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Soil salinization limits rice growth and is an important restriction on grain yield. Jacalin-related lectins are involved in multiple stress responses, but their role in salt stress responses and use as molecular markers for salt tolerance remain poorly understood. Salt stress treatments and RT-qPCR analyses of Sea Rice 86 (SR86), 9311, and Nipponbare (Nip) showed that OsJRL45 and OsJRL40 enhanced tolerance of salt stress in SR86. Molecular markers based on sequence differences in SR86 and the salt-sensitive variety, 9311, in the intergenic region between OsJRL45 and OsJRL40 were validated in recombinant inbred lines derived from SR86 and 9311, hybrid populations, and common rice varieties. Yeast two-hybrid and bimolecular fluorescence complementation demonstrated that OsJRL45 and OsJRL40 interacted. Co-transformation of Nip with OsJRL45 and OsJRL40 derived from SR86 had no effect on the mature phenotype in T2 plants; however, salt stress at the three-leaf stage led to significant increases in CAT, POD, SOD, and Pro contents, but reduced MDA content in transgenic plants. Transcriptomic analysis identified 834 differentially expressed genes in transgenic plants under salt stress. GO and KEGG enrichment analyses indicated that metabolic pathways related to antioxidant responses and osmotic balance were crucial for salt-stress tolerance. Thus, molecular markers based on nucleotide differences in OsJRL45 and OsJRL40 provide a novel method for identifying salt-tolerant rice varieties. [ABSTRACT FROM AUTHOR]

Receptor-like kinase FERONIA (FER) plays a crucial role in plant response to small molecule hormones [e.g., auxin and abscisic acid (ABA)] and peptide signals [e.g., rapid alkalinization factor (RALF)]. It remains unknown how FER integrates these different signaling events in the control of cell growth and stress responses. Under stress conditions, increased levels of ABA will inhibit cell elongation in the roots. In our previous work, we have shown that FER, through activation of the guanine nucleotide exchange factor 1 (GEF1)/4/10-Rho of Plant 11 (ROP11) pathway, enhances the activity of the phosphatase ABA Insensitive 2 (ABI2), a negative regulator of ABA signaling, thereby inhibiting ABA response. In this study, we found that both RALF and ABA activated FER by increasing the phosphorylation level of FER. The FER loss-of-function mutant displayed strong hypersensitivity to both ABA and abiotic stresses such as salt and cold conditions, indicating that FER plays a key role in ABA and stress responses. We further showed that ABI2 directly interacted with and dephosphorylated FER, leading to inhibition of FER activity. Several other ABI2-like phosphatases also function in this pathway, and ABA-dependent FER activation required PYRABACTIN RESISTANCE (PYR)/PYR1-LIKE (PYL)/REGULATORY COMPONENTS OF ABA RECEPTORS (RCAR)-A-type protein phosphatase type 2C (PP2CA) modules. Furthermore, suppression of RALF1 gene expression, similar to disruption of the FER gene, rendered plants hypersensitive to ABA. These results formulated a mechanism for ABA activation of FER and for cross-talk between ABA and peptide hormone RALF in the control of plant growth and responses to stress signals.

High salinity is a major stress factor affecting the quality and productivity of rice (Oryza sativa L.). Although numerous salt tolerance-related genes have been identified in rice, their molecular mechanisms remain unknown. Here, we report that OsJRL40, a jacalin-related lectin gene, confers remarkable salt tolerance in rice. The loss of function of OsJRL40 increased sensitivity to salt stress in rice, whereas its overexpression enhanced salt tolerance at the seedling stage and during reproductive growth. β-glucuronidase (GUS) reporter assays indicated that OsJRL40 is expressed to higher levels in roots and internodes than in other tissues, and subcellular localization analysis revealed that the OsJRL40 protein localizes to the cytoplasm. Further molecular analyses showed that OsJRL40 enhances antioxidant enzyme activities and regulates Na+-K+ homeostasis under salt stress. RNA-seq analysis revealed that OsJRL40 regulates salt tolerance in rice by controlling the expression of genes encoding Na+/K+ transporters, salt-responsive transcription factors, and other salt response-related proteins. Overall, this study provides a scientific basis for an in-depth investigation of the salt tolerance mechanism in rice and could guide the breeding of salt-tolerant rice cultivars. [ABSTRACT FROM AUTHOR]

Chilling stress has become a major limiting factor that reduces crop productivity worldwide. In this study, we identified a new gene bHLH57, whose product enhances chilling tolerance in rice at diverse developmental stages. bHLH57 was mainly expressed in leaves and anthers, and its protein was targeted to the nucleus. Overexpression of bHLH57 enhanced chilling tolerance by increasing trehalose synthesis, whereas its mutants by CRISPR/Cas9‐mediated mutagenesis were more sensitive to chilling and had reduced trehalose. Meanwhile, bHLH57 may regulate ROS metabolism and CBFs/DREBs‐ dependent pathways in response to chilling stress. In addition, the overexpression of bHLH57 resulted in increased grain yield under normal and chilling conditions, however, the disruption of bHLH57 displayed decreased grain size and seed setting rate, thus reduced grain yield. Phylogenetic and nucleotide diversity analyses suggested that bHLH57 is relatively conserved in monocotyledons, and may be selected during indica populations adaptation. Taken together, we have identified a new bHLH regulator involved rice chilling tolerance and grain yield, and provide a potential target gene for improving chilling tolerance and grain yield of rice. Summary statement: bHLH57 enhances chilling tolerance through regulation of trehalose synthase, ROS metabolism, and CBFs/DREBs‐ dependent pathways. In addition, the overexpressing of bHLH57 potentially improves grain yield by increasing the seed setting rate and grain size. Taken together, we provide a potential target gene for improving chilling tolerance and grain yield of rice [ABSTRACT FROM AUTHOR]

Preharvest sprouting (PHS) is an unfavorable trait in cereal crops and causes serious yield loss. However, the molecular mechanism underlying PHS remains largely elusive. Here, we identified a member of 9‐cis‐epoxycarotenoid dioxygenase family, OsNCED3, which regulates PHS and grain development in rice (Oryza sativa L.). OsNCED3 encodes a chloroplast‐localized abscisic acid (ABA) biosynthetic enzyme highly expressed in the embryo of developing seeds. Disruption of OsNCED3 by CRISPR/Cas9‐mediated mutagenesis led to a lower ABA and higher gibberellic acid (GA) levels (thus a skewed ABA/GA ratio) in the embryo, promoting embryos growth and breaking seed dormancy before seed maturity and harvest, thus decreased seed dormancy and enhanced PHS in rice. However, the overexpression of OsNCED3 enhanced PHS resistance by regulating proper ABA/GA ratio in the embryo. Intriguingly, the overexpression of OsNCED3 resulted in increased grain size and weight, whereas the disruption of OsNCED3 function decreased grain size and weight. Nucleotide diversity analyses suggested that OsNCED3 may be selected during japonica populations adaptation of seed dormancy and germination. Taken together, we have identified a new OsNCED regulator involved rice PHS and grain development, and provide a potential target gene for improving PHS resistance and grain development in rice. Summary statement: Preharvest sprouting (PHS) is an unfavorable trait in cereal crops and causes serious yield loss. However, the molecular mechanism underlying PHS remains largely elusive. Here, we identified that overexpression of OsNCED3 enhanced PHS resistance by regulating proper abscisic acidgibberellic acid ratio in the embryo. In addition, the overexpression of OsNCED3 resulted in increased grain size and weight. This study provides a potential target gene for improving PHS resistance and grain development in rice. [ABSTRACT FROM AUTHOR]

Zhu1S is a thermosensitive genic male-sterile (TGMS) line of rice possessing outstanding combining ability and low critical temperature, which has been extensively utilized as a female parent in two-line hybrid ricebreeding. However, the fertility of Zhu 1S during hybrid seed production is frequently affected by high temperature, thus leading to its fertility alteration and aborted hybrid seed production. To understand its fertility conversion mechanism under high temperature, we employed transcriptomics analyses on the anthers of young panicles of Zhu 1S during the fertility alternation sensitivity stage under high (Zhu 1S-H) and low (Zhu 1S-L) temperatures. The results showed that a total of 1119 differentially expressed genes (DEGs) were identified between Zhu 1S-H and Zhu1S-L anthers, including 680 up-regulated and 439 down-regulated genes. Bioinformatics analysis of these DEGs revealed that the high temperature induction caused fertility-sterility conversion in Zhu1S, mainly by decreasing the mRNA abundances of important genes closely related to plant hormone and MAPK signal pathway and transcriptional regulation factors, thereby impeding the growth and development of the anther of Zhu 1S, which ultimately affected the fertility transition of Zhu 1S under high temperature. The protein–protein interaction network analysis indicates that transcription factor OsTIFY11C possibility plays a central role in the fertility transition of Zhu 1S under high temperature.The present studies offer a theoretical foundation for further research into the molecular mechanism underlying fertility conversion in TGMS line Zhu 1S. [ABSTRACT FROM AUTHOR]

Soil salinity has become a major stress factor that reduces crop productivity worldwide. Sodium (Na+) toxicity in a number of crop plants is tightly linked with shoot Na+ overaccumulation, thus Na+ exclusion from shoot is crucial for salt tolerance in crops. In this study, we identified a member of the high-affinity K+ transport family (HAK), OsHAK12, which mediates shoots Na+ exclusion in response to salt stress in rice. The Oshak12 mutants showed sensitivity to salt toxicity and accumulated more Na+ in the xylem sap, leading to excessive Na+ in the shoots and less Na+ in the roots. Unlike typical HAK family transporters that transport K+, OsHAK12 is a Na+-permeable plasma membrane transporter. In addition, OsHAK12 was strongly expressed in the root vascular tissues and induced by salt stress. These findings indicate that OsHAK12 mediates Na+ exclusion from shoot, possibly by retrieving Na+ from xylem vessel thereby reducing Na+ content in the shoots. These findings provide a unique function of a rice HAK family member and provide a potential target gene for improving salt tolerance of rice. [ABSTRACT FROM AUTHOR]

Potassium (K+) levels in the soil often limit plant growth and development. As a result, crop production largely relies on the heavy use of chemical fertilizers, presenting a challenging problem in sustainable agriculture. To breed crops with higher K+-use efficiency (KUE), we must learn how K+ is acquired from the soil by the root system and transported to the rest of the plant through K+ transporters. In this study, we identified the function of the rice K+ transporter OsHAK8 , whose expression level is downregulated in response to low-K+ stress. When OsHAK8 was disrupted by CRISPR/Cas9-mediated mutagenesis, Oshak8 mutant plants showed stunted growth, especially under low-K+ conditions. Ion content analyses indicated that K+ uptake and root-to-shoot K+ transport were significantly impaired in Oshak8 mutants under low-K+ conditions. As the OsHAK8 gene was broadly expressed in different cell types in the roots and its protein was targeted to the plasma membrane, we propose that OsHAK8 serves as a major transporter for both uptake and root-to-shoot translocation in rice plants. [ABSTRACT FROM AUTHOR]