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srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans
Conidiation is an important reproductive process in Aspergillus. We previously reported, in A. nidulans, that the deletion of a putative glycosyltransferase gene, rseA/cpsA, causes an increase in the production of extracellular hydrolases and a severe reduction in conidiation. The aim of this study...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10017718/ https://www.ncbi.nlm.nih.gov/pubmed/36922566 http://dx.doi.org/10.1038/s41598-023-31363-8 |
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author | Ogawa, Masahiro Fukuda, Ryouichi Iwama, Ryo Koyama, Yasuji Horiuchi, Hiroyuki |
author_facet | Ogawa, Masahiro Fukuda, Ryouichi Iwama, Ryo Koyama, Yasuji Horiuchi, Hiroyuki |
author_sort | Ogawa, Masahiro |
collection | PubMed |
description | Conidiation is an important reproductive process in Aspergillus. We previously reported, in A. nidulans, that the deletion of a putative glycosyltransferase gene, rseA/cpsA, causes an increase in the production of extracellular hydrolases and a severe reduction in conidiation. The aim of this study was to obtain novel genetic factors involved in the repression of conidiation in the rseA deletion mutant. We isolated mutants in which the rseA deletion mutant conidiation defect is suppressed and performed a comparative genomic analysis of these mutants. A gene encoding a putative transcription factor was identified as the associated candidate causative gene. The candidate gene was designated as srdA (suppressor gene for the conidiation defect of the rseA deletion mutant). The conidiation efficiency of the rseAsrdA double-deletion mutant was increased. Introduction of wild-type srdA into the suppressor mutants caused a conidiation defect similar to that of the rseA deletion mutant. Notably, the conidiation efficiencies of the rseAsrdA double-deletion and srdA single-deletion mutants were higher than that of the wild-type strain. These results indicate that srdA is a novel genetic factor that strongly represses conidiation of the rseA deletion mutant, and a putative transcriptional regulator, SrdA is a negative regulator of conidiation in A. nidulans. |
format | Online Article Text |
id | pubmed-10017718 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-100177182023-03-17 srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans Ogawa, Masahiro Fukuda, Ryouichi Iwama, Ryo Koyama, Yasuji Horiuchi, Hiroyuki Sci Rep Article Conidiation is an important reproductive process in Aspergillus. We previously reported, in A. nidulans, that the deletion of a putative glycosyltransferase gene, rseA/cpsA, causes an increase in the production of extracellular hydrolases and a severe reduction in conidiation. The aim of this study was to obtain novel genetic factors involved in the repression of conidiation in the rseA deletion mutant. We isolated mutants in which the rseA deletion mutant conidiation defect is suppressed and performed a comparative genomic analysis of these mutants. A gene encoding a putative transcription factor was identified as the associated candidate causative gene. The candidate gene was designated as srdA (suppressor gene for the conidiation defect of the rseA deletion mutant). The conidiation efficiency of the rseAsrdA double-deletion mutant was increased. Introduction of wild-type srdA into the suppressor mutants caused a conidiation defect similar to that of the rseA deletion mutant. Notably, the conidiation efficiencies of the rseAsrdA double-deletion and srdA single-deletion mutants were higher than that of the wild-type strain. These results indicate that srdA is a novel genetic factor that strongly represses conidiation of the rseA deletion mutant, and a putative transcriptional regulator, SrdA is a negative regulator of conidiation in A. nidulans. Nature Publishing Group UK 2023-03-15 /pmc/articles/PMC10017718/ /pubmed/36922566 http://dx.doi.org/10.1038/s41598-023-31363-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Ogawa, Masahiro Fukuda, Ryouichi Iwama, Ryo Koyama, Yasuji Horiuchi, Hiroyuki srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title | srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title_full | srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title_fullStr | srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title_full_unstemmed | srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title_short | srdA mutations suppress the rseA/cpsA deletion mutant conidiation defect in Aspergillus nidulans |
title_sort | srda mutations suppress the rsea/cpsa deletion mutant conidiation defect in aspergillus nidulans |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10017718/ https://www.ncbi.nlm.nih.gov/pubmed/36922566 http://dx.doi.org/10.1038/s41598-023-31363-8 |
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