Abstract
Sprouting of sweet potato during transportation and storage is a serious problem leads to weight loss and quality degradation. In this study, the effect of piperitone in inhibiting sprouting of 'Yan 25' sweet potato was analyzed through physiological and transcriptomic analyses. The results showed that untreated 'Yan 25' sweet potatoes sprouted after 14 d at 30 °C. While sweet potatoes treated with 150 μL/23 L piperitone did not grow any sprouts after 14 d. Furthermore, the investigation into the effect of piperitone on established sweet potato sprouts showed that the sprouts were damaged with the MDA content increased by 35 % after 18 h of piperitone fumigation, which then died after 48 h. The transcriptomic analyses showed that genes from the pathways of somatic embryogenesis, plant hormone metabolism or signal transduction, cell wall synthesis, cell wall loosening and DNA replication in the storage roots or sprout were altered by piperitone treatment. It is worth mentioning that, genes related to cell apoptosis are up-regulated in the sprout such as 1-amino-cyclopropane-1-carboxylate synthase (ACS), ACC oxidase (ACO), ethylene insensitive 3 family protein (EIN), senescence-associated gene (SAG) and so on, which was associated with the herbicidal effects of piperitone on sweet potato sprout. To facilitate the understanding of the results, two conceptual models elucidate the molecular mechanism of piperitone inhibited sweet potato sprouting were provided. This study provides new insights for inhibiting the sprouting of sweet potato during post-harvest storage.