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Inhibition of Golgi function causes plastid starch accumulation

Little is known about possible interactions between chloroplasts and the Golgi apparatus, although there is increasing evidence for a direct Golgi to chloroplast transport pathway targeting proteins to their destinations within the membranes and stroma of plastids. Here data are presented showing th...

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Detalles Bibliográficos
Autores principales: Hummel, Eric, Osterrieder, Anne, Robinson, David G., Hawes, Chris
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882258/
https://www.ncbi.nlm.nih.gov/pubmed/20423939
http://dx.doi.org/10.1093/jxb/erq091
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author Hummel, Eric
Osterrieder, Anne
Robinson, David G.
Hawes, Chris
author_facet Hummel, Eric
Osterrieder, Anne
Robinson, David G.
Hawes, Chris
author_sort Hummel, Eric
collection PubMed
description Little is known about possible interactions between chloroplasts and the Golgi apparatus, although there is increasing evidence for a direct Golgi to chloroplast transport pathway targeting proteins to their destinations within the membranes and stroma of plastids. Here data are presented showing that a blockage of secretion results in a significant increase of starch within plastids. Golgi disassembly promoted either by the secretory inhibitor brefeldin A or through an inducible Sar1-GTP system leads to dramatic starch accumulation in plastids, thus providing evidence for a direct interaction between plastids and Golgi activity. The possibility that starch accumulation is due either to elevated levels of cytosolic sugars because of loss of secretory Golgi activity or even to a blockage of amylase transport from the Golgi to the chloroplast is discussed.
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spelling pubmed-28822582010-06-08 Inhibition of Golgi function causes plastid starch accumulation Hummel, Eric Osterrieder, Anne Robinson, David G. Hawes, Chris J Exp Bot Research Papers Little is known about possible interactions between chloroplasts and the Golgi apparatus, although there is increasing evidence for a direct Golgi to chloroplast transport pathway targeting proteins to their destinations within the membranes and stroma of plastids. Here data are presented showing that a blockage of secretion results in a significant increase of starch within plastids. Golgi disassembly promoted either by the secretory inhibitor brefeldin A or through an inducible Sar1-GTP system leads to dramatic starch accumulation in plastids, thus providing evidence for a direct interaction between plastids and Golgi activity. The possibility that starch accumulation is due either to elevated levels of cytosolic sugars because of loss of secretory Golgi activity or even to a blockage of amylase transport from the Golgi to the chloroplast is discussed. Oxford University Press 2010-06 2010-04-27 /pmc/articles/PMC2882258/ /pubmed/20423939 http://dx.doi.org/10.1093/jxb/erq091 Text en © 2010 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. This paper is available online free of all access charges (see http://jxb.oxfordjournals.org/open_access.html for further details)
spellingShingle Research Papers
Hummel, Eric
Osterrieder, Anne
Robinson, David G.
Hawes, Chris
Inhibition of Golgi function causes plastid starch accumulation
title Inhibition of Golgi function causes plastid starch accumulation
title_full Inhibition of Golgi function causes plastid starch accumulation
title_fullStr Inhibition of Golgi function causes plastid starch accumulation
title_full_unstemmed Inhibition of Golgi function causes plastid starch accumulation
title_short Inhibition of Golgi function causes plastid starch accumulation
title_sort inhibition of golgi function causes plastid starch accumulation
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882258/
https://www.ncbi.nlm.nih.gov/pubmed/20423939
http://dx.doi.org/10.1093/jxb/erq091
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