The Mutation of Rice MEDIATOR25, OsMED25, Induces Rice Bacterial Blight Resistance through Altering Jasmonate- and Auxin-Signaling.

Rice bacterial blight disease caused by Xanthomonas oryzae pv. oryzae (Xoo) is one of the most severe diseases of rice. However, the regulatory mechanisms of rice defense against Xoo remain poorly understood. The rice MEDIATOR25, OsMED25-a subunit of the mediator multiprotein complex that acts as a universal adaptor between transcription factors (TFs) and RNA polymerase II-plays an important role in jasmonic acid (JA)-mediated lateral root development in rice. In this study, we found that OsMED25 also plays an important role in JA- and auxin-mediated resistance responses against rice bacterial blight. The osmed25 loss-of-function mutant exhibited high resistance to Xoo. The expression of JA-responsive defense-related genes regulated by OsMYC2, which is a positive TF in JA signaling, was downregulated in osmed25 mutants. Conversely, expression of some OsMYC2-independent JA-responsive defense-related genes was upregulated in osmed25 mutants. Furthermore, OsMED25 interacted with some AUXIN RESPONSE FACTORS (OsARFs) that regulate auxin signaling, whereas the mutated osmed25 protein did not interact with the OsARFs. The expression of auxin-responsive genes was downregulated in osmed25 mutants, and auxin-induced susceptibility to Xoo was not observed in osmed25 mutants. These results indicate that OsMED25 plays an important role in the stable regulation of JA- and auxin-mediated signaling in rice defense response.

WUSCHEL-related homeobox family genes in rice control lateral root primordium size.

The development of a plastic root system is essential for stable crop production under variable environments. Rice plants have two types of lateral roots (LRs): S-type (short and thin) and L-type (long, thick, and capable of further branching). LR types are determined at the primordium stage, with a larger primordium size in L-types than S-types. Despite the importance of LR types for rice adaptability to variable water conditions, molecular mechanisms underlying the primordium size control of LRs are unknown. Here, we show that two WUSCHEL-related homeobox (WOX) genes have opposing roles in controlling LR primordium (LRP) size in rice. Root tip excision on seminal roots induced L-type LR formation with wider primordia formed from an early developmental stage. QHB/OsWOX5 was isolated as a causative gene of a mutant that is defective in S-type LR formation but produces more L-type LRs than wild-type (WT) plants following root tip excision. A transcriptome analysis revealed that OsWOX10 is highly up-regulated in L-type LRPs. OsWOX10 overexpression in LRPs increased the LR diameter in an expression-dependent manner. Conversely, the mutation in OsWOX10 decreased the L-type LR diameter under mild drought conditions. The qhb mutants had higher OsWOX10 expression than WT after root tip excision. A yeast one-hybrid assay revealed that the transcriptional repressive activity of QHB was lost in qhb mutants. An electrophoresis mobility shift assay revealed that OsWOX10 is a potential target of QHB. These data suggest that QHB represses LR diameter increase, repressing OsWOX10 Our findings could help improve root system plasticity under variable environments.

Morpho-physiological and molecular mechanisms of phenotypic root plasticity for rice adaptation to water stress conditions.

Different types of water stress severely affect crop production, and the plant root system plays a critical role in stress avoidance. In the case of rice, a cereal crop cultivated under the widest range of soil hydrologic conditions, from irrigated anaerobic conditions to rainfed conditions, phenotypic root plasticity is of particular relevance. Recently, important plastic root traits under different water stress conditions, and their physiological and molecular mechanisms have been gradually understood. In this review, we summarize these plastic root traits and their contributions to dry matter production through enhancement of water uptake under different water stress conditions. We also discuss the physiological and molecular mechanisms regulating the phenotypic plasticity of root systems.

Rice MEDIATOR25, OsMED25, is an essential subunit for jasmonate-mediated root development and OsMYC2-mediated leaf senescence.

The Mediator multiprotein complex acts as a universal adaptor between transcription factors (TFs) and RNA polymerase II. MEDIATOR25 (MED25) has an important role in jasmonic acid (JA) signaling in Arabidopsis. However, no research has been conducted on the role of MED25 in JA signaling in rice, which is one of the most important food crops globally and is a model plant for molecular studies in other monocotyledonous species. In the present study, we isolated the loss-of function mutant of MED25, osmed25, through the map-based cloning and phenotypic complementation analysis by the introduction of OsMED25 and investigated the role of OsMED25 in JA signaling in rice. The osmed25 mutants had longer primary (seminal) roots than those of the wild-type (WT) and exhibited JA-insensitive phenotypes. S-type lateral root densities in osmed25 mutants were lower than those in the WT, whereas L-type lateral root densities in osmed25 mutants were higher than those in the WT. Furthermore, the osmed25 mutants retarded JA-regulated leaf senescence under dark-induced senescence. Mutated osmed25 protein could not interact with OsMYC2, which is a positive TF in JA signaling in rice. The expression of JA-responsive senescence-associated genes was not upregulated in response to JA in the osmed25 mutants. The results suggest that OsMED25 participates in JA-mediated root development and OsMYC2-mediated leaf senescence in rice.

Mutation of OUR1/OsbZIP1, which encodes a member of the basic leucine zipper transcription factor family, promotes root development in rice through repressing auxin signaling.

A well-developed root system is essential for efficient water uptake, particularly in drought-prone environments. However, the molecular mechanisms underlying the promotion of root development are poorly understood. We identified and characterized a rice mutant, outstanding rooting1 (our1), which exhibited a well-developed root system. The our1 mutant displayed typical auxin-related phenotypes, including elongated seminal root and defective gravitropism. Seminal root elongation in the our1 mutant was accelerated via the promotion of cell division and elongation. In addition, compared with the wild type, the density of short and thin lateral roots (S-type LRs) was reduced in the our1 mutant, whereas that of long and thick LRs (L-type LRs) was increased. Expression of OUR1, which encodes OsbZIP1, a member of the basic leucine zipper transcription factor family, was observed in the seminal root tip and sites of LR emergence, wherein attenuation of reporter gene expression levels controlled by the auxin response promoter DR5 was also observed in the our1 mutant. Taken together, our results indicate that the our1 gene promotes root development by suppressing auxin signaling, which may be a key factor contributing to an improvement in root architecture.

The promoted lateral root 1 (plr1) mutation is involved in reduced basal shoot starch accumulation and increased root sugars for enhanced lateral root growth in rice.

Lateral roots (LRs) are indispensable for plant growth, adaptability and productivity. We previously reported a rice mutant, exhibiting a high density of thick and long LRs (L-type LRs) with long parental roots and herein referred to as promoted lateral root1 (plr1). In this study, we describe that the mutant exhibited decreased basal shoot starch accumulation, suggesting that carbohydrates might regulate the mutant root phenotype. Further analysis revealed that plr1 mutation gene regulated reduced starch accumulation resulting in increased root sugars for the regulation of promoted LR development. This was supported by the exogenous glucose application that promoted L-type LRs. Moreover, nitrogen (N) application was found to reduce basal shoot starch accumulation in both plr1 mutant and wild-type seedlings, which was due to the repressed expression of starch biosynthesis genes. However, unlike the wild-type that responded to N treatment only at seedling stage, the plr1 mutant regulated LR development under low to increasing N levels, both at seedling and higher growth stages. These results suggest that plr1 mutation gene is involved in reduced basal shoot starch accumulation and increased root sugar level for the promotion of L-type LR development, and thus would be very useful in improving rice root architecture.

WEG1, which encodes a cell wall hydroxyproline-rich glycoprotein, is essential for parental root elongation controlling lateral root formation in rice.

Lateral roots (LRs) determine the overall root system architecture, thus enabling plants to efficiently explore their underground environment for water and nutrients. However, the mechanisms regulating LR development are poorly understood in monocotyledonous plants. We characterized a rice mutant, wavy root elongation growth 1 (weg1), that produced higher number of long and thick LRs (L-type LRs) formed from the curvatures of its wavy parental roots caused by asymmetric cell growth in the elongation zone. Consistent with this phenotype, was the expression of the WEG1 gene, which encodes a putative member of the hydroxyproline-rich glycoprotein family that regulates cell wall extensibility, in the root elongation zone. The asymmetric elongation growth in roots is well known to be regulated by auxin, but we found that the distribution of auxin at the apical region of the mutant and the wild-type roots was symmetric suggesting that the wavy root phenotype in rice is independent of auxin. However, the accumulation of auxin at the convex side of the curvatures, the site of L-type LR formation, suggested that auxin likely induced the formation of L-type LRs. This was supported by the need of a high amount of exogenous auxin to induce the formation of L-type LRs. These results suggest that the MNU-induced weg1 mutated gene regulates the auxin-independent parental root elongation that controls the number of likely auxin-induced L-type LRs, thus reflecting its importance in improving rice root architecture.