miRNeye: a microRNA expression atlas of the mouse eye

Karali, Marianthi; Peluso, Ilaria; Gennarino, Vincenzo A.; Bilio, Marchesa; Verde, Roberta; Lago, Giampiero; Dollé, Pascal; Banfi, Sandro

doi:10.1186/1471-2164-11-715

Cited by 139 publications

(132 citation statements)

References 54 publications

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“…The developmental increase in expression of miR-9, miR125b, and let-7 family members that we observe in the retinal progenitors confirms and extends earlier analyses of retinal miRNAs (31)(32)(33)(34)(35)(36). The most recent comprehensive microarray and in situ analyses (31,35) show that miR-9, miR-125, and several members of the let-7 family (including let-7a, -b, -c, -d, -e, -f, -g, and -i) are expressed in the retina and increase over the developmental period that we have analyzed.…”

Section: Discussionsupporting

confidence: 90%

“…Moreover, previous in situ localization studies have demonstrated that there is widespread expression of let-7 family members in all retinal layers from E16.5 to adulthood (ref. 33; http://mirneye.tigem.it), and miR-9 is expressed from optic cup stages to all retinal layers at P0 (33,35). Our results now show that several members of the let-7 family, miR-9, and miR-125 increase quantitatively over the period of retinal development when the progenitors change their competence, consistent with the hypothesis that miRNAs regulate this process.…”

Section: Discussionsupporting

confidence: 88%

“…The most recent comprehensive microarray and in situ analyses (31,35) show that miR-9, miR-125, and several members of the let-7 family (including let-7a, -b, -c, -d, -e, -f, -g, and -i) are expressed in the retina and increase over the developmental period that we have analyzed. Moreover, previous in situ localization studies have demonstrated that there is widespread expression of let-7 family members in all retinal layers from E16.5 to adulthood (ref.…”

Section: Discussionmentioning

confidence: 87%

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Conserved microRNA pathway regulates developmental timing of retinal neurogenesis

Torre

Georgi²,

Reh

2013

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

196

189

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Most regions of the vertebrate central nervous system develop by the sequential addition of different classes of neurons and glia. This phenomenon has been best characterized in laminated structures like the retina and the cerebral cortex, in which the progenitor cells in these structures are thought to change in their competence as development proceeds to generate different types of neurons in a stereotypic sequence that is conserved across vertebrates. We previously reported that conditional deletion of Dicer prevents the change in competence of progenitors to generate later-born cell types, suggesting that specific microRNAs (miRNAs) are required for this developmental transition. In this report, we now show that three miRNAs, let-7, miR-125, and miR-9, are key regulators of the early to late developmental transition in retinal progenitors: (i) members of these three miRNA families increase over the relevant developmental period in normal retinal progenitors; (ii) inhibiting the function of these miRNAs produces changes in retinal development similar to Dicer CKO; (iii) overexpression of members of these three miRNA families in Dicer-CKO retinas can rescue the phenotype, allowing their progression to late progenitors; (iv) overexpression of these miRNAs can accelerate normal retinal development; (v) microarray and computational analyses of Dicer-CKO retinal cells identified two potential targets of the late-progenitor miRNAs: Protogenin (Prtg) and Lin28b; and (vi) overexpression of either Lin28 or Prtg can maintain the early progenitor state. Together, these data demonstrate that a conserved miRNA pathway controls a key step in the progression of temporal identity in retinal progenitors.heterochronic | progenitor competence

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 87%

See 1 more Smart Citation

Conserved microRNA pathway regulates developmental timing of retinal neurogenesis

Torre

Georgi²,

Reh

2013

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

196

189

View full text Add to dashboard Cite

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“…First, we performed miRNA array profiling of 84 miRNAs that have been assigned a role in vascular function and/or dysfunction. Overall, microarray results shown in Table 1 were concordant with previous surveys of the miRNA expression pattern in the retina using either microarrays or deep sequencing technologies (5,32). Several miRNAs with stricter cut-off criteria (log 2 Ͼ2 or ϽϪ2) were differentially expressed at P12 following hyperoxiainduced vaso-obliteration, including miR-103, miR-107, miR-125, miR-126, miR-155, miR-93, miR-16, and miR-195.…”

Section: Microrna Expression Profile In the Retina Of Oir Mice-supporting

confidence: 85%

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Yan

Lee

Lazzaro

et al. 2015

Journal of Biological Chemistry

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Background: MicroRNA-155 is a proinflammatory small RNA, but its function in pathological angiogenesis is unknown. Results: MicroRNA-155 deficiency increases angiogenic protein CCN1 expression, which harnesses retinal neovascularization by reducing both microglia activation and inflammation. Conclusion: The microRNA-155/CCN1 regulatory axis regulates angiogenic and inflammatory responses in the retina. Significance: Modulation of microRNA-155 and CCN1 interaction is potentially beneficial in retinal neovascularization therapy.

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“…The loss of ERG b-wave in KO mice indicated abnormalities at either pre-or postsynaptic levels. Previous studies detected the three miRNAs of the cluster in bipolar and ganglion cells in addition to photoreceptors (9,17). To resolve which cell populations are affected in the KO, retinas from adult wild-type Fig.…”

Section: Maturation Deficiency Of Cone and Rod Pathways As Measured Bymentioning

confidence: 99%

Maturation arrest in early postnatal sensory receptors by deletion of the miR-183/96/182 cluster in mouse

Fan

et al. 2017

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

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The polycistronic miR-183/96/182 cluster is preferentially and abundantly expressed in terminally differentiating sensory epithelia. To clarify its roles in the terminal differentiation of sensory receptors in vivo, we deleted the entire gene cluster in mouse germline through homologous recombination. The miR-183/96/ 182 null mice display impairment of the visual, auditory, vestibular, and olfactory systems, attributable to profound defects in sensory receptor terminal differentiation. Maturation of sensory receptor precursors is delayed, and they never attain a fully differentiated state. In the retina, delay in up-regulation of key photoreceptor genes underlies delayed outer segment elongation and possibly mispositioning of cone nuclei in the retina. Incomplete maturation of photoreceptors is followed shortly afterward by early-onset degeneration. Cell biologic and transcriptome analyses implicate dysregulation of ciliogenesis, nuclear translocation, and an epigenetic mechanism that may control timing of terminal differentiation in developing photoreceptors. In both the organ of Corti and the vestibular organ, impaired terminal differentiation manifests as immature stereocilia and kinocilia on the apical surface of hair cells. Our study thus establishes a dedicated role of the miR-183/96/182 cluster in driving the terminal differentiation of multiple sensory receptor cells. M ammalian sensory epithelia, such as those underlying vison, hearing, smell, and balance, consist of ciliated sensory receptor cells. Although highly specialized, similarities in embryonic origin underlie common features in their development (1). Following specification, lineage-restricted postmitotic precursors become structurally and functionally mature through a series of cellular differentiation events, collectively described as terminal differentiation (2). During maturation, sensory receptor cells typically develop microtubule-based primary cilia and in some cases actin-based membrane protrusions on apical membranes, which are sensory organelles, while maintaining apical basal polarity within sensory epithelia. In photoreceptors, for example, the extension of outer segments (OSs), specialized sensory cilia, is central to postmitotic differentiation and necessary for light sensitivity (3). In auditory and vestibular hair cells, the proper formation of hair bundles is indispensable for detecting sound and head positions (4). Similarly, olfactory sensory neurons (OSNs), the odorant receptor cells in the olfactory epithelium, project multiple dendritic cilia into the mucous membrane of the nasal epithelium where olfactory signaling is initiated (5). Mature sensory epithelia are highly structured with specific spatial organization that is tied to their functions. Synchronized planar cell polarity (PCP) of hair cells in the inner ear, for example, provides their directional sensitivity (6), whereas the development of laminar architecture in the retina restricts photoreceptors to proper compartments for efficient wiring with secondary neuro...

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miRNeye: a microRNA expression atlas of the mouse eye

Cited by 139 publications

References 54 publications

Conserved microRNA pathway regulates developmental timing of retinal neurogenesis

Conserved microRNA pathway regulates developmental timing of retinal neurogenesis

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Maturation arrest in early postnatal sensory receptors by deletion of the miR-183/96/182 cluster in mouse

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