miRNAs in brain development

Petri, Rebecca; Malmevik, Josephine; Fasching, Liana; Åkerblom, Malin; Jakobsson, Johan

doi:10.1016/j.yexcr.2013.09.022

Cited by 101 publications

(80 citation statements)

References 52 publications

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“…The pre-miRNA is then processed by Dicer [202] and the mature miRNA guides the miRNA-induced silencing complex to the target mRNA sequence, via complementary base pairing, to downregulate its expression through translational repression, mRNA degradation or mRNA cleavage [203]. Several miRNAs are specifically enriched in the brain and the necessity of miRNA regulation for normal brain development has been the subject of several recent reviews [204][205][206]. What is more, miRNAs are regulators of NSC proliferation and differentiation and several studies have linked deregulated miRNA expression or function in the brain or in NSCs with PD pathogenesis (reviewed in [207,208]).…”

Section: Overexpression Of Mutated Lrrk2mentioning

confidence: 99%

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

Grand

Gonzalez-Cano

Pavlou

et al. 2014

Cell. Mol. Life Sci.

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Parkinson's disease (PD) is the second most common neurodegenerative disorder, leading to a variety of motor and non-motor symptoms. Interestingly, nonmotor symptoms often appear a decade or more before the first signs of motor symptoms. Some of these non-motor symptoms are remarkably similar to those observed in cases of impaired neurogenesis and several PD-related genes have been shown to play a role in embryonic or adult neurogenesis. Indeed, animal models deficient in Nurr1, Pitx3, SNCA and PINK1 display deregulated embryonic neurogenesis and LRRK2 and VPS35 have been implicated in neuronal development-related processes such as Wnt/bcatenin signaling and neurite outgrowth. Moreover, adult neurogenesis is affected in both PD patients and PD animal models and is regulated by dopamine and dopaminergic (DA) receptors, by chronic neuroinflammation, such as that observed in PD, and by differential expression of wild-type or mutant forms of PD-related genes. Indeed, an increasing number of in vivo studies demonstrate a role for SNCA and LRRK2 in adult neurogenesis and in the generation and maintenance of DA neurons. Finally, the roles of PDrelated genes, SNCA, LRRK2, VPS35, Parkin, PINK1 and DJ-1 have been studied in NSCs, progenitor cells and induced pluripotent stem cells, demonstrating a role for some of these genes in stem/progenitor cell proliferation and maintenance. Together, these studies strongly suggest a link between deregulated neurogenesis and the onset and progression of PD and present strong evidence that, in addition to a neurodegenerative disorder, PD can also be regarded as a developmental disorder.

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Section: Overexpression Of Mutated Lrrk2mentioning

confidence: 99%

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

Grand

Gonzalez-Cano

Pavlou

et al. 2014

Cell. Mol. Life Sci.

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“…miRNAs are small (approximately 22 nucleotide long), highly conserved regulatory molecules that modulate gene expression, mainly by targeting mRNAs for translational repression or degradation (Lau et al, 2001;Berezikov, 2011). Since their discovery, these non-coding RNA molecules have been shown to play important roles in several biological processes, including vertebrate develop-ment (Gavalas et al, 1998;Petri et al, 2014;Pasquinelli, 2012).…”

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confidence: 99%

“…However, there have been several mice studies that explored the role of miRNAs in the development of heart, retina, brain and inner ear. These studies have shown a particular spatiotemporal pattern of miRNAs expression, where specific sets of miRNAs are expressed in the developmental processes of each structure (Petri et al, 2014;Sacheli et al, 2009).…”

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confidence: 99%

External ear microRNA expression profiles during mouse development

Torres¹,

Juárez²,

García³

et al. 2015

Int. J. Dev. Biol.

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MicroRNAs (miRNAs) comprise a class of approximately 22 nucleotide regulatory noncoding RNAs that play several roles in diverse biological processes. Recent reports suggest that embryonic development in mammals is accompanied by dynamic changes in miRNA expression; however, there is no information regarding the role of miRNAs in the development of the external ear. The aim of this study was to determine the stage-specific expression of miRNAs during mouse external ear development in order to identify potentially implicated miRNAs along with their possible targets. miRNA expression profiles from fetal mice pinnae and back skin tissues at 13.5 dpc and 14.5 dpc were obtained using an Affymetrix GeneChip miRNA 3.0 array. Biological triplicates for both tissues, each collected from a litter averaging 16 fetuses, were analyzed. The results were analyzed with Affymetrix's Transcriptome Analysis Console software to identify differentially expressed miRNAs. We observed differential expression of 40 miRNAs including some predicted to target genes implicated in external ear development, such as mmu-miR-10a, a miRNA known to modulate Hoxa1 mRNA levels, and mmu-miR-200c and mmu-miR-205. To our knowledge, this is the first miRNA expression profiling study of external ear development in mammals. These data could set the basis to understand the implications of miRNAs in normal external ear development KEY WORDS: miRNA, pinnae, auricle, microtia, GEO (GSE64945) In mammals, the outer ear is formed by the ear pinna (i.e., the auricle and the external ear), the external acoustic meatus (i.e., the ear canal), and the outer layer of the tympanic membrane (i.e., the eardrum). The outer ear develops as a result of complex tissue interactions between ectoderm and mesoderm during embryogenesis. Outer ear development is driven by the mesenchyme of the first and second pharyngeal arches and is controlled, at least in part, by the genes that determine the first and the second pharyngeal arch identity. The auricle is formed from six protuberances in the first and the second arches known as the auricular hillocks (Jones and Chuan, 1934;Mallo and Gridley, 1996). In mice, several genes involved in external ear development have been identified, including Hoxa2, Hoxa1, Hoxb1, Prrx1, Dlx1, Dlx5, Six1, Six4, Sall1, Tbx1, Bmp5, Fgf3, Fgf8, Fgf10 and Eya1. The genetic and cellular mechanisms underlying normal morphogenesis of the external Int.

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“…It has a maternal-specific methylation imprint acquired in oocytes and generates a population of large compartmentalized noncoding RNA species (58). Conditional KO studies of Dgcr8 have also demonstrated a crucial role for miRNAs in development of the brain (59), especially in the context of olfactory neuron morphogenesis (60). MeCP2 binds directly to Dgcr8, regulating gene expression posttranscriptionally by suppressing nuclear miRNA processing, and gain of function of MeCP2 strongly inhibits dendritic spine growth (61).…”

Section: Coadaptation Of Hypothalamus and Placenta: Consequences For mentioning

confidence: 99%

Genomic imprinting, action, and interaction of maternal and fetal genomes

Keverne

2014

Proc. Natl. Acad. Sci. U.S.A.

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Mammalian viviparity (intrauterine development of the fetus) introduced a new dimension to brain development, with the fetal hypothalamus and fetal placenta developing at a time when the fetal placenta engages hypothalamic structures of the maternal generation. Such transgenerational interactions provide a basis for ensuring optimal maternalism in the next generation. This success has depended on genomic imprinting and a biased role of the matriline. Maternal methylation imprints determine parent of origin expression of genes fundamental to both placental and hypothalamic development. The matriline takes a further leading role for transgenerational reprogramming of these imprints. Developmental errors are minimized by the tight control that imprinted genes have on regulation of downstream evolutionary expanded gene families important for placental and hypothalamic development. Imprinted genes themselves have undergone purifying selection, providing a framework of stability for in utero development with most growth variance occurring postnatally. Mothers, not fathers, take the lead in the endocrinological and behavior adaptations that nurture, feed, and protect the infant. In utero coadaptive development of the placenta and hypothalamus has thus required a concomitant development to ensure male masculinization. Only placental male mammals evolved the sex determining SRY, which activates Sox9 for testes formation. SRY is a hybrid gene of Dgcr8 expressed in the developing placenta and Sox3 expressed in hypothalamic development. This hybridization of genes that take their origin from the placenta and hypothalamus has enabled critical in utero timing for the development of fetal Leydig cells, and hence testosterone production for hypothalamic masculinization.genomic imprinting | genomic reprogramming | hypothalamus | placenta | development

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miRNAs in brain development

Cited by 101 publications

References 52 publications

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

External ear microRNA expression profiles during mouse development

Genomic imprinting, action, and interaction of maternal and fetal genomes

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