Synthesis of glucose‐β‐1,3‐fucose‐α‐O‐threonine/serine to identify critical epitope in Peters‐plus syndrome (792.1)

Abstract

Complex carbohydrates coat the cell surface and carry biological information for altering cell morphology and function during developmental processes and for the invasion of pathogens. Decoding of critical glycan patterns and their function is complex because of the redundancy of glycan biosynthetic machinery. Peters Plus Syndrome, a syndrome mainly affects the eyes, growth, and intellectual ability, is known to be caused by gene mutation of B3GALTL, an unusual O-linked fucose β-1,3 glucosyltransferase. The epitope glucose-β-1,3-fucose-α-O-threonine/serine is involved in the syndrome but cannot be observed. We synthesized this epitope and will generate monoclonal chicken antibody of the epitope to observe the way that glucose-β-1,3-fucose-α-O-threonine/serine influences the development of Peters Plus Syndrome. The disaccharide is synthesized by nucleophilic substitution of a protected trichloroacetimidate glucose acceptor and a protected fucose donor with trimethylsilyl trifluoromethanesulfonate (TMSOTf) in ether. After deprotection, the disaccharide is linked to keyhole limpet hemocyanin (KLH) by click chemistry and a substitution with a linker carrying both acetenyl and N-hydroxysuccinimide (NHS) active groups. Chicken monoclonal antibody will be made to recognize the epitope in studying the syndrome.