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During  C. elegans  development, microRNAs (miRNAs) function as molecular switches that define temporal gene expression and cell lineage patterns in a dosage-dependent manner. It is critical, therefore, that the expression of miRNAs be tightly regulated so that target mRNA expression is properly controlled. The molecular mechanisms that function to optimize or control miRNA levels during development are unknown. Here we find that mutations in  lin-42 , the  C. elegans  homolog of the circadian-related  period  gene, suppress multiple dosage-dependent miRNA phenotypes including those involved in developmental timing and neuronal cell fate determination. Analysis of mature miRNA levels in  lin-42  mutants indicates that  lin-42  functions to attenuate miRNA expression. Through the analysis of transcriptional reporters, we show that the upstream  cis- acting regulatory regions of several miRNA genes are sufficient to promote highly dynamic transcription that is coupled to the molting cycles of post-embryonic development. Immunoprecipitation of LIN-42 complexes indicates that LIN-42 binds the putative  cis- regulatory regions of both non-coding and protein-coding genes and likely plays a role in regulating their transcription. Consistent with this hypothesis, analysis of miRNA transcriptional reporters in  lin-42  mutants indicates that  lin-42  regulates miRNA transcription. Surprisingly, strong loss-of-function mutations in  lin-42  do not abolish the oscillatory expression patterns of  lin-4  and  let-7  transcription but lead to increased expression of these genes. We propose that  lin-42  functions to negatively regulate the transcriptional output of multiple miRNAs and mRNAs and therefore coordinates the expression levels of genes that dictate temporal cell fate with other regulatory programs that promote rhythmic gene expression.

LIN-42, the Caenorhabditis elegans PERIOD homolog, Negatively Regulates MicroRNA Transcription