High temperature defense-related pathways, mediating lodicule expansion and spikelet opening in maize tassel.

High temperature (HT) at flowering hinders pollen shedding, whereas mechanisms underlying stress-induced spikelet closure are poorly known in maize. Yield components, spikelet opening, and lodicule morphology/protein profiling upon HT stress during flowering were explored in maize inbred lines Chang 7-2 and Qi 319. HT induced spikelet closure and reduced pollen shed weight (PSW) and seed set. Qi 319 that had a 7-fold lower PSW than Chang 7-2 was more susceptible to HT. A small lodicule size reduced spikelet opening rate and angle, and more vascular bundles hastened lodicule shrinking in Qi 319. Lodicules were collected for proteomics. In HT-stressed lodicules, proteins involved in stress signal, cell wall, cell constructure, carbohydrate metabolism, and phytohormone signaling were associated with stress tolerance. Among these proteins, HT downregulated expression of ADP-ribosylation factor GTPase-activating protein domain2, SNAP receptor complex member11, and sterol methyltransferase2 in Qi 319 but not in Chang 7-2, agreeing well with protein abundance changes. Exogenous epibrassinolide enlarged spikelet opening angle and extended spikelet opening duration. These results suggest that dysfunction of actin cytoskeleton and membrane remodeling induced by HT likely limits lodicule expansion. Additionally, reduced vascular bundles in lodicule and application of epibrassinolide might confer spikelet tolerance to HT stress.