Energy status of kiwifruit stored under different temperatures or exposed to long-term anaerobic conditions or pure oxygen

• Long term N2 or 15 °C treatments delayed ripening and senescence of kiwifruit.
• Long term O2 accelerated ripening and senescence of kiwifruit.
• Ripening and senescence were closely related with energy level.
• Energy level was correlated positively with respiration activity.
• Energy level was coordinately regulated by the 5 energy-related genes.

Energy status is a key factor switching on ripening and senescence of fruit. In this study, kiwifruit was stored at 15 °C or 25 °C or exposed to long-term N2 and O2. Energy characteristics and transcript abundance of energy-related genes cloned from kiwifruit in relation to fruit quality, respiration rate and ethylene production rate were investigated. The concentrations of adenylate triphosphate (ATP), adenylate diphosphate (ADP) and adenylate monophosphate (AMP) peaked during storage in the following order: AMP, ADP and ATP. The transcript abundances of ADP/ATP carrier 1 (AdAAC1), ATP synthase β subunit (AdAtpB) and sucrose non-fermenting-1-related kinase 1 (AdSnRK1) fluctuated during storage. Transcript abundance peaks of alternative oxidase 2 (AdAOX2) and uncoupling protein (AdUCP) appeared after 2 days of storage, consistent with the peak in respiratory rate. Low temperature (15 °C) and long-term N2 treatment maintained higher firmness, blocked respiration and energy production, and lowered the total soluble solids (TSS) content, ATP level, and ATP/AMP ratio, whilst these treatments increased the transcript abundance of AdAAC1 and AdSnRK1. Furthermore, low temperature storage increased the transcript abundance of AdAtpB, AdAOX2 and AdAUCP. Long-term O2 application dramatically elevated the transcript abundance of AdAOX2 and AdUCP, especially at the beginning of storage. It was suggested that ripening and senescence of kiwifruit was closely related to the energy level, which in turn was positively correlated with respiration activity and regulated in coordination with AdAAC1, AdAtpB, AdAOX2, AdAUCP and AdSnRK1.