3 results about "Deficient mutant" patented technology

The invention belongs to the technical field of gene engineering, and particularly relates to application of an OsACX4 gene in regulation and control of rice salt tolerance. The gene related to the rice salt tolerance is identified for the first time and is named as OsACX4, under treatment of different salt concentrations, the salt tolerance of the OsACX4 gene editing function deletion mutant is remarkably improved, and the growth vigor and survival rate of the OsACX4 gene editing function deletion mutant are higher than those of a wild type and an overexpression strain. After salt treatment, the activity of the OsACX4 deletion mutant and ROS removal related enzymes is generally higher than that of a wild type, the ROS cumulant in vivo is lower than that of the wild type, the content of proline for maintaining cell osmotic equilibrium is higher than that of the wild type, and the content of MDA positively related to the cell membrane damage degree is lower than that of the wild type. The results show that the OsACX4 gene negatively regulates and controls the salt tolerance of the rice in the seedling stage, and is a key gene of the rice in response to salt stress in the seedling stage. The method has important application value in the aspects of analyzing a plant salt-tolerant mechanism and breeding salt-tolerant rice varieties.

This invention relates to the field of agricultural technology, specifically to a mutant Arabidopsis protein and gene that promotes chloroplast development, and their applications. The mutant Arabidopsis protein is the AtMurE protein in wild-type Arabidopsis Sig6 factor-deficient mutants, with mutations occurring at positions 89, 97, 106, 125, 126, 130, or 140. The mutant protein or gene provided by this invention, when introduced into wild-type Arabidopsis Sig6 factor-deficient mutants, can restore chlorophyll content and resolve the cotyledon yellowing problem in wild-type Arabidopsis Sig6 factor-deficient mutants.

The invention discloses a construction method and application of an exacerbated acute kidney injury model, and belongs to the technical field of biomedicine. In particular discloses application of an Atg7 phosphorylation deficient mutant Atg7-T82A / T562A in construction of an exacerbated acute kidney injury (AKI) model. The mutant is delivered to the kidney of a mouse through an adeno-associated virus (AAV), phosphorylation modification of AMPK on Atg7 is specifically blocked, and in combination with an acute renal ischemia (ARI) model, serum creatinine and urea nitrogen levels can be remarkably improved, renal tubular necrosis and apoptosis can be aggravated, autophagosome formation can be reduced, and mitochondrial injury can be induced. The method has high specificity and high efficiency, and provides a key tool for mechanism research, drug toxicity evaluation and treatment strategy development of autophagy-related renal injury.