Cultural advice

The Australian National University acknowledges, celebrates and pays our respects to the Ngunnawal and Ngambri people of the Canberra region and to all First Nations Australians on whose traditional lands we meet and work, and whose cultures are among the oldest continuing cultures in human history.

Aboriginal and Torres Strait Islander peoples are advised that ANU Library collections may include images, names, voices, and other representations of deceased persons.

Material in the collection may contain terms, language or views that reflect the period in which the item was created and may be considered inappropriate today.

Convergence of mitochondrial and chloroplastic ANAC017/PAP-dependent retrograde signalling pathways and suppression of programmed cell death

Loading...
Thumbnail Image

Date

Authors

Pogson, Barry
Van Aken, Olivier

Journal Title

Journal ISSN

Volume Title

Publisher

Stockton Press

Abstract

The energy-converting organelles mitochondria and chloroplasts are tightly embedded in cellular metabolism and stress response. To appropriately control organelle function, extensive regulatory mechanisms are at play that involve two-way exchange between the nucleus and mitochondria/chloroplasts. In recent years, our understanding of how mitochondria and chloroplasts provide â € retrograde' feedback to the nucleus, resulting in targeted transcriptional changes, has greatly increased. Nevertheless, mitochondrial and chloroplast retrograde signalling have largely been studied independently, and only few points of interaction have been found or proposed. Through reassessment of recent publications, this perspective proposes that two of the most well-studied retrograde signalling pathways in plants, those mediated by ANAC017 and those mediated by phosphoadenosine phosphate (PAP), are most likely convergent and can direct overlapping genes. Furthermore, at least part of this common retrograde response appears targeted towards suppression of programmed cell death (PCD) triggered by organellar defects. The identified target genes are discussed in light of their roles in PCD suppression and amplifying the signalling cascade via positive-feedback loops. Finally, a mechanism is proposed that may explain why the convergence of PAP/ANAC017-dependent signalling appears capable of suppressing some types of PCD lesions, but not others, based on the subcellular location of the initial PCD-inducing dysfunction

Description

Keywords

Citation

Source

Cell Death and Differentiation

Book Title

Entity type

Access Statement

License Rights

Restricted until

2099-12-31