MED18 interaction with distinct transcription factors regulates multiple plant functions

Abstract

Mediator is an evolutionarily conserved transcriptional regulatory complex. Mechanisms of Mediator function are poorly understood. Here we show that Arabidopsis MED18 is a multifunctional protein regulating plant immunity, flowering time and responses to hormones through interactions with distinct transcription factors. MED18 interacts with YIN YANG1 to suppress disease susceptibility genes glutaredoxins GRX480, GRXS13 and thioredoxin TRX-h5. Consequently, yy1 and med18 mutants exhibit deregulated expression of these genes and enhanced susceptibility to fungal infection. In addition, MED18 interacts with ABA INSEN-SITIVE 4 and SUPPRESSOR OF FRIGIDA4 to regulate abscisic acid responses and flowering time, respectively. MED18 associates with the promoter, coding and terminator regions of target genes suggesting its function in transcription initiation, elongation and termination. Notably, RNA polymerase II occupancy and histone H3 lysine tri-methylation of target genes are affected in the med18 mutant, reinforcing MED18 function in different mechanisms of transcriptional control. Overall, MED18 conveys distinct cues to engender transcription underpinning plant responses.

The Arabidopsis Mediator Complex Subunit16 Is a Key Component of Basal Resistance against the Necrotrophic Fungal Pathogen Sclerotinia sclerotiorum

“…1). Although med8, med13, and med18 have been shown to be more susceptible than the wild type to the necrotrophic fungal pathogens B. cinerea and A. brassicicola (Kidd et al, 2009;Lai et al, 2014;Zhu et al, 2014), they did not show enhanced susceptibility to S. sclerotiorum. This is probably because MED8, MED13, and MED18 do not play a major role in regulating S. sclerotiorum-induced transcriptome changes (Fig.…”

“…MED14, MED15, MED16, and MED19a have been shown to regulate the SA-triggered immunity against biotrophic and hemibiotrophic pathogens (Canet et al, 2012;Zhang et al, 2012Zhang et al, , 2013Caillaud et al, 2013), whereas MED8, MED12, MED13, MED16, MED21, MED25, and CDK8 have been found to function in JA/ET-mediated immunity against necrotrophic pathogens (Dhawan et al, 2009;Kidd et al, 2009;Zhang et al, 2012;Zhu et al, 2014). MED18 also functions in resistance to necrotrophic pathogens, but the resistance is independent of the JA/ET signaling (Lai et al, 2014). Interestingly, the Arabidopsis oomycete pathogen Hyaloperonospora arabidopsidis RXLR effector44 (HaRxL44) interacts with MED19a and promotes its degradation, which shifts the balance of defense transcription from SA to JA/ET signaling (Caillaud et al, 2013).…”

Chitin and chitin-related compounds in plant–fungal interactions

“…MED8, MED12, MED13, MED14, MED16, MED21, MED25 and CDK8 have been found to function in JA/ET-mediated immunity against necrotrophic pathogens (Dhawan et al 2009; Zhang et al 2012). MED18 also operates in resistance to necrotrophic pathogens, but the resistance appears to be independent of the JA/ET signalling (Lai et al 2014). Wang et al (2016) showed that MED33A/B contributed to the necrotrophic fungal pathogen Botrytis cinerea induced expression of the PDF1.2 defensin, HEVEIN-LIKE and BASIC CHITINASE defence genes and is required for full-scale basal resistance to B. cinerea , which demonstrated a decisive role for MED33 against necrotrophic fungal pathogens.…”

Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1

“…Chromatin associated with GFP-MOS1 was precipitated with anti-GFP antibodies and four FLC genomic sites ( Fig. 4d), including the SUF4-binding site 23 of the FLC promoter, were analysed for their abundance in the precipitated chromatins by quantitative (q)-PCR. Compared with the no antibody (Ab) IP sample, the Ab IP sample had a five-fold enrichment at the SUF4-binding site, while no significant enrichment was found at three other sites: TATA box, a coding fragment and the terminator (Fig.…”