Journal
CELL DEATH AND DIFFERENTIATION
Volume 23, Issue 9, Pages 1458-1470Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2016.27
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Funding
- Natural Sciences and Engineering Research Council of Canada (NSERC) [227937-2012]
- Canadian Institutes of Health Research [CHRP 462341-2014]
- Natural Sciences and Engineering Research Council of Canada [CPG 134747]
- Heart and Stroke Foundation of Ontario [CI 7418]
- Canadian Breast Cancer Foundation of Ontario
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MicroRNAs (miRNAs) and piwi-interacting RNAs (piRNAs) are two classes of small noncoding RNAs, both of which play roles in regulating tissue development. It is unknown whether these distinct classes of noncoding RNAs can regulate one another. Here we show that ectopic expression of miR-17 inhibited mouse fertility and early embryonic development. Specifically, we found that the piRNA amplification loop was repressed by miR-17-5p, leading to increased levels of transposition mutagenesis. This occurred by suppressing the amplification loop of piRNAs with an identical 5' sequence and by targeting Mili/Miwi2, an essential component of the piRNA amplification loop, and the DNA methyltransferase, Dnmt3a. We also found that increased levels of piRNAs could compete with miRNAs for target binding, resulting in increased expression of Dnmt3a and Mili. Increased Dnmt3a levels could in turn block miR-17-5p expression, while increased Mili expression could accelerate piRNA amplification and inhibit transposon generation, favoring embryonic development. We report for the first time the reciprocal regulation between miRNAs and piRNAs in mouse embryonic development.
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