Regulation of microRNA function in somatic stem cell proliferation and differentiation

Shenoy, Archana; Blelloch, Robert

doi:10.1038/nrm3854

Cited by 324 publications

(241 citation statements)

References 105 publications

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“…Mice-Loss of microRNAs could result in up-or down-regulation of mRNAs and the corresponding proteins depending on cell type and developmental status and for other reasons (75)(76)(77)(78). To test, how loss of DICER-dependent miRNAs affects gonadotropin synthesis in pituitaries of male mice, we first quantified gonadotropin subunit mRNAs by real time qPCR assays.…”

Section: Loss Of Dicer In Gonadotropes Results In Suppressed Gonadotrmentioning

confidence: 99%

Gonadotrope-specific Deletion of Dicer Results in Severely Suppressed Gonadotropins and Fertility Defects

Wang

Graham

Hastings

et al. 2015

Journal of Biological Chemistry

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Background: DICER mediates microRNA production, and its functional role in gonadotropes is not known. Results: Deletion of Dicer in gonadotropes leads to suppression of gonadotropin synthesis and secretion and results in fertility defects. Conclusion: DICER-dependent microRNAs are critical for gonadotropin homeostasis and fertility. Significance: Understanding how microRNAs regulate gonadotropin homeostasis provides a new approach to enhance or block fertility in mammals.

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Section: Loss Of Dicer In Gonadotropes Results In Suppressed Gonadotrmentioning

confidence: 99%

Gonadotrope-specific Deletion of Dicer Results in Severely Suppressed Gonadotropins and Fertility Defects

Wang

Graham

Hastings

et al. 2015

Journal of Biological Chemistry

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“…In the last decades, miRNAs have been postulated as important regulatory molecules in many cellular and developmental pathways (15,16). Numerous studies have focused on the assessment of miRNA expression and have shown considerable changes in their expression profiles in various diseases (17)(18)(19)(20), although the most remarkable changes have been observed in cancer (21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic regulation mechanisms of microRNA expression

Morales

Monzó

Navarro

2017

Biomolecular Concepts

121

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MicroRNAs (miRNAs) are single-stranded RNAs of 18-25 nucleotides that regulate gene expression at the post-transcriptional level. They are involved in many physiological and pathological processes, including cell proliferation, apoptosis, development and carcinogenesis. Because of the central role of miRNAs in the regulation of gene expression, their expression needs to be tightly controlled. Here, we summarize the different mechanisms of epigenetic regulation of miRNAs, with a particular focus on DNA methylation and histone modification.

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“…Mature miRNAs are small noncoding RNAs that interact with their targets by partial base pairing with complementary sequences commonly found within the 3′ untranslated region (3′ UTR) of the target mRNA. In the majority of cases, miRNA binding inhibits translation and/or destabilizes the target mRNA (20). Similar to lin-28, let-7 was initially identified in C. elegans as a heterochronic gene (10,21).…”

mentioning

confidence: 99%

The RNA-binding protein LIN28B regulates developmental timing in the mammalian cochlea

Golden

Benito-Gonzalez

Doetzlhofer

2015

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

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Proper tissue development requires strict coordination of proliferation, growth, and differentiation. Strict coordination is particularly important for the auditory sensory epithelium, where deviations from the normal spatial and temporal pattern of auditory progenitor cell (prosensory cell) proliferation and differentiation result in abnormal cellular organization and, thus, auditory dysfunction. The molecular mechanisms involved in the timing and coordination of auditory prosensory proliferation and differentiation are poorly understood. Here we identify the RNAbinding protein LIN28B as a critical regulator of developmental timing in the murine cochlea. We show that Lin28b and its opposing let-7 miRNAs are differentially expressed in the auditory sensory lineage, with Lin28b being highly expressed in undifferentiated prosensory cells and let-7 miRNAs being highly expressed in their progeny-hair cells (HCs) and supporting cells (SCs). Using recently developed transgenic mouse models for LIN28B and let-7g, we demonstrate that prolonged LIN28B expression delays prosensory cell cycle withdrawal and differentiation, resulting in HC and SC patterning and maturation defects. Surprisingly, let-7g overexpression, although capable of inducing premature prosensory cell cycle exit, failed to induce premature HC differentiation, suggesting that LIN28B's functional role in the timing of differentiation uses let-7 independent mechanisms. Finally, we demonstrate that overexpression of LIN28B or let-7g can significantly alter the postnatal production of HCs in response to Notch inhibition; LIN28B has a positive effect on HC production, whereas let-7 antagonizes this process. Together, these results implicate a key role for the LIN28B/let-7 axis in regulating postnatal SC plasticity.Lin28b | Let-7 | hair cell | cochlea | regeneration

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Regulation of microRNA function in somatic stem cell proliferation and differentiation

Cited by 324 publications

References 105 publications

Gonadotrope-specific Deletion of Dicer Results in Severely Suppressed Gonadotropins and Fertility Defects

Gonadotrope-specific Deletion of Dicer Results in Severely Suppressed Gonadotropins and Fertility Defects

Epigenetic regulation mechanisms of microRNA expression

The RNA-binding protein LIN28B regulates developmental timing in the mammalian cochlea

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