Comparative analyses of D-fenchone and MENA inhibited sprouting of sweet potato storage roots.

Postharvest sprouting is a major problem for the storage of sweet potato. This study compared the effect of D-fenchone with methyl naphthacetate (MENA) treatments on the sprouting of 'Yan 25′ sweet potato. The untreated control roots sprouted within 4 days however the roots fumigated with 200 μL / 23 L D-fenchone or MENA completely inhibited the sprouting of freshly harvested 'Yan 25′ during 14 days storage at 30 ℃. Furthermore, treating established sprouts (0.5 cm) with MENA or D-fenchone resulted in damaged sprouts after seven days following treatment with higher MDA content and these sprouts eventually died. Transcriptomic analyses revealed that both D-fenchone and MENA inhibited cell wall synthesis and disrupted auxin and cytokinin pathways in the storage roots, by which suppressed the sprouting. The RNA-seq results of established sprouts showed that both D-fenchone and MENA promoted ethylene and reactive oxidative species (ROS) pathways, which were correlated with the physical damage. In addition, D-fenchone and MENA inhibited auxin pathway, MENA changed cytokinin and D-fenchone disrupted polyamine, cell division and cellulose biosynthesis pathways which all may have contributed to sprout suppression. • D-fenchone works better than MENA in inhibiting sweet potato sprouting. • The inhibiting effect of D-fenchone on sprouting of sweet potato is reversible. • D-fenchone/MENA induced membrane damage and senescence in established shoots. • Plant hormones were associated with D-fenchone/MENA induced sprout suppression. • Transcriptional responses of established shoots to D-fenchone is quicker than MENA. [ABSTRACT FROM AUTHOR]