Rice (Oryza sativa) is a research model for monocotyledonous plants. Rice is also one of the major staple foods and the primary crop for more than half of the world’s population. Increasing industrial activities and the use of different fertilizers and pesticides containing heavy metals (HMs) contribute to the contamination of agriculture fields. HM contamination is among the leading causes that affect the health of rice plants by limiting their growth and causing plant death. Phytohormones have a crucial role in stress-coping mechanisms and in determining a range of plant development and growth aspects during heavy metal stress. This review summarizes the role of different exogenous applications of phytohormones including auxin, cytokinin, gibberellins, ethylene, abscisic acid, strigolactones, jasmonates, brassinosteroids, and salicylic acids in rice plants for mitigating heavy metal stress via manipulation of their stress-related physiological and biochemical processes, and alterations of signaling and biosynthesis of genes. Exogenous administration of phytohormones and regulation of endogenous levels by targeting their biosynthesis/signaling machineries is a potential strategy for protecting rice from HM stress. The current review primarily emphasizes the key mechanistic phytohormonal-mediated strategies for reducing the adverse effects of HM toxicity in rice. Herein, we have provided comprehensive evidence for the effective role of exogenous phytohormones in employing defense responses and tolerance in rice to the phytotoxic effects of HM toxicity along with endogenous hormonal crosstalk for modulation of subcellular mechanisms and modification of stress-related signaling pathways, and uptake and translocation of metals. Altogether, this information offers a systematic understanding of how phytohormones modulate a plant’s tolerance to heavy metals and may assist in directing the development of new approaches to strengthen rice plant resistance to HM toxicity.

Seed or pod shattering in rice (Oryza sativa) is considered to be one of the major factors involved in the domestication of rice as a crop. High seed shattering results in significant yield losses. In this study, we characterize the RICEHIGHSHATTERING 1 (RHS1) that corresponds to the locus LOC_Os04g41250 from a greenhouse screen, involving 145 Ac/Ds transposon mutant rice lines. The knockout mutant line rhs1 exhibited a significantly high shattering of grains in comparison to the wild-type plants. The exogenous application of nitric oxide (NO) resulted in a significant reduction in the expression of RHS1 in wild-type rice plants. The absence of RHS1, which encodes a putative armadillo/beta-catenin repeat family protein, resulted in high sensitivity of the rhs1 plants to nitrosative stress. Interestingly, the basal expression levels of QSH1 and SHAT1 genes (transcription factors that regulate seed-pod shattering in rice) were significantly lower in these plants than in wild-type plants; however, nitrosative stress negatively regulated the expression of QSH1 and SHAT1 in both WT and rhs1 plants, but positively regulated QSH4 expression in rhs1 plants alone. The expression levels of genes responsible for NO production (OsNIA1, OsNIA2, and OsNOA1) were lower in rhs1 plants than in WT plants under normal conditions. However, under nitrosative stress, the expression of OsNIA2 significantly increased in rhs1 plants. The expression of CPL1 (a negative regulator of seed shattering in rice) was significantly lower in rhs1 plants, and we found that CPL1 expression was correlated with S-nitrosothiol (SNO) alteration in rhs1. Interestingly noe1, a rice mutant with high SNO levels, exhibited low seed shattering, whereas rhs1 resulted in low SNO levels with high seed shattering. Therefore, RHS1 is a novel gene that negatively regulates the shattering trait in rice via regulation of endogenous SNO levels. However, the molecular mechanisms involved in the control of RHS1-mediated regulation of seed shattering and its interaction with nitric oxide and involvement in plant defense need to be investigated further.