Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans

Publication Date:
2018-02-09
Publisher:
Genetics Society of America (GSA)
Electronic ISSN:
2160-1836
Topics:
Biology
Published by:
_version_ 1836398785114144768
autor Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
beschreibung Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Cryptococcus neoformans . Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in C. neoformans . In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the had1 mutant was found to be compromised at 38° or higher. In addition, the had1 mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the had1 mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of C. neoformans .
citation_standardnr 6159760
datenlieferant ipn_articles
feed_id 169615
feed_publisher Genetics Society of America (GSA)
feed_publisher_url http://www.genetics-gsa.org/
insertion_date 2018-02-09
journaleissn 2160-1836
publikationsjahr_anzeige 2018
publikationsjahr_facette 2018
publikationsjahr_intervall 7984:2015-2019
publikationsjahr_sort 2018
publisher Genetics Society of America (GSA)
quelle G3: Genes, Genomes, Genetics
relation http://www.g3journal.org/cgi/content/short/8/2/643?rss=1
search_space articles
shingle_author_1 Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
shingle_author_2 Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
shingle_author_3 Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
shingle_author_4 Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
shingle_catch_all_1 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Cryptococcus neoformans . Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in C. neoformans . In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the had1 mutant was found to be compromised at 38° or higher. In addition, the had1 mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the had1 mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of C. neoformans .
Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
Genetics Society of America (GSA)
2160-1836
21601836
shingle_catch_all_2 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Cryptococcus neoformans . Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in C. neoformans . In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the had1 mutant was found to be compromised at 38° or higher. In addition, the had1 mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the had1 mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of C. neoformans .
Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
Genetics Society of America (GSA)
2160-1836
21601836
shingle_catch_all_3 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Cryptococcus neoformans . Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in C. neoformans . In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the had1 mutant was found to be compromised at 38° or higher. In addition, the had1 mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the had1 mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of C. neoformans .
Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
Genetics Society of America (GSA)
2160-1836
21601836
shingle_catch_all_4 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Cryptococcus neoformans . Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in C. neoformans . In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the had1 mutant was found to be compromised at 38° or higher. In addition, the had1 mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the had1 mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of C. neoformans .
Jung, W.-H., Son, Y.-E., Oh, S.-H., Fu, C., Kim, H. S., Kwak, J.-H., Cardenas, M. E., Heitman, J., Park, H.-S.
Genetics Society of America (GSA)
2160-1836
21601836
shingle_title_1 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
shingle_title_2 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
shingle_title_3 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
shingle_title_4 Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
timestamp 2025-06-30T23:32:35.981Z
titel Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
titel_suche Had1 Is Required for Cell Wall Integrity and Fungal Virulence in Cryptococcus neoformans
topic W
uid ipn_articles_6159760