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Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans
McrA is a key transcription factor that functions as a global repressor of fungal secondary metabolism in Aspergillus species. Here, we report that mcrA is one of the VosA-VelB target genes and McrA governs the cellular and metabolic development in Aspergillus nidulans. The deletion of mcrA resulted...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493923/ https://www.ncbi.nlm.nih.gov/pubmed/32934285 http://dx.doi.org/10.1038/s41598-020-72224-y |
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author | Lee, Mi-Kyung Son, Ye-Eun Park, Hee-Soo Alshannaq, Ahmad Han, Kap-Hoon Yu, Jae-Hyuk |
author_facet | Lee, Mi-Kyung Son, Ye-Eun Park, Hee-Soo Alshannaq, Ahmad Han, Kap-Hoon Yu, Jae-Hyuk |
author_sort | Lee, Mi-Kyung |
collection | PubMed |
description | McrA is a key transcription factor that functions as a global repressor of fungal secondary metabolism in Aspergillus species. Here, we report that mcrA is one of the VosA-VelB target genes and McrA governs the cellular and metabolic development in Aspergillus nidulans. The deletion of mcrA resulted in a reduced number of conidia and decreased mRNA levels of brlA, the key asexual developmental activator. In addition, the absence of mcrA led to a loss of long-term viability of asexual spores (conidia), which is likely associated with the lack of conidial trehalose and increased β-(1,3)-glucan levels in conidia. In supporting its repressive role, the mcrA deletion mutant conidia contain more amounts of sterigmatocystin and an unknown metabolite than the wild type conidia. While overexpression of mcrA caused the fluffy-autolytic phenotype coupled with accelerated cell death, deletion of mcrA did not fully suppress the developmental defects caused by the lack of the regulator of G-protein signaling protein FlbA. On the contrary to the cellular development, sterigmatocystin production was restored in the ΔflbA ΔmcrA double mutant, and overexpression of mcrA completely blocked the production of sterigmatocystin. Overall, McrA plays a multiple role in governing growth, development, spore viability, and secondary metabolism in A. nidulans. |
format | Online Article Text |
id | pubmed-7493923 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-74939232020-09-16 Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans Lee, Mi-Kyung Son, Ye-Eun Park, Hee-Soo Alshannaq, Ahmad Han, Kap-Hoon Yu, Jae-Hyuk Sci Rep Article McrA is a key transcription factor that functions as a global repressor of fungal secondary metabolism in Aspergillus species. Here, we report that mcrA is one of the VosA-VelB target genes and McrA governs the cellular and metabolic development in Aspergillus nidulans. The deletion of mcrA resulted in a reduced number of conidia and decreased mRNA levels of brlA, the key asexual developmental activator. In addition, the absence of mcrA led to a loss of long-term viability of asexual spores (conidia), which is likely associated with the lack of conidial trehalose and increased β-(1,3)-glucan levels in conidia. In supporting its repressive role, the mcrA deletion mutant conidia contain more amounts of sterigmatocystin and an unknown metabolite than the wild type conidia. While overexpression of mcrA caused the fluffy-autolytic phenotype coupled with accelerated cell death, deletion of mcrA did not fully suppress the developmental defects caused by the lack of the regulator of G-protein signaling protein FlbA. On the contrary to the cellular development, sterigmatocystin production was restored in the ΔflbA ΔmcrA double mutant, and overexpression of mcrA completely blocked the production of sterigmatocystin. Overall, McrA plays a multiple role in governing growth, development, spore viability, and secondary metabolism in A. nidulans. Nature Publishing Group UK 2020-09-15 /pmc/articles/PMC7493923/ /pubmed/32934285 http://dx.doi.org/10.1038/s41598-020-72224-y Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Lee, Mi-Kyung Son, Ye-Eun Park, Hee-Soo Alshannaq, Ahmad Han, Kap-Hoon Yu, Jae-Hyuk Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title | Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title_full | Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title_fullStr | Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title_full_unstemmed | Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title_short | Velvet activated McrA plays a key role in cellular and metabolic development in Aspergillus nidulans |
title_sort | velvet activated mcra plays a key role in cellular and metabolic development in aspergillus nidulans |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493923/ https://www.ncbi.nlm.nih.gov/pubmed/32934285 http://dx.doi.org/10.1038/s41598-020-72224-y |
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