Dauer larva quiescence alters the circuitry of microRNA pathways regulating cell fate progression in<i>C. elegans</i>

Karp, Xantha; Ambros, Victor R.

doi:10.1242/dev.075986

Cited by 52 publications

(75 citation statements)

References 49 publications

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“…If dauer larvae encounter an environment suitable for growth, they resume normal development such that postdauer cell divisions are identical to those occurring during continuous development (66,67). Robustness to developmental interruption by dauer is due, in part, to enhanced activity of lin-4 and let-7 family miRNAs, such that lin-4 can substitute for miR-48, miR-241, and miR-84 during postdauer development but not continuous development (68). Surprisingly, enhancement of miRNA activity occurs without alg-1, as heterochronic phenotypes of alg-1 mutants are efficiently suppressed postdauer (68).…”

Section: Cgh-1 Harbors Four Sites Matching the Ck2 Consensus Phosphormentioning

confidence: 99%

“…Robustness to developmental interruption by dauer is due, in part, to enhanced activity of lin-4 and let-7 family miRNAs, such that lin-4 can substitute for miR-48, miR-241, and miR-84 during postdauer development but not continuous development (68). Surprisingly, enhancement of miRNA activity occurs without alg-1, as heterochronic phenotypes of alg-1 mutants are efficiently suppressed postdauer (68). This suggests that modulatory proteins elevate the activity of the remaining ALG-2-containing miRISC.…”

Section: Cgh-1 Harbors Four Sites Matching the Ck2 Consensus Phosphormentioning

confidence: 99%

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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: Cgh-1 Harbors Four Sites Matching the Ck2 Consensus Phosphormentioning

confidence: 99%

Section: Cgh-1 Harbors Four Sites Matching the Ck2 Consensus Phosphormentioning

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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“…hbl-1 contains lin-4 family binding sites in its 39 UTR, making it a potential direct target of mir-237 (Abrahante et al 2003;Lin et al 2003). hbl-1 also appears to be the most proximal regulator of L2 cell fates, making its expression a valuable tool for studying this larval stage (Abbott et al 2005;Karp and Ambros 2012;Vadla et al 2012). During WT development, hbl-1::GFP is highly expressed in the hypodermis upon hatching and throughout the L1 (Figure 2, bar 1), but is downregulated as development proceeds, becoming undetectable by the L3 (Fay et al 1999;Abrahante et al 2003).…”

Section: Resultsmentioning

confidence: 99%

Stage-Specific Timing of the microRNA Regulation oflin-28by the Heterochronic Genelin-14inCaenorhabditis elegans

et al. 2017

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In normal development, the order and synchrony of diverse developmental events must be explicitly controlled. In the nematode Caenorhabditis elegans, the timing of larval events is regulated by hierarchy of proteins and microRNAs (miRNAs) known as the heterochronic pathway. These regulators are organized in feedforward and feedback interactions to form a robust mechanism for specifying the timing and execution of cell fates at successive stages. One member of this pathway is the RNA binding protein LIN-28, which promotes pluripotency and cell fate decisions in successive stages. Two genetic circuits control LIN-28 abundance: it is negatively regulated by the miRNA lin-4, and positively regulated by the transcription factor LIN-14 through a mechanism that was previously unknown. In this report, we used animals that lack lin-4 to elucidate LIN-14's activity in this circuit. We demonstrate that three let-7 family miRNAs-miR-48, miR-84, and miR-241-inhibit lin-28 expression. Furthermore, we show genetically that these miRNAs act between lin-14 and lin-28, and that they comprise the pathway by which lin-14 positively regulates lin-28. We also show that the lin-4 family member mir-237, also regulates early cell fates. Finally, we show that the expression of these miRNAs is directly inhibited by lin-14 activity, making them the first known targets of lin-14 that act in the heterochronic pathway.

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“…Interestingly, developmental timing in Caenorhabditis elegans is regulated by the miRNAs lin-4 and let-7. The induction of dauer larvae depends on environmental cues and both miRNAs are involved in its regulation (Karp and Ambros, 2012). Thus, environmental modulation of development through miRNAs appears to be a general mechanism in plants and animals.…”

Section: Discussionmentioning

confidence: 99%

Arabidopsis miR156 Regulates Tolerance to Recurring Environmental Stress through SPL Transcription Factors

et al. 2014

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Plants are sessile organisms that gauge stressful conditions to ensure survival and reproductive success. While plants in nature often encounter chronic or recurring stressful conditions, the strategies to cope with those are poorly understood. Here, we demonstrate the involvement of ARGONAUTE1 and the microRNA pathway in the adaptation to recurring heat stress (HS memory) at the physiological and molecular level. We show that miR156 isoforms are highly induced after HS and are functionally important for HS memory. miR156 promotes sustained expression of HS-responsive genes and is critical only after HS, demonstrating that the effects of modulating miR156 on HS memory do not reflect preexisting developmental alterations. miR156 targets SPL transcription factor genes that are master regulators of developmental transitions. SPL genes are posttranscriptionally downregulated by miR156 after HS, and this is critical for HS memory. Altogether, the miR156-SPL module mediates the response to recurring HS in Arabidopsis thaliana and thus may serve to integrate stress responses with development.

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Dauer larva quiescence alters the circuitry of microRNA pathways regulating cell fate progression inC. elegans

Cited by 52 publications

References 49 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

Stage-Specific Timing of the microRNA Regulation oflin-28by the Heterochronic Genelin-14inCaenorhabditis elegans

Arabidopsis miR156 Regulates Tolerance to Recurring Environmental Stress through SPL Transcription Factors

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