Publications by authors named "Rebeca Alonso-Monge"
As part of the intestinal microbiota, can elicit a humoral response in the gastrointestinal tract (GIT) that is mainly directed toward hyphal antigens. This response has been implicated in controlling the invasive form of the fungus and maintaining the yeast as an innocuous commensal. However, the specific targets of this response are still unknown.
View Article and Find Full Text PDFCandidaalbicans normally colonizes the human gastrointestinal tract as a commensal. Studying fungal factors involved in colonizing the mammalian gastrointestinal tract requires mouse models with altered microbiota. We have obtained strains of C.
View Article and Find Full Text PDFMorphogenetic transitions in the adaptation of Candida albicans to the mammalian gut.
Microbes Infect
March 2024
Article Synopsis
- * Its ability to change shape from yeast to filamentous form is linked to its transition from harmless to pathogenic, which is key to its virulence.
- * The review highlights the importance of these shape changes in how C. albicans grows in the gut and emphasizes the transcription factors that regulate these transformations.
Article Synopsis
- * Researchers created mutants lacking Hog1 MAP kinase that overproduce Wor1, enabling these mutants to establish themselves as commensals in the mouse gut and even compete with wild-type Candida cells.
- * The enhanced fitness of these Wor1 overproducing mutants is linked to better adherence to surfaces, increased production of enzymes like proteinase and phospholipase, and reduced filamentation in lab conditions, while showing no virulence in a systemic candidiasis model in mice.
Article Synopsis
- The study investigates how the transcription factor Wor1 impacts the commensal yeast's ability to thrive in the human gastrointestinal tract.
- Overexpressing Wor1 leads to significant changes in the yeast's lipid content and composition, affecting various aspects of cellular physiology.
- These alterations enhance the yeast's resistance to certain damaging agents and improve its ability to adapt to the unique conditions of the gut environment.
Identification of Clinical Isolates of with Increased Fitness in Colonization of the Murine Gut.
J Fungi (Basel)
August 2021
Article Synopsis
- The gastrointestinal tract serves as a key reservoir for a significant opportunistic pathogen that causes fungal diseases in humans, prompting research into the mechanisms that help it thrive as a commensal organism.
- This study involved barcoding 114 clinical isolates to find strains with enhanced survival in a mouse model, leading to the selection of eight strains that showed better colonization after antibiotic treatment.
- One strain, CaORAL3, demonstrated the ability to colonize the intestines of mice even without prior antibiotic treatment, suggesting its potential for becoming a stable commensal in various gut environments.
Article Synopsis
- A specific yeast species lives in the human gut and its ability to transition between two forms (white and opaque) is controlled by a key transcription factor, which affects its metabolism and commensal relationship with the host.* -
- Proteomic analysis shows that when this transcription factor is overexpressed, the yeast struggles to utilize certain sugars (like trehalose and xylose) due to lower levels of isocitrate lyase, linking these metabolic changes to its commensal status.* -
- Mutants lacking proper function of this transcription factor show reduced fitness in the mouse gut, indicating the glyoxylate shunt’s role in helping the yeast adapt as a commensal organism, independent of the transcription factor
Article Synopsis
- The Hog1 MAPK is crucial for answering osmotic stress and also helps the pathogen deal with various other stresses, influencing its survival and ability to flourish in different environments.
- The study reveals that Hog1 is vital for maintaining lipid balance, as mutants lacking Hog1 accumulate lipid droplets under osmotic stress, leading to cell permeability issues.
- Cek1, another MAPK related to osmotic stress response, does not affect lipid homeostasis, suggesting that Hog1 is the primary MAP kinase managing these processes and that lipid metabolism changes make mutants more susceptible to osmotic stress.
Article Synopsis
- The Mitogen-Activated Protein kinase (MAPK) pathways in fungi, particularly the HOG pathway, are crucial for responding to environmental changes and stress, impacting their survival and colonization in hosts.
- A study found that the antifungal Micafungin (MF) had the same minimum inhibitory concentration in both a parent strain and a mutant, indicating no difference in susceptibility, and both strains showed similar impaired cell viability after treatment.
- Unlike the positive control Amphotericin B, MF did not activate specific antioxidant genes or influence reactive oxygen species levels, suggesting that MF's toxic effects do not involve the Hog1 MAPK pathway or oxidative stress in affected cells.
Cooperative Role of MAPK Pathways in the Interaction of with the Host Epithelium.
Microorganisms
December 2019
is an important human fungal pathogen responsible for tens of millions of infections as well as hundreds of thousands of severe life-threatening infections each year. MAP kinase (MAPK) signal transduction pathways facilitate the sensing and adaptation to external stimuli and control the expression of key virulence factors such as the yeast-to-hypha transition, the biogenesis of the cell wall, and the interaction with the host. In the present study, we have combined molecular approaches and infection biology to analyse the role of MAPK pathways during an epithelial invasion.
View Article and Find Full Text PDFThe MAPK Hog1 mediates the response to amphotericin B in Candida albicans.
José Pedro Guirao-Abad
,
Ruth Sánchez-Fresneda
,
Elvira Román
,
Jesús Pla
,
Juan Carlos Argüelles
,
Rebeca Alonso-Monge
Fungal Genet Biol
March 2020
Article Synopsis
- The HOG MAP kinase pathway is essential for Candida albicans to respond to various stresses, particularly to the antifungal drug amphotericin B (AMB).
- Mutants lacking the Hog1 protein, part of this pathway, show increased susceptibility to AMB due to a failure in sensing and surviving oxidative stress induced by the drug.
- The study found that both the phosphorylation and kinase activity of Hog1 are crucial for survival during AMB treatment, while the drug also triggers Hog1-independent processes like trehalose synthesis and influences intracellular reactive oxygen species (ROS) levels.
Deletion of the Gene in a Mutant Reverts Virulence in .
Verónica Urrialde
,
Daniel Prieto
,
Susana Hidalgo-Vico
,
Elvira Román
,
Jesús Pla
,
Rebeca Alonso-Monge
J Fungi (Basel)
November 2019
displays the ability to adapt to a wide variety of environmental conditions, triggering signaling pathways and transcriptional regulation. Sko1 is a transcription factor that was previously involved in early hypoxic response, cell wall remodeling, and stress response. In the present work, the role of mutant in o and studies was explored.
View Article and Find Full Text PDFArticle Synopsis
- CRISPR-Cas systems are powerful tools for genome manipulation, particularly the Class 2 type II system, which has been widely studied across various organisms including mammalian cells, plants, fungi, and bacteria.
- * Pathogenic fungi are significant contributors to human diseases, making genetic manipulation crucial for developing new therapies and antifungal treatments.
- * The review focuses on advancements in using CRISPR systems for human pathogenic fungi, highlighting improvements in research utility and exploring potential future applications.*
Article Synopsis
- CRISPR is not just a gene-editing tool; it can also regulate gene expression by combining Cas9 with transcriptional repressors or activators.
- Researchers created a system in yeast that shows specific gene repression or activation, demonstrating success through various techniques like qPCR and flow cytometry.
- The study highlights the potential of CRISPR technology to manipulate complex regulatory traits in important fungal pathogens, enhancing our understanding of their virulence pathways.
Non-canonical Activities of Hog1 Control Sensitivity of to Killer Toxins From .
Ana Morales-Menchén
,
Federico Navarro-García
,
José P Guirao-Abad
,
Elvira Román
,
Daniel Prieto
,
Rebeca Alonso-Monge
Front Cell Infect Microbiol
February 2019
Article Synopsis
- - Certain yeasts produce killer toxins (mycocins) that can harm sensitive yeast and fungi, a phenomenon observed in various environmental species.
- - Recent research found cheese-derived yeast strains that produce these toxins and indicated that mutants lacking the MAPK Hog1 signal pathway are more susceptible to the mycocins, unlike other mutants.
- - The study revealed that while Hog1's phosphorylation is crucial for survival against these toxins and coping with osmotic and oxidative stresses, overactive catalase does not provide protection, hinting at other stress-related mechanisms involved.
Overexpression of the Transcriptional Regulator Increases Susceptibility to Bile Salts and Adhesion to the Mouse Gut Mucosa in .
Front Cell Infect Microbiol
June 2018
Article Synopsis
- The transcriptional regulator Wor1 plays a key role in the GUT transition, enhancing fitness in the mouse gastrointestinal tract in response to environmental changes.
- Researchers created strains with controlled Wor1 expression using a tetracycline promoter, which retained GUT cell characteristics but struggled in early colonization stages.
- These modified cells displayed unique colonization patterns and metabolic changes, suggesting they could be better at adhering to the mouse mucosa and thus enhance their long-term colonization capabilities.
Article Synopsis
- Arsenic is a toxic metalloid found in nature, and recent studies highlight the role of the transcription factor Pho4 in helping Candida albicans tolerate arsenic-derived compounds like arsenite and arsenate.
- In wild type Candida cells, exposure to arsenite and arsenate increases reactive oxygen species (ROS) production and activates protective enzymes, indicating the oxidative stress these compounds cause.
- Pho4 null mutants showed reduced ROS production and different responses to arsenic, suggesting Pho4 is crucial for the yeast's antioxidant defense, with arsenite triggering specific enzymes that arsenate does not.
Article Synopsis
- This text serves as a correction to an article appearing on page 2133 in volume 7.
- The article referenced has the PubMed Identifier (PMID) 28111572.
- The correction likely addresses errors or clarifications in the originally published work.
The Hog1 MAP Kinase Promotes the Recovery from Cell Cycle Arrest Induced by Hydrogen Peroxide in .
Front Microbiol
January 2017
Article Synopsis
- - Eukaryotic cell cycle progression is monitored by checkpoints and influenced by environmental stress, with MAPKs like Mkc1 and Hog1 being crucial for sensing oxidative stress, particularly from hydrogen peroxide.
- - Exposure to hydrogen peroxide leads to a temporary arrest in the G1 phase of the cell cycle, and certain mutant strains take longer to resume growth compared to wild type cells after stress, while some mutants progress faster under normal conditions.
- - The study reveals that Hog1 MAPK affects the expression of G1 cyclins differently during stress and standard conditions, impacting cell size and the overall cell cycle progression, highlighting its role in both scenarios.
Role of catalase overproduction in drug resistance and virulence in Candida albicans.
Elvira Román
,
Daniel Prieto
,
Ry Martin
,
Inês Correia
,
Ana Cecilia Mesa Arango
,
Rebeca Alonso-Monge
Future Microbiol
October 2016
Aim: To investigate the role of Cat1 overproduction in Candida albicans.
Materials & Methods: Strains overproducing the CAT1 gene were constructed.
Results: Cells overproducing CAT1 were found to be more resistant to some oxidants and mammalian phagocytic cells.
Article Synopsis
- The Pho4 transcription factor is essential for growth and stress response in the fungus Candida albicans, particularly under low phosphate conditions.
- Pho4 mutants showed increased susceptibility to osmotic and oxidative stress but maintained virulence comparable to wild type strains in infection models.
- Although Pho4 did not affect gut colonization abilities, it significantly influenced competition and adherence, revealing its critical role in stress adaptation and overall fitness.
The cell wall integrity pathway (CWI) plays an important role in the biogenesis of the cell wall in Candida albicans and other fungi. In the present work, the C. albicans MKK2 gene that encodes the putative MAPKK of this pathway was deleted in different backgrounds and the phenotypes of the resultant mutants were characterised.
View Article and Find Full Text PDFThe Pho4 transcription factor mediates the response to arsenate and arsenite in Candida albicans.
Front Microbiol
February 2015
Article Synopsis
- Arsenate (As (V)) is the main toxic form of arsenic, and the study investigates how the pathogenic fungus Candida albicans detects and responds to it.
- The research found that the Hog1 and Mkc1 signaling pathways respond to arsenate, with Hog1 phosphorylation dependent on another protein called Ssk1.
- A specific transcription factor, Pho4, was identified as crucial for the arsenate response, influencing Hog1 activity and showing sensitivity to both arsenate and arsenite due to its phosphorylation changes.
Article Synopsis
- Different MAP kinase pathways in Candida albicans respond to various stimuli, with Hog1 linked to stress and virulence, while Cek1 is associated with cell wall production, mating, and biofilm formation.!* -
- Mutants lacking both MAPK pathways showed issues like abnormal shape, cell polarity problems, and improper chitin distribution under osmotic stress, leading to decreased viability and signs of cell death, despite some normal phosphorylation and glycerol buildup.!* -
- The significance of these pathways in virulence is highlighted by the observation that certain mutants (ssk1 msb2 sho1 opy2) displayed no virulence in mice and weakened virulence in Galleria mellonella infections.!*