Natural changes in photoperiod, light quantity, and quality play a key role in plant signaling, enabling daily and seasonal adjustment of growth and development. Growing concern about the global climate crisis together with scattered reports about the interactive effects of temperature and light parameters on plants necessitates more detailed information about these effects. Furthermore, the actual light emitting diode (LED) lighting technology allows mimicking of light climate scenarios more similar to natural conditions, but to fully exploit this in plant cultivation, easy-to-apply knowledge about the natural variation in light quantity and spectral distribution is required. Here, we aimed to provide detailed information about short and long-term variation in the natural light climate, by recording the light quantity and quality at an open site in Switzerland every minute for a whole year, and to analyze its relationship to a set of previous tree seedling growth experiments. Changes in the spectral composition as a function of solar elevation angle and weather conditions were analyzed. At a solar elevation angle lower than 20°, the weather conditions have a significant effect on the proportions of blue (B) and red (R) light, whereas the proportion of green (G) light is almost constant. At a low solar elevation, the red to far red (R:FR) ratio fluctuates between 0.8 in cloudy conditions and 1.3 on sunny days. As the duration of periods with low solar angles increases with increasing latitude, an analysis of previous experiments on tree seedlings shows that the effect of the R:FR ratio correlates with the responses of plants from different latitudes to light quality. We suggest an evolutionary adaptation where growth in seedlings of selected tree species from high latitudes is more dependent on detection of light quantity of specific light qualities than in such seedlings originating from lower latitudes.

Whereas long days (LDs) sustain shoot elongation, short days (SDs) induce growth cessation and formation of dormant buds in young individuals of a wide range of temperate and boreal tree species. In specific conifers, including Norway spruce, photoperiodic control of bud development is associated with the formation of a plate of thick-walled cells, denoted as the crown, at the base of the bud. Information about cellular characteristics of this crown region is limited. We aimed to test whether the crown region is an important SD-induced barrier ensuring dehydration of the developing winter bud by preventing water influx. Using microscopy and synchrotron techniques, we show here that under LD, cell walls in growing shoot tips had highly methyl-esterified homogalacturonan pectin. During SD-induced bud development, the homogalacturonan in the crown region was de-methyl-esterified, enabling Ca²⁺ binding and crosslinking, a process known to decrease cell wall water permeability by reducing pectin pore size. In addition, there was abundant callose deposition at plasmodesmata in the crown region, and xylem connections between the bud and the subtending shoot were blocked. Consistent with reduced water transport across the crown region into the bud, uptake of fluorescein in shoot tips was blocked at the base of the bud under SD. Upon transfer from SD to bud-break-inducing LD, these processes were reversed, and aquaporin transcript levels significantly increased in young stem tissue after 4 weeks under LD. These findings indicate that terminal bud development is associated with reduced water transport through decreased cell wall permeability and blocking of plasmodesmata and xylem connections in the crown structure. This provides further understanding of the regulatory mechanism for growth-dormancy cycling in coniferous tree species such as Norway spruce.

Gymnosperms are long-lived, cone-bearing seed plants that include some of the most ancient extant plant species. These relict land plants have evolved to survive in habitats marked by chronic or episodic stress. Their ability to thrive in these environments is partly due to their phenotypic flexibility, and epigenetic regulation likely plays a crucial part in this plasticity. We review the current knowledge on abiotic and biotic stress memory in gymnosperms and the possible epigenetic mechanisms underlying long-term phenotypic adaptations. We also discuss recent technological improvements and new experimental possibilities that likely will advance our understanding of epigenetic regulation in these ancient and hard-to-study plants.

Exposure to ambient UV-B radiation may prime protective responses towards various stressors in plants, though information about interactive effects of UV-B and gamma radiation is scarce. Here, we aimed to test whether UV-B exposure could prime acclimatisation mechanisms contributing to tolerance to low-moderate gamma radiation levels in Scots pine seedlings, and concurrently whether simultaneous UV-B and gamma exposure may have an additive adverse effect on seedlings that had previously not encountered either of these stressors. Responses to simultaneous UV-B (0.35 W m⁻²) and gamma radiation (10.2–125 mGy h⁻¹) for 6 days with or without UV-B pre-exposure (0.35 W m⁻², 4 days) were studied across various levels of organisation, as compared to effects of either radiation type. In contrast to UV-B, and regardless of UV-B presence, gamma radiation at ≥42.9 mGy h⁻¹ caused increased formation of reactive oxygen species and reduced shoot length, and reduced root length at 125 mGy h⁻¹. In all experiments there was a gamma dose rate-dependent increase in DNA damage at ≥10.8 mGy h⁻¹, generally with additional UV-B-induced damage. Gamma-induced growth inhibition and gamma- and UV-B-induced DNA damage were still visible 44 days post-irradiation, even at 20.7 mGy h⁻¹, probably due to genomic instability, but this was reversed after 8 months. In conclusion, there was no evidence of a protective effect of UV-B on gamma-induced growth inhibition and DNA damage in Scots pine, and no additive adverse effect of gamma and UV-B radiation on growth in spite of the additional UV-B-induced DNA damage.