Heat stress and sexual reproduction in maize: unveiling the most pivotal factors and the greatest opportunities.

The escalation in the intensity, frequency, and duration of high-temperature (HT) stress is currently unparalleled, which aggravates the challenges for crop production. Yet, the stage-dependent responses of reproductive organs to HT stress at the morphological, physiological, and molecular levels remain inadequately explored in pivotal staple crops. This review synthesized current knowledge regarding the mechanisms by which HT stress induces abnormalities and aberrations in reproductive growth and development, as well as by which it alters the morphology and function of florets, flowering patterns, and the processes of pollination and fertilization in maize (Zea mays L.). We identified the stage-specific sensitivities to HT stress and accurately defined the sensitive period from a time scale of days to hours. The microspore tetrad phase of pollen development and anthesis (especially shortly after pollination) are most sensitive to HT stress, and even brief temperature spikes during these stages can lead to significant kernel loss. The impetuses behind the heat-induced impairments in seed set are closely related to carbon, reactive oxygen species, phytohormone signals, ion (e.g. Ca2+) homeostasis, plasma membrane structure and function, and others. Recent advances in understanding the genetic mechanisms underlying HT stress responses during maize sexual reproduction have been systematically summarized.

Heat-dependent postpollination limitations on maize pollen tube growth and kernel sterility.

Heat stress has a negative impact on pollen development in maize (Zea mays L.) but the postpollination events that determine kernel sterility are less well characterised. The impact of short-term (hours) heat exposure during postpollination was therefore assessed in silks and ovaries. The temperatures inside the kernels housed within the husks was significantly lower than the imposed heat stress. This protected the ovaries and possibly the later phase of pollen tube growth from the adverse effects of heat stress. Failure of maize kernel fertilization was observed within 6 h of heat stress exposure postpollination. This was accompanied by a significant restriction of early pollen tube growth rather than pollen germination. Limitations on early pollen tube growth were therefore a major factor contributing to heat stress-induced kernel sterility. Exposure to heat stress altered the sugar composition of silks, suggesting that hexose supply contributed to the limitations on pollen tube growth. Moreover, the activities of sucrose metabolising enzymes, the expression of sucrose degradation and trehalose biosynthesis genes were decreased following heat stress. Significant increases in reactive oxygen species, abscisic acid and auxin levels accompanied by altered expression of phytohormone-related genes may also be important in the heat-induced suppression of pollen tube growth.

High temperature defense pathways mediate lodicule expansion and spikelet opening in maize tassels.

High temperature (HT) at flowering hinders pollen shedding, but the mechanisms underlying stress-induced spikelet closure are poorly understood in maize. In this study, yield components, spikelet opening, and lodicule morphology/protein profiling upon HT stress during flowering were examined in two contrasting maize inbred lines, Chang 7-2 and Qi 319. HT induced spikelet closure and reduced pollen shed weight (PSW) and seed set in both lines, but Qi 319 had a 7-fold lower PSW than Chang 7-2, and was thus more susceptible to HT. In Qi 319, a smaller lodicule size reduced the spikelet opening rate and angle, and relatively more vascular bundles hastened lodicule shrinking compared with Chang 7-2. Lodicules were collected for proteomics analysis. In lodicules of HT-stressed plants, proteins involved in stress signals, cell wall, cell constructure, carbohydrate metabolism, and phytohormone signaling were associated with stress tolerance. HT down-regulated the 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, which was in good agreement with the observed changes in protein abundance. Exogenous epibrassinolide increased the spikelet opening angle and extended the duration of spikelet opening. These results suggest that dysfunction of the actin cytoskeleton and membrane remodeling induced by HT probably limits lodicule expansion. In addition, a reduction in the vascular bundles in the lodicules and application of epibrassinolide might confer spikelet tolerance to HT stress.