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GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7
Golgi Arf1-guanine nucleotide exchange factors (GEFs) belong to two subfamilies: GBF/Gea and BIG/Sec7. Both are conserved across eukaryotes, but the physiological role of each is not well understood. Aspergillus nidulans has a single member of the early Golgi GBF/Gea-subfamily, geaA, and the late Go...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266534/ https://www.ncbi.nlm.nih.gov/pubmed/25451223 http://dx.doi.org/10.1016/j.febslet.2014.11.014 |
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author | Arst, Herbert N. Hernandez-Gonzalez, Miguel Peñalva, Miguel A. Pantazopoulou, Areti |
author_facet | Arst, Herbert N. Hernandez-Gonzalez, Miguel Peñalva, Miguel A. Pantazopoulou, Areti |
author_sort | Arst, Herbert N. |
collection | PubMed |
description | Golgi Arf1-guanine nucleotide exchange factors (GEFs) belong to two subfamilies: GBF/Gea and BIG/Sec7. Both are conserved across eukaryotes, but the physiological role of each is not well understood. Aspergillus nidulans has a single member of the early Golgi GBF/Gea-subfamily, geaA, and the late Golgi BIG/Sec7-subfamily, hypB. Both geaA and hypB are essential. hypB5 conditionally blocks secretion. We sought extragenic hypB5 suppressors and obtained geaA1. geaA1 results in Tyr1022Cys within a conserved GBF/Gea-specific S(Y/W/F)(L/I) motif in GeaA. This mutation alters GeaA localization. Remarkably, geaA1 suppresses hypBΔ, indicating that a single mutant Golgi Arf1-GEF suffices for growth. |
format | Online Article Text |
id | pubmed-4266534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | John Wiley & Sons Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-42665342014-12-20 GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 Arst, Herbert N. Hernandez-Gonzalez, Miguel Peñalva, Miguel A. Pantazopoulou, Areti FEBS Lett Article Golgi Arf1-guanine nucleotide exchange factors (GEFs) belong to two subfamilies: GBF/Gea and BIG/Sec7. Both are conserved across eukaryotes, but the physiological role of each is not well understood. Aspergillus nidulans has a single member of the early Golgi GBF/Gea-subfamily, geaA, and the late Golgi BIG/Sec7-subfamily, hypB. Both geaA and hypB are essential. hypB5 conditionally blocks secretion. We sought extragenic hypB5 suppressors and obtained geaA1. geaA1 results in Tyr1022Cys within a conserved GBF/Gea-specific S(Y/W/F)(L/I) motif in GeaA. This mutation alters GeaA localization. Remarkably, geaA1 suppresses hypBΔ, indicating that a single mutant Golgi Arf1-GEF suffices for growth. John Wiley & Sons Ltd 2014-12-20 /pmc/articles/PMC4266534/ /pubmed/25451223 http://dx.doi.org/10.1016/j.febslet.2014.11.014 Text en © 2014 The Authors https://creativecommons.org/licenses/by/3.0/This work is licensed under a Creative Commons Attribution 3.0 Unported License (https://creativecommons.org/licenses/by/3.0/) . |
spellingShingle | Article Arst, Herbert N. Hernandez-Gonzalez, Miguel Peñalva, Miguel A. Pantazopoulou, Areti GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title | GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title_full | GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title_fullStr | GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title_full_unstemmed | GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title_short | GBF/Gea mutant with a single substitution sustains fungal growth in the absence of BIG/Sec7 |
title_sort | gbf/gea mutant with a single substitution sustains fungal growth in the absence of big/sec7 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266534/ https://www.ncbi.nlm.nih.gov/pubmed/25451223 http://dx.doi.org/10.1016/j.febslet.2014.11.014 |
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