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Article|19 Jan 2022|OPEN
An ARF1-binding factor triggering programmed cell death and periderm development in pear russet fruit skin
Yuezhi Wang1 , , Meisong Dai1 , Xinyi Wu2 , Shujun Zhang1 , Zebin Shi1 , Danying Cai1 and Lixiang Miao,1 ,
1Institute of Horticulture, Zhejiang Academy of Agricultural Sciences, Shiqiao Road No. 139, Hangzhou, Zhejiang Province, 310021, China
2Institute of Vegetable, Zhejiang Academy of Agricultural Sciences, Desheng Middle Road No. 298, Hangzhou, Zhejiang Province, 310021, China
*Corresponding author. E-mail: yzwang2010@zaas.ac.cn,shizebinszb@126.com

Horticulture Research 9,
Article number: uhab061 (2022)
doi: https://doi.org/10.1093/hr/uhab061
Views: 182

Received: 19 Apr 2021
Accepted: 28 Oct 2021
Published online: 19 Jan 2022

Abstract

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 includes suberized cells stacked externally 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 russet fruit skin of pear. PyPPCD1.1 showed preferential expression in pear fruit skin, and the encoded protein shares a structural similarity to that of the viral capsid proteins. Aspartic acid deletion in PyPPCD1.1 weakened its nuclear localization but increased its accumulation in the chloroplast. The products of both PyPPCD1.1 and its recessive allele directly interact with ADP-ribosylation factor 1 (ARF1). PyPPCD1.1 triggered programmed cell death in an ARF1-dependent manner. Thus, this study identified the switch gene for programmed cell death and periderm development and provided a new molecular regulatory mechanism underlying the development of this trait.