Human TRIM71 and Its Nematode Homologue Are Targets of let-7 MicroRNA and Its Zebrafish Orthologue Is Essential for Development

Lin, You‐Yu; Hsieh, Li-Ching; Kuo, Ming‐Tse; Yu, John Yuh-Lin; Kuo, H.P.; Lo, Wan‐Lin; Lin, Ruey‐Jen; Yu, Alice L.; Li, Wen-Hsiung

doi:10.1093/molbev/msm195

Cited by 80 publications

(62 citation statements)

References 60 publications

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“…In C. elegans, let-7 triggers the rapid degradation of lin-41 mRNA at the L4-to-adult transition (50,51). lin-41 encodes a TRIM/RBCC family protein, homologous to human TRIM71 (52), that negatively regulates expression of LIN-29, a transcription factor required for adult cell fate specification (50). Depletion of alg-1 leads to significant derepression of lin-41 mRNA compared with empty vector RNAi (Fig.…”

Section: Resultsmentioning

confidence: 99%

Casein kinase II promotes target silencing by miRISC through direct phosphorylation of the DEAD-box RNA helicase CGH-1

Alessi

Khivansara

Han

et al. 2015

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

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MicroRNAs (miRNAs) play essential, conserved roles in diverse developmental processes through association with the miRNA-induced silencing complex (miRISC). Whereas fundamental insights into the mechanistic framework of miRNA biogenesis and target gene silencing have been established, posttranslational modifications that affect miRISC function are less well understood. Here we report that the conserved serine/threonine kinase, casein kinase II (CK2), promotes miRISC function in Caenorhabditis elegans. CK2 inactivation results in developmental defects that phenocopy loss of miRISC cofactors and enhances the loss of miRNA function in diverse cellular contexts. Whereas CK2 is dispensable for miRNA biogenesis and the stability of miRISC cofactors, it is required for efficient miRISC target mRNA binding and silencing. Importantly, we identify the conserved DEAD-box RNA helicase, CGH-1/DDX6, as a key CK2 substrate within miRISC and demonstrate phosphorylation of a conserved N-terminal serine is required for CGH-1 function in the miRNA pathway.

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Section: Resultsmentioning

confidence: 99%

Casein kinase II promotes target silencing by miRISC through direct phosphorylation of the DEAD-box RNA helicase CGH-1

Alessi

Khivansara

Han

et al. 2015

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

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“…In addition to Lin28b, we characterized the expression of the high mobility group transcription factor Hmga2, which has been shown to promote organismal growth and stemness in other systems (28,29). Similar to Lin28b, both human and murine Hmga2 harbor let-7 binding sites in their 3′ UTRs and are negatively regulated by the let-7 miRNAs (23,24,30,31). In the mammalian cochlea, prosensory cell differentiation follows a steep basal-to-apical gradient, whereby midbasally located HCs differentiate before more apically located HCs.…”

Section: Resultsmentioning

confidence: 99%

“…Similar to lin-28, let-7 was initially identified in C. elegans as a heterochronic gene (10,21). Let-7 miRNAs inhibit stem cell/ progenitor cell proliferation and promote differentiation by targeting cell cycle and growth-associated genes (22)(23)(24). The Lin28 genes possess multiple let-7 binding sites in their 3′ UTR and are subject to negative regulation by let-7 miRNAs, establishing a double negative feedback loop (19).…”

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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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“…Of the 55 putative targets, we found that only eight have been empirically validated: miR-378-SUFU, miR-101- MYCN,, and let-7c-TRIM71 (Lewis et al 2003(Lewis et al , 2005Yekta et al 2004;Lee et al 2007;Lin et al 2007;Mitomo et al 2008). Interestingly, many of the 47 remaining putative targets have known CSR functions: proteolysis (miR-101-UBE2A); molecular chaperones (miR-125b-DNAJB2, miR-424-HSPA4L, miR-424-DNAJB4, miR-125b-TTC7A, miR-452-TTC7A, miR-378-TTC7A, miR-378-HSP90AB1, miR-138-CCT5, miR-138-HSPA4L, miR-376a-HSPA6, miR-let-7c-HSPB2, and miR-196a-HSPH1) (Kojima et al 2004;White et al 2005); protein trafficking (miR-125-ZFYVE1); metabolism (miR-382-KYNU, miR-378-KLK4, miR-376a-MAN1C1, miR-let-7c-GALE, and miR-let-7c-RNF20); cell cycle progression (miR-101-MYCN, miR-196a-HOXC8, and miR-196b-HOXC8) (Deraison et al 2007;Kamel et al 2009) (Tables 1 and 2).…”

Section: Resultsmentioning

confidence: 99%

Identification of microRNAs associated with hyperthermia-induced cellular stress response

Wilmink

Roth

Ibey

et al. 2010

Cell Stress and Chaperones

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MicroRNAs (miRNAs) are a class of small RNAs that play a critical role in the coordination of fundamental cellular processes. Recent studies suggest that miRNAs participate in the cellular stress response (CSR), but their specific involvement remains unclear. In this study, we identify a group of thermally regulated miRNAs (TRMs) that are associated with the CSR. Using miRNA microarrays, we show that dermal fibroblasts differentially express 123 miRNAs when exposed to hyperthermia. Interestingly, only 27 of these miRNAs are annotated in the current Sanger registry. We validated the expression of the annotated miRNAs using qPCR techniques, and we found that the qPCR and microarray data was in well agreement. Computational target-prediction studies revealed that putative targets for the TRMs are heat shock proteins and Argonaute-2-the core functional unit of RNA silencing. These results indicate that cells express a specific group of miRNAs when exposed to hyperthermia, and these miRNAs may function in the regulation of the CSR. Future studies will be conducted to determine if other cells lines differentially express these miRNAs when exposed to hyperthermia.

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Human TRIM71 and Its Nematode Homologue Are Targets of let-7 MicroRNA and Its Zebrafish Orthologue Is Essential for Development

Cited by 80 publications

References 60 publications

Casein kinase II promotes target silencing by miRISC through direct phosphorylation of the DEAD-box RNA helicase CGH-1

Casein kinase II promotes target silencing by miRISC through direct phosphorylation of the DEAD-box RNA helicase CGH-1

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

Identification of microRNAs associated with hyperthermia-induced cellular stress response

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