An ARF1-binding factor triggering programmed cell death and periderm development in pear russet fruit skin.

Plants have a cuticular membrane (CM) and periderm membrane (PM), which act as barriers to terrestrial stresses. The CM covers primary organs with a continuous hydrophobic layer of waxes embedded in cutin, while the PM stacks with suberized cells outermost to the secondary tissues. The formation of native periderm is regulated by a postembryonic meristem phellogen that produces suberized phellem (cork) outwardly. However, the mechanism controlling phellogen differentiation to phellem remains to be clarified. Here, map-based cloning in a pear F1 population with segregation for periderm development in fruit skin facilitated the identification of an aspartic acid repeat deletion in Pyrus Periderm Programmed Cell Death 1.1 (PyPPCD1.1) that triggers phellogen activity for cork formation in pear russet fruit skin. PyPPCD1.1 showed preferential expression in pear fruit skin, and the encoded protein shares a structural similarity to that of the viral capsid proteins. Asp deletion in PyPPCD1.1 weakened its nuclear localization but increased its accumulation in the chloroplast. Both PyPPCD1.1 and its recessive allele directly interact with ADP-ribosylation factor 1 (ARF1). PyPPCD1.1 triggered PCD in an ARF1-dependent manner. Thus, this study identified the switch gene for PCD and periderm development and provided a new molecular regulatory mechanism underlying the development of this trait.