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Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.

Endosidin 2 (ES2) is a cell-permeable drug that binds to the Exo70 subunit of the exocyst complex, disrupting the final stages of exocytosis. This allows for a dose-dependent control over the process of exocytosis and greater ease in studying exocytic-dependent processes such as polarized cell growt...

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Autores principales: Bormann, Eric, Xu, Rholee, Nargi, Clare, Wu, Min, Vidali, Luis
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674970/
https://www.ncbi.nlm.nih.gov/pubmed/36411798
http://dx.doi.org/10.17912/micropub.biology.000655
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author Bormann, Eric
Xu, Rholee
Nargi, Clare
Wu, Min
Vidali, Luis
author_facet Bormann, Eric
Xu, Rholee
Nargi, Clare
Wu, Min
Vidali, Luis
author_sort Bormann, Eric
collection PubMed
description Endosidin 2 (ES2) is a cell-permeable drug that binds to the Exo70 subunit of the exocyst complex, disrupting the final stages of exocytosis. This allows for a dose-dependent control over the process of exocytosis and greater ease in studying exocytic-dependent processes such as polarized cell growth. ES2 was utilized in studying polarized cell growth in the moss Physcomitrium patens , in which plants were exposed to increasing concentrations of ES2 with an IC50 between 8.8 and 12.3 µM. At 50 µM, tip-growing cells ruptured close to their tips, an indication that ES2 inhibits the deposition of new cell wall material via exocytosis. This data serves to further support the use of ES2 as a tool to interfere with exocytosis with lethality only seen at high levels of ES2.
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spelling pubmed-96749702022-11-20 Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens. Bormann, Eric Xu, Rholee Nargi, Clare Wu, Min Vidali, Luis MicroPubl Biol New Finding Endosidin 2 (ES2) is a cell-permeable drug that binds to the Exo70 subunit of the exocyst complex, disrupting the final stages of exocytosis. This allows for a dose-dependent control over the process of exocytosis and greater ease in studying exocytic-dependent processes such as polarized cell growth. ES2 was utilized in studying polarized cell growth in the moss Physcomitrium patens , in which plants were exposed to increasing concentrations of ES2 with an IC50 between 8.8 and 12.3 µM. At 50 µM, tip-growing cells ruptured close to their tips, an indication that ES2 inhibits the deposition of new cell wall material via exocytosis. This data serves to further support the use of ES2 as a tool to interfere with exocytosis with lethality only seen at high levels of ES2. Caltech Library 2022-11-04 /pmc/articles/PMC9674970/ /pubmed/36411798 http://dx.doi.org/10.17912/micropub.biology.000655 Text en Copyright: © 2022 by the authors https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle New Finding
Bormann, Eric
Xu, Rholee
Nargi, Clare
Wu, Min
Vidali, Luis
Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title_full Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title_fullStr Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title_full_unstemmed Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title_short Inhibition of the Exocyst Complex with Endosidin 2 Reduces Polarized Growth in Physcomitrium patens.
title_sort inhibition of the exocyst complex with endosidin 2 reduces polarized growth in physcomitrium patens.
topic New Finding
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674970/
https://www.ncbi.nlm.nih.gov/pubmed/36411798
http://dx.doi.org/10.17912/micropub.biology.000655
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