A critical review of pre‐harvest sprouting in barley

Pre‐harvest sprouting (PHS) in barley ( Hordeum vulgare ) threatens grain quality and malting performance. This review synthesizes current knowledge on genetic, environmental, physiological, and management factors influencing PHS susceptibility. Seed dormancy, governed by loci including Qsd1 and Qsd2 (where Qsd is quantitative seed dormancy ) and genes including mitogen‐activated protein kinase gene, ABSCISIC ACID INSENSITIVE 3 , VIVIPAROUS 1 , and DELLA (named for its conserved D‐E‐L‐L‐A amino acid motif), underpins PHS resistance. Environmental triggers, particularly rainfall, temperature, and humidity, act independently and synergistically with morphological features, including spike orientation, epicuticular waxes, and glume tenacity, to influence dormancy loss and germination. Starch composition and degradation, governed by granule‐bound starch synthase 1 , starch‐branching enzyme 2b , and isoamylase 1 , further impact sprouting risk and malting quality, with early enzymatic activity undermining functional grain properties. The hormonal regulation of dormancy involves abscisic acid and gibberellic acid as central antagonists, while brassinosteroids, ethylene, auxin, cytokinin, jasmonates, salicylic acid, and strigolactones also contribute through intricate signaling networks. Limited data exist on hormonal cross‐talk and seed tissue‐specific responses in barley. Finally, agronomic strategies, such as cultivar selection, early harvesting, windrowing, nitrogen application, and disease management, can either mitigate or exacerbate PHS, though their effectiveness is context dependent. This review identifies critical knowledge gaps, particularly regarding barley‐specific mechanisms and interactions, and emphasizes the need for integrated breeding and management approaches to enhance PHS resistance without compromising malting performance.