PR10/Bet v1-like Proteins as Novel Contributors to Plant Biochemical Diversity.

Autor: Morris JS; Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N N4, Canada., Caldo KMP; Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N N4, Canada., Liang S; Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N N4, Canada., Facchini PJ; Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N N4, Canada.
Jazyk: angličtina
Zdroj: Chembiochem : a European journal of chemical biology [Chembiochem] 2021 Jan 15; Vol. 22 (2), pp. 264-287. Date of Electronic Publication: 2020 Sep 07.
DOI: 10.1002/cbic.202000354
Abstrakt: Pathogenesis-related (PR) proteins constitute a broad class of plant proteins with analogues found throughout nature from bacteria to higher eukaryotes. PR proteins were first noted in plants as part of the hypersensitive response, but have since been assigned an array of biological roles. The PR10/Bet v1-like proteins are a subset of PR proteins characterized by an ability to bind a wide range of lipophilic ligands, uniquely positioning them as contributors to specialized biosynthetic pathways. PR10/Bet v1-like proteins participate in the production of plant alkaloids and phenolics including flavonoids, both as general binding proteins and in special cases as catalysts. Owing initially to the perceived allergenic properties of PR10/Bet v1-like proteins, many were studied at the structural level to elucidate the basis for ligand binding. These studies provided a foundation for more recent efforts to understand higher-level structural order and how PR10/Bet v1-like proteins catalyse key reactions in plant pathways. Synthetic biology aimed at reconstituting plant-specialized metabolism in microorganisms uses knowledge of these proteins to fine-tune performance in new systems.
(© 2020 Wiley-VCH GmbH.)
Databáze: MEDLINE
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