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Research article2025Peer reviewedOpen access

TYPHON proteins are RAB-dependent mediators of the trans-Golgi network secretory pathway

Baral, Anirban; Gendre, Delphine; Aryal, Bibek; Fougere, Louise; Di Fino, Luciano Martin; Ohori, Chihiro; Sztojka, Bernadette; Uemura, Tomohiro; Ueda, Takashi; Marhavy, Peter; Boutte, Yohann; Bhalerao, Rishikesh P.

Abstract

The trans-Golgi network (TGN), a key compartment in endomembrane trafficking, participates in both secretion to and endocytosis from the plasma membrane. Consequently, the TGN plays a key role in plant growth and development. Understanding how proteins are sorted for secretion or endocytic recycling at the TGN is critical for elucidating mechanisms of plant development. We previously showed that the protein ECHIDNA is essential for phytohormonal control of hypocotyl bending because it mediates secretion of cell wall components and the auxin influx carrier AUXIN RESISTANT 1 (AUX1) from the TGN. Despite the critical role of ECHIDNA in TGN-mediated trafficking, its mode of action remains unknown in Arabidopsis ( Arabidopsis thaliana). We therefore performed a suppressor screen on the ech mutant. Here, we report the identification of TGN-localized TYPHON 1(TPN1) and TPN2 proteins. A single amino acid change in either TPN protein causes dominant suppression of the ech mutant's defects in growth and AUX1 secretion, while also restoring wild-type (WT)-like ethylene-responsive hypocotyl bending. Importantly, genetic and cell biological evidence shows that TPN1 acts through RASASSOCIATED BINDING H1b (RABH1b), a TGN-localized RAB-GTPase. These results provide insights into ECHIDNA-mediated secretory trafficking of cell wall and auxin carriers at the TGN, as well as its role in controlling plant growth.

Published in

Plant Cell
2025, volume: 37, number: 1, article number: koae280
Publisher: OXFORD UNIV PRESS INC

SLU Authors

UKÄ Subject classification

Cell Biology
Botany

Publication identifier

  • DOI: https://doi.org/10.1093/plcell/koae280

Permanent link to this page (URI)

https://res.slu.se/id/publ/133193