Bernardo Ramirez-Zavala

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About Bernardo Ramirez-Zavala:

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SEEK ID: https://funginet.hki-jena.de/people/107

Location: Germany

ORCID: Not specified

Joined: 6th May 2016

Expertise: Molecular Biology, Candida albicans, Protein Kinases

Tools: Molecular Biology, Biochemistry and protein analysis

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Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

The yeast Candida albicans and the filamentous fungus Aspergillus fumigatus are by far the most important causes of life-threatening invasive mycoses in Europe. Despite the increasing incidence of these infections, the current diagnosis is still difficult and often too late, and options for therapies are limited. Moreover, A. fumigatus and C. albicans have developed multiple sophisticated, specific and unique pathogenicity mechanisms. Many of these mechanisms are not well understood. Research on ...

Projects: FungiNet total, FungiNet A - Aspergillus projects, FungiNet B - Bioinformatics projects, FungiNet C - Candida projects, INF, A1, A2, A3, A4 (E), A5, B1, B2, B3 (E), B4, C1, C2, C3, C4 (E), C5, C6 (E), Z2, Z1, B5, A6, A7, A8, C7

Web page: http://www.funginet.de/home.html

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FungiNet total

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Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/home.html

Organisms: Aspergillus fumigatus, Candida albicans

Regulation of Candida albicans virulence traits by protein kinases

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-c2.html

Organisms: Candida albicans

FungiNet C - Candida projects

No description specified

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-area-c.html

Organisms: Candida albicans

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Julius Maximilians University Würzburg, Institute for Molecular Infection Biology

Country: Germany

City: Würzburg

Web page: http://www.imib-wuerzburg.de/imib

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Candida albicans SR-Like Protein Kinases Regulate Different Cellular Processes: Sky1 Is Involved in Control of Ion Homeostasis, While Sky2 Is Important for Dipeptide Utilization.

INF, C2, Z2, B5

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Protein kinases play a crucial role in regulating cellular processes such as growth, proliferation, environmental adaptation and stress responses. Serine-arginine (SR) protein kinases are highly conserved …

Authors: P. Brandt, F. Gerwien, L. Wagner, T. Kruger, B. Ramirez-Zavala, M. H. Mirhakkak, S. Schauble, O. Kniemeyer, G. Panagiotou, A. A. Brakhage, J. Morschhauser, S. Vylkova

Date Published: 23rd May 2022

Publication Type: Journal

PubMed ID: 35601106

Citation: Front Cell Infect Microbiol. 2022 May 6;12:850531. doi: 10.3389/fcimb.2022.850531. eCollection 2022.

Created: 19th Jan 2024 at 12:17

The zinc cluster transcription factor Czf1 regulates cell wall architecture and integrity in Candida albicans.

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The fungal cell wall is essential for the maintenance of cellular integrity and mediates interactions of the cells with the environment. It is a highly flexible organelle whose composition and organization …

Authors: A. Mottola, B. Ramirez-Zavala, K. Hunniger, O. Kurzai, J. Morschhauser

Date Published: 15th Apr 2021

Publication Type: Not specified

PubMed ID: 33860578

Citation: Mol Microbiol. 2021 Apr 15. doi: 10.1111/mmi.14727.

Created: 14th May 2021 at 10:22, Last updated: 17th Jan 2024 at 10:24

Evolution of Fluconazole-Resistant Candida albicans Strains by Drug-Induced Mating Competence and Parasexual Recombination.

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The clonal population structure of Candida albicans suggests that (para)sexual recombination does not play an important role in the lifestyle of this opportunistic fungal pathogen, an assumption that … is strengthened by the fact that most C. albicans strains are heterozygous at the mating type locus (MTL) and therefore mating-incompetent. On the other hand, mating might occur within clonal populations and allow the combination of advantageous traits that were acquired by individual cells to adapt to adverse conditions. We have investigated if parasexual recombination may be involved in the evolution of highly drug-resistant strains exhibiting multiple resistance mechanisms against fluconazole, an antifungal drug that is commonly used to treat infections by C. albicans Growth of strains that were heterozygous for MTL and different fluconazole resistance mutations in the presence of the drug resulted in the emergence of derivatives that had become homozygous for the mutated allele and the mating type locus and exhibited increased drug resistance. When MTL a/a and MTLalpha/alpha cells of these strains were mixed in all possible combinations, we could isolate mating products containing the genetic material from both parents. The initial mating products did not exhibit higher drug resistance than their parental strains, but further propagation under selective pressure resulted in the loss of the wild-type alleles and increased fluconazole resistance. Therefore, fluconazole treatment not only selects for resistance mutations but also promotes genomic alterations that confer mating competence, which allows cells in an originally clonal population to exchange individually acquired resistance mechanisms and generate highly drug-resistant progeny.IMPORTANCE Sexual reproduction is an important mechanism in the evolution of species, since it allows the combination of advantageous traits of individual members in a population. The pathogenic yeast Candida albicans is a diploid organism that normally propagates in a clonal fashion, because heterozygosity at the mating type locus (MTL) inhibits mating between cells. Here we show that C. albicans cells that have acquired drug resistance mutations during treatment with the commonly used antifungal agent fluconazole rapidly develop further increased resistance by genome rearrangements that result in simultaneous loss of heterozygosity for the mutated allele and the mating type locus. This enables the drug-resistant cells of a population to switch to the mating-competent opaque morphology and mate with each other to combine different individually acquired resistance mechanisms. The tetraploid mating products reassort their merged genomes and, under selective pressure by the drug, generate highly resistant progeny that have retained the advantageous mutated alleles. Parasexual propagation, promoted by stress-induced genome rearrangements that result in the acquisition of mating competence in cells with adaptive mutations, may therefore be an important mechanism in the evolution of C. albicans populations.

Authors: C. Popp, B. Ramirez-Zavala, S. Schwanfelder, I. Kruger, J. Morschhauser

Date Published: 5th Feb 2019

Publication Type: Not specified

PubMed ID: 30723130

Citation: mBio. 2019 Feb 5;10(1). pii: mBio.02740-18. doi: 10.1128/mBio.02740-18.

Created: 16th Feb 2021 at 13:55, Last updated: 17th Jan 2024 at 10:24

A Hyperactive Form of the Zinc Cluster Transcription Factor Stb5 Causes YOR1 Overexpression and Beauvericin Resistance in Candida albicans.

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Gain-of-function mutations in the zinc cluster transcription factors Mrr1, Tac1, and Upc2, which result in constitutive overexpression of their target genes, are a frequent cause of fluconazole resistance …

Authors: B. Ramirez-Zavala, H. Manz, F. Englert, P. D. Rogers, J. Morschhauser

Date Published: 27th Sep 2018

Publication Type: Not specified

PubMed ID: 30249688

Citation: Antimicrob Agents Chemother. 2018 Nov 26;62(12). pii: AAC.01655-18. doi: 10.1128/AAC.01655-18. Print 2018 Dec.

Created: 16th Feb 2021 at 13:56, Last updated: 17th Jan 2024 at 10:24

The Snf1-activating kinase Sak1 is a key regulator of metabolic adaptation and in vivo fitness of Candida albicans.

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The metabolic flexibility of the opportunistic fungal pathogen Candida albicans is important for colonisation and infection of different host niches. Complex regulatory networks, in which protein kinases …

Authors: B. Ramirez-Zavala, A. Mottola, J. Haubenreisser, S. Schneider, S. Allert, S. Brunke, K. Ohlsen, B. Hube, J. Morschhauser

Date Published: 25th Mar 2017

Publication Type: Not specified

PubMed ID: 28337802

Citation: Mol Microbiol. 2017 Jun;104(6):989-1007. doi: 10.1111/mmi.13674. Epub 2017 Apr 18.

Created: 16th Feb 2021 at 14:03, Last updated: 17th Jan 2024 at 10:24

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