scholarly journals The Control of Developmental Phase Transitions by microRNAs and Their Targets in Seed Plants

2020 ◽  
Vol 21 (6) ◽  
pp. 1971
Author(s):  
Jingyi Ma ◽  
Pan Zhao ◽  
Shibiao Liu ◽  
Qi Yang ◽  
Huihong Guo
Keyword(s):  
Phase Transitions ◽  
Target Genes ◽  
Seed Plants ◽  
Transcriptional Level ◽  
Developmental Phase ◽  
Tissue Formation ◽  
Research Directions ◽  
Developmental Transitions ◽  
Organ Tissue ◽  
Cumulative Evidence

Seed plants usually undergo various developmental phase transitions throughout their lifespan, mainly including juvenile-to-adult and vegetative-to-reproductive transitions, as well as developmental transitions within organ/tissue formation. MicroRNAs (miRNAs), as a class of small endogenous non-coding RNAs, are involved in the developmental phase transitions in plants by negatively regulating the expression of their target genes at the post-transcriptional level. In recent years, cumulative evidence has revealed that five miRNAs, miR156, miR159, miR166, miR172, and miR396, are key regulators of developmental phase transitions in plants. In this review, the advanced progress of the five miRNAs and their targets in regulating plant developmental transitions, especially in storage organ formation, are summarized and discussed, combining our own findings with the literature. In general, the functions of the five miRNAs and their targets are relatively conserved, but their functional divergences also emerge to some extent. In addition, potential research directions of miRNAs in regulating plant developmental phase transitions are prospected.

Exogenous application of RNAs as a silencing tool for discovering gene function.

2021 ◽  
pp. 14-24
Author(s):  
Barbara Molesini ◽  
Tiziana Pandolfini
Keyword(s):  
Gene Expression ◽  
Gene Function ◽  
Rna Silencing ◽  
Target Genes ◽  
Specific Gene ◽  
Transcriptional Level ◽  
Fruit Setting ◽  
Organ Tissue ◽  
Specific Regulation ◽  
Time Specific

Abstract This chapter focuses on the importance of the RNA silencing technique in unraveling the function of genes by inhibiting gene expression at the post-transcriptional level, and is particularly appropriate for studying developmental processes such as fruit setting and growth that require a tight organ/tissue and time-specific regulation of the expression of target genes. Some methods used for establishing the function of a specific gene altering gene expression at either the genomic or post-transcriptional level are also presented.

The search of CAR, AhR, ESRs binding sites in promoters of intronic and intergenic microRNAs

2018 ◽  
Vol 16 (01) ◽  
pp. 1750029 ◽  
Author(s):  
Vladimir Y. Ovchinnikov ◽  
Denis V. Antonets ◽  
Lyudmila F. Gulyaeva
Keyword(s):  
Transcriptional Activation ◽  
Binding Sites ◽  
In Silico ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Regulation Of Gene Expression ◽  
Experimental Studies ◽  
Transcriptional Level ◽  
Aryl Hydrocarbon ◽  
Exogenous Compounds

MicroRNAs (miRNAs) play important roles in the regulation of gene expression at the post-transcriptional level. Many exogenous compounds or xenobiotics may affect microRNA expression. It is a well-established fact that xenobiotics with planar structure like TCDD, benzo(a)pyrene (BP) can bind aryl hydrocarbon receptor (AhR) followed by its nuclear translocation and transcriptional activation of target genes. Another chemically diverse group of xenobiotics including phenobarbital, DDT, can activate the nuclear receptor CAR and in some cases estrogen receptors ESR1 and ESR2. We hypothesized that such chemicals can affect miRNA expression through the activation of AHR, CAR, and ESRs. To prove this statement, we used in silico methods to find DRE, PBEM, ERE potential binding sites for these receptors, respectively. We have predicted AhR, CAR, and ESRs binding sites in 224 rat, 201 mouse, and 232 human promoters of miRNA-coding genes. In addition, we have identified a number of miRNAs with predicted AhR, CAR, and ESRs binding sites that are known as oncogenes and as tumor suppressors. Our results, obtained in silico, open a new strategy for ongoing experimental studies and will contribute to further investigation of epigenetic mechanisms of carcinogenesis.

Drugs used to treat bipolar disorder act via microRNAs to regulate expression of genes involved in neurite outgrowth

2020 ◽  
Vol 34 (3) ◽  
pp. 370-379 ◽  
Author(s):  
Srisaiyini Kidnapillai ◽  
Ben Wade ◽  
Chiara C Bortolasci ◽  
Bruna Panizzutti ◽  
Briana Spolding ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Neurite Outgrowth ◽  
Neural Plasticity ◽  
Drug Combination ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Drug Effects ◽  
Differentially Expressed ◽  
Transcriptional Level ◽  
Expression Of Genes

Background: The drugs commonly used to treat bipolar disorder have limited efficacy and drug discovery is hampered by the paucity of knowledge of the pathophysiology of this disease. This study aims to explore the role of microRNAs in bipolar disorder and understand the molecular mechanisms of action of commonly used bipolar disorder drugs. Methods: The transcriptional effects of bipolar disorder drug combination (lithium, valproate, lamotrigine and quetiapine) in cultured human neuronal cells were studied using next generation sequencing. Differential expression of genes ( n=20) and microRNAs ( n=6) was assessed and the differentially expressed microRNAs were confirmed with TaqMan MicroRNA Assays. The expression of the differentially expressed microRNAs were inhibited to determine bipolar disorder drug effects on their target genes ( n=8). Independent samples t-test was used for normally distributed data and Kruskal-Wallis/Mann-Whitney U test was used for data not distributed normally. Significance levels were set at p<0.05. Results: We found that bipolar disorder drugs tended to increase the expression of miR-128 and miR-378 ( p<0.05). Putative target genes of these microRNAs targeted pathways including those identified as “neuron projection development” and “axonogenesis”. Many of the target genes are inhibitors of neurite outgrowth and neurogenesis and were downregulated following bipolar disorder drug combination treatment (all p<0.05). The bipolar disorder drug combination tended to decrease the expression of the target genes ( NOVA1, GRIN3A, and VIM), however this effect could be reversed by the application of microRNA inhibitors. Conclusions: We conclude that at a transcriptional level, bipolar disorder drugs affect several genes in concert that would increase neurite outgrowth and neurogenesis and hence neural plasticity, and that this effect is mediated (at least in part) by modulation of the expression of these two key microRNAs.

Circular RNAs as microRNA sponges: evidence and controversies

2021 ◽  
Author(s):  
Morten T. Jarlstad Olesen ◽  
Lasse S. Kristensen
Keyword(s):  
Gene Regulation ◽  
Target Genes ◽  
Research Field ◽  
Circular Rnas ◽  
Transcriptional Level ◽  
Additional Layer ◽  
Complex Process ◽  
Non Coding Rnas ◽  
New Research ◽  
Microrna Sponges

Abstract Gene expression in eukaryotic cells is a complex process encompassing several layers of regulation at the transcriptional and post-transcriptional levels. At the post-transcriptional level, microRNAs (miRs) are key regulatory molecules that function by binding directly to mRNAs. This generally leads to less efficient translation of the target mRNAs. More recently, an additional layer of gene regulation has been discovered, as other molecules, including circular RNAs (circRNAs), may bind to miRs and thereby function as sponges or decoys resulting in increased expression of the corresponding miR target genes. The circRNAs constitute a large class of mainly non-coding RNAs, which have been extensively studied in recent years, in particular in the cancer research field where many circRNAs have been proposed to function as miR sponges. Here, we briefly describe miR-mediated gene regulation and the extra layer of regulation that is imposed by the circRNAs. We describe techniques and methodologies that are commonly used to investigate potential miR sponging properties of circRNAs and discuss major pitfalls and controversies within this relatively new research field.

scholarly journals Regulatory Mechanism of MicroRNA Expression in Cancer

2020 ◽  
Vol 21 (5) ◽  
pp. 1723 ◽  
Author(s):  
Zainab Ali Syeda ◽  
Siu Semar Saratu’ Langden ◽  
Choijamts Munkhzul ◽  
Mihye Lee ◽  
Su Jung Song
Keyword(s):  
Molecular Mechanism ◽  
Mirna Expression ◽  
Messenger Rna ◽  
Target Genes ◽  
Regulatory Mechanism ◽  
Physiological Role ◽  
Mirna Biogenesis ◽  
Transcriptional Level ◽  
Detailed Knowledge ◽  
Cancer Pathogenesis

Altered gene expression is the primary molecular mechanism responsible for the pathological processes of human diseases, including cancer. MicroRNAs (miRNAs) are virtually involved at the post-transcriptional level and bind to 3′ UTR of their target messenger RNA (mRNA) to suppress expression. Dysfunction of miRNAs disturbs expression of oncogenic or tumor-suppressive target genes, which is implicated in cancer pathogenesis. As such, a large number of miRNAs have been found to be downregulated or upregulated in human cancers and to function as oncomiRs or oncosuppressor miRs. Notably, the molecular mechanism underlying the dysregulation of miRNA expression in cancer has been recently uncovered. The genetic deletion or amplification and epigenetic methylation of miRNA genomic loci and the transcription factor-mediated regulation of primary miRNA often alter the landscape of miRNA expression in cancer. Dysregulation of the multiple processing steps in mature miRNA biogenesis can also cause alterations in miRNA expression in cancer. Detailed knowledge of the regulatory mechanism of miRNAs in cancer is essential for understanding its physiological role and the implications of cancer-associated dysfunction and dysregulation. In this review, we elucidate how miRNA expression is deregulated in cancer, paying particular attention to the cancer-associated transcriptional and post-transcriptional factors that execute miRNA programs.

scholarly journals Cross-Kingdom Regulation by Plant microRNAs Provides Novel Insight into Gene Regulation

2020 ◽  
Author(s):  
Abdul Fatah A Samad ◽  
Mohd Farizal Kamaroddin ◽  
Muhammad Sajad
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Current Knowledge ◽  
Circulatory System ◽  
Dietary Therapy ◽  
Transcriptional Level ◽  
Plant Mirnas ◽  
Health Issues ◽  
Plant Mirna ◽  
Potential Applications

ABSTRACT microRNAs (miRNAs) are well known as major players in mammalian and plant genetic systems that act by regulating gene expression at the post-transcriptional level. These tiny molecules can regulate target genes (mRNAs) through either cleavage or translational inhibition. Recently, the discovery of plant-derived miRNAs showing cross-kingdom abilities to regulate mammalian gene expression has prompted exciting discussions among researchers. After being acquired orally through the diet, plant miRNAs can survive in the digestive tract, enter the circulatory system, and regulate endogenous mRNAs. Here, we review current knowledge regarding the cross-kingdom mechanisms of plant miRNAs, related controversies, and potential applications of these miRNAs in dietary therapy, which will provide new insights for plant miRNA investigations related to health issues in humans.

scholarly journals One Function—Multiple Mechanisms: The Manifold Activities of p53 as a Transcriptional Repressor

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Levin Böhlig ◽  
Karen Rother
Keyword(s):  
Tumor Suppressor ◽  
Target Genes ◽  
Transcriptional Repressor ◽  
Underlying Mechanism ◽  
Transcriptional Level ◽  
Suppressor Activity ◽  
Tumor Suppressor Activity ◽  
Functional Inactivation ◽  
Tumor Suppressive Function ◽  
Transcription Factor P53

Maintenance of genome integrity is a dynamic process involving complex regulation systems. Defects in one or more of these pathways could result in cancer. The most important tumor-suppressor is the transcription factor p53, and its functional inactivation is frequently observed in many tumor types. The tumor suppressive function of p53 is mainly attributed to its ability to regulate numerous target genes at the transcriptional level. While the mechanism of transcriptional induction by p53 is well characterized, p53-dependent repression is not understood in detail. Here, we review the manifold mechanisms of p53 as a transcriptional repressor. We classify two different categories of repressed genes based on the underlying mechanism, and novel mechanisms which involve regulation through noncoding RNAs are discussed. The complete elucidation of p53 functions is important for our understanding of its tumor-suppressor activity and, therefore, represents the key for the development of novel therapeutic approaches.

Response to “No evidence of functional co-adaptation between clustered microRNAs”

2018 ◽  
Author(s):  
Yirong Wang ◽  
Hong Zhang ◽  
Jian Lu
Keyword(s):  
Target Genes ◽  
Long Term Evolution ◽  
Significant Feature ◽  
Transcriptional Level ◽  
Model Based ◽  
Term Evolution ◽  
Non Coding Rnas ◽  
Genomic Locations ◽  
Adaptation Model

AbstractmicroRNAs (miRNAs) are a class of endogenously expressed small non-coding RNAs that regulate target genes at the post-transcriptional level. One significant feature of miRNA is that their genomic locations are often clustered together in the genome. In a previous study (Wang, et al. 2016), we proposed a “functional co-adaptation” model to explain how clustering helps new miRNAs survive and develop functions during long-term evolution. In a manuscript recently posted at bioRxiv (doi:10.1101/274811), Marco claimed that he re-analyzed our data and came to a different conclusion. However, we found his analyses were conducted in an inappropriate approach. He also claimed that the absence of substitution in highly conserved miRNAs does not support the “functional co-adaption” model based on the misunderstanding of our model. In summary, the analyses and claims of Marco, which are flawed, do not refute our model.

scholarly journals Developmental Phase Transitions in Spatial Organization of Spontaneous Activity in Postnatal Barrel Cortex Layer 4

2020 ◽  
Vol 40 (40) ◽  
pp. 7637-7650 ◽  
Author(s):  
Shingo Nakazawa ◽  
Yumiko Yoshimura ◽  
Masahiro Takagi ◽  
Hidenobu Mizuno ◽  
Takuji Iwasato
Keyword(s):  
Phase Transitions ◽  
Spontaneous Activity ◽  
Spatial Organization ◽  
Barrel Cortex ◽  
Developmental Phase ◽  
Layer 4

scholarly journals Physiological and Receptor-selective Retinoids Modulate Interferon γ Signaling by Increasing the Expression, Nuclear Localization, and Functional Activity of Interferon Regulatory Factor-1

2005 ◽  
Vol 280 (43) ◽  
pp. 36228-36236 ◽  
Author(s):  
Xin M. Luo ◽  
A. Catharine Ross
Keyword(s):  
Retinoic Acid ◽  
Nuclear Localization ◽  
Target Genes ◽  
Interferon Γ ◽  
Epithelial Cell Line ◽  
Transcriptional Level ◽  
Signal Transducer ◽  
Regulatory Factor

Synergistic actions between all-trans-retinoic acid (atRA) and interferon γ (IFNγ) on modulation of cellular functions have been reported both in vitro and in vivo. However, the mechanism of atRA-mediated regulation of IFNγ signaling is poorly understood. In this study, we have used the human lung epithelial cell line A549 to examine the effect of atRA on IFNγ-induced expression of IFN regulatory factor-1 (IRF-1), an important transcription factor involved in cell growth and apoptosis, differentiation, and antiviral and antibacterial immune responses. At least 4 h of pretreatment with atRA followed by suboptimal concentrations of IFNγ induced a faster, higher, and more stable expression of IRF-1 than IFNγ alone. Actinomycin D completely blocked the induction of IRF-1 by the combination, suggesting regulation at the transcriptional level. Further, we found that activation of signal transducer and activator of transcription-1 was induced more dramatically by atRA and IFNγ than by IFNγ alone. Expression of IFNγ receptor-1 on the cell surface was also increased upon atRA pretreatment. Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-α (RARα), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNγ receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARα antagonist was able to inhibit the effects of atRA and Am580. In addition, atRA pretreatment affected the transcriptional functions of IFNγ-induced IRF-1, increasing its nuclear localization and DNA binding activity as well as the transcript levels of IRF-1 target genes. These results suggest that atRA, an RARα ligand, regulates IFNγ-induced IRF-1 by affecting multiple components of the IFNγ signaling pathway, from the plasma membrane to the nuclear transcription factors.

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