Down-regulation of nitrogen/carbon metabolism coupled with coordinative hormone modulation contributes to developmental inhibition of the maize ear under nitrogen limitation.

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CONCLUSION: Developmental inhibition of the maize ear by nitrogen limitation is due to overall down-regulation of nitrogen/carbon metabolism, coordinative hormonal modulation, and probable early senescence. The kernel number is primarily determined from 2 weeks pre-silking to 3 weeks post-silking, largely depending on dynamic nitrogen (N) and carbohydrate metabolism and accumulation in the maize ear. Underlying physiological and molecular mechanisms of kernel abortion caused by N limitation needs to be further investigated. Using a widely grown maize hybrid ZD958, we found that the N deficient ear was shorter, with less biomass accumulation, lower N concentrations, and overall lower concentrations of N assimilates and soluble sugars at 1- or 2-week after silking. Such negative alterations were probably due to significant decreases in activities of nitrate reductase, glutamine synthetase, sucrose phosphate synthetase, and sucrose synthetase in the N deficient maize ear especially after silking. Compensatory up-regulation of corresponding gene expression, together with co-downregulation of gene expression and enzyme activities in certain circumstances, suggested regulatory complexity and mechanistic differentiation from gene expression to functioning at physiological and molecular levels in quickly developing maize ear in counteracting N deficiency. Importantly, auxin, gibberellin, cytokinin, and abscisic acid may act in a coordinative manner to negatively modulate ear development under N limitation, as indicated by their concentration variations and substantial up-regulation of IAA14, GA2-ox1, and CKX12. Lastly, early senescence may occur in the low-N ear driven by interplay of hormone functioning and senescence-related gene regulation.