Abstract
Autophagy is a conserved quality control pathway that mediates the degradation of cellular components by targeting them to the lysosomes or vacuoles.1 Autophagy has been implicated in the regulation of some regulated cell death processes in animal systems.2 However, its function in developmentally controlled programmed cell death (dPCD) in plants remains little studied and controversial.3 Some studies have reported autophagy pro-survival roles,4,5 while others have suggested pro-death functions for autophagy,6,7 calling for further detailed investigations. Here, we investigated the role of autophagy in dPCD using the Arabidopsis root cap as an accessible and genetically tractable model system.8 In Arabidopsis, dPCD is an integral part of root cap differentiation, restricting root cap organ size to the root meristem.9 The root cap consists of two distinct tissues: the proximally positioned columella that is located at the very root tip and the lateral root cap (LRC) that flanks the root meristem up to its distal end at the start of the root elongation zone.10 We show that autophagic flux strongly increased prior to dPCD execution in both root cap tissues and depends on the key autophagy genes ATG2, ATG5, and ATG7. Systemic and organ-specific mutation of these genes shows delayed PCD execution and lack of postmortem corpse clearance in the columella but no defects in dPCD execution or corpse clearance in the distal LRC. Our results reveal a high degree of cell-type specificity in autophagy functions and suggest that autophagy roles in dPCD can considerably diverge between different cell types of the same plant organ.