Pectin remodeling belongs to a homeostatic system and triggers trasncriptomic and hormonal modulations

Pectins occur in primary cell walls and consist of multiblock co-polymers among which homogalacturonan (HG) is the simplest and most abundant form. Methylesterification patterns of HG are tuned by pectin methylesterases (PMEs), the activities of which are controlled by specific inhibitors (PMEIs). By impacting cell wall mechanical properties, PMEmediated regulation of HG methylesterification plays a major role in several developmental processes, including seed germination and dark-grown hypocotyl elongation. Arabidopsis PME36 is preferentially expressed during the late stage of seed development and, using the knock-out mutants pme36-1 and pme36-2, we show here that PME36 is required to implement the characteristic pattern of de-methylesterified pectin in the mature seed. Surprisingly, while this pattern is strongly impaired in pme36-1 mature seed, no phenotypical effect is observed in the mutant during seed germination and dark-grown hypocotyl elongation, suggesting the existence of a compensatory mechanism overcoming the defect in pectin de-methylesterification. By analyzing hormone contents and gene expression, a strong, dynamic, and long-lasting physiological disorder is revealed in the mutant. These results suggest the existence of complex connections between pectin remodeling, transcriptomic regulations and hormonal homeostasis, modulating several physiological parameters to ensure the maintenance of a normal seed-to-seedling developmental program in pme36-1.Considered for a long time as an end-point passive effector mainly involved in modification of cell wall mechanics, the role of pectin methylesterification needs to be reconsidered as amodulator acting upstream of diverse regulatory pathways involved in plant development.