scholarly journals TaWRKY40 transcription factor positively regulate the expression of TaGAPC1 to enhance drought tolerance

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Lin Zhang ◽  
Zhiyong Xu ◽  
Haikun Ji ◽  
Ye Zhou ◽  
Shushen Yang
Keyword(s):  
Transcription Factor ◽  
Abiotic Stress ◽  
Drought Stress ◽  
Wheat Yield ◽  
Luciferase Reporter ◽  
Limited Information ◽  
Major Factors ◽  
Direct Regulator ◽  
Dual Luciferase Reporter Assay

Abstract Backgrounds Drought stress is one of the major factors that affects wheat yield. Glyceraldehyde-3-Phosphate dehydrogenase (GAPDH) is a multifunctional enzyme that plays the important role in abiotic stress and plant development. However, in wheat, limited information about drought-responsive GAPC genes has been reported, and the mechanism underlying the regulation of the GAPC protein is unknown. Results In this study, we evaluated the potential role of GAPC1 in drought stress in wheat and Arabidopsis. We found that the overexpression of TaGAPC1 could enhance the tolerance to drought stress in transgenic Arabidopsis. Yeast one-hybrid library screening and EMSA showed that TaWRKY40 acts as a direct regulator of the TaGAPC1 gene. A dual luciferase reporter assay indicated that TaWRKY40 improved the TaGAPC1 promoter activity. The results of qRT-PCR in wheat protoplast cells with instantaneous overexpression of TaWRKY40 indicated that the expression level of TaGAPC1 induced by abiotic stress was upregulated by TaWRKY40. Moreover, TaGAPC1 promoted H2O2 detoxification in response to drought. Conclusion These results demonstrate that the inducible transcription factor TaWRKY40 could activate the transcription of the TaGAPC1 gene, thereby increasing the tolerance of plants to drought stress.

scholarly journals Hsa_circ_0026628 promotes the development of colorectal cancer by targeting SP1 to activate the Wnt/β-catenin pathway

2021 ◽  
Vol 12 (9) ◽  
Author(s):  
Xuexiu Zhang ◽  
Jianning Yao ◽  
Haoling Shi ◽  
Bing Gao ◽  
Haining Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcription Factor ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Transcriptional Level ◽  
Sp1 Transcription Factor ◽  
Reporter Assays ◽  
Sphere Formation

AbstractCircular RNAs (circRNAs) have been reported to play crucial roles in the progression of various cancers, including colorectal cancer (CRC). SP1 (Sp1 transcription factor) is a well-recognized oncogene in CRC and is deemed to trigger the Wnt/β-catenin pathway. The present study was designed to investigate the role of circRNAs which shared the same pre-mRNA with SP1 in CRC cells. We identified that hsa_circ_0026628 (circ_0026628), a circular RNA that originated from SP1 pre-mRNA, was upregulated in CRC cells. Sanger sequencing and agarose gel electrophoresis verified the circular characteristic of circ_0026628. Functional assays including CCK-8, colony formation, transwell, immunofluorescence staining, and sphere formation assay revealed the function of circ_0026628. RNA pull-down and mass spectrometry disclosed the proteins interacting with circ_0026628. Mechanistic assays including RIP, RNA pull-down, CoIP, ChIP, and luciferase reporter assays demonstrated the interplays between molecules. The results depicted that circ_0026628 functioned as a contributor to CRC cell proliferation, migration, EMT, and stemness. Mechanistically, circ_0026628 served as the endogenous sponge of miR-346 and FUS to elevate SP1 expression at the post-transcriptional level, thus strengthening the interaction between SP1 and β-catenin to activate the Wnt/β-catenin pathway. In turn, the downstream gene of Wnt/β-catenin signaling, SOX2 (SRY-box transcription factor 2), transcriptionally activated SP1 and therefore boosted circ_0026628 level. On the whole, SOX2-induced circ_0026628 sponged miR-346 and recruited FUS protein to augment SP1, triggering the downstream Wnt/β-catenin pathway to facilitate CRC progression.

scholarly journals Unsafe medication administration experience in nursing practice at Public Hospitals of Harari region, eastern Ethiopia: Phenomenological Study.

2020 ◽  
Author(s):  
Gelana Fekadu ◽  
Amanuel Oljira ◽  
Biftu Geda ◽  
Gudina Egata
Keyword(s):  
Nursing Practice ◽  
Phenomenological Study ◽  
Organizational Factors ◽  
Medication Administration ◽  
Public Hospitals ◽  
Limited Information ◽  
Contributing Factors ◽  
Eastern Ethiopia ◽  
Major Factors

Abstract Background: The unsafe medication administration is one of the most medication related problems which causes harm and death to the patients and threatens the healthcare system. Given medication administration is predominantly the role of nurses. This study was aimed to explore the nurse’s experience of unsafe medication administration at public hospitals in Harari region, eastern Ethiopia. Methods: A phenomenological study design was conducted and the data were collected from 11 nurses from March 1 to March 31, 2019. The tape recorder and note taking was used to collect the data by in-depth interviews and key informant interviews. Open code software version 3.4 was used to write memos, coding and categorizing under their inductive thematic areas. Thematic analysis method were used.Result: The study had explored nurse’s experience and contributing factors for unsafe medication administration. Nurses have reported that they have ever experienced unsafe medication administration like, wrong time, medication, patient and self-stick injury during their practice. i) Organizational factors: inadequate resource, lack of clear policy and job description, lack of supervision and poor collaboration among staffs. The identified themes were, ii) Precondition challenges: expensive medication, frequently changed and too much prescription for a single patient, new medications with limited information. iii) Individual nurses factor: work absenteeism, lack of training and knowledge gap.Conclusion: The organizational culture, precondition challenges and individual nurse’s factors was found to be a major factors linked to unsafe medication administration practice. So tailored intervention is needed to reduce the unsafe medication administration in nursing practice.

scholarly journals Expression of miR159 Is Altered in Tomato Plants Undergoing Drought Stress

Plants ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 201 ◽  
Author(s):  
María José López-Galiano ◽  
Inmaculada García-Robles ◽  
Ana I. González-Hernández ◽  
Gemma Camañes ◽  
Begonya Vicedo ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Drought Stress ◽  
Regulatory Networks ◽  
Crop Yields ◽  
Insect Pest ◽  
Regulatory Function ◽  
Myb Transcription Factor ◽  
Regulation Of Transcription ◽  
Tomato Plants

In a scenario of global climate change, water scarcity is a major threat for agriculture, severely limiting crop yields. Therefore, alternatives are urgently needed for improving plant adaptation to drought stress. Among them, gene expression reprogramming by microRNAs (miRNAs) might offer a biotechnologically sound strategy. Drought-responsive miRNAs have been reported in many plant species, and some of them are known to participate in complex regulatory networks via their regulation of transcription factors involved in water stress signaling. We explored the role of miR159 in the response of Solanum lycopersicum Mill. plants to drought stress by analyzing the expression of sly-miR159 and its target SlMYB transcription factor genes in tomato plants of cv. Ailsa Craig grown in deprived water conditions or in response to mechanical damage caused by the Colorado potato beetle, a devastating insect pest of Solanaceae plants. Results showed that sly-miR159 regulatory function in the tomato plants response to distinct stresses might be mediated by differential stress-specific MYB transcription factor targeting. sly-miR159 targeting of SlMYB33 transcription factor transcript correlated with accumulation of the osmoprotective compounds proline and putrescine, which promote drought tolerance. This highlights the potential role of sly-miR159 in tomato plants’ adaptation to water deficit conditions.

Controlled nuclear import of the transcription factor NTL6 reveals a cytoplasmic role of SnRK2.8 in the drought-stress response

2012 ◽  
Vol 448 (3) ◽  
pp. 353-363 ◽  
Author(s):  
Mi Jung Kim ◽  
Mi-Jeong Park ◽  
Pil Joon Seo ◽  
Jin-Su Song ◽  
Hie-Joon Kim ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Drought Stress ◽  
Transgenic Plants ◽  
Drought Resistance ◽  
Nuclear Import ◽  
Proteolytic Processing ◽  
Transcriptional Responses ◽  
Resistance Response ◽  
Proteolytic Activation

Controlled proteolytic activation of membrane-anchored transcription factors provides an adaptation strategy that guarantees rapid transcriptional responses to abrupt environmental stresses in both animals and plants. NTL6 is a plant-specific NAC [NAM/ATAF1/2/CUC2] transcription factor that is expressed as a dormant plasma membrane-associated form in Arabidopsis. Proteolytic processing of NTL6 is triggered by abiotic stresses and ABA (abscisic acid). In the present study, we show that NTL6 is linked directly with SnRK (Snf1-related protein kinase) 2.8-mediated signalling in inducing a drought-resistance response. SnRK2.8 phosphorylates NTL6 primarily at Thr142. NTL6 phosphorylation by SnRK2.8 is required for its nuclear import. Accordingly, a mutant NTL6 protein, in which Thr142 was mutated to an alanine, was poorly phosphorylated and failed to enter the nucleus. In accordance with the role of SnRK2.8 in drought-stress signalling, transgenic plants overproducing either NTL6 or its active form 6ΔC (35S:NTL6 and 35S:6ΔC) exhibited enhanced resistance to water-deficit conditions such as those overproducing SnRK2.8 (35S:SnRK2.8). In contrast, NTL6 RNAi (RNA interference) plants were susceptible to dehydration as observed in the SnRK2.8-deficient snrk2.8-1 mutant. Furthermore, the dehydration-resistant phenotype of 35S:NTL6 transgenic plants was compromised in 35S:NTL6 X snrk2.8-1 plants. These observations indicate that SnRK2.8-mediated protein phosphorylation, in addition to a proteolytic processing event, is important for NTL6 function in inducing a drought-resistance response.

scholarly journals (456) Abiotic Stress Responses in Cucumber (Cucumis sativus L.) Plants Expressing the Arabidopsis thaliana Transcriptional Activators-CBF1and CBF3

HortScience ◽  
2005 ◽  
Vol 40 (4) ◽  
pp. 1036E-1037
Author(s):  
Mohamed Tawfik ◽  
Alejandra Ferenczi ◽  
Daniel Enter ◽  
Rebecca Grumet
Keyword(s):  
Oxidative Stress ◽  
Abiotic Stress ◽  
Drought Stress ◽  
Stress Responses ◽  
Stress Resistance ◽  
Photochemical Efficiency ◽  
Leaf Damage ◽  
Cucumis Sativus L ◽  
Oxidative Stresses ◽  
Major Factors

Abiotic stresses (e.g., salinity, drought, cold, oxidative stress) can be major factors limiting plant productivity worldwide. We sought to increase abiotic stress resistance in cucumber by expressing the A. thaliana transcription factors CBF1and CBF3, which regulate genes responsible for enhanced dehydration-stress resistance in Arabidopsis. Our previous studies in the greenhouse and field demonstrated increased salinity tolerance in CBF-expressing cucumber lines. In the current studies, we tested response of CBF-cucumber plants to drought, chilling, and oxidative stresses. Transgenic cucumber plants subjected to drought stress in the greenhouse showed elevated levels of the stress-inducible compatible solute, proline, compared to the nontransgenic controls. Preliminary results also indicate greater photochemical efficiency in CBF-expressing plants under drought stress conditions compared to the nontransgenic controls. Under nonstressed conditions, there were no significant differences in growth between the transgenic and the nontransgenic cucumber plants; however, after a cycle of drought stress, CBF-cucumber lines had less growth reduction compared to the nontransgenic counterparts. The advantage in growth was less pronounced after a second cycle of drought. We also evaluated the transgenic cucumber plants under chilling conditions (i.e., low, nonfreezing temperatures within the 0 to 12 °C range). Based on plant height and cotyledon and leaf damage measurements, transgenic cucumber seedlings did not show chilling tolerance compared to the wild-type control. The response of transgenic CBF-cucumber plants to oxidative stress using methyl viologen is also being evaluated.

scholarly journals Knockdown of LincRNA PADNA Promotes Bupivacaine-Induced Neurotoxicity by miR-194/FBXW7 Axis

2020 ◽  
Author(s):  
Fan Yuning ◽  
Chen Liang ◽  
Wang Tenghuan ◽  
Nan Zhenhua ◽  
Shengkai Gong
Keyword(s):  
Functional Analysis ◽  
Western Blot ◽  
Cell Viability ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Drg Neurons ◽  
Dual Luciferase Reporter Assay

Abstract The aim of the study was to explore the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Mouse DRG neurons were cultured in vitro and treated with bupivacaine to establish the neurotoxicity model. Caspase3 activity, cell viability, tunel assay were analyzed to assess the role of lincRNA PADNA. Dual-luciferase reporter assay was used to determine the binding target of lincRNA PANDA. The expression of lincRNA PADNA was significantly increased with the increasing concentration of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA accelerated the caspase3 activity and inhibited the cell viability. Western blot showed that knockdown of lincRNA PADNA promoted the occurrence of cleaved-caspase3. We also proved that lincRNA PADNA may bind with miR-194. Overexpression of miR-194 could rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidences that lincRNA PADNA/miR-194/FBXW7 axis play an important role in the neurotoxicity process. We performed comprehensive experiments to verify the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Our study provided new evidences and clues for prevention of neurotoxicity.

scholarly journals Transcription Factor FOXK1 Regulates the lncRNA NEAT1 to Promote Glioma Development Through Mediating KDM3A

2020 ◽  
Author(s):  
Feng Liu ◽  
Hao Wu ◽  
Guangyong Wu ◽  
Jun Long ◽  
Jin Dai ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Viability ◽  
Rna Binding ◽  
Luciferase Reporter ◽  
Normal Brain ◽  
Invasion And Migration ◽  
Gene Assay ◽  
And Migration ◽  
Lncrna Neat1

Abstract Background: Long noncoding RNAs are widely studied in glioma. However, the role of the lncRNA NEAT1 and KDM3A in glioma has not yet been reported. We aimed to reveal the role of these two lncRNAs in the development of glioma through this study.Methods: Samples from glioma patients and normal brain tissues were collected, and the expression of NEAT1 was detected by qRT-PCR. A dual-luciferase reporter gene assay, chromatin immunoprecipitation (ChIP), RNA-binding protein immunoprecipitation (RIP), and RNA pulldown experiments were used to identify the relationship between FOXK1, NEAT1, miR-128, and KDM3A. The CCK8 assay, Transwell assay and flow cytometry were used to detect cell viability, invasion and migration ability, and the cell cycle and apoptosis, respectively. Tumor formation experiments verified the effect of NEAT1 on gliomas in vivo.Results: FOXK1 and NEAT1 were significantly overexpressed in glioma tissues and cells, and NEAT1 was significantly related to WHO classification. FOXK1 bound the NEAT1 gene promoter region in glioma cells, and interference with FOXK1 inhibited NEAT1 expression. NEAT1 inhibited miR-128 expression by binding miR-128; significantly improved cell viability and invasion and migration capabilities; increased the expression of KDM3A and activated the Wnt signaling pathway. Interference with KDM3A reversed the above results. In addition, interference with NEAT1 decreased KDM3A expression and inhibited tumor growth.Conclusion: Interference with NEAT1 promoted the expression of miR-128, thereby suppressing the expression of KDM3A and inhibiting the occurrence and development of glioma, while the expression of NEAT1 was shown to be regulated by the upstream transcription factor FOXK1.

scholarly journals LncRNA LINC01303 Promotes the Progression of Oral Squamous Cell Carcinomas via the miR-429/ZEB1/EMT Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Bo Sun ◽  
Xianyu Zheng ◽  
Weilong Ye ◽  
Pengcheng Zhao ◽  
Guowu Ma
Keyword(s):  
Squamous Cell ◽  
Luciferase Reporter ◽  
Real Time Quantitative Pcr ◽  
Qrt Pcr ◽  
Cytoplasmic Rna ◽  
Transwell Invasion Assay ◽  
Dual Luciferase Reporter Assay

Objectives. The aim of this research was to uncover the biological role and mechanisms of LINC01303 in oral squamous cell carcinoma (OSCC). Materials and Methods. Real-time quantitative PCR (qRT-PCR) was used to determine LINC01303 expression in OSCC tissues. Subcellular distribution of LINC01303 was examined by nuclear/cytoplasmic RNA fractionation and FISH experiments. The role of LINC01303 in the growth of TSCCA and SCC-25 was examined by CCK-8 assay, colony formation, transwell invasion assay in vitro, and xenograft tumor experiment in vivo. Dual-luciferase reporter assay was used to verify the interaction between LINC01303 and miR-429. RNA pull‐down assay was used to discover miR-429‐interacted protein, which was further examined by qRT-PCR, western blot, and rescue experiments. Results. LINC01303 expression was higher in OSCC tissues compared with adjacent nontumor tissues. LINC01303 was found to be localized in the cytoplasm of OSCC cells. Knockdown of LINC01303 inhibited OSCC cell proliferation and invasion, whereas increasing the expression of LINC01303 showed the opposite effects. Furthermore, LINC01303 served as a miR-429 “sponge” and positively regulated ZEB1 expression. Moreover, LINC01303 promoted OSCC through miR-429/ZEB1 axis both in vivo and in vitro. Conclusions. LINC01303 plays an oncogenic role in OSCC and is a promising biomarker for OSCC patients.

scholarly journals GATA1-induced upregulation of LINC01503 promotes carboplatin resistance in ovarian carcinoma by upregulating PD-L1 via sponging miR-766-5p

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yao Li ◽  
Yan Zhai ◽  
Yuxuan Chen
Keyword(s):  
Ovarian Carcinoma ◽  
Inhibitory Concentration ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Invasive Ability ◽  
Protein Levels ◽  
Reverse Transcription Quantitative Pcr ◽  
Non Coding Rnas ◽  
Dual Luciferase Reporter Assay

Abstract Background Ovarian Carcinoma (OCa) is a high-mortality malignancy derived from female reproductive system. Increasing evidence has identified long non-coding RNAs (lncRNAs) as important regulators in OCa chemoresistance. In this study, we intended to explore the role of LINC01503 in OCa resistance to carboplatin (CBP). Methods Gene expression was measured by reverse transcription-quantitative PCR (RT-qPCR) in OCa cells. Western blot was adopted to detect protein levels of GATA1, PD-L1, E-cadherin, N-cadherin, Vimentin, Bcl-2, Bax, cleaved caspase-3. To assess the effects of LINC01503 on the resistance of OCa cells to CBP, Cell Counting Kit-8 (CCK-8), colony formation, Transwell, and flow cytometry experiments were performed to evaluate half-maximal inhibitory concentration (IC50), cell viability, migrative and invasive ability, as well as cell apoptosis. Dual-luciferase reporter assay was employed to assess the associations between the genes. Results LINC01503 was upregulated in CBP-resistant OCa cells. LINC01503 knockdown reduced CBP resistance in OCa cells. Besides, GATA-binding protein 1 (GATA1) activated LINC01503 transcription in CBP-resistant OCa cells. MiR-766-5p was lowly expressed in CBP-resistant cells and confirmed as a target for LINC01503. In addition, miR-766-5p overexpression increased CBP sensitivity in OCa cells. PD-L1 was verified as the target of miR-766-5p. Besides, LINC01503 upregulated PD-L1 level by regulating miR-766-5p. Furthermore, rescue experiments showed that PD-L1 overexpression abrogated the inhibited impacts of blocking LINC01503 on CBP resistance in OCa cells. Conclusion GATA1-induced LINC01503 expedited CBP resistance in OCa cells via the miR-766-5p/PD-L1 axis, providing a new target for improving the efficacy of OCa chemotherapy. Graphical Abstract

scholarly journals LncRNA SNHG14 regulates the DDP-resistance of non-small cell lung cancer cell through miR-133a/HOXB13 pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Li Xu ◽  
Yan Xu ◽  
Min Yang ◽  
Jia Li ◽  
Fang Xu ◽  
...  
Keyword(s):  
Cell Line ◽  
A549 Cells ◽  
Parental Cell ◽  
Luciferase Reporter ◽  
Inhibitory Effects ◽  
Through Flow ◽  
Non Coding Rnas ◽  
Apoptosis Related Protein ◽  
Dual Luciferase Reporter Assay

Abstract Background Recently, long non-coding RNAs (lncRNAs) have been reported to be involved in regulating chemo-resistance of NSCLC, however, the role of lncRNA SNHG14 in the DDP-resistance of NSCLC remains unexplored. Methods Relative expression of SNHG14, HOXB13 and miR-133a in DDP-resistant A549 (A549/DDP) cell and its parental cell A549 were measured using qRT-PCR. Cell proliferation viability of indicated A549/DDP cell was estimated via CCK-8 and colony formation experiments. Cell cycle and apoptosis were analyzed through flow cytometry. Expression of apoptosis-related protein and HOXB13 were detected via western blot. The interaction among SNHG14, HOXB13 and miR-133a was predicted by bioinformatics and validated by dual-luciferase reporter assay. Results LncRNA SNHG14 and HOXB13 were upregulated while miR-133a was downregulated in A549/DDP cell line compared to A549 cell line. SNHG14 knockdown or miR-133a overexpression was demonstrated to increase the DDP-sensitivity of A549/DDP cells. SNHG14 was revealed to compete with HOXB13 for miR-133a binding in A549/DDP cells. Inhibition of miR-133a in A549 cells could reverse the promotive effects of SNHG14 knockdown on DDP-sensitivity, as well as the inhibitory effects on HOXB13 expression. HOXB13 overexpression was revealed to abolish the enhanced effects of miR-133a on the sensitivity of A549/DDP cell to DDP. Conclusion Our findings demonstrated that SNHG14 was involved in the development of DDP-resistance of A549/DDP cells through miR-133a/HOXB13 axis, which may present a path to novel therapeutic stratagems for DDP resistance of NSCLC.

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