Germostatin resistance locus 1 encodes a PHD finger protein involved in auxin‐mediated seed dormancy and germination

Abstract

SUMMARYSeed dormancy and germination are important physiological processes during the life cycle of a seed plant. Recently, auxin has been characterized as a positive regulator that functions during seed dormancy and as a negative regulator during germination. Through chemical genetic screenings, we have identified a small molecule, germostatin (GS), which effectively inhibits seed germination in Arabidopsis. GSR1 (germostatin resistance locus 1) encodes a tandem plant homeodomain (PHD) finger protein, identified by screening GSresistant mutants. Certain PHD fingers of GSR1 are capable of binding unmethylated H3K4, which has been reported as an epigenetic mark of gene transcriptional repression. Biochemical studies show that GSR1 physically interacts with the transcriptional repressor ARF16 and attenuates the intensity of interaction of IAA17/ARF16 by directly interacting with IAA17 to release ARF16. Further results show that axr3-1, arf10 arf16 are hyposensitive to GS, and gsr1 not only resists auxin-mediated inhibition of seed germination but also displays decreased dormancy. We therefore propose that GSR1 may form a co-repressor with ARF16 to regulate seed germination. Besides promoting auxin biosynthesis via upregulating expression of YUCCA1, GS also enhances auxin responses by inducing degradation of DΙΙ-VENUS and upregulating expression of DR5-GFP. In summary, we identified GSR1 as a member of the auxin-mediated seed germination genetic network, and GS, a small non-auxin molecule that specifically acts on auxin-mediated seed germination.

Triplin, a small molecule, reveals copper ion transport in ethylene signaling from ATX1 to RAN1

“…We believe that a copper ion chelator with such a property would be useful for investigating the mechanisms of copper ion transport to the ethylene receptors. More ever, chemical genetics approaches are powerful in dealing with the function redundancy of components involved in phytohormone signaling, and have helped scientists to identify ABA receptors and novel signaling components involving in auxin and other phytohormones [29–32]. …”

Plant Chemical Genetics: From Phenotype-Based Screens to Synthetic Biology

“…Similarly, a recent screen for compounds that alter leaf vein patterns in Arabidopsis produced chemical hits affecting hormone signaling, endomembrane trafficking, and MAPK function, among others (Carland et al, 2016). The more general phenotype-based screens have been especially valuable for the identification of small molecules acting in signaling cross talk (He et al, 2011;Kim et al, 2011;Ye et al, 2016). For instance, a chemical screen for compounds activating mitochondrial retrograde signaling uncovered an inhibitor of auxin responses, 2-furylacrylic acid (Armstrong et al, 2004;Sungur et al, 2007), exposing an unexpected link between mitochondrial function and auxin signaling (Kerchev et al, 2014).…”

“…Chembridge also provides focused or targeted small-molecule libraries (Poretska et al, 2016). Additional libraries include the Maybridge Hitfinder (Nishimura et al, 2012(Nishimura et al, , 2014, the Life Chemicals, Inc., collection (Zhao, 2012;Ye et al, 2016), the Korean Chemical Bank (Kim et al, 2010), and the RIKEN Natural Products Depository (Noutoshi et al, 2012a;Ito et al, 2015). Several smaller libraries also can be combined, resulting in screens of sometimes more than 50,000 small molecules (Drakakaki et al, 2011;Okamoto et al, 2013;Knoth and Eulgem, 2014).…”

“…Seed germination inhibitory screens have led to the identification of hypostatins, cell expansion inhibitors with an unknown MoA (Zhao et al, 2007), and auxin response-promoting compounds, such as germostatin (Ye et al, 2016).…”

“…For instance, the screen for germostatin-resistant mutants revealed a mutation in the GERMOSTATIN RESISTANCE1 (GRS1) gene. This GRS1 allele encodes a mutation in the PHD finger protein GSR1, which interacts physically with IAA17 and ADP-RIBOSYLATION FACTOR10 (ARF10)/ARF16 to form a corepressor complex and to enhance auxin signaling, but it is not a direct target of germostatin (Ye et al, 2016). A screen for naxillin-resistant mutants uncovered the NAXILLIN RESISTANT1 locus containing INDOLE-3-BUTYRIC ACID RESPONSE3, which codes for a protein implicated in the peroxisomal b-oxidation pathway in which IBA is converted into IAA17, confirming that a defect in this step is responsible for the naxillin resistance phenotype (De Rybel et al, 2012).…”