• Nitrogen and NO regulate plant flowering through different pathways. • Both nitrogen and sucrose suppress circadian transcript oscillation. • NO treatments increased CRY1 , LHY , CCA1 and TOC1 , but decreased CO and GI oscillation. • Among circadian oscillators, only GI and CO can be S-nitrosylated by NO treatments. • Sucrose supplementation counteracted the effects of NO, but not the effects of nitrogen. Both nitrogen (N) and nitric oxide (NO) postpone plant flowering. However, we still don't know whether N and NO trigger the same signaling pathways leading to flowering delay. Our previous study found that ferredoxin NADP+ oxidoreductase (FNR1) and the blue-light receptor cryptochrome 1 (CRY1) are involved in nitrogen-regulated flowering-time control. However, NO-induced late-flowering does not require FNR1 or CRY1. Sucrose supply counteracts the flowering delay induced by NO. However high-N-induced late-flowering could not be reversed by 5% sucrose supplementation. The high nitrogen condition decreased the amplitudes of all transcripts of the circadian clock. While NO increased the amplitudes of circadian transcripts of CRY1 , LHY (LATE ELONGATED HYPOCOTYL), CCA1 (CIRCADIAN CLOCK ASSOCIATED 1) and TOC1 (TIMING OF CAB EXPRESSION 1), but decreased the amplitudes of circadian transcripts of CO (CONSTANS) and GI (GIGANTEA). 5% sucrose supplementation reversed the declines in amplitudes of circadian transcripts of CO and GI after the NO treatment. NO induced S-nitrosation modification on oscillators CO and GI, but not on the other oscillators of the circadian clock. Sucrose supply interestingly reduced S-nitrosation levels of GI and CO proteins. Thus N and NO rely on overlapping but distinct signaling pathways on plant flowering. [ABSTRACT FROM AUTHOR]