Growth-inhibiting effects of the unconventional plant APYRASE 7 of Arabidopsis thaliana influences the LRX/RALF/FER growth regulatory module.

Plant cell growth involves coordination of numerous processes and signaling cascades among the different cellular compartments to concomitantly enlarge the protoplast and the surrounding cell wall. The cell wall integrity-sensing process involves the extracellular LRX (LRR-Extensin) proteins that bind RALF (Rapid ALkalinization Factor) peptide hormones and, in vegetative tissues, interact with the transmembrane receptor kinase FERONIA (FER). This LRX/RALF/FER signaling module influences cell wall composition and regulates cell growth. The numerous proteins involved in or influenced by this module are beginning to be characterized. In a genetic screen, mutations in Apyrase 7 (APY7) were identified to suppress growth defects observed in lrx1 and fer mutants. APY7 encodes a Golgi-localized NTP-diphosphohydrolase, but opposed to other apyrases of Arabidopsis, APY7 revealed to be a negative regulator of cell growth. APY7 modulates the growth-inhibiting effect of RALF1, influences the cell wall architecture and -composition, and alters the pH of the extracellular matrix, all of which affect cell growth. Together, this study reveals a function of APY7 in cell wall formation and cell growth that is connected to growth processes influenced by the LRX/RALF/FER signaling module.

Role of Flavonol Synthesized by Nucleus FLS1 in Arabidopsis Resistance to Pb Stress.

Lead (Pb) is an important pollutant of worldwide concern with respect to extensive pollution sources and highly toxic effect. Flavonol can improve plant resistance to abiotic stress and is also responsible for the alleviating effect under Pb stress. The relationship between Pb stress and flavonol and the knowledge about the mechanisms of flavonol function are very limited. Pb affected the energy metabolism process and, thus, inhibited plant growth and development. Flavonol accumulation controlled by FLS1 (flavonol synthase) could alleviate the toxic effect. Importantly, nes (mutant of NES that allows FLS1 to enter the nucleus expression) showed better growth status and lighter oxidative damage than NES (N-terminal nucleus exclusion signal peptide prevents FLS1 from entering the nucleus expression), which indicated that nucleus flavonol synthesized by nucleus FLS1 plays a key role in plant resistance to Pb stress. Although FLS1 signals were detected in the cell membrane, cytoplasm, and nucleus, membrane flavonol, cytoplasm flavonol, and nucleus flavonol were not exercising their function in the corresponding position. The expression of nucleus FLS1 intervened in the total content and composition of flavonol. The results also revealed that nucleus flavonol could regulate the ascorbate metabolism for alleviating the damage on the chloroplast, thus maintaining the photophosphorylation pathway. Our findings provided new insights for the molecular basis of Pb tolerance and response mechanism of the plant.

Mutations in the Arabidopsis ROL17/isopropylmalate synthase 1 locus alter amino acid content, modify the TOR network, and suppress the root hair cell development mutant lrx1.

The growth and development of organisms must be tightly controlled and adjusted to nutrient availability and metabolic activities. The Target of Rapamycin (TOR) network is a major control mechanism in eukaryotes and influences processes such as translation, mitochondrial activity, production of reactive oxygen species, and the cytoskeleton. In Arabidopsis thaliana, inhibition of the TOR kinase causes changes in cell wall architecture and suppression of phenotypic defects of the cell wall formation mutant lrx1 (leucine-rich repeat extensin 1). The rol17 (repressor of lrx1 17) mutant was identified as a new suppressor of lrx1 that induces also a short root phenotype. The ROL17 locus encodes isopropylmalate synthase 1, a protein involved in leucine biosynthesis. Dependent on growth conditions, mutations in ROL17 do not necessarily alter the level of leucine, but always cause development of the rol17 mutant phenotypes, suggesting that the mutation does not only influence leucine biosynthesis. Changes in the metabolome of rol17 mutants are also found in plants with inhibited TOR kinase activity. Furthermore, rol17 mutants show reduced sensitivity to the TOR kinase inhibitor AZD-8055, indicating a modified TOR network. Together, these data suggest that suppression of lrx1 by rol17 is the result of an alteration of the TOR network.