Over the past few years, three photorespiratory bypasses have been introduced into plants, two of which led to observable increases in photosynthesis and biomass yield. However, most of the experiments were carried out using Arabidopsis under controlled environmental conditions, and the increases were only observed under low-light and short-day conditions. In this study, we designed a new photorespiratory bypass (called GOC bypass), characterized by no reducing equivalents being produced during a complete oxidation of glycolate into CO 2 catalyzed by three rice-self-originating enzymes, i.e., glycolate oxidase, oxalate oxidase, and catalase. We successfully established this bypass in rice chloroplasts using a multi-gene assembly and transformation system. Transgenic rice plants carrying GOC bypass (GOC plants) showed significant increases in photosynthesis efficiency, biomass yield, and nitrogen content, as well as several other CO 2 -enriched phenotypes under both greenhouse and field conditions. Grain yield of GOC plants varied depending on seeding season and was increased significantly in the spring. We further demonstrated that GOC plants had significant advantages under high-light conditions and that the improvements in GOC plants resulted primarily from a photosynthetic CO 2 -concentrating effect rather than from improved energy balance. Taken together, our results reveal that engineering a newly designed chloroplastic photorespiratory bypass could increase photosynthetic efficiency and yield of rice plants grown in field conditions, particularly under high light.

An ultra-light porous 3D Ti3C2Txaerogel electrode was prepared by freeze-drying the wet hydrogel, which has an ultrahigh rate capability and excellent cycling life.

In this study, the dense polycrystalline Ti2AlC was synthesized by self-propagating high-temperature combustion synthesis with the pseudo–hot isostatic pressing process (SHS/PHIP). The resultant phase purity is highly dependent on the mol ratio of raw powders. The Ti2AlC was densified by applying pressure after the SHS reaction. The resultant sample mainly contains typical plate-like nonstoichiometric Ti2AlCx (x = 0.69) with grain size of ∼6 µm. The sample shows the Vickers hardness of 5.5 GPa, highest flexural strength of 431 MPa, compressive strength of 1033 MPa, and fracture toughness of 6.5 MPa·m1/2. No indentation cracks in Ti2AlCx were observed, indicative of a damage material nature. The reaction mechanism for the formation of SHS/PHIP-derived Ti2AlC is also discussed based on differential thermal analysis and x-ray diffraction results.

Although modifier genes are extensively studied in various diseases, little is known about modifier genes that regulate autoimmune diseases. Autoimmune disease caused by the Faslpr mutation depends on the genetic background of mouse strains, suggesting a crucial role of modifier genes. MRL/MpJ-Faslpr (MRL/lpr) and AKR/lpr mice develop severe and mild lupus-like autoimmune disease, respectively, whereas this mutation does not cause disease on C57BL/6 (B6) or C3H background. Both MRL and AKR carry the same haplotype of the Cd72 gene encoding an inhibitory BCR coreceptor (CD72c), and CD72c contains several amino acid substitutions and a deletion in the extracellular region compared with CD72a and CD72b. To address the role of Cd72c locus in the regulation of Faslpr-induced autoimmune disease, we generated B6.CD72c/lpr and MRL.CD72b/lpr congenic mice. Introduction of the chromosomal interval containing Cd72c did not cause disease in B6 mice by itself, but caused development of lupus-like disease in the presence of Faslpr on B6 background, clearly demonstrating that this interval contains the modifier gene that regulates Faslpr-induced autoimmune disease. Conversely, MRL.CD72b/lpr congenic mice showed milder disease compared with MRL/lpr mice. We further demonstrated that Cd72c is a hypofunctional allele in BCR signal inhibition and that CD72 deficiency induces severe autoimmune disease in the presence of Faslpr. These results strongly suggest that the Cd72c is a crucial modifier gene that regulates Faslpr-induced autoimmune disease due to its reduced activity of B cell signal regulation.

No abstract