Corn nitrogen rate recommendation tools’ performance across eight US midwest corn belt states

Determining which corn (Zea mays L.) N fertilizer rate recommendation tools best predict crop N need would be valuable for maximizing profits and minimizing environmental consequences. Simultaneous comparisons of multiple tools across various environmental conditions have been limited. The objectives of this research were to evaluate the performance of publicly‐available N fertilizer recommendation tools across diverse soil and weather conditions for: (i) prescribing N rates for planting and split‐fertilizer applications, and (ii) economic and environmental effects. Corn N‐response trials using standardized methods were conducted at 49 sites, spanning eight US Midwest states and three growing seasons. Nitrogen applications included eight rates in 45 kg N ha−1 increments all at‐planting and matching rates with 45 kg N ha−1 at‐planting plus at the V9 development stage. Tool performances were compared to the economically optimal N rate (EONR). Over this large geographic region, only 10 of 31 recommendation tools (mainly soil nitrate tests) produced N rate recommendations that weakly correlated to EONR (P ≤ .10; r2 ≤ .20). With other metrics of performance, the Maximum Return to N (MRTN) soil nitrate tests, and canopy reflectance sensing came close to matching EONR. Economically, all tools but the Maize‐N crop growth model had similar returns compared to EONR. Environmentally, yield goal based tools resulted in the highest environmental costs. Results show that no tool was universally reliable over this study\u27s diverse growing environments, suggesting that additional tool development is needed to better represent N inputs and crop utilization at a larger regional level

Gβγ and the C Terminus of SNAP-25 Are Necessary for Long-Term Depression of Transmitter Release

Short-term presynaptic inhibition mediated by G protein-coupled receptors involves a direct interaction between G proteins and the vesicle release machinery. Recent studies implicate the C terminus of the vesicle-associated protein SNAP-25 as a molecular binding target of Gβγ that transiently reduces vesicular release. However, it is not known whether SNAP-25 is a target for molecular modifications expressing long-term changes in transmitter release probability.This study utilized two-photon laser scanning microscopy for real-time imaging of action potential-evoked [Ca(2+)] increases, in single Schaffer collateral presynaptic release sites in in vitro hippocampal slices, plus simultaneous recording of Schaffer collateral-evoked synaptic potentials. We used electroporation to infuse small peptides through CA3 cell bodies into presynaptic Schaffer collateral terminals to selectively study the presynaptic effect of scavenging the G-protein Gβγ. We demonstrate here that the C terminus of SNAP-25 is necessary for expression of LTD, but not long-term potentiation (LTP), of synaptic strength. Using type A botulinum toxin (BoNT/A) to enzymatically cleave the 9 amino acid C-terminus of SNAP-25 eliminated the ability of low frequency synaptic stimulation to induce LTD, but not LTP, even if release probability was restored to pre-BoNT/A levels by elevating extracellular [Ca(2+)]. Presynaptic electroporation infusion of the 14-amino acid C-terminus of SNAP-25 (Ct-SNAP-25), to scavenge Gβγ, reduced both the transient presynaptic inhibition produced by the group II metabotropic glutamate receptor stimulation, and LTD. Furthermore, presynaptic infusion of mSIRK, a second, structurally distinct Gβγ scavenging peptide, also blocked the induction of LTD. While Gβγ binds directly to and inhibit voltage-dependent Ca(2+) channels, imaging of presynaptic [Ca(2+)] with Mg-Green revealed that low-frequency stimulation only transiently reduced presynaptic Ca(2+) influx, an effect not altered by infusion of Ct-SNAP-25.The C-terminus of SNAP-25, which links synaptotagmin I to the SNARE complex, is a binding target for Gβγ necessary for both transient transmitter-mediated presynaptic inhibition, and the induction of presynaptic LTD