Table 1.

Circadian aspects of miRNAs, lncRNAs and proteins involved in chromatin remodeling. Findings discussed in Section 2, Section 6 and Section 8 are omitted. ¹ ICR = imprinting control region; ² Mico = maternal intergenic circadian oscillating; NAMPT = nicotinamide phosphoribosyltransferase; os = opposite strand; ³ ZT = Zeitgeber time; ⁴ PSF = polypyrimidine tract-binding protein-associated splicing factor; ⁵ NONO = non-POU domain-containing octamer binding protein; ⁶ SFPQ = splicing factor proline/glutamine-rich.

Organism/Tissue or Cells	Main Findings	References
Mouse/SCN	Circadian rhythms of miR-219 and miR-132; miR-219; knockdown lengthens circadian period; Cry1/Cry2 double knockout abolishes rhythms of pre-miR-219-1 and miR-219-1; CLOCK/BMAL1 over-expression stimulates pre-miR-219-1; miR-132 is induced by light (also by LAN) via ERK/MAPK, but acts as negative regulator of photic entrainment; miR-132 is presumably target of CBP (CREB binding protein)	[46,47]
Rat/primary cortical neurons	miR-219 over-expression suppresses NMDA-induced Ca2+ influx	[46]
Mouse/brain and P19 cells	miR-219 down-regulates NMDA signaling by targeting CamkII subunit γ mRNA	[48]
Mouse/SCN	miR-132 targets mRNAs of proteins involved in chromatin remodeling (Mecp2, Ep300, Jarid1a) and translational control (Btg2, Paip2a); MeCP2 binds to Per1 and Per2 promoters; BTG2 and PAIP2A enhance decay of Per1 and Per2 mRNAs	[49]
Mouse/retina	Circadian rhythms of 16 lincRNAs	[50]
Mouse/retina	Circadian rhythms of 12 miRNAs, including those from miR-183-96-182 cluster	[47,51]
Mouse/brain	Two overlapping imprinted ncRNAs from intergenic region Dlk1–Gtl2 that contains an ICR 1 are exclusively expressed at maternal chromosome, from both strands: Mico1 and Mico1os 2; both oscillate in a circadian fashion	[52]
Mouse/hypothalamus, hindbrain, forebrain, cortex, hippocampus, cerebellum; neurons but not glia	Transcript of Prader–Willis locus SNORD116 is spliced into multiple snoRNAs and the lncRNA 116HG; 116HG forms subnuclear clouds that increase postnatally and are associated with large-scale chromatin decondensation; size of clouds smaller at ZT16 3 than at ZT6; in SNORD116−/− mice, expression of 6467 genes is altered at ZT6, of 3240 genes at ZT16; relative to WT, Clock, Cry1 and Per2 are up-regulated at ZT6, Cry1, Cry2 and Per1 down-regulated at ZT16	[53]
Mouse/serum	Circadian rhythms of miR-152 and miR-494; circulating miRNAs may influence oscillators via microvesicles	[54]
Human/HEK293 cells	Bmal1 is targeted at 3'-UTR by miR-494 and miR-142-3p	[54]
HTC116, HT29 and NIH3T3 cells	miR-192/194 cluster targets Per1, Per2, and Per3 and alters circadian rhythms	[55]
Mouse/liver	Circadian rhythms of 85 miRNAs; several miRNA/mRNA target pairs identified, including core oscillator mRNAs; miR-181d and miR-191 are inversely correlated with Clock/Bmal1 and presumably involved in peripheral clocks; miR-328 and miR-383 positively correlated with Per1/Cry1	[47,56]
Mouse/liver	REV-ERBα drives miR-122 transcription; knockdown of miR-122 alters expression of hundreds of hepatic mRNAs	[57]
Mouse/liver	miR-122 targets Noc mRNA; miR-122 knockdown increases the amplitude of the nocturnin rhythm	[58]
Mouse/various organs	Noc mRNA is rhythmic in several brain regions, retina, heart, kidney, spleen, and liver	[59,60]
Mouse/liver	Several hundred mRNAs exhibit circadian rhythms in poly(A) tail length, even in cases in which mRNA levels are not rhythmic	[61]
Mouse/liver	CLOCK controls rhythmic transcription of Noc; Clock mutants exhibit dampened Noc rhythms	[62]
Human/Huh7 hepatoma cells	Binding of CLOCK/BMAL1 to E-box in Noc promoter	[63]
Mouse/liver	NOC stabilizes iNOS mRNA; NOC deficiency blunts the nocturnal peak of iNOS mRNA	[33]
Mouse/liver	Circadian rhythms of 54 miRNAs, 16 lincRNAs and several antisense transcripts, including a Per2 antisense RNA (asPer2); rhythms in histone modifications: especially, H3K4me3, but also H3K4me1, H3K9ac, H3K27ac (at active enhancers), and H3K36me3 enriched in actively transcribed genes	[64]
Mouse/embryo fibroblasts, liver	SIRT1, an accessory circadian oscillator protein, histone deacetylase and aging suppressor, promotes PER2 degradation by deacetylation, is required for high amplitudes of Per2, Cry1, Bmal1 and RORγ transcription rhythms, is recruited to the BMAL1/CLOCK complex and controls the expression of E-box-containing genes such as Per2, Cry1 and NAMPT via cycling NAD+ concentration	[65,66,67,68,69]
Mouse/liver, lung, fibroblasts	PER proteins form complexes that include PSF 4, which recruits the scaffold SIN3A associated with a HDAC that rhythmically suppresses Per1 transcription by deacetylating histones at the promoter	[70]
Mouse/liver, 3T3 cells	NONO 5 interacts with PER1 and modulates its activity	[71]
Mouse/liver, brain areas incl. SCN	NONO associates with PER1 or PER2 at Rev-erbα and Dbp promoters; NONO couples the oscillator to cell cycle; NONO also interacts with ncRNAs	[72,73]
Rat/GH4C1 cells	NONO and SFPQ 6 induce chromatin remodeling at prolactin promoter and couple Prl expression to circadian oscillator; NONO/SFPQ over-expression decreases promoter activity and disrupts circadian Prl rhythm	[74]