A novel class of small RNAs bind to MILI protein in mouse testes

Aravin, Alexei A.; Gaidatzis, Dimos; Pfeffer, Sébastien; Lagos-Quintana, Mariana; Landgraf, Pablo; Iovino, Nicola; Morris, Patricia L.; Brownstein, Michael J.; Kuramochi‐Miyagawa, Satomi; Nakano, Toru; Chien, Minchen; Russo, James J.; Ju, Jingyue; Sheridan, Robert P.; Sander, Chris; Zavolan, Mihaela; Tuschl, Thomas

doi:10.1038/nature04916

Cited by 1,325 publications

(1,323 citation statements)

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“…Alternatively, does this mean that the biologically most important dsRNA targets for A→I RNA editing have yet to be discovered? A large new class of small RNAs (∼26-30 nucleotides) in complex with PIWI-family proteins (piRNAs, PIWI-interacting RNAs) has been reported in mammalian testes 92,[101][102][103] . It would be interesting to determine whether A→I RNA editing is at all involved in the suppression of piRNA biogenesis.…”

Section: Concluding Remarks and Outlookmentioning

confidence: 99%

Editor meets silencer: crosstalk between RNA editing and RNA interference

Nishikura

2006

Nat Rev Mol Cell Biol

257

263

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The most prevalent type of RNA editing is mediated by ADAR (adenosine deaminase acting on RNA) enzymes, which convert adenosines to inosines (a process known as A→I RNA editing) in double-stranded (ds)RNA substrates. A→I RNA editing was long thought to affect only selected transcripts by altering the proteins they encode. However, genome-wide screening has revealed numerous editing sites within inverted Alu repeats in introns and untranslated regions. Also, recent evidence indicates that A→I RNA editing crosstalks with RNA-interference pathways, which, like A→I RNA editing, involve dsRNAs. A→I RNA editing therefore seems to have additional functions, including the regulation of retrotransposons and gene silencing, which adds a new urgency to the challenges of fully understanding ADAR functions.An RNA transcript is subjected to various maturation processes, such as 5′ capping, splicing, 3′ processing and polyadenylation, after it is transcribed from the gene. Post-transcriptional processing of primary transcripts is essential to generate mature messenger RNAs that are ready to be translated into proteins 1 . RNA editing is a post-transcriptional-processing mechanism that results in an RNA sequence that is different from the one encoded by the genome, and thereby contributes to the diversity of gene products. There are different types of RNA-editing mechanism that either add or delete nucleotides, or that change one nucleotide into another 2 (BOX 1).The type of RNA editing that is most prevalent in higher eukaryotes converts adenosine (A) residues into inosine (I) in double-stranded (ds)RNAs through the action of ADAR (adenosine deaminase acting on RNA) enzymes [3][4][5] . A→I RNA editing of a short dsRNA that has formed between a coding exon and nearby intron sequences can lead to a codon change and an alteration in the protein function. However, it was recently discovered that the most frequent targets of A→I RNA editing seem to be long, but partially double-stranded, RNAs that are formed from inverted Alu repeats and long interspersed element (LINE) repeats located in introns and untranslated regions (UTRs) of mRNAs [6][7][8][9] . Global editing of non-coding RNA might control the expression of genes that harbour these repeat sequences of retrotransposon origin.Post-transcriptional gene regulation can also occur through RNA interference (RNAi), an evolutionarily conserved phenomenon that involves dsRNA molecules 10,11 . Small interfering RNAs (siRNAs) and microRNAs (miRNAs) are non-coding RNAs that are generated by a class of RNase III ribonucleases (specifically, Dicer and Drosha). These small RNAs are incorporated into the RNA-induced silencing complex (RISC), which mediates the RNAi process [12][13][14][15][16] . The idea that the RNAi and A→I RNA editing pathways might compete for a Competing interests statement: The author declares no competing financial interests. [23][24][25] . NIH Public AccessIn this review, I discuss recent findings on new functions of A→I RNA editing in the regulation of non...

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Section: Concluding Remarks and Outlookmentioning

confidence: 99%

Editor meets silencer: crosstalk between RNA editing and RNA interference

Nishikura

2006

Nat Rev Mol Cell Biol

257

263

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“…MIWI, MIWI2 and MILI are members of the argonaute proteins and Piwi subfamily in mice. The Piwi proteins are present in the germline and play an essential role in piRNA production [18,19]. According to research, the lack of MIWI, MIWI2 or MILI proteins in knockout mice causes meiotic arrest in spermatogenesis [18,20].…”

Section: Introductionmentioning

confidence: 99%

Association of MOV10L1 gene polymorphisms and male infertility in azoospermic men with complete maturation arrest

Sarkardeh

Totonchi

Asadpour

et al. 2014

J Assist Reprod Genet

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Purpose The present research was undertaken to study probable genetic variations of MOV10L1 in 30 infertile men that had complete maturation arrest in their spermatocyte levels and 70 fertile men as the control group. Methods We performed polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) on extracted DNAs and sequencing was used to confirm the results.Identified polymorphisms in the MOV10L1 were further subjected to a haplotype analysis. Results We identified eight single nucleotide polymorphisms (SNPs): one missense (rs2272837) and four nonsense polymorphisms (rs2272836, rs11704548, rs2272838, rs138271) in the exonic sequences and three polymorphisms (rs12170772, rs2272840, rs17248147) in the intronic regions. With the exception of rs2272838, there was a statistically significant association in all polymorphisms between study population (P<0.05). The result of haplotyping analysis showed ten possible haplotypes, from which five were significantly increased in infertile patients compared with the control group. Conclusions Our results suggest that MOV10L1 gene polymorphisms in the studied infertile males with complete maturation arrest are linked to infertility.

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“…Les résultats de séquençages modernes montrent que les millions de piARN différents proviennent d'un nombre limité de locus, une centaine chez les mammifères, dans lesquels la plupart sont regroupés en clusters. Dans ces clusters, les piARN sont issus d'un des deux brins, mais ne se chevauchent pas [4,5]. Ces clusters sont majoritairement localisés dans des régions riches en répétitions ou encore dans les régions intergéniques.…”

Section: Biogenèse Des Piarnunclassified

“…De plus, il existe chez les mammifères une fenêtre critique, de la fin de l'embryogenèse jusqu'à quelques jours après la naissance, pendant laquelle la méthylation du génome des cellules germinales est remodelée, ce qui rend ces cellules, qui sont en cours de différenciation, particulièrement vulnérables à l'envahissement par les éléments transposables. Durant cette période, le génome peut bénéficier de la présence du système de défense particulier basé sur l'utilisation de petits ARN appelés piARN (PIWIinteracting RNA) [4][5][6][7]38, 39], dont l'action pou rrait être comparée à celle d'un système immunitaire à l'échelle du génome. Cette revue résume les connaissances que nous avons de cette classe d'ARN dont la caractérisation a débuté en 2006.…”

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