ABSTRACT
Nitrogen (N) is a critical factor for crop growth and yield. Improving N use efficiency (NUE) in agricultural systems is crucial for sustainable food production. However, the underlying regulation of N uptake and utilization in crops is not well known. Here, we identified OsSNAC1 (stress-responsive NAC 1) as an upstream regulator of OsNRT2.1 (nitrate transporter 2.1) in rice (Oryza sativa) by yeast 1-hybridization screening. OsSNAC1 was mainly expressed in roots and shoots and induced by N deficiency. We observed similar expression patterns of OsSNAC1, OsNRT2.1/2.2, and OsNRT1.1A/B in response to NO3- supply. Overexpression of OsSNAC1 resulted in increased concentrations of free NO3- in roots and shoots, as well as higher N uptake, higher NUE, and N use index (NUI) in rice plants, which conferred increased plant biomass and grain yield. On the contrary, mutations in OsSNAC1 resulted in decreased N uptake and lower NUI, which inhibited plant growth and yield. OsSNAC1 overexpression significantly upregulated OsNRT2.1/2.2 and OsNRT1.1A/B expression, while the mutation in OsSNAC1 significantly downregulated OsNRT2.1/2.2 and OsNRT1.1A/B expression. Y1H, transient co-expression, and ChIP assays showed OsSNAC1 directly binds to the upstream promoter regions of OsNRT2.1/2.2 and OsNRT1.1A/1.1B. In conclusion, we identified a NAC transcription factor in rice, OsSNAC1, with a positive role in regulating NO3- uptake through direct binding to the upstream promoter regions of OsNRT2.1/2.2 and OsNRT1.1A/1.1B and activating their expression. Our results provide a potential genetic approach for improving crop NUE in agriculture.
Subject(s)
Nitrate Transporters , Oryza , Oryza/metabolism , Anion Transport Proteins/genetics , Anion Transport Proteins/metabolism , Plant Proteins/genetics , Plant Proteins/metabolism , Transcription Factors/genetics , Transcription Factors/metabolism , Gene Expression Regulation, Plant , Nitrogen/metabolism , Gene Expression , Nitrates/metabolismABSTRACT
Endogenous synthesis of PUFAs is mediated by genes controlling fatty acid elongases 2 and 5 (ELOVL2 and ELOVL5) and by exogenous DHA intake. Associations between elongases and PUFA levels probably involve genetic variants of ELOVL and changes in DHA intake, but data about their combined effect on PUFA levels are sparse. We hypothesized that each factor would directly affect PUFAs and that interactions between haplotypes and DHA intake would influence PUFAs. We explored four levels of DHA intake in pregnant Chinese Han women and 10 SNPs in the ELOVL genes to determine associations with PUFAs in breast milk. The SNP rs3798713 and 3-SNP haplotype (rs2281591, rs12332786, and rs3798713) in ELOVL2 were associated with linoleic acid (LA) concentrations. However, carriers of the 3-SNP haplotype with higher DHA intake (second quartile: 14.58-43.15 mg/day) had higher concentrations of LA, arachidonic acid, EPA, and DHA compared with the interaction baseline. In ELOVL5, five SNPs (rs2294867, rs9357760, rs2397142, rs209512, and rs12207094) correlated with PUFA changes. Compared with those who had the 5-SNP haplotype C-A-C-G-A and low DHA intake (<14.58 mg/day), carriers with other haplotypes (A-A-C-A-A or C-A-C-A-A) and high DHA intake (≥118.82 mg/day) had increased EPA levels after adjustments for age and BMI. This study showed that maternal genetic variants in ELOVL2 and ELOVL5 were associated with PUFA levels in breast milk and that the combination of SNP haplotypes and higher DHA intake increased PUFA concentrations.
