The present invention relates to barley plant or a part thereof, wherein the kernels of said barley plant have a reduced (1,3;1,4)-β-glucan content. The barley plant may carry a mutation in the CslF6 gene, wherein said mutated CslF6 gene encodes a mutant CslF6 polypeptide.

The present invention relates to vectors and compositions for the treatment of glycogen storage disease III.

Methods of preparing novel steviol glycosides are described herein. The methods utilize biocatalysts for converting a starting steviol glycoside to a target steviol glycoside. Compositions and consumables comprising said novel steviol glycosides as well as methods of purifying and using said novel steviol glycosides, are also provided.

The present invention relates to a group of glycosyltransferase, and an application thereof. Specifically, provided is using glycosyltransferase GT29-32, GT29-33, GT29-34, GT29-4, GT29-5, GT29-7, GT29-9, GT29-11, GT29-13, GT29-17, GT29-18, GT29-19, GT29-20, GT29-21, GT29-22, GT29-23, GT29-24, GT29-25, GT29-36, GT29-37, GT29-42, GT29-43, GT29-45, GT29-46, PNUGT29-1, PNUGT29-2, PNUGT29-3, PNUGT29-4, PNUGT29-5, PNUGT29-6, PNUGT29-7, PNUGT29-8, PNUGT29-9, PNUGT29-14, and PNUGT29-15, as well as derived polypeptides thereof to catalyze the first glycosyl at position C-20, the first glycosyl at position C-6, and the first glycosyl at position C-3 of a tetracyclic triterpene compound substrate to elongate a carbohydrate chain, thereby obtaining a catalytic reaction of ginsenoside products such as ginsenoside Rg3, ginsenoside Rd, ginsenoside Rb1, ginsenoside Rb3, saponin DMGG, saponin DMGX, gypenoside LXXV, gypenoside XVII, gypenoside XIII, gypenoside IX, notoginsenoside U, and notoginsenoside R1, notoginsenoside R2, notoginsenoside R3, 3-O-β-(D-xylopyranosyl)-β-(D-glucopyranosyl)-PPD, 3-O-β-(D-xylopyranosyl)-β-(D-glucopyranosyl)-CK, 20-O-Glucosylginsenoside Rf, and Ginsenoside F3. Glycosyltransferase in the present invention can further be applied to construction of artificially synthesized ginsenoside, novel ginsenoside, and derivatives thereof.

Improved production of recombinant proteins in E. coli, reliant on tightly controlled autoinduction, triggered by phosphate depletion in stationary phase. The process also provides an optimized autoinduction media, enabling routine batch production at various culture volumes where cells densities routinely reach ˜5-7 g cell dry weight per liter and offer protein titers above 2 g/L. The methodology has been validated with a set of diverse heterologous proteins and is of general use for the facile optimization of routine protein expression from high throughput screens to fed-batch fermentation.

A truncated hyaluronan synthase (HAS) comprising an exemplary amino acid sequence having at least 95% identity with SEQ ID NO: 2. The truncated HAS may be encoded by an exemplary nucleic acid sequence set forth in SEQ ID NO: 3.

Methods and compositions for modifying glycans (e.g., glycans expressed on the surface of live cells or cell particles) are provided herein.

In one aspect, the invention relates to an immunogenic composition that includes a mutant Clostridium difficile toxin A and/or a mutant Clostridium difficile toxin B. Each mutant toxin includes a glucosyltransferase domain having at least one mutation and a cysteine protease domain having at least one mutation, relative to the corresponding wild-type C. difficile toxin. The mutant toxins may further include at least one amino acid that is chemically crosslinked. In another aspect, the invention relates to antibodies or binding fragments thereof that binds to said immunogenic compositions. In further aspects, the invention relates to isolated nucleotide sequences that encode any of the foregoing, and methods of use of any of the foregoing compositions.

This disclosure relates to mRNA therapy for the treatment of Crigler-Najjar Syndrome Type 1 (CN-1). mRNAs for use in the invention, when administered in vivo, encode uridine diphosphate glycosyltransferase 1 family, polypeptide A1 (UGT1A1). mRNA therapies of the disclosure increase and/or restore deficient levels of UGT1A1 expression and/or activity in subjects. mRNA therapies of the disclosure further decrease abnormal accumulation of bilirubin associated with deficient UGT1A1 activity in subjects.

This disclosure is in the technical field of synthetic biology and metabolic engineering. The disclosure provides engineered viable bacteria having a reduced or abolished synthesis of poly-N-acetyl-glucosamine (PNAG), Enterobacterial Common Antigen (ECA), cellulose, colanic acid, core oligosaccharides, Osmoregulated Periplasmic Glucans and Glucosylglycerol (O), glycan, and trebalose. The disclosure further provides methods for the production of bioproduct by the viable bacteria and uses thereof. Furthermore, the disclosure is in the technical field of fermentation of metabolically engineered microorganisms producing bioproduct.