Explore the vast range of titles available.

Nodulation in legumes is regulated to maintain carbon–nitrogen homeostasis. A systemic negative feedback pathway, Autoregulation of Nodulation (AON) controls nodule number by suppressing further nodulation as early as 48–72 h post inoculation. In order to identify new genes involved in AON, a screen for suppressors of sunn-1 , a Medicago truncatula AON mutant with a hypernodulation phenotype, was performed and identified a gene not previously associated with signaling in the legume-rhizobia symbiosis . We discovered that sunn-1 plants carrying the mutation s uppressor o f s unn-1 ( sos1 ) displayed wild-type nodule numbers. At 3 days post inoculation (dpi), sos1 sunn-1 plants make many nodulation foci and infection threads but lack the emerging nodules observed in wild-type and sunn-1 mutants. At 10 dpi, in contrast to sunn-1 , no significance in nodule number was observed between wildtype and the sos1 sunn-1 plants. Using grafting, we showed that sos1 suppression of the sunn-1 nodule phenotype is dependent on the genotype of the root. The lesion a C to T transition resulting in an R to H a change mapped to Mediator 16A (MED16A) and expression of this gene in composite hairy roots led to recovery of hypernodulation in sos1 sunn-1 plants. Induction of expression of the MtNIN transcription factor involved in regulating nodulation is reduced in sos1 sunn-1 compared to sunn-1. Furthermore, sos1 plants display fewer nodules than wild-type but higher arbuscular density when colonized by an arbuscular mycorrhizal fungus, and shorter roots in the absence of rhizobia. Collectively, our findings show that effects of mutation of Mediator 16A are not specific for symbiosis but involve multiple root response pathways, making the sos1 mutant an important tool for dissection of regulons controlling rhizobial and mycorrhizal responses, root growth and possibly other response pathways.

The Mediator complex controls transcription of most eukaryotic genes with individual subunits required for the control of particular gene regulons in response to various perturbations. In this study, we reveal the roles of the plant Mediator subunits MED16, MED14, and MED2 in regulating transcription in response to the phytohormone abscisic acid (ABA) and we determine which cis elements are under their control. Using synthetic promoter reporters we established an effective system for testing relationships between subunits and specific cis- acting motifs in protoplasts. Our results demonstrate that MED16, MED14, and MED2 are required for the full transcriptional activation by ABA of promoters containing both the ABRE (ABA-responsive element) and DRE (drought-responsive element). Using synthetic promoter motif concatamers, we showed that ABA-responsive activation of the ABRE but not the DRE motif was dependent on these three Mediator subunits. Furthermore, the three subunits were required for the control of water loss from leaves but played no role in ABA-dependent growth inhibition, highlighting specificity in their functions. Our results identify new roles for three Mediator subunits, provide a direct demonstration of their function and highlight that our experimental approach can be utilized to identify the function of subunits of plant transcriptional regulators.

• Arabidopsis SENSITIVE TO FREEZING6 (SFR6) controls cold‐ and drought‐inducible gene expression and freezing‐ and osmotic‐stress tolerance. Its identification as a component of the MEDIATOR transcriptional co‐activator complex led us to address its involvement in other transcriptional responses. • Gene expression responses to Pseudomonas syringae, ultraviolet‐C (UV‐C) irradiation, salicylic acid (SA) and jasmonic acid (JA) were investigated in three sfr6 mutant alleles by quantitative real‐time PCR and susceptibility to UV‐C irradiation and Pseudomonas infection were assessed. • sfr6 mutants were more susceptible to both Pseudomonas syringae infection and UV‐C irradiation. They exhibited correspondingly weaker PR (pathogenesis‐related) gene expression than wild‐type Arabidopsis following these treatments or after direct application of SA, involved in response to both UV‐C and Pseudomonas infection. Other genes, however, were induced normally in the mutants by these treatments. sfr6 mutants were severely defective in expression of plant defensin genes in response to JA; ectopic expression of defensin genes was provoked in wild‐type but not sfr6 by overexpression of ERF5. • SFR6/MED16 controls both SA‐ and JA‐mediated defence gene expression and is necessary for tolerance of Pseudomonas syringae infection and UV‐C irradiation. It is not, however, a universal regulator of stress gene transcription and is likely to mediate transcriptional activation of specific regulons only.

Mediator is a highly conserved protein complex that functions as a transcriptional coactivator in RNA polymerase II (RNAPII)-mediated transcription. The Mediator complex has recently been implicated in plant immune responses. Here, we compared salicylic acid (SA)-, methyl jasmonate (MeJA)-, and the ethylene (ET) precursor 1-aminocyclopropane-1-carboxylic acid (ACC)-induced defense and/or wound-responsive gene expression in 14 Mediator subunit mutants. Our results show that MED14, MED15, and MED16 are required for SA-activated expression of the defense marker gene , MED25 is required for MeJA-induced expression of the wound-responsive marker gene ( ), MED8, MED14, MED15, MED16, MED18, MED20a, MED25, MED31, and MED33A/B (MED33a and MED33B) are required for MeJA-induced expression of the defense maker gene ( ), and MED8, MED14, MED15, MED16, MED25, and MED33A/B are also required for ACC-triggered expression of . Furthermore, we investigated the involvement of MED14, MED15, and MED16 in plant defense signaling crosstalk and found that MED14, MED15, and MED16 are required for SA- and ET-mediated suppression of MeJA-induced expression. This result suggests that MED14, MED15, and MED16 not only relay defense signaling from the SA and JA/ET defense pathways to the RNAPII transcription machinery, but also fine-tune defense signaling crosstalk. Finally, we show that MED33A/B contributes to the necrotrophic fungal pathogen induced expression of the defense genes , and and is required for full-scale basal resistance to , demonstrating a positive role for MED33 in plant immunity against necrotrophic fungal pathogens.

Recent studies have shown that the mediator complex (MED) plays a vital role in tumorigenesis and development, but the role of MED16 (mediator complex subunit 16) in breast cancer (BC) is not clear. Increasing evidence has shown that the mTOR pathway is important for tumour progression and therapy. In this study, we demonstrated that the mTOR signalling pathway is regulated by the expression level of MED16 in ER+ breast cancer. With the analysis of bioinformatics data and clinical specimens, we revealed an elevated expression of MED16 in luminal subtype tumours. We found that MED16 knockdown significantly inhibited cell proliferation and promoted G1 phase cell cycle arrest in ER+ BC cell lines. Downregulation of MED16 markedly reduced the sensitivity of ER+ BC cells to tamoxifen and increased the stemness and autophagy of ER+ BC cells. Bioinformatic analysis of similar genes to MED16 were mainly enriched in autophagy, endocrine therapy and mTOR signalling pathways, and the inhibition of mTOR-mediated autophagy restored sensitivity to tamoxifen by MED16 downregulation in ER+ BC cells. These results suggest an important role of MED16 in the regulation of tamoxifen sensitivity in ER+ BC cells, crosstalk between the mTOR signalling pathway-induced autophagy, and together, with the exploration of tamoxifen resistance, may indicate a new therapy option for endocrine therapy-resistant patients.

Mediator is a central transcriptional coactivator that connects sequence-specific transcription factors with RNA polymerase II to control inducible gene expression in plants. MED16 is a Mediator tail module subunit that functions as a context-dependent integrator, helping coordinate developmental programs with environmental adaptation. This review summarizes current evidence for MED16 function from structural and evolutionary perspectives to physiological outputs, with emphasis on how MED16 interacts with transcription factors and other Mediator subunits to shape RNA polymerase II engagement at target loci. In terms of development, MED16 contributes to organ growth and root system architecture, and comparative studies have revealed that it plays conserved roles in lineage-specific wiring. Under abiotic stress, MED16 supports the efficient activation of stress-inducible transcription, including cold acclimation and nutrient stress responses such as phosphate starvation-dependent root remodeling. In immunity, MED16 modulates salicylic acid- and jasmonate/ethylene-associated defence outputs and can be targeted by plant viruses, which is consistent with its role in antiviral transcriptional responses. Mechanistically, MED16 participates in cooperative and competitive interactions within the Mediator complex that tune hormone-responsive outputs, exemplified by MED25-related competition in abscisic acid signalling. We highlight key limitations and future directions, including the need for mechanistic validation beyond Arabidopsis, clearer models of dosage control in crops, improved understanding of context-dependent tail configurations, and high-resolution mapping of MED16 interaction interfaces.