NADPH oxidases (NOXs), mostly known as respiratory burst oxidase homologs (RBOHs), are the key producers of reactive oxygen species (ROS) in plants. A lot of literature has addressed ROS signaling in plant development regulation and stress responses as well as on the enzyme’s structure, evolution, function, regulation and associated mechanisms, manifesting the role of NOXs/RBOHs as the vital performers and center hubs during plant growth and signaling. This review focuses on recent advances of NOXs/RBOHs on cell growth, hormone interaction, calcium signaling, abiotic stress responses, and immunity. Several primary particles, including Ca2+, CDPKs, BIK1, ROPs/RACs, CERK, FER, ANX, SnRK and SIK1-mediated regulatory mechanisms, are fully summarized to illustrate the signaling behavior of NOXs/RBOHs and their sophisticated and dexterous crosstalks. Diverse expression and activation regulation models endow NOXs/RBOHs powerful and versatile functions in plants to maintain innate immune homeostasis and development integrity. NOXs/RBOHs and their related regulatory items are the ideal targets for crop improvement in both yield and quality during agricultural practices.
NADPH oxidases (NOXs), also known as respiratory burst oxidase homologs (RBOHs), are the major source of reactive oxygen species (ROS), and are involved in many important processes in plants such as regulation of acclimatory signaling and programmed cell death (PCD). Increasing evidence shows that NOXs play crucial roles in plant immunity and their functions in plant immune responses are not as separate individuals but with other signal molecules such as kinases, Rac/Rop small GTPases and hormones, mediating a series of signal transmissions. In a similar way, NOX-mediated signaling also participates in abiotic stress response of plants. We summarized here the complex role and regulation mechanism of NOXs in mediating plant immune response, and the viewpoint that abiotic stress response of plants may be a kind of special plant immunity is also proposed.
Background: NAD kinases (NADKs) are the only known enzymes that directly phosphorylate NAD(H) to generate NADP(H) in different subcellular compartments. They participate in multiple life activities, such as modulating the NADP/NAD ratio, maintaining the intracellular redox balance and responding to environmental stresses. However, the functions of individual NADK in plants are still under investigation. Here, a rice NADK, namely, OsNADK1, was identified, and its functions in plant growth regulation and stress tolerance were analysed by employing a series of transgenic plant lines. Results: OsNADK1 is a cytosol-localized NADK in rice. It was expressed in all rice tissues examined, and its transcriptional expression could be stimulated by a number of environmental stress treatments. Compared with wild-type (WT) rice, the mutant plant osnadk1 in which OsNADK1 was knocked out was a dwarf at the heading stage and had decreased NADP(H)/NAD(H), ascorbic acid (ASA)/dehydroascorbate (DHA) and reduced glutathione (GSH)/oxidized glutathione (GSSG) ratios, which led to increased oxidation states in the rice cells and sensitivity to drought. Moreover, certain stress-related genes showed differential expression patterns in osnadk1 under both normal growth and drought-stress conditions compared with WT. Among these genes, OsDREB1B and several WRKY family transcription factors, e.g., OsWRKY21 and OsWRKY42, showed correlated co-expression patterns with OsNADK1 in osnadk1 and the plants overexpressing or underexpressing OsNADK1, implying roles for these transcription factors in OsNADK1-mediated processes. In addition, overexpression of OsNADK1 enhanced the drought tolerance of rice plants, whereas loss of function of the gene reduced the tolerance. Furthermore, the proline content was dramatically increased in the leaves of the OsNADK1-overexpressing lines under drought conditions. Conclusions: Altogether, the results suggest that an OsNADK1-mediated intracellular redox balance is involved in the tolerance of rice plants to drought.
Fusarium head blight (FHB), or scab, caused by Fusarium species, is an extremely destructive fungal disease in wheat worldwide. In recent decades, researchers have made unremitting efforts in genetic breeding and control technology related to FHB and have made great progress, especially in the exploration of germplasm resources resistant to FHB; identification and pathogenesis of pathogenic strains; discovery and identification of disease-resistant genes; biochemical control, and so on. However, FHB burst have not been effectively controlled and thereby pose increasingly severe threats to wheat productivity. This review focuses on recent advances in pathogenesis, resistance quantitative trait loci (QTLs)/genes, resistance mechanism, and signaling pathways. We identify two primary pathogenetic patterns of Fusarium species and three significant signaling pathways mediated by UGT, WRKY, and SnRK1, respectively; many publicly approved superstar QTLs and genes are fully summarized to illustrate the pathogenetic patterns of Fusarium species, signaling behavior of the major genes, and their sophisticated and dexterous crosstalk. Besides the research status of FHB resistance, breeding bottlenecks in resistant germplasm resources are also analyzed deeply. Finally, this review proposes that the maintenance of intracellular ROS (reactive oxygen species) homeostasis, regulated by several TaCERK-mediated theoretical patterns, may play an important role in plant response to FHB and puts forward some suggestions on resistant QTL/gene mining and molecular breeding in order to provide a valuable reference to contain FHB outbreaks in agricultural production and promote the sustainable development of green agriculture.
Temporal response is an important factor limiting the performance of two-dimensional (2D) material photodetectors. The deep trap states caused by intrinsic defects are the main factor to prolong the response time. In this work, it is demonstrated that the trap states in 2D molybdenum disulfide (MoS2) can be efficiently modulated by defect engineering through mild oxygen plasma treatment. The response time of the few-layer MoS2 photodetector is accelerated by 2–3 orders of magnitude, which is mainly attributed to the deep trap states that can be easily filled when O2 or oxygen ions are chemically bonded with MoS2 at sulfur vacancies (SV) sites. We characterized the defect engineering of plasma-exposed MoS2 by Raman, PL and electric properties. Under the optimal processing conditions of 30 W, 50 Pa and 30 s, we found 30-fold enhancements in photoluminescence (PL) intensity and a nearly 2-fold enhancement in carrier field-effect mobility, while the rise and fall response times reached 110 ms and 55 ms, respectively, at the illumination wavelength of 532 nm. This work would, therefore, offer a practical route to improve the performance of 2D dichalcogenide-based devices for future consideration in optoelectronics research.