7 research outputs found

    Transcription Factor SiDi19-3 Enhances Salt Tolerance of Foxtail Millet and <i>Arabidopsis</i>

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    Salt stress is an important limiting factor of crop production. Foxtail millet (Setaria italica L.) is an important model crop for studying tolerance to various abiotic stressors. Therefore, examining the response of foxtail millet to salt stress at the molecular level is critical. Herein, we discovered that SiDi19-3 interacts with SiPLATZ12 to control salt tolerance in transgenic Arabidopsis and foxtail millet seedlings. SiDi19-3 overexpression increased the transcript levels of most Na+/H+ antiporter (NHX), salt overly sensitive (SOS), and calcineurin B-like protein (CBL) genes and improved the salt tolerance of foxtail millet and Arabidopsis. Six SiDi19 genes were isolated from foxtail millet. Compared with roots, stems, and leaves, panicles and seeds had higher transcript levels of SiDi19 genes. All of them responded to salt, alkaline, polyethylene glycol, and/or abscisic acid treatments with enhanced expression levels. These findings indicate that SiDi19-3 and other SiDi19 members regulate salt tolerance and other abiotic stress response in foxtail millet

    Halomonas ventosae JPT10 promotes salt tolerance in foxtail millet (Setaria italica) by affecting the levels of multiple antioxidants and phytohormones

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    Abstract Plant growth‐promoting bacterias (PGPBs) can increase crop output under normal and abiotic conditions. However, the mechanisms underlying the plant salt tolerance‐promoting role of PGPBs still remain largely unknown. In this study, we demonstrated that Halomonas ventosae JPT10 promoted the salt tolerance of both dicots and monocots. Physiological analysis revealed that JPT10 reduced reactive oxygen species accumulation by improving the antioxidant capability of foxtail millet seedlings. The metabolomic analysis of JPT10‐inoculated foxtail millet seedlings led to the identification of 438 diversely accumulated metabolites, including flavonoids, phenolic acids, lignans, coumarins, sugar, alkaloids, organic acids, and lipids, under salt stress. Exogenous apigenin and chlorogenic acid increased the salt tolerance of foxtail millet seedlings. Simultaneously, JPT10 led to greater amounts of abscisic acid (ABA), indole‐3‐acetic acid (IAA), salicylic acid (SA), and their derivatives but lower levels of 12‐oxo‐phytodienoic acid (OPDA), jasmonate (JA), and JA‐isoleucine (JA‐Ile) under salt stress. Exogenous JA, methyl‐JA, and OPDA intensified, whereas ibuprofen or phenitone, two inhibitors of JA and OPDA biosynthesis, partially reversed, the growth inhibition of foxtail millet seedlings caused by salt stress. Our results shed light on the response of foxtail millet seedlings to H. ventosae under salt stress and provide potential compounds to increase salt tolerance in foxtail millet and other crops

    A Current Sensing Biosensor for BOD Rapid Measurement

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    In order to improve the practicality of the rapid biochemical oxygen demand (BOD) method, a highly sensitive rapid detection method for BOD that is based on establishing the correlation between current and dissolved oxygen (DO) was developed. In this experiment, Bacillus subtilis was used as the test microorganism, and the embedding method was used to achieve quantitative fixation of microorganisms, which could increase the content of microorganisms and prolong the service life of the biological element. The conductivity (COND) probe is used as a sensing element, so that the testing value can be read every second. In the program, the moving average method is used to process the collected data so that the value can be read every minute. National standard samples were detected to test the accuracy and stability of the method. The results showed that relative error and analytical standard deviations were less than 5%. Different polluted water was tested to evaluate its application range. The results showed that relative error was less than 5%. The results of the method are consistent with the results of the wastewater sample obtained by the BOD5 standard method. The proposed rapid BOD current sensing biosensor method should be promising in practical application of wastewater monitoring

    Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells

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    Nephron progenitor cells surround around the ureteric bud tips (UB) and inductively interact with the UB to originate nephrons, the basic units of renal function. This process is determined by the internal balance between self-renewal and consumption of the nephron progenitor cells, which is depending on the complicated regulation networks. It has been reported that Zeb1 regulates the proliferation of mesenchymal cells in mouse embryos. However, the role of Zeb1 in nephrons generation is not clear, especially in metanephric mesenchyme (MM). Here, we detected cell proliferation, apoptosis and migration in MM cells by EdU assay, flow cytometry assay and wound healing assay, respectively. Meanwhile, Western and RT-PCR were used to measure the expression level of Zeb1 and Six2 in MM cells and developing kidney. Besides, the dual-luciferase assay was conducted to study the molecular relationship between Zeb1 and Six2. We found that knock-down of Zeb1 decreased cell proliferation, migration and promoted cell apoptosis in MM cells and Zeb1 overexpression leaded to the opposite data. Western-blot and RT-PCR results showed that knock-down of Zeb1 decreased the expression of Six2 in MM cells and Zeb1 overexpression contributed to the opposite results. Similarly, Zeb1 promoted Six2 promoter reporter activity in luciferase assays. However, double knock-down of Zeb1 and Six2 did not enhance the apoptosis of MM cells compared with control cells. Nevertheless, double silence of Zeb1 and Six2 repressed cell proliferation. In addition, we also found that Zeb1 and Six2 had an identical pattern in distinct developing phases of embryonic kidney. These results indicated that there may exist a complicated regulation network between Six2 and Zeb1. Together, we demonstrate Zeb1 promotes proliferation and apoptosis and inhibits the migration of MM cells, in association with Six2

    Six2 Is a Coordinator of LiCl-Induced Cell Proliferation and Apoptosis

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    The metanephric mesenchyme (MM) cells are a subset of kidney progenitor cells and play an essential role in mesenchymal-epithelial transition (MET), the key step of nephron generation. Six2, a biological marker related to Wnt signaling pathway, promotes the proliferation, inhibits the apoptosis and maintains the un-differentiation of MM cells. Besides, LiCl is an activator of Wnt signaling pathway. However, the role of LiCl in cellular regulation of MM cells remains unclear, and the relationship between LiCl and Six2 in this process is also little known. Here, we performed EdU assay and flow cytometry assay to, respectively, detect the proliferation and apoptosis of MM cells treated with LiCl of increasing dosages. In addition, reverse transcription-PCR (RT-PCR) and Western-blot were conducted to measure the expression of Six2 and some maker genes of Wnt and bone-morphogenetic-protein (BMP) signaling pathway. Furthermore, luciferase assay was also carried out to detect the transcriptional regulation of Six2. Then we found LiCl promoted MM cell proliferation at low-concentration (10, 20, 30, and 40 mM). The expression of Six2 was dose-dependently increased in low-concentration (10, 20, 30, and 40 mM) at both mRNA and protein level. In addition, both of cell proliferation and Six2 expression in MM cells declined when dosage reached high-concentration (50 mM). However, Six2 knock-down converted the proliferation reduction at 50 mM. Furthermore, Six2 deficiency increased the apoptosis of MM cells, compared with negative control cells at relative LiCl concentration. However, the abnormal rise of apoptosis at 30 mM of LiCl concentration implies that it might be the reduction of GSK3β that increased cell apoptosis. Together, these demonstrate that LiCl can induce the proliferation and apoptosis of MM cells coordinating with Six2
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