scholarly journals Natural Antisense Transcript PEBP1P3 Regulates the RNA Expression, DNA Methylation and Histone Modification of CD45 Gene

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 759
Author(s):  
Zhongjing Su ◽  
Guangyu Liu ◽  
Bin Zhang ◽  
Ze Lin ◽  
Dongyang Huang
Keyword(s):  
Dna Methylation ◽  
Alternative Splicing ◽  
Histone Modification ◽  
Antisense Rna ◽  
Noncoding Rna ◽  
Antisense Transcript ◽  
Natural Antisense Transcript ◽  
Regulation Of Expression ◽  
Splicing Isoforms ◽  
Intron 2

The leukocyte common antigen CD45 is a transmembrane phosphatase expressed on all nucleated hemopoietic cells, and the expression levels of its splicing isoforms are closely related to the development and function of lymphocytes. PEBP1P3 is a natural antisense transcript from the opposite strand of CD45 intron 2 and is predicted to be a noncoding RNA. The genotype-tissue expression and quantitative PCR data suggested that PEBP1P3 might be involved in the regulation of expression of CD45 splicing isoforms. To explore the regulatory mechanism of PEBP1P3 in CD45 expression, DNA methylation and histone modification were detected by bisulfate sequencing PCR and chromatin immunoprecipitation assays, respectively. The results showed that after the antisense RNA PEBP1P3 was knocked down by RNA interference, the DNA methylation of CD45 intron 2 was decreased and histone H3K9 and H3K36 trimethylation at the alternative splicing exons of CD45 DNA was increased. Knockdown of PEBP1P3 also increased the binding levels of chromatin conformation organizer CTCF at intron 2 and the alternative splicing exons of CD45. The present results indicate that the natural antisense RNA PEBP1P3 regulated the alternative splicing of CD45 RNA, and that might be correlated with the regulation of histone modification and DNA methylation.

Long noncoding RNA FGFR3-AS1 promotes osteosarcoma growth through regulating its natural antisense transcript FGFR3

2016 ◽  
Vol 43 (5) ◽  
pp. 427-436 ◽  
Author(s):  
Jiabing Sun ◽  
Xuming Wang ◽  
Chunjiang Fu ◽  
Xiaoyu Wang ◽  
Jilong Zou ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Antisense Transcript ◽  
Natural Antisense Transcript

scholarly journals Control of seed dormancy inArabidopsisby acis-acting noncoding antisense transcript

2016 ◽  
Vol 113 (48) ◽  
pp. E7846-E7855 ◽  
Author(s):  
Halina Fedak ◽  
Malgorzata Palusinska ◽  
Katarzyna Krzyczmonik ◽  
Lien Brzezniak ◽  
Ruslan Yatusevich ◽  
...  
Keyword(s):  
Seed Dormancy ◽  
Antisense Rna ◽  
Noncoding Rna ◽  
Major Quantitative Trait Locus ◽  
Antisense Transcript ◽  
Evolutionary Conservation ◽  
Allele Specific ◽  
Trait Locus ◽  
High Level ◽  
Do So

Seed dormancy is one of the most crucial process transitions in a plant’s life cycle. Its timing is tightly controlled by the expression level of the Delay of Germination 1 gene (DOG1).DOG1is the major quantitative trait locus for seed dormancy inArabidopsisand has been shown to control dormancy in many other plant species. This is reflected by the evolutionary conservation of the functional short alternatively polyadenylated form of theDOG1mRNA. Notably, the 3′ region ofDOG1, including the last exon that is not included in this transcript isoform, shows a high level of conservation at the DNA level, but the encoded polypeptide is poorly conserved. Here, we demonstrate that this region ofDOG1contains a promoter for the transcription of a noncoding antisense RNA,asDOG1, that is 5′ capped, polyadenylated, and relatively stable. This promoter is autonomous andasDOG1has an expression profile that is different from knownDOG1transcripts. Using several approaches we show thatasDOG1strongly suppressesDOG1expression during seed maturation incis, but is unable to do so intrans. Therefore, the negative regulation of seed dormancy byasDOG1incisresults in allele-specific suppression ofDOG1expression and promotes germination. Given the evolutionary conservation of theasDOG1promoter, we propose that thiscis-constrained noncoding RNA-mediated mechanism limiting the duration of seed dormancy functions across the Brassicaceae.

scholarly journals Epigenetic Mechanisms of Paternal Stress in Offspring Development and Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xingyun Xu ◽  
Zhigang Miao ◽  
Miao Sun ◽  
Bo Wan
Keyword(s):  
Dna Methylation ◽  
Histone Modification ◽  
Epidemiological Study ◽  
Noncoding Rna ◽  
Sperm Cell ◽  
Biological Function ◽  
Rna Expression ◽  
Epigenetic Mechanisms ◽  
Paternal Stress ◽  
Offspring Health

The major biological function of the sperm cell is to transmit the paternal genetic and epigenetic information to the embryo as well as the following offspring. Sperm has a unique epigenome. An increasing body of epidemiological study supports that paternal stress induced by environmental exposures and lifestyle can modulate the sperm epigenome (including histone modification, DNA methylation, and noncoding RNA expression), sperm-egg fusion, embryo development, and offspring health. Based on the existing literature, we have summarized the paternal exposure on sperm epigenome along with the representative phenotypes of offspring and the possible mechanism involved.

Epigenetic modifications in acute lymphoblastic leukemia: From cellular mechanisms to therapeutics

2020 ◽  
Vol 20 ◽  
Author(s):  
Ezzatollah Fathi ◽  
Raheleh Farahzadi ◽  
Soheila Montazersaheb ◽  
Yasin Bagheri
Keyword(s):  
Dna Methylation ◽  
Acute Lymphoblastic Leukemia ◽  
Histone Modification ◽  
Epigenetic Modification ◽  
Lymphoblastic Leukemia ◽  
Underlying Mechanism ◽  
Methylation Pattern ◽  
Epigenetic Alterations ◽  
Cellular Mechanisms ◽  
Novel Treatments

Background:: Epigenetic modification pattern is considered as a characteristic feature in blood malignancies. Modifications in the DNA methylation modulators are recurrent in lymphoma and leukemia, so that, the distinct methylation pattern defines different types of leukemia. Generally, the role of epigenetics is less understood and most investigations are focused on genetic abnormalities and cytogenic studies to develop novel treatments for patients with hematologic disorders. Recently, understanding the underlying mechanism of acute lymphoblastic leukemia (ALL), especially epigenetic altera-tions as a driving force in the development of ALL opens a new era of investigation for developing promising strategy, be-yond available conventional therapy. Objective:: This review will focus on a better understanding of the epigenetic mechanisms in cancer development and pro-gression, with an emphasis on epigenetic alterations in ALL including, DNA methylation, histone modification, and mi-croRNA alterations. Other topics that will be discussed include the use of epigenetic alterations as a promising therapeutic target in order to develop novel well-suited approaches against ALL. Conclusion:: According to the literature review, leukemogenesis of ALL is extensively influenced by epigenetic modifica-tions, particularly DNA hyper-methylation, histone modification, and miRNA alteration.

scholarly journals LncRNA CRNDE attenuates chemoresistance in gastric cancer via SRSF6-regulated alternative splicing of PICALM

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Feifei Zhang ◽  
Hui Wang ◽  
Jiang Yu ◽  
Xueqing Yao ◽  
Shibin Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Alternative Splicing ◽  
Noncoding Rna ◽  
De Novo ◽  
Acquired Resistance ◽  
Genetic Alterations ◽  
Clinical Samples ◽  
Autophagy Flux ◽  
Resistance To Chemotherapy

AbstractDe novo and acquired resistance, which are mainly mediated by genetic alterations, are barriers to effective routine chemotherapy. However, the mechanisms underlying gastric cancer (GC) resistance to chemotherapy are still unclear. We showed that the long noncoding RNA CRNDE was related to the chemosensitivity of GC in clinical samples and a PDX model. CRNDE was decreased and inhibited autophagy flux in chemoresistant GC cells. CRNDE directly bound to splicing protein SRSF6 to reduce its protein stability and thus regulate alternative splicing (AS) events. We determined that SRSF6 regulated the PICALM exon 14 skip splice variant and triggered a significant S-to-L isoform switch, which contributed to the expression of the long isoform of PICALM (encoding PICALML). Collectively, our findings reveal the key role of CRNDE in autophagy regulation, highlighting the significance of CRNDE as a potential prognostic marker and therapeutic target against chemoresistance in GC.

scholarly journals An antisense noncoding RNA enhances translation via localised structural rearrangements of its cognate mRNA

2021 ◽  
Author(s):  
Rodrigo S Reis ◽  
Jules Deforges ◽  
Romy R Schmidt ◽  
Jos H M Schippers ◽  
Yves Poirier
Keyword(s):  
Antisense Rna ◽  
Noncoding Rna ◽  
Regulatory Region ◽  
Structural Rearrangement ◽  
Start Codon ◽  
Structural Rearrangements ◽  
Eukaryotic Genes ◽  
Inhibitory Region ◽  
Rna Interaction

Abstract A large portion of eukaryotic genes are associated with noncoding, natural antisense transcripts (NATs). Despite sharing extensive sequence complementarity with their sense mRNAs, mRNA-NAT pairs elusively often evade dsRNA-cleavage and siRNA-triggered silencing. More surprisingly, some NATs enhance translation of their sense mRNAs by yet unknown mechanism(s). Here we show that translation enhancement of the rice (Oryza sativa) PHOSPHATE1.2 (PHO1.2) mRNA is enabled by specific structural rearrangements guided by its noncoding antisense RNA (cis-NATpho1.2). Their interaction in vitro revealed no evidence of widespread intermolecular dsRNA formation, but rather specific local changes in nucleotide base-pairing, leading to higher flexibility of PHO1.2 mRNA at a key high GC regulatory region inhibiting translation, approximately 350 nucleotides downstream of the start codon. Sense-antisense RNA interaction increased formation of the 80S complex in PHO1.2, possibly by inducing structural rearrangement within this inhibitory region, thus making this mRNA more accessible to 60S. This work presents a framework for nucleotide-resolution studies of functional mRNA-antisense pairs. One-sentence summary: Interaction between PHO1.2 mRNA and its cis-natural antisense transcript enhances translation via a mechanism involving a local conformational shift and disruption of a key inhibitory region.

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