TYPHON proteins are RAB-dependent mediators of the trans-Golgi network secretory pathway. Baral, A., Gendre, D., Aryal, B., Fougère, L., Di Fino, L. M., Ohori, C., Sztojka, B., Uemura, T., Ueda, T., Marhavý, P., Boutté, Y., & Bhalerao, R. P The Plant Cell, October, 2024. ![TYPHON proteins are RAB-dependent mediators of the trans-Golgi network secretory pathway [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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-like ethylene-responsive hypocotyl bending. Importantly, genetic and cell biological evidence shows that TPN1 acts through RAS-ASSOCIATED 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.
@article{baral_typhon_2024,
title = {{TYPHON} proteins are {RAB}-dependent mediators of the trans-{Golgi} network secretory pathway},
issn = {1040-4651},
url = {https://doi.org/10.1093/plcell/koae280},
doi = {10.1093/plcell/koae280},
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-like ethylene-responsive hypocotyl bending. Importantly, genetic and cell biological evidence shows that TPN1 acts through RAS-ASSOCIATED 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.},
urldate = {2024-10-16},
journal = {The Plant Cell},
author = {Baral, Anirban and Gendre, Delphine and Aryal, Bibek and Fougère, Louise and Di Fino, Luciano Martin and Ohori, Chihiro and Sztojka, Bernadette and Uemura, Tomohiro and Ueda, Takashi and Marhavý, Peter and Boutté, Yohann and Bhalerao, Rishikesh P},
month = oct,
year = {2024},
pages = {koae280},
}
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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-like ethylene-responsive hypocotyl bending. Importantly, genetic and cell biological evidence shows that TPN1 acts through RAS-ASSOCIATED 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.","urldate":"2024-10-16","journal":"The Plant Cell","author":[{"propositions":[],"lastnames":["Baral"],"firstnames":["Anirban"],"suffixes":[]},{"propositions":[],"lastnames":["Gendre"],"firstnames":["Delphine"],"suffixes":[]},{"propositions":[],"lastnames":["Aryal"],"firstnames":["Bibek"],"suffixes":[]},{"propositions":[],"lastnames":["Fougère"],"firstnames":["Louise"],"suffixes":[]},{"propositions":[],"lastnames":["Di","Fino"],"firstnames":["Luciano","Martin"],"suffixes":[]},{"propositions":[],"lastnames":["Ohori"],"firstnames":["Chihiro"],"suffixes":[]},{"propositions":[],"lastnames":["Sztojka"],"firstnames":["Bernadette"],"suffixes":[]},{"propositions":[],"lastnames":["Uemura"],"firstnames":["Tomohiro"],"suffixes":[]},{"propositions":[],"lastnames":["Ueda"],"firstnames":["Takashi"],"suffixes":[]},{"propositions":[],"lastnames":["Marhavý"],"firstnames":["Peter"],"suffixes":[]},{"propositions":[],"lastnames":["Boutté"],"firstnames":["Yohann"],"suffixes":[]},{"propositions":[],"lastnames":["Bhalerao"],"firstnames":["Rishikesh","P"],"suffixes":[]}],"month":"October","year":"2024","pages":"koae280","bibtex":"@article{baral_typhon_2024,\n\ttitle = {{TYPHON} proteins are {RAB}-dependent mediators of the trans-{Golgi} network secretory pathway},\n\tissn = {1040-4651},\n\turl = {https://doi.org/10.1093/plcell/koae280},\n\tdoi = {10.1093/plcell/koae280},\n\tabstract = {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-like ethylene-responsive hypocotyl bending. Importantly, genetic and cell biological evidence shows that TPN1 acts through RAS-ASSOCIATED 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.},\n\turldate = {2024-10-16},\n\tjournal = {The Plant Cell},\n\tauthor = {Baral, Anirban and Gendre, Delphine and Aryal, Bibek and Fougère, Louise and Di Fino, Luciano Martin and Ohori, Chihiro and Sztojka, Bernadette and Uemura, Tomohiro and Ueda, Takashi and Marhavý, Peter and Boutté, Yohann and Bhalerao, Rishikesh P},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {koae280},\n}\n\n\n\n\n\n\n\n","author_short":["Baral, A.","Gendre, D.","Aryal, B.","Fougère, L.","Di Fino, L. M.","Ohori, C.","Sztojka, B.","Uemura, T.","Ueda, T.","Marhavý, P.","Boutté, Y.","Bhalerao, R. 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