promoting the synthesis of proteins related to the interpretation system, promoting RNA helicase activity, and maintaining normal vulcanized tRNA levels, respectively. OsUBP21 negatively regulates heat tolerance by mediating protein deubiquitylation, while TT1, OsHIRP1, and OsHTAS degrade ubiquitin-binding proteins through the ubiquitin/26S proteasome system. OsHTAS and OsMDHAR4 regulate heat tolerance by mediating the stomatal state induced by H₂O₂. HTH5 may reduce the damage to mitochondrial metabolism under HS by regulating ROS homeostasis. OsANN1, MSD1, SNAC3, and OsRab7 maintain ROS homeostasis by promoting the expression of ROS scavengers.