scholarly journals Waterlogging-Stress-Responsive LncRNAs, Their Regulatory Relationships with MiRNAs and Target Genes in Cucumber (Cucumis sativus L.)

2021 ◽  
Vol 22 (15) ◽  
pp. 8197
Author(s):  
Kinga Kęska ◽  
Michał Wojciech Szcześniak ◽  
Adela Adamus ◽  
Małgorzata Czernicka
Keyword(s):  
Target Genes ◽  
Recovery Period ◽  
Sufficient Information ◽  
Low Oxygen ◽  
Waterlogging Tolerance ◽  
Cucumis Sativus L ◽  
Waterlogging Stress ◽  
Non Coding Rna

Low oxygen level is a phenomenon often occurring during the cucumber cultivation period. Genes involved in adaptations to stress can be regulated by non-coding RNA. The aim was the identification of long non-coding RNAs (lncRNAs) involved in the response to long-term waterlogging stress in two cucumber haploid lines, i.e., DH2 (waterlogging tolerant—WL-T) and DH4 (waterlogging sensitive—WL-S). Plants, at the juvenile stage, were waterlogged for 7 days (non-primed, 1xH), and after a 14-day recovery period, plants were stressed again for another 7 days (primed, 2xH). Roots were collected for high-throughput RNA sequencing. Implementation of the bioinformatic pipeline made it possible to determine specific lncRNAs for non-primed and primed plants of both accessions, highlighting differential responses to hypoxia stress. In total, 3738 lncRNA molecules were identified. The highest number (1476) of unique lncRNAs was determined for non-primed WL-S plants. Seventy-one lncRNAs were depicted as potentially being involved in acquiring tolerance to hypoxia in cucumber. Understanding the mechanism of gene regulation under long-term waterlogging by lncRNAs and their interactions with miRNAs provides sufficient information in terms of adaptation to the oxygen deprivation in cucumber. To the best of our knowledge, this is the first report concerning the role of lncRNAs in the regulation of long-term waterlogging tolerance by priming application in cucumber.

scholarly journals Identification and Functional Analysis of ThADH1 and ThADH4 Genes Involved in Tolerance to Waterlogging Stress in Taxodium hybrid ‘Zhongshanshan 406’

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 225
Author(s):  
Lei Xuan ◽  
Jianfeng Hua ◽  
Fan Zhang ◽  
Zhiquan Wang ◽  
Xiaoxiao Pei ◽  
...  
Keyword(s):  
Ethanol Metabolism ◽  
Flooding Tolerance ◽  
Transcriptome Data ◽  
Low Oxygen ◽  
Anaerobic Conditions ◽  
Waterlogging Tolerance ◽  
Waterlogging Stress ◽  
Adh Genes ◽  
Oxygen Conditions ◽  
Stems And Leaves

The Taxodium hybrid ‘Zhongshanshan 406’ (T. hybrid ‘Zhongshanshan 406’) [Taxodium mucronatum Tenore × Taxodium distichum (L.). Rich] has an outstanding advantage in flooding tolerance and thus has been widely used in wetland afforestation in China. Alcohol dehydrogenase genes (ADHs) played key roles in ethanol metabolism to maintain energy supply for plants in low-oxygen conditions. Two ADH genes were isolated and characterized—ThADH1 and ThADH4 (GenBank ID: AWL83216 and AWL83217—basing on the transcriptome data of T. hybrid ‘Zhongshanshan 406’ grown under waterlogging stress. Then the functions of these two genes were investigated through transient expression and overexpression. The results showed that the ThADH1 and ThADH4 proteins both fall under ADH III subfamily. ThADH1 was localized in the cytoplasm and nucleus, whereas ThADH4 was only localized in the cytoplasm. The expression of the two genes was stimulated by waterlogging and the expression level in roots was significantly higher than those in stems and leaves. The respective overexpression of ThADH1 and ThADH4 in Populus caused the opposite phenotype, while waterlogging tolerance of the two transgenic Populus significantly improved. Collectively, these results indicated that genes ThADH1 and ThADH4 were involved in the tolerance and adaptation to anaerobic conditions in T. hybrid ‘Zhongshanshan 406’.

scholarly journals Long-Term Waterlogging as Factor Contributing to Hypoxia Stress Tolerance Enhancement in Cucumber: Comparative Transcriptome Analysis of Waterlogging Sensitive and Tolerant Accessions

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 189
Author(s):  
Kinga Kęska ◽  
Michał Wojciech Szcześniak ◽  
Izabela Makałowska ◽  
Małgorzata Czernicka
Keyword(s):  
Stress Tolerance ◽  
De Novo ◽  
Average Length ◽  
Marker Genes ◽  
Long Term Memory ◽  
Low Oxygen ◽  
Waterlogging Tolerance ◽  
Pre Treatment ◽  
Waterlogging Treatment

Waterlogging (WL), excess water in the soil, is a phenomenon often occurring during plant cultivation causing low oxygen levels (hypoxia) in the soil. The aim of this study was to identify candidate genes involved in long-term waterlogging tolerance in cucumber using RNA sequencing. Here, we also determined how waterlogging pre-treatment (priming) influenced long-term memory in WL tolerant (WL-T) and WL sensitive (WL-S) i.e., DH2 and DH4 accessions, respectively. This work uncovered various differentially expressed genes (DEGs) activated in the long-term recovery in both accessions. De novo assembly generated 36,712 transcripts with an average length of 2236 bp. The results revealed that long-term waterlogging had divergent impacts on gene expression in WL-T DH2 and WL-S DH4 cucumber accessions: after 7 days of waterlogging, more DEGs in comparison to control conditions were identified in WL-S DH4 (8927) than in WL-T DH2 (5957). Additionally, 11,619 and 5007 DEGs were identified after a second waterlogging treatment in the WL-S and WL-T accessions, respectively. We identified genes associated with WL in cucumber that were especially related to enhanced glycolysis, adventitious roots development, and amino acid metabolism. qRT-PCR assay for hypoxia marker genes i.e., alcohol dehydrogenase (adh), 1-aminocyclopropane-1-carboxylate oxidase (aco) and long chain acyl-CoA synthetase 6 (lacs6) confirmed differences in response to waterlogging stress between sensitive and tolerant cucumbers and effectiveness of priming to enhance stress tolerance.

scholarly journals Maternal Exposure to High-Fat Diet Induces Long-Term Derepressive Chromatin Marks in the Heart

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 181 ◽  
Author(s):  
Guillaume Blin ◽  
Marjorie Liand ◽  
Claire Mauduit ◽  
Hassib Chehade ◽  
Mohamed Benahmed ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Heart Development ◽  
High Fat Diet ◽  
Target Genes ◽  
Critical Role ◽  
Maternal Exposure ◽  
High Fat ◽  
Cardiac Alterations

Heart diseases are a leading cause of death. While the link between early exposure to nutritional excess and heart disease risk is clear, the molecular mechanisms involved are poorly understood. In the developmental programming field, increasing evidence is pointing out the critical role of epigenetic mechanisms. Among them, polycomb repressive complex 2 (PRC2) and DNA methylation play a critical role in heart development and pathogenesis. In this context, we aimed at evaluating the role of these epigenetic marks in the long-term cardiac alterations induced by early dietary challenge. Using a model of rats exposed to maternal high-fat diet during gestation and lactation, we evaluated cardiac alterations at adulthood. Expression levels of PRC2 components, its histone marks di- and trimethylated histone H3 (H3K27me2/3), associated histone mark (ubiquitinated histone H2A, H2AK119ub1) and target genes were measured by Western blot. Global DNA methylation level and DNA methyl transferase 3B (DNMT3B) protein levels were measured. Maternal high-fat diet decreased H3K27me3, H2Ak119ub1 and DNA methylation levels, down-regulated the enhancer of zeste homolog 2 (EZH2), and DNMT3B expression. The levels of the target genes, isl lim homeobox 1 (Isl1), six homeobox 1 (Six1) and mads box transcription enhancer factor 2, polypeptide C (Mef2c), involved in cardiac pathogenesis were up regulated. Overall, our data suggest that the programming of cardiac alterations by maternal exposure to high-fat diet involves the derepression of pro-fibrotic and pro-hypertrophic genes through the induction of EZH2 and DNMT3B deficiency.

scholarly journals Hematopoietic stem cells fail to regenerate following inflammatory challenge

2020 ◽  
Author(s):  
Ruzhica Bogeska ◽  
Paul Kaschutnig ◽  
Malak Fawaz ◽  
Ana-Matea Mikecin ◽  
Marleen Büchler-Schäff ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Recovery Period ◽  
Cumulative Impact ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Inflammatory Stress ◽  
Kinetics Of

AbstractHematopoietic stem cells (HSCs) are canonically defined by their capacity to maintain the HSC pool via self-renewal divisions. However, accumulating evidence suggests that HSC function is instead preserved by sustaining long-term quiescence. Here, we study the kinetics of HSC recovery in mice, following an inflammatory challenge that induces HSCs to exit dormancy. Repeated inflammatory challenge resulted in a progressive depletion of functional HSCs, with no sign of later recovery. Underlying this observation, label retention experiments demonstrated that self-renewal divisions were absent or extremely rare during challenge, as well as during any subsequent recovery period. While depletion of functional HSCs held no immediate consequences, young mice exposed to inflammatory challenge developed blood and bone marrow hypocellularity in old age, similar to elderly humans. The progressive, irreversible attrition of HSC function demonstrates that discreet instances of inflammatory stress can have an irreversible and therefore cumulative impact on HSC function, even when separated by several months. These findings have important implications for our understanding of the role of inflammation as a mediator of dysfunctional tissue maintenance and regeneration during ageing.

scholarly journals Inhibition of a transcriptional repressor rescues hearing in a splicing factor–deficient mouse

2020 ◽  
Vol 3 (12) ◽  
pp. e202000841
Author(s):  
Yoko Nakano ◽  
Susan Wiechert ◽  
Bernd Fritzsch ◽  
Botond Bánfi
Keyword(s):  
Alternative Splicing ◽  
Target Genes ◽  
Transcriptional Repressor ◽  
Dominant Negative ◽  
Splicing Factor ◽  
Loss Of Function ◽  
Transgenic Expression ◽  
Mechanosensory Hair Cells

In mechanosensory hair cells (HCs) of the ear, the transcriptional repressor REST is continuously inactivated by alternative splicing of its pre-mRNA. This mechanism of REST inactivation is crucial for hearing in humans and mice. Rest is one of many pre-mRNAs whose alternative splicing is regulated by the splicing factor SRRM4; Srrm4 loss-of-function mutation in mice (Srrm4bv/bv) causes deafness, balance defects, and degeneration of all HC types other than the outer HCs (OHCs). The specific splicing alterations that drive HC degeneration in Srrm4bv/bv mice are unknown, and the mechanism underlying SRRM4-independent survival of OHCs is undefined. Here, we show that transgenic expression of a dominant-negative REST fragment in Srrm4bv/bv mice is sufficient for long-term rescue of hearing, balancing, HCs, alternative splicing of Rest, and expression of REST target genes including the Srrm4 paralog Srrm3. We also show that in HCs, SRRM3 regulates many of the same exons as SRRM4; OHCs are unique among HCs in that they transiently down-regulate Rest transcription as they mature to express Srrm3 independently of SRRM4; and simultaneous SRRM4–SRRM3 deficiency causes complete HC loss by preventing inactivation of REST in all HCs. Thus, our data reveal that REST inactivation is the primary and essential role of SRRM4 in the ear, and that OHCs differ from other HCs in the SRRM4-independent expression of the functionally SRRM4-like splicing factor SRRM3.

Defining the waterlogging tolerance of Ornithopus spp. for the temperate pasture zone of southern Australia

2020 ◽  
Vol 71 (5) ◽  
pp. 506
Author(s):  
D. R. Kidd ◽  
C. E. Di Bella ◽  
L. Kotula ◽  
T. D. Colmer ◽  
M. H. Ryan ◽  
...  
Keyword(s):  
Nutrient Solution ◽  
Tissue Concentration ◽  
Recovery Period ◽  
Dry Mass ◽  
Waterlogging Tolerance ◽  
Root Porosity ◽  
High Rainfall ◽  
Productivity Losses ◽  
Pasture Legumes

Increasing the area sown to Ornithopus spp. (serradella) can reduce overall fertiliser requirements in Australian permanent pastures owing to their greater nutrient-acquisition efficiency than that of more widely used pasture legumes such as Trifolium spp. However, uncertainty regarding waterlogging tolerance of Ornithopus spp. may restrict their adoption in the high-rainfall zone of southern Australia. The waterlogging tolerance of cultivars and accessions of three species of Ornithopus (O. compressus, O. sativus and O. pinnatus) was determined by comparing root and shoot growth of plants in deoxygenated, stagnant agar nutrient solution (simulated waterlogging) with growth in aerated nutrient solution. The responses were benchmarked against the known waterlogging-tolerant pasture legume Trifolium michelianum. All Ornithopus cultivars were highly impacted by the deoxygenated stagnant treatment, including those of the anecdotally waterlogging-tolerant O. pinnatus. The 14-day stagnant treatment reduced root dry mass by 32–62% and relative growth rate (RGR) of roots by 36–73%. At the same time, root porosity increased from 1.4% to 8.8%. Following a 14-day recovery period, during which plants were returned to aerated nutrient solution, Ornithopus spp. failed to increase their shoot RGR (particularly for O. sativus cultivars); however, root RGR returned to that of the aerated controls. The stagnant conditions inhibited transport of potassium (K+) to the shoots in all species, as evidenced by lower shoot tissue K+ concentrations, with O. compressus and O. sativus most adversely affected (45% and 48% of the tissue concentration of aerated control plants). We conclude that the suggested area for Ornithopus spp. adaptation should not preclude areas of high rainfall because they have root adaptations that would assist them in coping with transient water excess; however, soil types and surface profiles conducive to long-term waterlogging should be avoided to negate significant productivity losses.

Involvement of Transcriptional Mediator Subunit TRAP220/MED1 in Action of Niche Cells to Support Hematopoietic Stem/Progenitor Cells

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3581-3581
Author(s):  
Kana Inoue ◽  
Akiko Sumitomo ◽  
Natsumi Hasegawa ◽  
Ayuko Kasai ◽  
Kenji Yonezawa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Synthesis ◽  
Progenitor Cells ◽  
Target Genes ◽  
Bone Marrow Cells ◽  
Live Cells ◽  
Hematopoietic Stem ◽  
Marrow Cells

Abstract The mammalian TRAP/Mediator complex is a master transcriptional regulatory complex that integrates signals of diverse activators and recruits RNA polymerase II and other general factors to activate transcription. The TRAP220/MED1 subunit was originally identified as a ligand-dependent coactivator specific for nuclear receptors. We have previously shown through biochemical and mouse genetic studies that MED1 is essential for embryogenesis, cell growth/differentiation and homeostasis, and that it stimulates nuclear receptor-mediated myelomonopoiesis. MED1 also integrates other activators such as GATA-1 and C/EBPβ and appears to mediate erythropoiesis as well. The niche cells in the bone marrow plays a pivotal role in the maintenance of hematopoietic stem/progenitor cells (HSPCs). In this study, we employed mouse embryonic fibroblasts (MEFs) as a model to analyze the role of MED1 in the niche, since MEFs have a mesenchymal feature with the osteoblastic precursor lineage and are known to support HSPCs. To establish an experimental system, we crossed Med1 and p53 double knockouts to obtain Med1+/+/p53−/− and Med1−/−/p53−/− E10.0 embryos from a single female and prepared stable MEF lines. Then the Med1−/−/p53−/− MEFs were stably transfected with a MED1 expression vector (Rev-Med1−/− MEFs) or a control empty vector. When normal mouse bone marrow cells were cocultured with these MEFs treated with mitomycin C for a short period of 2 weeks, cell counts, live cells (MTT assay) and a DNA synthesis (BrdU incorporation) of marrow cells were measured. The number of live cells as well as DNA synthesis on Med1−/− MEFs was significantly decreased during this period, but those on Rev-Med1−/− MEFs recovered to the control levels. Thus the growth stress on MEFs appears to be attenuated on Med1−/− MEFs. When apoptosis of the marrow cells was measured, both the FITC-dUTP incorporation by TdT and annexin V/PI double positive cells were lower for Med1−/− MEFs, indicating that apoptosis was also attenuated. We next assessed the role of MED1 in MEFs to support long-term bone marrow culture. After bone marrow cells were cultured on mitomycin C-treated MEFs for 8 weeks in Myelocult M5300 (StemCell Technologies) or IMDM supplemented with BIT9500 (StemCell Technologies) and LDL, progenitor cells (adherent and nonadherent) were collected and cultured in complete methylcellulose (Methocult M3434; StemCell Technologies), and colonies were counted. The number of both myeloid and erythroid colonies were significantly attenuated (0 to 40% depending on experimental conditions) for cells on Med1−/− MEFs, but colonies for cells cultured on Rev-Med1−/− MEFs recovered to the control level. In order to exclude the possibility that lot differences among MEFs or p53 depletion might have affected the results, we next prepared primary Med1+/+ and Med1−/− MEFs by crossing Med1+/− mice and conducted the long-term culture experiments using these MEFs. The attenuated number of colonies for cells cocultured with Med1−/− MEFs (circa 10% of the control) was reproduced repeatedly, indicating that the observed role of MED1 in MEFs to support HSPCs is intrinsic. Since MED1 converges signals from a series of activators on specific promoters and activates transcription, one or some products of the downstream target genes in MEFs may be responsible for the observed activity to maintain HSPCs. In search for candidate MED1 target gene products among a series of known molecules that possess an activity on HSPCs, only the expression of osteopontin was found to be attenuated in Med1−/− MEFs and reverted in Rev-Med1−/− MEFs. Other factors including Angiopoietin-1 and Jagged-1 were comparable. This fact contrasts with the previous observation of osteopontin knockouts where the null niche cells that restricted the size of HSPC number overexpressed these factors. We next assessed the role of MED1 on the osteopontin promoter. We focused on vitamin D receptor (VDR) and Runx2 among the activators and tested MEFs by luciferase reporter assays. The basal level of transcription without any activators in Med1−/− MEFs was about half of the control. Moreover, both the activation by Runx2 and the liganddependent VDR function were significantly attenuated in Med1−/− MEFs. These results indicate that transcriptional coactivator MED1 in niche cells plays an important role in HSPCs support, and that osteopontin may be one of the downstream candidate target genes for MED1.

scholarly journals Obesity, leptin, and deregulation of microRNA in lipid metabolisms: their contribution to breast cancer prognosis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Kartika W. Taroeno-Hariadi ◽  
Mardiah S. Hardianti ◽  
Hemi Sinorita ◽  
Teguh Aryandono
Keyword(s):  
Breast Cancer ◽  
Metabolic Syndrome ◽  
Target Genes ◽  
Breast Cancer Prognosis ◽  
Cancer Prognosis ◽  
Regulate Gene Expression ◽  
Non Coding Rna ◽  
Post Menopause ◽  
Points Of View

AbstractObesity and Metabolic Syndrome have been associated with cardiovascular, diabetes and cancer incidence. Obesity is a state of inflammation. There are cross-talks between adipocyte, adipokines, pro-inflammatory cytokines, insulin, leptin, and other growth factors to initiate signals for proliferation, anti-apoptosis, and angiogenesis. Those networks lead to cancer initiation, promotion, progression, and metastasis. Post menopause women with breast cancer commonly have overweight, obesity, and metabolic syndrome, which are previously reported as conditions to be associated with breast cancer prognosis. MicroRNAs (miRNAs), small non-coding RNA that regulate gene expression, are known to play important roles either in metabolic or carcinogenesis process in patients with breast cancer. Some miRNAs expressions are deregulated in persons either with obesity, breast cancer, or breast cancer with co-morbid obesity. This literature review aimed at reviewing recent publications on the role of obesity, leptin, and microRNA deregulation in adverse prognosis of breast cancer. Understanding the influence of deregulated miRNAs and their target genes in patients with breast cancer and obesity will direct more studies to explore the potential prognostic role of obesity in breast cancer from epigenetic points of view.

scholarly journals GPER1 and microRNA: Two Players in Breast Cancer Progression

2020 ◽  
Vol 22 (1) ◽  
pp. 98
Author(s):  
Adele Vivacqua
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Target Genes ◽  
Current Knowledge ◽  
Breast Cancer Progression ◽  
Non Coding Rna ◽  
Anti Cancer ◽  
G Protein Coupled ◽  
Breast Tumor Progression

Breast cancer is the main cause of morbidity and mortality in women worldwide. However, the molecular pathogenesis of breast cancer remains poorly defined due to its heterogeneity. Several studies have reported that G Protein-Coupled Estrogen Receptor 1 (GPER1) plays a crucial role in breast cancer progression, by binding to estrogens or synthetic agonists, like G-1, thus modulating genes involved in diverse biological events, such as cell proliferation, migration, apoptosis, and metastasis. In addition, it has been established that the dysregulation of short sequences of non-coding RNA, named microRNAs (miRNAs), is involved in various pathophysiological conditions, including breast cancer. Recent evidence has indicated that estrogens may regulate miRNA expression and therefore modulate the levels of their target genes, not only through the classical estrogen receptors (ERs), but also activating GPER1 signalling, hence suggesting an alternative molecular pathway involved in breast tumor progression. Here, the current knowledge about GPER1 and miRNA action in breast cancer is recapitulated, reporting recent evidence on the liaison of these two players in triggering breast tumorogenic effects. Elucidating the role of GPER1 and miRNAs in breast cancer might provide new tools for innovative approaches in anti-cancer therapy.

The human Ah receptor: hints from dioxin toxicities to deregulated target genes and physiological functions

2013 ◽  
Vol 394 (6) ◽  
pp. 729-739 ◽  
Author(s):  
Karl Walter Bock
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Target Genes ◽  
Intestinal Inflammation ◽  
Ah Receptor ◽  
Physiological Functions ◽  
Interleukin 22 ◽  
Transient Activation ◽  
Dioxin Toxicity

Abstract Marked species differences of dioxin toxicity prompted the review of three well-studied human dioxin toxicities (chloracne, inflammation and cancer) and deregulated Ah receptor (AhR) target genes to obtain hints as to the physiological functions of this receptor. Dioxin here stands for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Microarray analysis of dermal cysts from a dioxin-poisoned patient revealed, in addition to induced CYP1A1, increased expression of gremlin, an antagonist of bone morphogenetic proteins. Dioxin-mediated skin and intestinal inflammation is associated with deregulated T cell differentiation. In the supernatant of CD4+ T cells obtained from the dioxin-poisoned patient, increased interleukin-22 was detected, a cytokine that may be controlled in part by AhR-regulated Notch. Cancer is one of the long-term consequences of chronic inflammation. In line with dioxin-sensitive lymphoid tissue, enhanced death of lymphoid cancer was observed in the dioxin-exposed Seveso population 25 years after poisoning. Accumulating evidence suggests that endogenous AhR ligands, notably the tryptophan photoproduct 6-formylindolo[3,2-b]carbazole, in contrast to TCDD, is rapidly metabolized by AhR-induced CYP1A1. The feedback loop between 6-formylindolo[3,2-b]carbazole, AhR and CYP1A1 guarantees transient activation that, in contrast to sustained activation by TCDD, may be essential for a putative role of the AhR in stem/progenitor cell homeostasis.

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