The OsWRKY72-OsAAT30/OsGSTU26 module mediates reactive oxygen species scavenging to drive heterosis for salt tolerance in hybrid rice.

Hybrid rice (Oryza sativa) generally outperforms its inbred parents in yield and stress tolerance, a phenomenon termed heterosis, but the underlying mechanism is not completely understood. Here, we combined transcriptome, proteome, physiological, and heterosis analyses to examine the salt response of super hybrid rice Chaoyou1000 (CY1000). In addition to surpassing the mean values for its two parents (mid-parent heterosis), CY1000 exhibited a higher reactive oxygen species scavenging ability than both its parents (over-parent heterosis or heterobeltiosis). Nonadditive expression and allele-specific gene expression assays showed that the glutathione S-transferase gene OsGSTU26 and the amino acid transporter gene OsAAT30 may have major roles in heterosis for salt tolerance, acting in an overdominant fashion in CY1000. Furthermore, we identified OsWRKY72 as a common transcription factor that binds and regulates OsGSTU26 and OsAAT30. The salt-sensitive phenotypes were associated with the OsWRKY72paternal genotype or the OsAAT30maternal genotype in core rice germplasm varieties. OsWRKY72paternal specifically repressed the expression of OsGSTU26 under salt stress, leading to salinity sensitivity, while OsWRKY72maternal specifically repressed OsAAT30, resulting in salinity tolerance. These results suggest that the OsWRKY72-OsAAT30/OsGSTU26 module may play an important role in heterosis for salt tolerance in an overdominant fashion in CY1000 hybrid rice, providing valuable clues to elucidate the mechanism of heterosis for salinity tolerance in hybrid rice.

The RNA m6A landscape of mouse oocytes and preimplantation embryos.

Despite the significance of N6-methyladenosine (m6A) in gene regulation, the requirement for large amounts of RNA has hindered m6A profiling in mammalian early embryos. Here we apply low-input methyl RNA immunoprecipitation and sequencing to map m6A in mouse oocytes and preimplantation embryos. We define the landscape of m6A during the maternal-to-zygotic transition, including stage-specifically expressed transcription factors essential for cell fate determination. Both the maternally inherited transcripts to be degraded post fertilization and the zygotically activated genes during zygotic genome activation are widely marked by m6A. In contrast to m6A-marked zygotic ally-activated genes, m6A-marked maternally inherited transcripts have a higher tendency to be targeted by microRNAs. Moreover, RNAs derived from retrotransposons, such as MTA that is maternally expressed and MERVL that is transcriptionally activated at the two-cell stage, are largely marked by m6A. Our results provide a foundation for future studies exploring the regulatory roles of m6A in mammalian early embryonic development.

Epigenetic regulation of nitrogen and phosphorus responses in plants.

Nitrogen (N) and phosphorus (P) are two of the most important nutrients for plant growth and crop yields. In the last decade, plenty of studies have revealed the genetic factors and their regulatory networks which are involved in N and/or P uptake and utilization in different model plant species, especially in Arabidopsis and rice. However, increasing evidences have shown that epigenetic regulation also plays a vital role in modulating plant responses to nutrient availability. In this review, we make a brief summary of epigenetic regulation including histone modifications, DNA methylation, and other chromatin structure alterations in tuning N and P responses. We also give an outlook for future research directions to comprehensively dissect the involvement of epigenetic regulation in modulating nutrient response in plants.

Posttranslational Modifications: Regulation of Nitrogen Utilization and Signaling.

Nitrogen is the most important macroelement required for the composition of key molecules, such as nucleic acids, proteins and other organic compounds. As sessile organisms, plants have evolved sophisticated mechanisms to acquire nitrogen for their normal growth and development. Besides the transcriptional and translational regulation of nitrogen uptake, assimilation, remobilization and signal transduction, posttranslational modifications (PTMs) are shown to participate in these processes in plants. In addition to alterations in protein abundance, PTMs may dramatically increase the complexity of the proteome without the concomitant changes in gene transcription and have emerged as an important type of protein regulation in terms of protein function, subcellular localization and protein activity and stability. Herein, we briefly summarize recent advances on the posttranslational regulation of nitrogen uptake, assimilation, remobilization and nitrogen signaling and discuss the underlying mechanisms of PTMs as well as the signal output of such PTMs. Understanding these regulation mechanisms will provide novel insights for improving the nitrogen use efficiency of plants.

Genomic basis of geographical adaptation to soil nitrogen in rice.

The intensive application of inorganic nitrogen underlies marked increases in crop production, but imposes detrimental effects on ecosystems1,2: it is therefore crucial for future sustainable agriculture to improve the nitrogen-use efficiency of crop plants. Here we report the genetic basis of nitrogen-use efficiency associated with adaptation to local soils in rice (Oryza sativa L.). Using a panel of diverse rice germplasm collected from different ecogeographical regions, we performed a genome-wide association study on the tillering response to nitrogen-the trait that is most closely correlated with nitrogen-use efficiency in rice-and identified OsTCP19 as a modulator of this tillering response through its transcriptional response to nitrogen and its targeting to the tiller-promoting gene DWARF AND LOW-TILLERING (DLT)3,4. A 29-bp insertion and/or deletion in the OsTCP19 promoter confers a differential transcriptional response and variation in the tillering response to nitrogen among rice varieties. The allele of OsTCP19 associated with a high tillering response to nitrogen is prevalent in wild rice populations, but has largely been lost in modern cultivars: this loss correlates with increased local soil nitrogen content, which suggests that it might have contributed to geographical adaptation in rice. Introgression of the allele associated with a high tillering response into modern rice cultivars boosts grain yield and nitrogen-use efficiency under low or moderate levels of nitrogen, which demonstrates substantial potential for rice breeding and the amelioration of negative environment effects by reducing the application of nitrogen to crops.

Modulation of nitrate-induced phosphate response by the MYB transcription factor RLI1/HINGE1 in the nucleus.

The coordinated utilization of nitrogen (N) and phosphorus (P) is vital for plants to maintain nutrient balance and achieve optimal growth. Previously, we revealed a mechanism by which nitrate induces genes for phosphate utilization; this mechanism depends on NRT1.1B-facilitated degradation of cytoplasmic SPX4, which in turn promotes cytoplasmic-nuclear shuttling of PHR2, the central transcription factor of phosphate signaling, and triggers the nitrate-induced phosphate response (NIPR) and N-P coordinated utilization in rice. In this study, we unveiled a fine-tuning mechanism of NIPR in the nucleus regulated by Highly Induced by Nitrate Gene 1 (HINGE1, also known as RLI1), a MYB-transcription factor closely related to PHR2. RLI1/HINGE1, which is transcriptionally activated by PHR2 under nitrate induction, can directly activate the expression of phosphate starvation-induced genes. More importantly, RLI1/HINGE1 competes with PHR2 for binding to its repressor proteins in the nucleus (SPX proteins), and consequently releases PHR2 to further enhance phosphate response. Therefore, RLI1/HINGE1 amplifies the phosphate response in the nucleus downstream of the cytoplasmic SPX4-PHR2 cascade, thereby enabling fine-tuning of N-P balance when nitrate supply is sufficient.

NRT1.1s in plants: functions beyond nitrate transport.

Arabidopsis AtNRT1.1 (CHL1/AtNPF6.3) is the first nitrate transporter identified in plants and was initially found to play a role in nitrate uptake and transport. AtNRT1.1 also displays auxin transport activity and mediates nitrate-modulated root development, suggesting that it has transport capacity for multiple substrates. Subsequent work revealed that AtNRT1.1 can respond to environmental nitrate fluctuations by altering its nitrate transport activity, modulated by phosphorylation, leading to the critical finding that AtNRT1.1 acts as a transceptor for nitrate sensing. Recent studies have revealed how OsNRT1.1B, the functional homologue of AtNRT1.1 in rice, mediates nitrate signal transduction from the plasma membrane to the nucleus, and how OsNRT1.1B integrates the nitrate and phosphate signaling networks. OsNRT1.1B has also been shown to be involved in regulating the root microbiota to facilitate organic nitrogen mineralization in soil, thus mediating plant-microbe interactions. Furthermore, the divergent functions of OsNRT1.1A and OsNRT1.1B in regulating nitrogen use in rice suggest that the function of NRT1.1 is still far from fully understood. In this review, we focus on the most recent progress on the molecular mechanisms of NRT1.1s in plants, with the aim of providing an up-to-date view of the versatile functions of NRT1.1 in nitrogen utilization in plants.

Author Correction: Nitrate-NRT1.1B-SPX4 cascade integrates nitrogen and phosphorus signalling networks in plants.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Nitrate-NRT1.1B-SPX4 cascade integrates nitrogen and phosphorus signalling networks in plants.

To ensure high crop yields in a sustainable manner, a comprehensive understanding of the control of nutrient acquisition is required. In particular, the signalling networks controlling the coordinated utilization of the two most highly demanded mineral nutrients, nitrogen and phosphorus, are of utmost importance. Here, we reveal a mechanism by which nitrate activates both phosphate and nitrate utilization in rice (Oryza sativa L.). We show that the nitrate sensor NRT1.1B interacts with a phosphate signalling repressor SPX4. Nitrate perception strengthens the NRT1.1B-SPX4 interaction and promotes the ubiquitination and degradation of SPX4 by recruiting NRT1.1B interacting protein 1 (NBIP1), an E3 ubiquitin ligase. This in turn allows the key transcription factor of phosphate signalling, PHR2, to translocate to the nucleus and initiate the transcription of phosphorus utilization genes. Interestingly, the central transcription factor of nitrate signalling, NLP3, is also under the control of SPX4. Thus, nitrate-triggered degradation of SPX4 activates both phosphate- and nitrate-responsive genes, implementing the coordinated utilization of nitrogen and phosphorus.

Melatonin Regulates Root Architecture by Modulating Auxin Response in Rice.

It has been suggested that melatonin acts as an important regulator in controlling root growth and development, but the underlying molecular mechanism driving this relationship remains undetermined. In this study, we demonstrated that melatonin acts as a potent molecule to govern root architecture in rice. Treatments with melatonin significantly inhibited embryonic root growth, and promoted lateral root formation and development. Genome-wide expression profiling by RNA-sequencing revealed auxin-related genes were significantly activated under melatonin treatment. Moreover, several transcription factors and candidate cis-regulatory elements involved in root growth and developments, as well as auxin-related processes, were over-represented in both co-up and -down differentially expressed genes, suggesting that melatonin-mediated root growth occurs in an auxin signal pathway-dependent manner. Further, gravitropic response analysis determined that melatonin affects auxin-regulated processes in rice root. These data show that melatonin shapes root architecture by directly or indirectly activating the auxin signaling pathway.