A novel long intergenic noncoding
            <scp>RNA</scp>
            indispensable for the cleavage of mouse two‐cell embryos

Wang, Jiaqiang; X, Li; Wang, Leyun; Li, Jingyu; Zhao, Yanhua; Bou, Gerelchimeg; Li, Yufei; Jiao, Guanyi; Shen, Xiaopei; Wei, Renyue; Liu, Shichao; Xie, Bingteng; Lei, Lei; Li, Wei; Zhou, Qi

doi:10.15252/embr.201642051

Cited by 58 publications

(50 citation statements)

References 82 publications

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“…Consistent with this hypothesis, transient siRNA-mediated depletion of a subset of ERVK- and MaLR-derived long noncoding RNAs (lncRNA) highly expressed in mouse ESCs leads to reduced expression of cellular pluripotency markers, suggesting that these lncRNAs exert some form of control over the maintenance of a pluripotent state [54]. Similarly, a recent biochemical study showed that a lncRNA derived from a MERV-L locus, called LincGET , is required for in vitro embryonic development to proceed beyond the 2C stage [49]. Biochemical experiments and reporter assays suggest that LincGET functions as a scaffold for the recruitment of TFs and splicing factors (Figure 3C), some of which are known to be important for embryonic development [49,55].…”

Section: Erv Choreography In Early Embryonic Developmentmentioning

confidence: 99%

“…Similarly, a recent biochemical study showed that a lncRNA derived from a MERV-L locus, called LincGET , is required for in vitro embryonic development to proceed beyond the 2C stage [49]. Biochemical experiments and reporter assays suggest that LincGET functions as a scaffold for the recruitment of TFs and splicing factors (Figure 3C), some of which are known to be important for embryonic development [49,55]. …”

Section: Erv Choreography In Early Embryonic Developmentmentioning

confidence: 99%

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Co-option of endogenous viral sequences for host cell function

Frank

Feschotte

2017

Current Opinion in Virology

143

126

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Eukaryotic genomes are littered with sequences of diverse viral origins, termed endogenous viral elements (EVEs). Here we used examples primarily drawn from mammalian endogenous retroviruses to document how the influx of EVEs has provided a source of prefabricated coding and regulatory sequences that were formerly utilized for viral infection and replication, but have been occasionally repurposed for cellular function. While EVE co-option has benefited a variety of host biological functions, there appears to be a disproportionate contribution to immunity and antiviral defense. The mammalian embryo and placenta offer opportunistic routes of viral transmission to the next host generation and as such they represent hotbeds for EVE cooption. Based on these observations, we propose that EVE cooption is initially driven as a mean to mitigate conflicts between host and viruses, which in turn acts as a stepping-stone toward the evolution of cellular innovations serving host physiology and development.

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Section: Erv Choreography In Early Embryonic Developmentmentioning

confidence: 99%

Section: Erv Choreography In Early Embryonic Developmentmentioning

confidence: 99%

Co-option of endogenous viral sequences for host cell function

Frank

Feschotte

2017

Current Opinion in Virology

143

126

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“…The existence of such evolutionary-established mechanisms of regulation of ontogenesis with the help of TE can be confirmed if the suppression of the activity of specific TE required for further regulation of cell differentiation will stop the further development of the organism. Indeed, in experiments on mouse embryos, it was shown that depletion of the long LincGET ncRNA associated with LTR-RE leads to a complete arrest of further development at the two-cell stage (Wang et al, 2016). In this stage, many transcripts are initiated from the LTR-RE (Macfarlan et al, 2012) and are associated with enhancers that support the polypotency (Fort et al, 2014).…”

Section: Tissue-specific and Stage-specific Activation Of Transposonsmentioning

confidence: 99%

“…The literature provides enough data to suggest that transposons (TE, transposable elements) can serve as hidden genetic structures capable of changing the expression of specific genes in response to certain ES (which overcome resistance to the constancy of the phenotype). This is due to the fact that TEs play an important role in the regulation of gene expression in ontogenesis (de Souza et al, 2013;Pavlicev et al, 2015;Wang et al, 2016;Ito et al, 2017;Ramsay et al, 2017;Saze, 2018) and serve as sources of changes in epigenetic (EG) factors (Li et al, 2011;Ito, 2012;Kapusta et al, 2013;Gim et al, 2014;Cho, 2018).…”

Section: Introductionmentioning

confidence: 99%

The role of transposable elements in the ecological morphogenesis under the influence of stress

Мустафин

Khusnutdinova

2019

Vestn. VOGiS

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In natural selection, insertional mutagenesis is an important source of genome variability. Transposons are sensors of environmental stress effects, which contribute to adaptation and speciation. These effects are due to changes in the mechanisms of morphogenesis, since transposons contain regulatory sequences that have cis and trans effects on specific protein-coding genes. In variability of genomes, the horizontal transfer of transposons plays an important role, because it contributes to changing the composition of transposons and the acquisition of new properties. Transposons are capable of site-specific transpositions, which lead to the activation of stress response genes. Transposons are sources of non-coding RNA, transcription factors binding sites and protein-coding genes due to domestication, exonization, and duplication. These genes contain nucleotide sequences that interact with non-coding RNAs processed from transposons transcripts, and therefore they are under the control of epigenetic regulatory networks involving transposons. Therefore, inherited features of the location and composition of transposons, along with a change in the phenotype, play an important role in the characteristics of responding to a variety of environmental stressors. This is the basis for the selection and survival of organisms with a specific composition and arrangement of transposons that contribute to adaptation under certain environmental conditions. In evolution, the capability to transpose into specific genome sites, regulate gene expression, and interact with transcription factors, along with the ability to respond to stressors, is the basis for rapid variability and speciation by altering the regulation of ontogenesis. The review presents evidence of tissue-specific and stage-specific features of transposon activation and their role in the regulation of cell differentiation to confirm their role in ecological morphogenesis.

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“…depletion of the LincGET lncRNA causes a total arrest of the late G2-phase of bicellular stage in mice. This effect is determined by LincGET inability to bind the ILF2, FUBP1and hnRNP-U proteins and form a complex necessary for the cis-regulatory activity of LTR-containing retro-ТЕ GLN, MERVL, ERVK (Wang et al, 2016). TEs can also be used as lncRNA genes, e.g.…”

Section: Transposon and Noncoding Rna Activity In Brainmentioning

confidence: 99%

Interrelation of Prions With Non-Coding Rnas

Мустафин¹,

Хуснутдинова²

2018

Vestn. VOGiS

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Prions are alternative infectious conformations for some cellular proteins. For the protein PrPC (PrP – prion protein, С – common), a prion conformation, called PrPSc (S – scrapie), is pathological. For example, in mammals the PrPSc prion causes transmissible spongiform encephalopathies accumulating in the brain tissues of PrPSc aggregates that have amyloid properties. MicroRNAs and long non-coding RNAs can be translated into functional peptides. These peptides can have a regulatory effect on genes from which their non-coding RNAs are transcribed. It has been assumed that prions, like peptides, due to the presence of specific domains, can also activate certain non-coding RNAs. Some of the activated non-coding RNAs can catalyze the formation of new prions from normal protein, playing their role in the pathogenesis of prion diseases. Confirmation of this assumption is the presence of the association of alleles of microRNA with the development of the disease, which indicates the role of the specific sequences of noncoding RNAs in the catalysis of prion formation. In the brain tissues of patients with prion diseases, as well as in exosomes containing an abnormal PrPSc isoform, changes in the levels of microRNA have been observed. A possible cause is the interaction of the spatial domains of PrPSc with the sequences of the non-coding RNA genes, which causes a change in their expression. MicroRNAs, in turn, affect the synthesis of long non-coding RNAs. We hypothesize that long noncoding RNAs and possibly microRNAs can interact with PrPC catalyzing its transformation into PrPSc. As a result, the number of PrPSc increases exponentially. In the brain of animals and humans, transposon activity has been observed, which has a regulatory effect on the differentiation of neuronal stem cells. Transposons form the basis of domain structures of long non-coding RNAs. In addition, they are important sources of microRNA. Since prion diseases can arise as sporadic and hereditary cases, and hereditary predisposition is important for the development of pathology, we hypothesize the role of individual features of activation of transposons in the pathogenesis of prion diseases. The activation of transposons in the brain at certain stages of development, as well as under the influence of stress, is reflected in the peculiarities of expression of specific non-coding RNAs that are capable of catalyzing the transition of the PrPC protein to PrPSc. Research in this direction can be the basis for targeted anti-microRNA therapy of prion diseases.

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A novel long intergenic noncoding RNA indispensable for the cleavage of mouse two‐cell embryos

Cited by 58 publications

References 82 publications

Co-option of endogenous viral sequences for host cell function

Co-option of endogenous viral sequences for host cell function

The role of transposable elements in the ecological morphogenesis under the influence of stress

Interrelation of Prions With Non-Coding Rnas

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