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Plastic upcycling, which involves making plastic-derived products with unique or improved properties from discarded plastic materials, is a promising alternative to recycling and disposal to help reduce the overall production of waste. However, recycled and reused materials typically have inferior mechanical, thermal, optical, and barrier properties compared with virgin plastics. Upcycled plastic materials could improve these properties while addressing future waste accumulation. In this study, we use waste poly(ethylene terephthalate) (PET) collected from disposable food packaging to create a repurposed plastic graphene oxide (GO) composite with a goal of upcycling. We developed a one-pot “dynamic depolymerization” to break down PET in the presence of GO and successfully enabled transesterification of the polymer onto GO. Covalent attachment of PET onto GO and tailorable plastic content was confirmed by thermogravimetric analysis, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and scanning electron microscopy. These covalent composites (PET-GO) were found to be relatively impermeable to water vapor, showing promise for applications in packaging materials. Aqueous degradation experiments on the composite materials demonstrated that, in bulk conditions, PET-GOs remain mechanically robust while in contact with water over appropriate time scales for packaging applications, while beginning to break down in accelerated conditions. The use of depolymerization methods to promote polymer grafting concurrently with polymer deconstruction could provide a more general method for grafting waste polymers onto oxidized carbonaceous substrates with further study. 

Stomatal pores close rapidly in response to low-air-humidity-induced leaf-to-air vapor pressure difference (VPD) increases, thereby reducing excessive water loss. The hydroactive signal-transduction mechanisms mediating high VPD–induced stomatal closure remain largely unknown. The kinetics of stomatal high-VPD responses were investigated by using time-resolved gas-exchange analyses of higher-order mutants in guard-cell signal-transduction branches. We show that the slow-type anion channel SLAC1 plays a relatively more substantial role than the rapid-type anion channel ALMT12/QUAC1 in stomatal VPD signaling. VPD-induced stomatal closure is not affected in mpk12 / mpk4GC double mutants that completely disrupt stomatal CO 2 signaling, indicating that VPD signaling is independent of the early CO 2 signal-transduction pathway. Calcium imaging shows that osmotic stress causes cytoplasmic Ca 2+ transients in guard cells. Nevertheless, osca1-2 / 1.3 / 2.2 / 2.3 / 3.1 Ca 2+ -permeable channel quintuple, osca1.3 / 1.7 -channel double, cngc5 / 6 -channel double, cngc20 -channel single, cngc19 / 20crispr -channel double, glr3.2 / 3.3 -channel double, cpk- kinase quintuple, cbl1 / 4 / 5 / 8 / 9 quintuple, and cbl2 / 3rf double mutants showed wild-type-like stomatal VPD responses. A B3-family Raf-like mitogen-activated protein (MAP)-kinase kinase kinase, M3Kδ5/RAF6, activates the OST1/SnRK2.6 kinase in plant cells. Interestingly, B3 Raf-kinase m3kδ5 and m3kδ1 / δ5 / δ6 / δ7 ( raf3 / 6 / 5 / 4 ) quadruple mutants, but not a 14-gene raf-kinase mutant including osmotic stress-linked B4-family Raf-kinases, exhibited slowed high-VPD responses, suggesting that B3-family Raf-kinases play an important role in stomatal VPD signaling. Moreover, high VPD–induced stomatal closure was impaired in receptor-like pseudokinase GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1) mutant alleles. Notably, the classical transient “wrong-way” VPD response was absent in ghr1 mutant alleles. These findings reveal genes and signaling mechanisms in the elusive high VPD–induced stomatal closing response pathway.