scholarly journals Comprehensive Mechanism of Gene Silencing and Its Role in Plant Growth and Development

2021 ◽  
Vol 12 ◽  
Author(s):  
Ahmed H. El-Sappah ◽  
Kuan Yan ◽  
Qiulan Huang ◽  
Md. Monirul Islam ◽  
Quanzi Li ◽  
...  

Gene silencing is a negative feedback mechanism that regulates gene expression to define cell fate and also regulates metabolism and gene expression throughout the life of an organism. In plants, gene silencing occurs via transcriptional gene silencing (TGS) and post-transcriptional gene silencing (PTGS). TGS obscures transcription via the methylation of 5′ untranslated region (5′UTR), whereas PTGS causes the methylation of a coding region to result in transcript degradation. In this review, we summarized the history and molecular mechanisms of gene silencing and underlined its specific role in plant growth and crop production.

2020 ◽  
Vol 13 (1) ◽  
pp. 294
Author(s):  
Khadija Nawaz ◽  
Rimsha Chaudhary ◽  
Ayesha Sarwar ◽  
Bushra Ahmad ◽  
Asma Gul ◽  
...  

Melatonin, a multifunctional signaling molecule, is ubiquitously distributed in different parts of a plant and responsible for stimulating several physiochemical responses against adverse environmental conditions in various plant systems. Melatonin acts as an indoleamine neurotransmitter and is primarily considered as an antioxidant agent that can control reactive oxygen and nitrogen species in plants. Melatonin, being a signaling agent, induces several specific physiological responses in plants that might serve to enhance photosynthesis, growth, carbon fixation, rooting, seed germination and defense against several biotic and abiotic stressors. It also works as an important modulator of gene expression related to plant hormones such as in the metabolism of indole-3-acetic acid, cytokinin, ethylene, gibberellin and auxin carrier proteins. Additionally, the regulation of stress-specific genes and the activation of pathogenesis-related protein and antioxidant enzyme genes under stress conditions make it a more versatile molecule. Because of the diversity of action of melatonin, its role in plant growth, development, behavior and regulation of gene expression it is a plant’s master regulator. This review outlines the main functions of melatonin in the physiology, growth, development and regulation of higher plants. Its role as anti-stressor agent against various abiotic stressors, such as drought, salinity, temperatures, UV radiation and toxic chemicals, is also analyzed critically. Additionally, we have also identified many new aspects where melatonin may have possible roles in plants, for example, its function in improving the storage life and quality of fruits and vegetables, which can be useful in enhancing the environmentally friendly crop production and ensuring food safety.


Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1887
Author(s):  
Inbal Dagan ◽  
Raz Palty

Calcium (Ca2+) signaling plays a dichotomous role in cellular biology, controlling cell survival and proliferation on the one hand and cellular toxicity and cell death on the other. Store-operated Ca2+ entry (SOCE) by CRAC channels represents a major pathway for Ca2+ entry in non-excitable cells. The CRAC channel has two key components, the endoplasmic reticulum Ca2+ sensor stromal interaction molecule (STIM) and the plasma-membrane Ca2+ channel Orai. Physical coupling between STIM and Orai opens the CRAC channel and the resulting Ca2+ flux is regulated by a negative feedback mechanism of slow Ca2+ dependent inactivation (SCDI). The identification of the SOCE-associated regulatory factor (SARAF) and investigations of its role in SCDI have led to new functional and molecular insights into how SOCE is controlled. In this review, we provide an overview of the functional and molecular mechanisms underlying SCDI and discuss how the interaction between SARAF, STIM1, and Orai1 shapes Ca2+ signaling in cells.


2010 ◽  
Vol 38 (4) ◽  
pp. 1144-1149 ◽  
Author(s):  
Andreas Werner ◽  
Daniel Swan

NATs (natural antisense transcripts) are important regulators of eukaryotic gene expression. Interference between the expression of protein-coding sense transcripts and the corresponding NAT is well documented. In the present review, we focus on an additional, higher-order role of NATs that is currently emerging. The recent discovery of endogenous siRNAs (short interfering RNAs), as well as NAT-induced transcriptional gene silencing, are key to the proposed novel function of NATs.


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 5266-5266
Author(s):  
Michael Koldehoff ◽  
Nina K. Steckel ◽  
Rudolf Trenschel ◽  
Dietrich W. Beelen ◽  
Ahmet H. Elmaagacli

Abstract Multiple myeloma (MM) is a clonal B-cell malignancy characterized by the accumulation of malignant plasma cells within the bone marrow (BM). Vascular endothelial growth factor (VEGF), a glycoprotein produced by normal and neoplastic cells is an important regulator of physiological and pathological angiogenesis. MM cells secrete VEGF, which promotes production of cytokines in bone marrow stromal cells, as well as migration and proliferation of the tumor cells. Inhibition of VEGF activity or disabling the function of its receptors has been shown to inhibit both tumor growth and spread of metastases in a variety of animal tumor models. RNA interference (RNAi) is rapidly being established as a post-transcriptional gene silencing method and holds promise to specifically inhibit gene expression in mammals. Another novel class of antitumor agents is based on the inhibition of the ubiquitin-proteosomal system which represents the major nonlysosomal pathway through which intracellular proteins are degraded in eukaryotic cells. Bortezomib, a reversible proteosome inhibitor, shows remarkable anticancer activity in various malignant cell types, including MM cells that are resistant to conventional therapies. We studied the effect of transfection with small interfering RNA (siRNA) targeting VEGF in MM cells in terms of proliferation, induction of apoptosis, and cell differentiation. Further, we evaluated if the effects of post-transcriptional gene silencing by VEGF specific siRNA can be augmented by bortezomib and/or steroids in the cell line OPM-2. A mean reduction of VEGF gene expression to 38% as determined by real-time PCR was observed with 0.8 ug VEGF siRNA in OPM-2 cells compared to controls (controls were set up to 100%). Simultaneous administration of bortezomib and siRNA was able to reduce VEGF gene expression down to 23% compared to VEGF siRNA alone demonstrating a synergistic effect of combined bortezomib and siRNA treatment. We found a 2.5-fold increase in induced apoptosis in OPM-2 cells subsequent to VEGF siRNA administration but we saw no additional stimulation of apoptosis after combination of VEGF siRNA with bortezomib and/or steroids. Proliferation in OPM-2 cells was strongly inhibited (about 91%) following combination treatment as opposed to only 62% after administration of VEGF siRNA alone. The transfection of VEGF siRNA in OPM-2 cells had no influence on the expression levels of differentiation markers such as CD38, CD138, CD19, CD34, CD45, and CD7AAD. Our findings suggest that synergistic effects of VEGF siRNA with bortezomib and dexamethason may offer new therapeutic options in the treatment of MM.


2019 ◽  
Author(s):  
Ruihong Wang ◽  
Hongbo Guo ◽  
Juane Dong

Abstract Background: Our previous study found that male sterility in Salvia miltiorrhiza could result in stunted growth, decrease biomass, inhibit primary metabolism, and promote secondary metabolism, but their molecular mechanisms have not yet been elucidated. In this article, we investigated the underlying mechanism of plant growth and metabolism by using physiological analysis and mRNA sequencing (RNA-Seq). Results: In this study, transcriptomic and physiological analyses were performed to identify the effect on plant growth and metabolic production in male sterile mutants. Through GO and KEGG analysis it was found that the pathways were mainly enriched in processes including organ development, primary metabolic process and secondary metabolic process. Physiological analyses showed that the chloroplast structure of male sterile mutants of Salvia miltiorrhiza was abnormally developed, which could result in decrease in leaf gas exchange (A, E and gs), chlorophyll fluorescence (Fv, Fm and Fv/Fm), and the chlorophyll content. Transcriptomic analyses indicated that disproportionating enzyme 1 (DPE1) catalyzed the degradation of starch, while sucrose synthase 3 (SUS3) and cytosolic invertase 2 (CINV2) catalyzed the degradation of sucrose in S. miltiorrhiza. The results suggested that phenylalanine ammonialyase (PAL) played an important role in the biosynthesis of rosmarinic acid and salvianolic acid B, and flavone synthase (FLS) was an important enzyme catalyzing steps of flavonoid biosynthesis. High expression level of these enzyme genes in male sterile mutants resulted in high content of secondary metabolites. Conclusions: Our results from the physiological and transcriptome analyses reveal underlying mechanism of plant growth and metabolism in male sterile mutants, and provide insight into the crop production of S. miltiorrhiza.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Imke Kirste ◽  
Tilanthi M Jayawardena ◽  
J. A Payne ◽  
Victor J Dzau ◽  
Maria Mirotsou

Rationale: Regeneration of damaged cardiac tissue after injury presents a daunting challenge in cardiovascular medicine. Recent developments in reprogramming of somatic cells directly to cells of other lineages have raised the possibility of using this approach for cardiac regenerative therapy. Our group recently demonstrated successful miRNA mediated cardiac reprogramming in vitro and in vivo using a combination of miRNAs 1, 133, 206 and 499. Although, the molecular mechanisms underlying miRNA mediated fibroblast reprogramming to cardiomyocytes are yet unknown, accumulating evidence suggest that reprogramming acts through distinct phases and that histone modifications play an important role in these processes. Objective: Identify key genes involved in initiating miRNA mediated reprogramming via histone modifications. Methods and Results: For this, we analyzed the expression levels of 81 different genes involved in chromatin modification 4 days after miRNA transfection using PCR arrays. This analysis revealed that 6 of the 81 tested genes showed differential gene expression (≤-1.5-fold and p <0.02). JAK inhibitor-1 treatment, known for increasing reprogramming efficiency, further enhanced gene expression changes in 5 of these 6 genes. Setdb2, an H3K9 methyltransferase, was one of the most down-regulated targets 4 days after miRNA transfection (-1.4 fold, p<0.001). This effect was enhanced further when miRNAs were combined with the JAK inhibitor-1 (-2.6 fold, p<0.001). Silencing of Setdb2 using siRNAs further accentuated miRNA cardiac reprogramming as measured by cardiac transcription factor expression at 3 days and 6 days post treatment. Similar trends were observed by FACS analysis detecting increased percentage of αMHC-positive cells in siRNA treated fibroblasts compared to control treated only with the miRNA combination. Interestingly, our data showed that Setdb2 silencing alone was sufficient to initiate cardiac reprogramming, suggesting that Setdb2 might play a crucial role in defining cardiac cell fate. Conclusion: In conclusion our results indicate that Setdb2 down-regulation plays an important role in the direct reprogramming of fibroblasts to cardiomyocyte-like cells.


2014 ◽  
Author(s):  
Qingxin Song ◽  
Xueying Guan ◽  
Z. Jeffrey Chen

Cotton is the largest source of renewable textile fiber and a successful model of transgenic applications in crop production. However, improving cotton production using fiber-related transgenes is somewhat difficult. This is probably related to unique epigenetic and gene expression changes during fiber development. Here we show that inhibiting DNA methylation impairs fiber development. Genome-wide methylcytosine-, mRNA-, and small RNA-sequencing analyses reveal minor changes in CG and CHG methylation and distinct changes in CHH methylation among different tissues. In ovules CHH hypermethyaltion is associated with small RNA-directed DNA methylation (RdDM) and expression changes of nearby genes in euchromatin. Remarkably, ovule-derived fiber cells not only maintain euchromatic CHH methylation, but also generate additional heterochromatic CHH hypermethylation independent of RdDM, which represses transposable elements (TEs) and nearby genes including fiber-related genes. Furthermore, DNA methylation contributes to the expression bias of homoeologous genes in ovules and fibers. This spatiotemporal DNA methylation in promoters could act as a double-lock feedback mechanism to regulate TE and gene expression, which could be translated into genomic and biotechnological improvement of agronomic traits.


2015 ◽  
Vol 112 (32) ◽  
pp. 10026-10031 ◽  
Author(s):  
Han L. Tan ◽  
Bridget N. Queenan ◽  
Richard L. Huganir

Homeostatic plasticity is a negative feedback mechanism that stabilizes neurons during periods of perturbed activity. The best-studied form of homeostatic plasticity in the central nervous system is the scaling of excitatory synapses. Postsynaptic AMPA-type glutamate receptors (AMPARs) can be inserted into synapses to compensate for neuronal inactivity or removed to compensate for hyperactivity. However, the molecular mechanisms underlying the homeostatic regulation of AMPARs remain elusive. Here, we show that the expression of GRIP1, a multi-PDZ (postsynaptic density 95/discs large/zona occludens) domain AMPAR-binding protein, is bidirectionally altered by neuronal activity. Furthermore, we observe a subcellular redistribution of GRIP1 and a change in the binding of GRIP1 to GluA2 during synaptic scaling. Using a combination of biochemical, genetic, and electrophysiological methods, we find that loss of GRIP1 blocks the accumulation of surface AMPARs and the scaling up of synaptic strength that occur in response to chronic activity blockade. Collectively, our data point to an essential role of GRIP1-mediated AMPAR trafficking during inactivity-induced synaptic scaling.


2011 ◽  
Vol 208 (10) ◽  
pp. 1963-1976 ◽  
Author(s):  
Patrick Viatour ◽  
Ursula Ehmer ◽  
Louis A. Saddic ◽  
Craig Dorrell ◽  
Jesper B. Andersen ◽  
...  

Hepatocellular carcinoma (HCC) is the third cancer killer worldwide with &gt;600,000 deaths every year. Although the major risk factors are known, therapeutic options in patients remain limited in part because of our incomplete understanding of the cellular and molecular mechanisms influencing HCC development. Evidence indicates that the retinoblastoma (RB) pathway is functionally inactivated in most cases of HCC by genetic, epigenetic, and/or viral mechanisms. To investigate the functional relevance of this observation, we inactivated the RB pathway in the liver of adult mice by deleting the three members of the Rb (Rb1) gene family: Rb, p107, and p130. Rb family triple knockout mice develop liver tumors with histopathological features and gene expression profiles similar to human HCC. In this mouse model, cancer initiation is associated with the specific expansion of populations of liver stem/progenitor cells, indicating that the RB pathway may prevent HCC development by maintaining the quiescence of adult liver progenitor cells. In addition, we show that during tumor progression, activation of the Notch pathway via E2F transcription factors serves as a negative feedback mechanism to slow HCC growth. The level of Notch activity is also able to predict survival of HCC patients, suggesting novel means to diagnose and treat HCC.


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