Search for the missing lncs: gene regulatory networks in neural crest development and long non-coding RNA biomarkers of Hirschsprung's disease

2016 ◽  
Vol 28 (2) ◽  
pp. 161-166 ◽  
Author(s):  
J. M. Rogers
Keyword(s):  
Neural Crest ◽  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Neural Crest Development ◽  
Non Coding Rna ◽  
Gene Regulatory ◽  
Long Non Coding Rna ◽  
Rna Biomarkers

scholarly journals Molecular Mediators of RNA Loading into Extracellular Vesicles

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3355
Author(s):  
Chiara Corrado ◽  
Maria Magdalena Barreca ◽  
Chiara Zichittella ◽  
Riccardo Alessandro ◽  
Alice Conigliaro
Keyword(s):  
Gene Expression ◽  
Extracellular Vesicles ◽  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Translation Regulation ◽  
Circular Rnas ◽  
Non Coding Rna ◽  
Gene Regulatory ◽  
Non Coding Rnas ◽  
Different Levels

In the last decade, an increasing number of studies have demonstrated that non-coding RNA (ncRNAs) cooperate in the gene regulatory networks with other biomolecules, including coding RNAs, DNAs and proteins. Among them, microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) are involved in transcriptional and translation regulation at different levels. Intriguingly, ncRNAs can be packed in vesicles, released in the extracellular space, and finally internalized by receiving cells, thus affecting gene expression also at distance. This review focuses on the mechanisms through which the ncRNAs can be selectively packaged into extracellular vesicles (EVs).

scholarly journals Premature Ovarian Insufficiency: Past, Present, and Future

2021 ◽  
Vol 9 ◽  
Author(s):  
Seung Joo Chon ◽  
Zobia Umair ◽  
Mee-Sup Yoon
Keyword(s):  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Genetic Basis ◽  
Ovarian Function ◽  
Premature Ovarian Insufficiency ◽  
Ovarian Insufficiency ◽  
Non Coding Rna ◽  
Gene Regulatory ◽  
Near Future ◽  
Selection Of

Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by amenorrhea with hypoestrogenic and hypergonadotropic conditions, in some cases, causing loss of fertility. Heterogeneity of POI is registered by genetic and non-genetic causes, such as autoimmunity, environmental toxins, and chemicals. The identification of possible causative genes and selection of candidate genes for POI confirmation remain to be elucidated in cases of idiopathic POI. This review discusses the current understanding and future prospects of heterogeneous POI. We focus on the genetic basis of POI and the recent studies on non-coding RNA in POI pathogenesis as well as on animal models of POI pathogenesis, which help unravel POI mechanisms and potential targets. Despite the latest discoveries, the crosstalk among gene regulatory networks and the possible therapies targeting the same needs to explore in near future.

scholarly journals Long non-coding RNA FAL1 functions as a ceRNA to antagonize the effect of miR-637 on the down-regulation of AKT1 in Hirschsprung's disease

2018 ◽  
Vol 51 (5) ◽  
pp. e12489 ◽  
Author(s):  
Yang Li ◽  
Lingling Zhou ◽  
Changgui Lu ◽  
Qiyang Shen ◽  
Yang Su ◽  
...  
Keyword(s):  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Down Regulation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The conserved and divergent roles of Prdm3 and Prdm16 in zebrafish and mouse craniofacial development

2019 ◽  
Author(s):  
Lomeli Shull ◽  
Rwik Sen ◽  
Johannes Menzel ◽  
Kristin Bruk Artinger
Keyword(s):  
Neural Crest ◽  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Cleft Lip ◽  
Neural Crest Cell ◽  
Early Embryo ◽  
Craniofacial Development ◽  
Histone 3 ◽  
Gene Regulatory ◽  
Craniofacial Defects

The formation of the craniofacial skeleton is a highly dynamic process that requires proper orchestration of various cellular processes in cranial neural crest cell (cNCC) development, including cell migration, proliferation, differentiation, polarity and cell death. Alterations that occur during cNCC development result in congenital birth defects and craniofacial abnormalities such as cleft lip with or without cleft palate. While the gene regulatory networks facilitating neural crest development have been extensively studied, the epigenetic mechanisms by which these pathways are activated or repressed in a temporal and spatially regulated manner remain largely unknown. Chromatin modifers can precisely modify gene expression through a variety of mechanisms including histone modifications such as methylation. Here, we investigated the role of two members of the PRDM (Positive regulatory domain) histone methyltransferase family, Prdm3 and Prdm16 in craniofacial development using genetic models in zebrafish and mice. Loss of prdm3 or prdm16 in zebrafish causes craniofacial defects including hypoplasia of the craniofacial cartilage elements, undefined posterior ceratobranchials, and decreased mineralization of the parasphenoid. In mice, while conditional loss of Prdm3 in the early embryo proper causes mid-gestation lethality, loss of Prdm16 caused craniofacial defects including anterior mandibular hypoplasia, clefting in the secondary palate and severe middle ear defects. In zebrafish, prdm3 and prdm16 compensate for each other as well as a third Prdm family member, prdm1a. Combinatorial loss of prdm1a, prdm3, and prdm16 alleles results in severe hypoplasia of the anterior cartilage elements, abnormal formation of the jaw joint, complete loss of the posterior ceratobranchials, and clefting of the ethmoid plate. We further determined that loss of prdm3 and prdm16 reduces methylation of histone 3 lysine 9 (repression) and histone 3 lysine 4 (activation) in zebrafish. In mice, loss of Prdm16 significantly decreased histone 3 lysine 9 methylation in the palatal shelves but surprisingly did not change histone 3 lysine 4 methylation. Taken together, Prdm3 and Prdm16 play an important role in craniofacial development by maintaining temporal and spatial regulation of gene regulatory networks necessary for proper cNCC development and these functions are both conserved and divergent across vertebrates.

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