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Nocturnin is a member of the CCR4 deadenylase family, and its expression is under circadian control with peak levels at night. Because it can remove poly(A) tails from mRNAs, it is presumed to play a role in post-transcriptional control of circadian gene expression, but its target mRNAs are not known. Here we demonstrate that  Nocturnin  expression is acutely induced by the endotoxin lipopolysaccharide (LPS). Mouse embryo fibroblasts (MEFs) lacking  Nocturnin  exhibit normal patterns of acute induction of  TNFα  and  iNOS  mRNAs during the first three hours following LPS treatment, but by 24 hours, while  TNFα  mRNA levels are indistinguishable from WT cells,  iNOS  message is significantly reduced 20-fold. Accordingly, analysis of the stability of the mRNAs showed that loss of  Nocturnin  causes a significant decrease in the half-life of the  iNOS  mRNA (t 1/2  = 3.3 hours in Nocturnin knockout MEFs vs. 12.4 hours in wild type MEFs), while having no effect on the  TNFα  message. Furthermore, mice lacking  Nocturnin  lose the normal nighttime peak of hepatic  iNOS  mRNA, and have improved survival following LPS injection. These data suggest that Nocturnin has a novel stabilizing activity that plays an important role in the circadian response to inflammatory signals.

The Circadian Deadenylase Nocturnin Is Necessary for Stabilization of the iNOS mRNA in Mice