ABSTRACTThe Arabidopsis (Arabidopsis thaliana) seed coat mucilage is a specialized cell wall with pectin as its major component. Pectin is synthesized in the Golgi apparatus with homogalacturonan fully methylesterified, but it must undergo de-methylesterification by pectin methylesterase (PME) after being secreted into the cell wall. This reaction is critical for pectin maturation, but the mechanisms of its transcriptional regulation remain largely unknown. Here, we show that the Arabidopsis ERF4 transcription factor positively regulates pectin de-methylesterification during seed development and directly suppresses the expression of PME INHIBITOR13 (PMEI13), 14, 15 and SUBTILISIN-LIKE SERINE PROTEASE 1.7 (SBT1.7). The erf4 mutant seeds showed repartitioning of mucilage between soluble and adherent layers as a result of decreased PME activity and increased degree of pectin methylesterification. ERF4 physically associates with and antagonizes MYB52 in activating PMEI6, 14 and SBT1.7 and MYB52 also antagonizes ERF4 activity in the regulation of downstream targets. Gene expression studies revealed that ERF4 and MYB52 have opposite effects on pectin de-methylesterification. Genetic analysis indicated that the erf4-2 myb52 double mutant seeds show mucilage phenotype similar to wild-type. Taken together, this study demonstrates that ERF4 and MYB52 antagonize each other’s activity to maintain the appropriate degree of pectin methylesterification, expanding our understanding of how pectin de-methylesterification is fine-tuned by the ERF4-MYB52 transcriptional complex in the seed mucilage.One-sentence summaryArabidopsis ERF4 and MYB52 transcription factors interact and play antagonistic roles in regulating homogalacturonan de-methylesterification related genes in the seed coat mucilage.
Sticking to cellulose: exploiting Arabidopsis seed coat mucilage to understand cellulose biosynthesis and cell wall polysaccharide interactions