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Summary: In plant species, anthocyanin accumulation is specifically regulated by light signaling. Although the CONSTITUTIVELY PHOTOMORPHOGENIC1/SUPPRESSOR OF PHYA‐105 (COP1/SPA) complex is known to control anthocyanin biosynthesis in response to light, the precise mechanism underlying this process remains largely unknown.Here, we report that Increase in BONSAI Methylation 1 (IBM1), a JmjC domain‐containing histone demethylase, participates in the regulation of light‐induced anthocyanin biosynthesis in Arabidopsis.The expression of IBM1 was induced by high light (HL) stress, and loss‐of‐function mutations in IBM1 led to accelerated anthocyanin accumulation under HL conditions. We further identified that IBM1 is directly associated with SPA1/3/4 chromatin in vivo to establish a hypomethylation status on H3K9 and DNA non‐CG at these loci under HL, thereby releasing their expression. Genetic analysis showed that quadruple mutants of IBM1 and SPA1/3/4 resemble spa134 mutants. Overexpression of SPA1 in ibm1 mutants complements the mutant phenotype.Our results elucidate the significance and mechanism of IBM1 histone demethylase in the epigenetic regulation of anthocyanin biosynthesis in Arabidopsis under HL conditions. [ABSTRACT FROM AUTHOR]

Summary: Trichomes are specialized epidermal cells that contribute to plant resistance against herbivores. Their formation is controlled precisely by multiple genetic and environmental signals. Previous studies have shown that microRNA319 (miR319) and gibberellin (GA) signaling are involved in trichome development in Arabidopsis, but little is known about their interaction between these factors.Here we reported that the miR319a/TEOSINTE BRANCHED/CYCLOIDEA/PCF (TCP) module participates in trichome initiation synergistically with GA signaling in Populus tomentosa. We demonstrated that overexpression of miR319a decreased transcription levels of its targeted TCPs and significantly elevated leaf trichome density in transgenic poplar, resulting in decreasing insect herbivory. Conversely, repressing miR319a by short tandem target mimics (STTM) elevated TCP expression levels and decreased trichome density in transgenic plants.The trichome phenotype of 35S:miR319a plants could be abolished by introducing a miR319a‐resistant form of TCP19. Furthermore, the miR319a‐targeted TCP19 interacted directly with REPRESSOR OF ga1‐3 (RGA), a downstream repressor of GA signaling. TCP19 and RGA synergistically inhibited the GLABROUS1 (GL1)‐induced expression of trichome marker gene GLABRA2 (GL2), thereby repressing leaf trichome initiation.Our results provide an insight into the molecular mechanism by which miR319/TCP19 module and GA signaling coordinated regulating trichome initiation in P. tomentosa. [ABSTRACT FROM AUTHOR]

Summary: Wood development is strictly regulated by various phytohormones and auxin plays a central regulatory role in this process. However, how the auxin signaling is transducted in developing secondary xylem during wood formation in tree species remains unclear.Here, we identified an Aux/INDOLE‐3‐ACETIC ACID 9 (IAA9)‐AUXIN RESPONSE FACTOR 5 (ARF5) module in Populus tomentosa as a key mediator of auxin signaling to control early developing xylem development.PtoIAA9, a canonical Aux/IAA gene, is predominantly expressed in vascular cambium and developing secondary xylem and induced by exogenous auxin. Overexpression of PtoIAA9m encoding a stabilized IAA9 protein significantly represses secondary xylem development in transgenic poplar. We further showed that PtoIAA9 interacts with PtoARF5 homologs via the C‐terminal III/IV domains. The truncated PtoARF5.1 protein without the III/IV domains rescued defective phenotypes caused by PtoIAA9m. Expression analysis showed that the PtoIAA9‐PtoARF5 module regulated the expression of genes associated with secondary vascular development in PtoIAA9m‐ and PtoARF5.1‐overexpressing plants. Furthermore, PtoARF5.1 could bind to the promoters of two Class III homeodomain‐leucine zipper (HD‐ZIP III) genes, PtoHB7 and PtoHB8, to modulate secondary xylem formation.Taken together, our results suggest that the Aux/IAA9‐ARF5 module is required for auxin signaling to regulate wood formation via orchestrating the expression of HD‐ZIP III transcription factors in poplar. [ABSTRACT FROM AUTHOR]