Postharvest trehalose application alleviates chilling injuring of cold storage guava through upregulation of SnRK1 and energy charge

Abstract

Listen

Translate article

Sucrose non-fermenting-1-related protein kinases-1 (SnRK1) plays a crucial role in response to energy homeostasis for plant survival during exposure to environmental stresses. Trehalose has been reported as chilling injury alleviating agent of postharvest guava (Psidium guajava cv. Kim Ju), but the mechanism related to energy homeostasis have not been elucidated. This research is focusing on the influence of exogenous trehalose on SnRK1 activation associated with energy homeostasis and chilling injury incidence of ‘Kim Ju’ guava fruit during low temperature storage. The fruits were treated with 0 and 200 mM of trehalose for 30 min and kept at 8 °C for 14 d. It was demonstrated that PgSnRK1 expression and SnRK1 activity increased after trehalose treatment, reaching maximum within 1–2 d. Trehalose treatment upregulated the expression of energy producing related genes including adenosine triphosphate synthase subunit β and adenosine diphosphate/adenosine triphosphate carrier and increased the enzyme activities of nicotinamide adenine dinucleotide dehydrogenase, succinate dehydrogenase and cytochrome c oxidase. These events were accompanied by higher energy charge and lower chilling injury throughout storage. The increase in SnRK1 activity by exogenous trehalose was closely associated with an increase in sucrose level during the first 2 d of storage. The SnRK1 activation was induced apparently by 50–200 mM exogenous sucrose within 3–12 h after treatment while exogenous trehalose treatment induced SnRK1 activation slightly and slowly within 2 d. Moreover, validamycin A combined with exogenous trehalose enhanced the cellular trehalose accumulation while sucrose level remained constant which lowered PgSnRK1 expression. Our results suggested that exogenous trehalose induces a transient rise in sucrose content at the early storage for providing the sugar signaling to SnRK1 activation which is required for maintaining energy homeostasis accompanied by retarding chilling injury.