Energy status regulates disease development and respiratory metabolism of Lasiodiplodia theobromae (Pat.) Griff. & Maubl.-infected longan fruit

- DNP accelerated the disease development of harvested longans caused by L. theobromae.
- ATP retarded the disease development of harvested longans caused by L. theobromae.
- DNP raised activities of CCO, AAO and PPO, while ATP showed the reversed effects.
- DNP decreased energy level and PPP respiratory pathway, whereas raised EMP-TCA cycle.
- ATP raised energy level and PPP respiratory pathway, whereas reduced EMP-TCA cycle.

Lasiodiplodia theobromae (Pat.) Griff. & Maubl. is a major pathogen causing decay of harvested longan fruit. The roles of energy status regulated by 2,4-dinitrophenol (DNP) and adenosine triphosphate (ATP) in disease development regarding respiratory metabolism of L. theobromae-inoculated “Fuyan” longan fruit were studied. Compared with L. theobromae-inoculated longans, DNP treatment could promote the index of fruit disease, accelerate the decrease in energy charge, increase respiration rate and the activities of respiratory terminal oxidases like CCO, AAO and PPO, elevate contents of NAD and NADH, but decrease NAD kinase activity, as well as contents of NADP and NADPH; however, exogenous ATP supply acted contrarily. Above results suggested the different energy status caused by DNP and ATP treatments accelerated or delayed the disease development of L. theobromae-inoculated longans via regulating Embden-Meyerhof pathway (EMP) and tricarboxylic acid (TCA) cycle, pentose phosphate pathway (PPP) and activities of respiratory terminal oxidases.