The COP1/SPA complex is a central regulator of photomorphogenesis in Arabidopsis. COP1 is required for the elongation response of the hypocotyl to a low red light to far-red light ratio (R:FR ratio), which is caused by close neighbours in natural habitats. In this study, it was shown that SPA genes were also essential for elongation responses to low R:FR conditions. SPA1 and SPA4 were the main SPA genes that regulate the responses of seedlings. Close neighbours also trigger an elongation response of leaf petioles. Here, the SPA genes and COP1 were essential. Flowering is accelerated by low R:FR conditions and the COP1/SPA complex is a regulator of flowering time in SD. It was shown that neither COP1 nor SPA genes had a function in the acceleration of flowering in response to low R:FR conditions. A promoter-swap analysis of SPA1 and SPA2 revealed a function for SPA2 in the elongation response of the hypocotyl to simulated shade, but only when expressed from the SPA1 promoter. Furthermore, genetic interaction studies showed that spa mutations interacted with the hfr1 mutation in the elongation response of the hypocotyl to low R:FR, indicating that over-accumulation of HFR1 may contribute to the lack of elongation response of spa and cop1 mutants. Genetic interaction studies also revealed a genetic interaction of the cop1 mutation with the phyB mutation and of spa mutations with the phyA mutation in the hypocotyl elongation response to low R:FR. Moreover, a tissue-specific function for SPA1 in the elongation response to low R:FR was found in the epidermis, while seedling growth in darkness and light was largely controlled by expression of SPA1 in the phloem. Furthermore, it was shown that the increase of the auxin signalling by low R:FR conditions was absent from two spa mutants and that the transcript levels of YUC8, an auxin biosynthesis gene, were unresponsive to low R:FR in a spa mutant, while up-regulated in the WT. Moreover, auxin signalling was found to be altered in spa mutants at the seedling stage in darkness and light and in adult leaves, which suggests that altered auxin signalling may contribute to the aberrant seedling phenotype and dwarfed growth of spa mutants. It is known that a number of auxin-induced genes are light-repressed, but whether the light-regulation is indirect via auxin or direct is not fully resolved. Here, two G-Box core motifs of the IAA19 promoter were shown to contribute to the light-regulation of the IAA19 gene, while an auxin response element (AuxRE), but not the G-Box present in the SAUR-AC1-l promoter was contributing to the light-regulation of the SAUR-AC1-l gene. This supports the notion that light signalling can directly act on promoter activity of target genes, but can also regulate genes via manipulation of hormonal pathways
