Abstract During Arabidopsis thaliana photomorphogenesis, light promotes cotyledon expansion and inhibits hypocotyl elongation. This process involves transcriptional reprogramming controlled by various factors, including the Elongator complex which regulates gene expression at the level of transcription and translation via epigenetic and tRNA modifications, respectively. The elo3–6 mutant, lacking Elongator activity, exhibited photomorphogenic defects: less open, hyponastic cotyledons and an elongated hypocotyl. RNA-Seq and miRNA-Seq revealed distinct dysregulated gene sets in elo3–6 hypocotyl and cotyledons. In hypocotyl, the elo3–6 defect affected expression of genes involved in chloroplast physiology, circadian regulation, and auxin responses. Impaired chloroplast biogenesis apparently triggered retrograde signaling and a hypoxia-like state, preventing full inhibition of hypocotyl elongation. The defective elo3–6 cotyledon development is likely due to compromised translation. This was supported by the presence of similar morphological defects in urm11 urm12, defective in the same type of tRNA modification as in elo3–6, and the synergism observed in the elo3–6 urm11 urm12 (euu) triple mutant showing seedling lethality. Moreover, elo3–6 and urm11 urm12 showed increased tolerance to translation inhibitors, including hygromycin B which prevented the narrower cotyledon opening in elo3–6, suggesting that strong Elongator-dependent codon-anticodon interactions are required for proper cotyledon development. Interestingly, the genes enriched in codons recognized by tRNA anticodons modified by Elongator showed decreased mRNA abundance in elo3–6, suggesting a feedback mechanism downregulating the abundance of inefficiently translated mRNAs. Our results suggest that Elongator’s transcriptional role is more important in hypocotyl growth, while its translational role is more prominent in cotyledon development.
Jarosz-Ostrówka et al. (2026) studied this question.