Developmental Anatomy of Russet of `McIntosh' Apple Fruit Induced by the Fungus Aureobasidium pullulans

Abstract

The fungus Aureobasidium pullulans is ubiquitous and can cause russet of fruit in New York orchards. The details of russet induction by this fungus are not well known. We inoculated `McIntosh' apple fruits with a suspension of A. pullulans spores (10 million colony-forming units/mL) 1–2 weeks postbloom or later at about 30 days postbloom. We dropped inoculum into plastic “microwells” attached to the fruit surface. The cuticle of uninoculated fruit (wells filled with water only) had no russet by autumn. Skin susceptibility to russet diminished with fruit age. The cuticle of inoculated young fruit began to break down in a few days, likely through direct cuticular digestion. Further erosion and breaching of the protective cuticle caused underlying epidermal cells to die. Within 1–2 weeks, cuticle disruption and epidermal cell death were widespread. This stimulated the fruit to initiate a repair process that involved periderm formation (russet), where many rows of cells were produced in nearby tissue to seal off the injury. This type of repair is not stretchable, so as young fruit expanded, additional skin splits and checks developed. This breakdown–repair process repeated itself, which created a scurfy skin. Older fruit did not expand as much after inoculation as did young fruit, and so they developed few obvious leathery patches of periderm. Older cuticle also resisted digestion better than did the young fruit cuticle, but we do not know if resistance resulted from increased cuticle thickness in older fruit or a change in cuticular compounds during fruit growth. Regardless, A. pullulans applied to older fruit did not progress beyond the early phase of cuticle digestion, even after 3 weeks postinoculation.