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1. The pathobiology of human fungal infections

Author

Brown, Gordon D., Ballou, Elizabeth R., Bates, Steven, Bignell, Elaine M., Borman, Andrew M., Brand, Alexandra C., Brown, Alistair J. P., Coelho, Carolina, Cook, Peter C., Farrer, Rhys A., Govender, Nelesh P., Gow, Neil A. R., Hope, William, Hoving, J. Claire, Dangarembizi, Rachael, Harrison, Thomas S., Johnson, Elizabeth M., Mukaremera, Liliane, Ramsdale, Mark, Thornton, Christopher R., Usher, Jane, Warris, Adilia, and Wilson, Duncan

Published
2024
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10. Divergent functions of three Candida albicans zinc-cluster transcription factors (CTA4, ASG1 and CTF1) complementing pleiotropic drug resistance in Saccharomyces cerevisiae

Author

Coste, Alix T., Ramsdale, Mark, Ischer, Francoise, and Sanglard, Dominique

Subjects
Brewer's yeast -- Genetic aspects, Drug resistance in microorganisms -- Genetic aspects, Candida albicans -- Genetic aspects, DNA binding proteins -- Physiological aspects, Biological sciences
Abstract

One of the mediators of pleiotropic drug resistance in Saccharomyces cerevisiae is the ABC-transporter gene PDR5. This gene is regulated by at least two transcription factors with Zn(2)-Cys(6) finger DNA-binding motifs, Pdr1p and Pdr3p. In this work, we searched for functional homologues of these transcription factors in Candida albicans. A C. albicans gene library was screened in a S. cerevisiae mutant lacking PDR1 and PDR3 and clones resistant to azole antifungals were isolated. From these clones, three genes responsible for azole resistance were identified. These genes (CTA4, ASG1 and CTF1) encode proteins with Zn(2)-Cys(6)-type zinc finger motifs in their N-terminal domains. The C. albicans genes expressed in S. cerevisiae could activate the transcription of a PDR5-lacZ reporter system and this reporter activity was PDRE-dependent. They could also confer resistance to azoles in a S. cerevisiae strain lacking PDR1, PDR3 and PDR5, suggesting that CTA4-, ASG1- and CTF1-dependent azole resistance can be caused by genes other than PDR5 in S. cerevisiae. Deletion of CTA4, ASG1 and CTF1 in C. albicans had no effect on fluconazole susceptibility and did not alter the expression of the ABC-transporter genes CDR1 and CDR2 or the major facilitator gene MDR1, which encode multidrug transporters known as mediators of azole resistance in C. albicans. However, additional phenotypic screening tests on the C. albicans mutants revealed that the presence of ASG1 was necessary to sustain growth on non-fermentative carbon sources (sodium acetate, acetic acid, ethanol). In conclusion, C. albicans possesses functional homologues of the S. cerevisiae Pdr1p and Pdr3p transcription factors; however, their properties in C. albicans have been rewired to other functions.

Published
2008

11. Guidelines and recommendations on yeast cell death nomenclature

Author

Carmona-Gutierrez, Didac, Bauer, Maria Anna, Zimmermann, Andreas, Aguilera, Andres, Austriaco, Nicanor, Ayscough, Kathryn, Balzan, Rena, Bar-Nun, Shoshana, Barrientos, Antonio, Belenky, Peter, Blondel, Marc, Braun, Ralf J., Breitenbach, Michael, Burhans, William C., Büttner, Sabrina, Cavalieri, Duccio, Chang, Michael, Cooper, Katrina F., Corte-Real, Manuela, Costa, Vitor, Cullin, Christophe, Dawes, Ian, Dengjel, Jorn, Dickman, Martin B., Eisenberg, Tobias, Fahrenkrog, Birthe, Fasel, Nicolas, Frohlich, Kai-Uwe, Gargouri, Ali, Giannattasio, Sergio, Goffrini, Paola, Gourlay, Campbell W., Grant, Chris M., Greenwood, Michael T., Guaragnella, Nicoletta, Heger, Thomas, Heinisch, Juergen, Herker, Eva, Herrmann, Johannes M., Hofer, Sebastian, Jimenez-Ruiz, Antonio, Jungwirth, Helmut, Kainz, Katharina, Kontoyiannis, Dimitrios P., Ludovico, Paula, Manon, Stephen, Martegani, Enzo, Mazzoni, Cristina, Megeney, Lynn A., Meisinger, Chris, Nielsen, Jens, Nystrom, Thomas, Osiewacz, Heinz D., Outeiro, Tiago F., Park, Hay-Oak, Pendl, Tobias, Petranovic, Dina, Picot, Stephane, Polcic, Peter, Powers, Ted, Ramsdale, Mark, Rinnerthaler, Mark, Rockenfeller, Patrick, Ruckenstuhl, Christoph, Schaffrath, Raffael, Segovia, Maria, Severin, Fedor F., Sharon, Amir, Sigrist, Stephan J., Sommer-Ruck, Cornelia, Sousa, Maria Joao, Thevelein, Johan M., Thevissen, Karin, Titorenko, Vladimir, Toledano, Michel B., Tuite, Mick, Voegtle, F. -Nora, Westermann, Benedikt, Winderickx, Joris, Wissing, Silke, Woelfl, Stefan, Zhang, Zhaojie J., Zhao, Richard Y., Zhou, Bing, Galluzzi, Lorenzo, Kroemer, Guido, Madeo, Frank, Carmona-Gutierrez, Didac, Bauer, Maria Anna, Zimmermann, Andreas, Aguilera, Andres, Austriaco, Nicanor, Ayscough, Kathryn, Balzan, Rena, Bar-Nun, Shoshana, Barrientos, Antonio, Belenky, Peter, Blondel, Marc, Braun, Ralf J., Breitenbach, Michael, Burhans, William C., Büttner, Sabrina, Cavalieri, Duccio, Chang, Michael, Cooper, Katrina F., Corte-Real, Manuela, Costa, Vitor, Cullin, Christophe, Dawes, Ian, Dengjel, Jorn, Dickman, Martin B., Eisenberg, Tobias, Fahrenkrog, Birthe, Fasel, Nicolas, Frohlich, Kai-Uwe, Gargouri, Ali, Giannattasio, Sergio, Goffrini, Paola, Gourlay, Campbell W., Grant, Chris M., Greenwood, Michael T., Guaragnella, Nicoletta, Heger, Thomas, Heinisch, Juergen, Herker, Eva, Herrmann, Johannes M., Hofer, Sebastian, Jimenez-Ruiz, Antonio, Jungwirth, Helmut, Kainz, Katharina, Kontoyiannis, Dimitrios P., Ludovico, Paula, Manon, Stephen, Martegani, Enzo, Mazzoni, Cristina, Megeney, Lynn A., Meisinger, Chris, Nielsen, Jens, Nystrom, Thomas, Osiewacz, Heinz D., Outeiro, Tiago F., Park, Hay-Oak, Pendl, Tobias, Petranovic, Dina, Picot, Stephane, Polcic, Peter, Powers, Ted, Ramsdale, Mark, Rinnerthaler, Mark, Rockenfeller, Patrick, Ruckenstuhl, Christoph, Schaffrath, Raffael, Segovia, Maria, Severin, Fedor F., Sharon, Amir, Sigrist, Stephan J., Sommer-Ruck, Cornelia, Sousa, Maria Joao, Thevelein, Johan M., Thevissen, Karin, Titorenko, Vladimir, Toledano, Michel B., Tuite, Mick, Voegtle, F. -Nora, Westermann, Benedikt, Winderickx, Joris, Wissing, Silke, Woelfl, Stefan, Zhang, Zhaojie J., Zhao, Richard Y., Zhou, Bing, Galluzzi, Lorenzo, Kroemer, Guido, and Madeo, Frank

Abstract

Elucidating the biology of yeast in its full complexity has major implications for science, medicine and industry. One of the most critical processes determining yeast life and physiology is cellular demise. However, the investigation of yeast cell death is a relatively young field, and a widely accepted set of concepts and terms is still missing. Here, we propose unified criteria for the definition of accidental, regulated, and programmed forms of cell death in yeast based on a series of morphological and biochemical criteria. Specifically, we provide consensus guidelines on the differential definition of terms including apoptosis, regulated necrosis, and autophagic cell death, as we refer to additional cell death routines that are relevant for the biology of (at least some species of) yeast. As this area of investigation advances rapidly, changes and extensions to this set of recommendations will be implemented in the years to come. Nonetheless, we strongly encourage the authors, reviewers and editors of scientific articles to adopt these collective standards in order to establish an accurate framework for yeast cell death research and, ultimately, to accelerate the progress of this vibrant field of research.

Published
2018
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12. Guidelines and recommendations on yeast cell death nomenclature

Author

Carmona-Gutierrez, D, Bauer, M, Zimmermann, A, Aguilera, A, Austriaco, N, Ayscough, K, Balzan, R, Bar-Nun, S, Barrientos, A, Belenky, P, Blondel, M, Braun, R, Breitenbach, M, Burhans, W, Buettner, S, Cavalieri, D, Chang, M, Cooper, K, Côrte-Real, M, Costa, V, Cullin, C, Dawes, I, Dengjel, J, Dickman, M, Eisenberg, T, Fahrenkrog, B, Fasel, N, Froehlich, K, Gargouri, A, Giannattasio, S, Goffrini, P, Gourlay, C, Grant, C, Greenwood, M, Guaragnella, N, Heger, T, Heinisch, J, Herker, E, Herrmann, J, Hofer, S, Jiménez-Ruiz, A, Jungwirth, H, Kainz, K, Kontoyiannis, D, Ludovico, P, Manon, S, Martegani, E, Mazzoni, C, Megeney, L, Meisinger, C, Nielsen, J, Nystroem, T, Osiewacz, H, Outeiro, T, Park, H, Pendl, T, Petranovic, D, Picot, S, Polčic, P, Powers, T, Ramsdale, M, Rinnerthaler, M, Rockenfeller, P, Ruckenstuhl, C, Schaffrath, R, Segovia, M, Severin, F, Sharon, A, Sigrist, S, Sommer-Ruck, C, Sousa, M, Thevelein, J, Thevissen, K, Titorenko, V, Toledano, M, Tuite, M, Voegtle, F, Westermann, B, Winderickx, J, Wissing, S, Woelfl, S, Zhang, Z, Zhao, R, Zhou, B, Galluzzi, L, Kroemer, G, Madeo, F, Carmona-Gutierrez, Didac, Bauer, Maria Anna, Zimmermann, Andreas, Aguilera, Andrés, Austriaco, Nicanor, Ayscough, Kathryn, Balzan, Rena, Bar-Nun, Shoshana, Barrientos, Antonio, Belenky, Peter, Blondel, Marc, Braun, Ralf J., Breitenbach, Michael, Burhans, William C., Buettner, Sabrina, Cavalieri, Duccio, Chang, Michael, Cooper, Katrina F., Côrte-Real, Manuela, Costa, Vítor, Cullin, Christophe, Dawes, Ian, Dengjel, Jörn, Dickman, Martin B., Eisenberg, Tobias, Fahrenkrog, Birthe, Fasel, Nicolas, Froehlich, Kai-Uwe, Gargouri, Ali, Giannattasio, Sergio, Goffrini, Paola, Gourlay, Campbell W., Grant, Chris M., Greenwood, Michael T., Guaragnella, Nicoletta, Heger, Thomas, Heinisch, Juergen, Herker, Eva, Herrmann, Johannes M., Hofer, Sebastian, Jiménez-Ruiz, Antonio, Jungwirth, Helmut, Kainz, Katharina, Kontoyiannis, Dimitrios P., Ludovico, Paula, Manon, Stéphen, Martegani, Enzo, Mazzoni, Cristina, Megeney, Lynn A., Meisinger, Chris, Nielsen, Jens, Nystroem, Thomas, Osiewacz, Heinz D., Outeiro, Tiago F., Park, Hay-Oak, Pendl, Tobias, Petranovic, Dina, Picot, Stephane, Polčic, Peter, Powers, Ted, Ramsdale, Mark, Rinnerthaler, Mark, Rockenfeller, Patrick, Ruckenstuhl, Christoph, Schaffrath, Raffael, Segovia, Maria, Severin, Fedor F., Sharon, Amir, Sigrist, Stephan J., Sommer-Ruck, Cornelia, Sousa, Maria João, Thevelein, Johan M., Thevissen, Karin, Titorenko, Vladimir, Toledano, Michel B., Tuite, Mick, Voegtle, F. -Nora, Westermann, Benedikt, Winderickx, Joris, Wissing, Silke, Woelfl, Stefan, Zhang, Zhaojie J., Zhao, Richard Y., Zhou, Bing, Galluzzi, Lorenzo, Kroemer, Guido, Madeo, Frank, Carmona-Gutierrez, D, Bauer, M, Zimmermann, A, Aguilera, A, Austriaco, N, Ayscough, K, Balzan, R, Bar-Nun, S, Barrientos, A, Belenky, P, Blondel, M, Braun, R, Breitenbach, M, Burhans, W, Buettner, S, Cavalieri, D, Chang, M, Cooper, K, Côrte-Real, M, Costa, V, Cullin, C, Dawes, I, Dengjel, J, Dickman, M, Eisenberg, T, Fahrenkrog, B, Fasel, N, Froehlich, K, Gargouri, A, Giannattasio, S, Goffrini, P, Gourlay, C, Grant, C, Greenwood, M, Guaragnella, N, Heger, T, Heinisch, J, Herker, E, Herrmann, J, Hofer, S, Jiménez-Ruiz, A, Jungwirth, H, Kainz, K, Kontoyiannis, D, Ludovico, P, Manon, S, Martegani, E, Mazzoni, C, Megeney, L, Meisinger, C, Nielsen, J, Nystroem, T, Osiewacz, H, Outeiro, T, Park, H, Pendl, T, Petranovic, D, Picot, S, Polčic, P, Powers, T, Ramsdale, M, Rinnerthaler, M, Rockenfeller, P, Ruckenstuhl, C, Schaffrath, R, Segovia, M, Severin, F, Sharon, A, Sigrist, S, Sommer-Ruck, C, Sousa, M, Thevelein, J, Thevissen, K, Titorenko, V, Toledano, M, Tuite, M, Voegtle, F, Westermann, B, Winderickx, J, Wissing, S, Woelfl, S, Zhang, Z, Zhao, R, Zhou, B, Galluzzi, L, Kroemer, G, Madeo, F, Carmona-Gutierrez, Didac, Bauer, Maria Anna, Zimmermann, Andreas, Aguilera, Andrés, Austriaco, Nicanor, Ayscough, Kathryn, Balzan, Rena, Bar-Nun, Shoshana, Barrientos, Antonio, Belenky, Peter, Blondel, Marc, Braun, Ralf J., Breitenbach, Michael, Burhans, William C., Buettner, Sabrina, Cavalieri, Duccio, Chang, Michael, Cooper, Katrina F., Côrte-Real, Manuela, Costa, Vítor, Cullin, Christophe, Dawes, Ian, Dengjel, Jörn, Dickman, Martin B., Eisenberg, Tobias, Fahrenkrog, Birthe, Fasel, Nicolas, Froehlich, Kai-Uwe, Gargouri, Ali, Giannattasio, Sergio, Goffrini, Paola, Gourlay, Campbell W., Grant, Chris M., Greenwood, Michael T., Guaragnella, Nicoletta, Heger, Thomas, Heinisch, Juergen, Herker, Eva, Herrmann, Johannes M., Hofer, Sebastian, Jiménez-Ruiz, Antonio, Jungwirth, Helmut, Kainz, Katharina, Kontoyiannis, Dimitrios P., Ludovico, Paula, Manon, Stéphen, Martegani, Enzo, Mazzoni, Cristina, Megeney, Lynn A., Meisinger, Chris, Nielsen, Jens, Nystroem, Thomas, Osiewacz, Heinz D., Outeiro, Tiago F., Park, Hay-Oak, Pendl, Tobias, Petranovic, Dina, Picot, Stephane, Polčic, Peter, Powers, Ted, Ramsdale, Mark, Rinnerthaler, Mark, Rockenfeller, Patrick, Ruckenstuhl, Christoph, Schaffrath, Raffael, Segovia, Maria, Severin, Fedor F., Sharon, Amir, Sigrist, Stephan J., Sommer-Ruck, Cornelia, Sousa, Maria João, Thevelein, Johan M., Thevissen, Karin, Titorenko, Vladimir, Toledano, Michel B., Tuite, Mick, Voegtle, F. -Nora, Westermann, Benedikt, Winderickx, Joris, Wissing, Silke, Woelfl, Stefan, Zhang, Zhaojie J., Zhao, Richard Y., Zhou, Bing, Galluzzi, Lorenzo, Kroemer, Guido, and Madeo, Frank

Abstract

Elucidating the biology of yeast in its full complexity has major implications for science, medicine and industry. One of the most critical processes determining yeast life and physiology is cellular demise. However, the investigation of yeast cell death is a relatively young field, and a widely accepted set of concepts and terms is still missing. Here, we propose unified criteria for the definition of accidental, regulated, and programmed forms of cell death in yeast based on a series of morphological and biochemical criteria. Specifically, we provide consensus guidelines on the differential definition of terms including apoptosis, regulated necrosis, and autophagic cell death, as we refer to additional cell death routines that are relevant for the biology of (at least some species of) yeast. As this area of investigation advances rapidly, changes and extensions to this set of recommendations will be implemented in the years to come. Nonetheless, we strongly encourage the authors, reviewers and editors of scientific articles to adopt these collective standards in order to establish an accurate framework for yeast cell death research and, ultimately, to accelerate the progress of this vibrant field of research.

Published
2018

14. Guidelines and recommendations on yeast cell death nomenclature

Author

Carmona-Gutierrez, Didac, primary, Bauer, Maria Anna, additional, Zimmermann, Andreas, additional, Aguilera, Andrés, additional, Austriaco, Nicanor, additional, Ayscough, Kathryn, additional, Balzan, Rena, additional, Bar-Nun, Shoshana, additional, Barrientos, Antonio, additional, Belenky, Peter, additional, Blondel, Marc, additional, Braun, Ralf J., additional, Breitenbach, Michael, additional, Burhans, William C., additional, Buettner, Sabrina, additional, Cavalieri, Duccio, additional, Chang, Michael, additional, Cooper, Katrina F., additional, Côrte-Real, Manuela, additional, Costa, Vítor, additional, Cullin, Christophe, additional, Dawes, Ian, additional, Dengjel, Jörn, additional, Dickman, Martin B., additional, Eisenberg, Tobias, additional, Fahrenkrog, Birthe, additional, Fasel, Nicolas, additional, Froehlich, Kai-Uwe, additional, Gargouri, Ali, additional, Giannattasio, Sergio, additional, Goffrini, Paola, additional, Gourlay, Campbell W., additional, Grant, Chris M., additional, Greenwood, Michael T., additional, Guaragnella, Nicoletta, additional, Heger, Thomas, additional, Heinisch, Juergen, additional, Herker, Eva, additional, Herrmann, Johannes M., additional, Hofer, Sebastian, additional, Jiménez-Ruiz, Antonio, additional, Jungwirth, Helmut, additional, Kainz, Katharina, additional, Kontoyiannis, Dimitrios P., additional, Ludovico, Paula, additional, Manon, Stéphen, additional, Martegani, Enzo, additional, Mazzoni, Cristina, additional, Megeney, Lynn A., additional, Meisinger, Chris, additional, Nielsen, Jens, additional, Nystroem, Thomas, additional, Osiewacz, Heinz D., additional, Outeiro, Tiago F., additional, Park, Hay-Oak, additional, Pendl, Tobias, additional, Petranovic, Dina, additional, Picot, Stephane, additional, Polčic, Peter, additional, Powers, Ted, additional, Ramsdale, Mark, additional, Rinnerthaler, Mark, additional, Rockenfeller, Patrick, additional, Ruckenstuhl, Christoph, additional, Schaffrath, Raffael, additional, Segovia, Maria, additional, Severin, Fedor F., additional, Sharon, Amir, additional, Sigrist, Stephan J., additional, Sommer-Ruck, Cornelia, additional, Sousa, Maria João, additional, Thevelein, Johan M., additional, Thevissen, Karin, additional, Titorenko, Vladimir, additional, Toledano, Michel B., additional, Tuite, Mick, additional, Voegtle, F.-Nora, additional, Westermann, Benedikt, additional, Winderickx, Joris, additional, Wissing, Silke, additional, Woelfl, Stefan, additional, Zhang, Zhaojie J., additional, Zhao, Richard Y., additional, Zhou, Bing, additional, Galluzzi, Lorenzo, additional, Kroemer, Guido, additional, and Madeo, Frank, additional

Published
2018
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15. Apoptosis of Candida albicans during the Interaction with Murine Macrophages: Proteomics and Cell-Death Marker Monitoring

Author

Cabezón, Virginia, primary, Vialás, Vital, additional, Gil-Bona, Ana, additional, Reales-Calderón, Jose A., additional, Martínez-Gomariz, Montserrat, additional, Gutiérrez-Blázquez, Dolores, additional, Monteoliva, Lucía, additional, Molero, Gloria, additional, Ramsdale, Mark, additional, and Gil, Concha, additional

Published
2016
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24. Apoptosis of Candida albicansduring the Interaction with Murine Macrophages: Proteomics and Cell-Death Marker Monitoring

Author

Cabezón, Virginia, Vialás, Vital, Gil-Bona, Ana, Reales-Calderón, Jose A., Martínez-Gomariz, Montserrat, Gutiérrez-Blázquez, Dolores, Monteoliva, Lucía, Molero, Gloria, Ramsdale, Mark, and Gil, Concha

Abstract

Macrophages may induce fungal apoptosis to fight against C. albicans, as previously hypothesized by our group. To confirm this hypothesis, we analyzed proteins from C. albicanscells after 3 h of interaction with macrophages using two quantitative proteomic approaches. A total of 51 and 97 proteins were identified as differentially expressed by DIGE and iTRAQ, respectively. The proteins identified and quantified were different, with only seven in common, but classified in the same functional categories. The analyses of their functions indicated that an increase in the metabolism of amino acids and purine nucleotides were taking place, while the glycolysis and translation levels dropped after 3 h of interaction. Also, the response to oxidative stress and protein translation were reduced. In addition, seven substrates of metacaspase (Mca1) were identified (Cdc48, Fba1, Gpm1, Pmm1, Rct1, Ssb1, and Tal1) as decreased in abundance, plus 12 proteins previously described as related to apoptosis. Besides, the monitoring of apoptotic markers along 24 h of interaction (caspase-like activity, TUNEL assay, and the measurement of ROS and cell examination by transmission electron microscopy) revealed that apoptotic processes took place for 30% of the fungal cells, thus supporting the proteomic results and the hypothesis of macrophages killing C. albicansby apoptosis.

Published
2016
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28. Endoplasmic reticulum involvement in yeast cell death.

Author

Austriaco, Nicanor, Gourlay, Campbell, Winderickx, Joris, and Ramsdale, Mark

Subjects
ENDOPLASMIC reticulum, CELL death, EUKARYOTES, MEMBRANE proteins, POLYPEPTIDES, GLYCOSYLATION
Abstract

In all eukaryotes the endoplasmic reticulum (ER) has a central role in protein folding and maturation of secretory and membrane proteins. Upon translocation into the ER polypeptides are immediately subjected to folding and modifications involving the formation of disulfide bridges, assembly of subunits to multi-protein complexes, and glycosylation. During these processes incompletely folded, terminally misfolded, and unassembled proteins can accumulate which endanger the cellular homeostasis and subsequently the survival of cells and tissues. Consequently, organisms have developed a quality control system to cope with this problem and remove the unwanted protein load from the ER by a process collectively referred to as ER-associated degradation (ERAD) pathway. Recent studies in Arabidopsis have identified plant ERAD components involved in the degradation of aberrant proteins and evidence was provided for a specific role in abiotic stress tolerance. In this short review we discuss our current knowledge about this important cellular pathway. [ABSTRACT FROM AUTHOR]

Published
2012
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29. Divergent functions of three Candida albicans zinc-cluster transcription factors (CTA4, ASG1 and CTF1) complementing pleiotropic drug resistance in Saccharomyces cerevisiae.

Author

Caste, Alix T., Ramsdale, Mark, Ischer, Françoise, and Sanglard, Dominique

Subjects
*CANDIDA albicans, *TRANSCRIPTION factors, *NUCLEAR receptors (Biochemistry), *SACCHAROMYCES cerevisiae, *GENE silencing, *GENETIC regulation, *GENE expression, *GENETIC translation, *CANDIDA, *ZINC
Abstract

The article offers information on the role of three Candida albicans zinc-cluster transcription factors, including CTA4, ASG1 and CTF1, complementing pleiotropic drug resistance in Saccharomyces cerevisiae. A study was conducted to determine the functional homologues of transcription factors in Candida albicans. ABC-transporter gene PDR5 is one of the mediators of pleiotropic drug resistance in Saccharomyces cerevisiae. Three zinc-cluster transcription factors, namely CTA4, ASG1 and CTF1, were identified. It is revealed that C. albicans possesses functional homologues of the S,. cerevisiae Pdr1p and Pdr3p transcription factors. The properties of three transcription factors have been rewired to other functions.

Published
2008
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30. Opinion: Letter - PR degrees should be a recruitment must

Author

Ramsdale, Mark

Subjects
Public relations -- Study and teaching, Universities and colleges -- Graduate work, Advertising, marketing and public relations, Business, Business, international
Abstract

Kirsty O'Connor's letter ('Forget English grads and hire PR students', 23 March) expresses an opinion that has been long-felt by PR graduates. PR is a strategic business function and requires [...]

Published
2007

31. Imbalanced nuclear ratios, post-germination mortality and phenotype-genotype relationships in allopatrically-derived heterokaryons of <em>Heterobasidion annosum</em>.

Author

Ramsdale, Mark and Rayner, Alan D. M.

Subjects
*HETEROBASIDION annosum, *CONIDIA, *MYCELIUM, *PLANT-fungus relationships, *GERMINATION, *PLANT physiology, *PLANT genetics
Abstract

Twelve heterokaryotic strains of Heterobasidion annosum (Fr.) Bref. containing nuclei and mitochondria derived from British and North European populations were prepared by pairing homokaryotic strains and isolating hyphal tips from either side of interaction interfaces. Conidia derived from the heterokaryons had high germinability and were predominantly uninucleate. The nuclear genotypes recovered from these conidia were predominantly non-resident in origin, reflecting the marked asymmetry in nuclear ratios (as high as 9:1) in favour of invasive nuclei that developed in the mycelium. In spite of this asymmetry, the heterokaryons had similar phenotypes to the resident homokaryons that they were derived from. Whereas the relative ability of sib-related nuclei to become established in a homokaryon was about equal in sympatric protoplasm, it could be very different in allopatric protoplasm. Post-germination mortality due to the cessation of development following transfer of germlings to fresh medium was on average similar for allopatric and sympatric conidia, but there was a marked trend for reduction in mortality as nuclear ratio asymmetry increased. Homokaryons derived via conidia from a common heterokaryon exhibited less somatic incompatibility when paired together than did the original, basidiospore-derived strains. These findings indicate that phenotype--genotype relationships resulting from allopatric matings, such as could occur following geographical transposition, are liable to differ radically from those in sympatric matings and so have potentially profound effects on resident population structure. [ABSTRACT FROM AUTHOR]

Published
1996
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32. MNL1Regulates Weak Acid–induced Stress Responses of the Fungal Pathogen Candida albicans

Author

Ramsdale, Mark, Selway, Laura, Stead, David, Walker, Jan, Yin, Zhikang, Nicholls, Susan M., Crowe, Jonathan, Sheils, Emma M., and Brown, Alistair J.P.

Abstract

MNL1, the Candida albicanshomologue of an orphan Msn2-like gene (YER130cin Saccharomyces cerevisiae) has no known function. Here we report that MNL1regulates weak acid stress responses. Deletion of MNL1prevents the long-term adaptation of C. albicanscells to weak acid stresses and compromises their global transcriptional response under these conditions. The promoters of Mnl1-dependent genes contain a novel STRE-like element (SLE) that imposes Mnl1-dependent, weak acid stress–induced transcription upon a lacZreporter in C. albicans.The SLE (HHYYCCCCTTYTY) is related to the Nrg1 response element (NRE) element recognized by the transcriptional repressor Nrg1. Deletion of NRG1partially restores the ability of C. albicans mnl1cells to adapt to weak acid stress, indicating that Mnl1 and Nrg1 act antagonistically to regulate this response. Molecular, microarray, and proteomic analyses revealed that Mnl1-dependent adaptation does not occur in cells exposed to proapoptotic or pronecrotic doses of weak acid, suggesting that Ras-pathway activation might suppress the Mnl1-dependent weak acid response in dying cells. Our work defines a role for this YER130corthologue in stress adaptation and cell death.

Published
2008
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33. MNL1 Regulates Weak Acid–induced Stress Responses of the Fungal Pathogen Candida albicans

Author

Ramsdale, Mark, Selway, Laura, Stead, David, Walker, Jan, Yin, Zhikang, Nicholls, Susan M., Crowe, Jonathan, Sheils, Emma M., and Brown, Alistair J.P.

Abstract

MNL1, the Candida albicans homologue of an orphan Msn2-like gene (YER130c in Saccharomyces cerevisiae) has no known function. Here we report that MNL1 regulates weak acid stress responses. Deletion of MNL1 prevents the long-term adaptation of C. albicans cells to weak acid stresses and compromises their global transcriptional response under these conditions. The promoters of Mnl1-dependent genes contain a novel STRE-like element (SLE) that imposes Mnl1-dependent, weak acid stress–induced transcription upon a lacZ reporter in C. albicans. The SLE (HHYYCCCCTTYTY) is related to the Nrg1 response element (NRE) element recognized by the transcriptional repressor Nrg1. Deletion of NRG1 partially restores the ability of C. albicans mnl1 cells to adapt to weak acid stress, indicating that Mnl1 and Nrg1 act antagonistically to regulate this response. Molecular, microarray, and proteomic analyses revealed that Mnl1-dependent adaptation does not occur in cells exposed to proapoptotic or pronecrotic doses of weak acid, suggesting that Ras-pathway activation might suppress the Mnl1-dependent weak acid response in dying cells. Our work defines a role for this YER130c orthologue in stress adaptation and cell death.

Published
2008

34. Community Development between Porphyromonas gingivalisand Candida albicansMediated by InlJ and Als3

Author

Sztukowska, Maryta N., Dutton, Lindsay C., Delaney, Christopher, Ramsdale, Mark, Ramage, Gordon, Jenkinson, Howard F., Nobbs, Angela H., and Lamont, Richard J.

Abstract

ABSTRACTThe pleiomorphic yeast Candida albicansis a significant pathogen in immunocompromised individuals. In the oral cavity, C. albicansis an inhabitant of polymicrobial communities, and interspecies interactions promote hyphal formation and biofilm formation. C. albicanscolonizes the subgingival area, and the frequency of colonization increases in periodontal disease. In this study, we investigated the interactions between C. albicansand the periodontal pathogen Porphyromonas gingivalis. C. albicansand P. gingivaliswere found to coadhere in both the planktonic and sessile phases. Loss of the internalin-family protein InlJ abrogated adhesion of P. gingivalisto C. albicans, and recombinant InlJ protein competitively inhibited interspecies binding. A mutant of C. albicansdeficient in expression of major hyphal protein Als3 showed diminished binding to P. gingivalis, and InlJ interacted with Als3 heterologously expressed in Saccharomyces cerevisiae. Transcriptional profiling by RNA sequencing (RNA-Seq) established that 57 genes were uniquely upregulated in an InlJ-dependent manner in P. gingivalis-C. albicanscommunities, with overrepresentation of those corresponding to 31 gene ontology terms, including those associated with growth and division. Of potential relevance to the disease process, C. albicansinduced upregulation of components of the type IX secretion apparatus. Collectively, these findings indicate that InlJ-Als3-dependent binding facilitates interdomain community development between C. albicansand P. gingivalisand that P. gingivalishas the potential for increased virulence within such communities.IMPORTANCEMany diseases involve the concerted actions of microorganisms assembled in polymicrobial communities. Inflammatory periodontal diseases are among the most common infections of humans and result in destruction of gum tissue and, ultimately, in loss of teeth. In periodontal disease, pathogenic communities can include the fungus Candida albicans; however, the contribution of C. albicansto the synergistic virulence of the community is poorly understood. Here we characterize the interactions between C. albicansand the keystone bacterial pathogen Porphyromonas gingivalisand show that coadhesion mediated by specific proteins results in major changes in gene expression by P. gingivalis, which could serve to increase pathogenic potential. The work provides significant insights into interdomain interactions that can enhance our understanding of diseases involving a multiplicity of microbial pathogens.

Published
2018
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35. The functional significance of allelic diversity in Candida albicans

Author

Shaw, Sophie and Ramsdale, Mark

Subjects
500, Candida albicans, Allelic expression imbalance
Abstract

Allelic expression imbalance, or AEI, is the term given to differences in the expression levels of the two alleles of a gene. AEI has been previously identified in a number of species using various techniques. Here, the genome-wide extent of allelic expression imbalance in the pathogenic yeast species, Candida albicans, was examined through use of RNA sequencing in combination with a novel computational pipeline based around the diploid reference genome. Techniques for validating these results were investigated, and the difficulties surrounding specificity and quantification are discussed. As C. albicans is a highly heterozygous species, it was hypothesised that polymorphisms within alleles lead to differences in allele expression, which are further linked to differences in allele function. The functional consequences of AEI were therefore interrogated through investigation of Gene Ontology, identification of condition specific responses in AEI, and targeted construction and phenotypic screening of heterozygous knockout strains. Together, these results strongly suggest that divergence in allele expression is not linked to differences in allele function. Investigations of the possible control mechanisms behind the differences in allele expression were considered, with a focus upon structural factors such as chromosomal location, GC content, allele length and codon usage. However, issues with establishing causality are present, and difficulties lie in distinguishing between functional differences and consequences of bias in sequencing technologies. This piece of research has advanced the understanding of gene expression mechanisms within a medically important pathogen, paving the way for further investigations into the functional consequences of allelic expression imbalance in Candida albicans.

Published
2014

36. Proteases and programmed cell death in fungi

Author

Wilkinson, Derek and Ramsdale, Mark

Subjects
571.936, Apoptosis, Programmed Cell Death, Fungi, Protease, Metacaspase, Mca1, Mass Spectometry, LC MS.MS, Candida albicans, Saccharomyces cerevisiae, Acetic Acid, Yeast, Degradomic, Degradome, Proteolysis, Caspase, Cell Death
Abstract

Programmed cell death in animals, plants and protists is in part regulated by a variety of proteases, including cysteine aspartyl proteases, (caspases, paracaspases and metacaspases), cathepsins, subtilisin-like serine proteases, vacuolar processing enzymes and the proteasome. The role of different proteases in the cell death responses of the fungi is however largely unknown. A greater understanding of the fungal cell death machinery may provide new insights into the mechanisms and evolution of PCD and potentially reveal novel targets for a new generation of antifungal drugs. The role of a metacaspase encoding gene, MCA1, in the cell death response of the human pathogen Candida albicans pathogen has been investigated by functional analysis. MCA1 deletion not only alters the sensitivity of cells to a number of cell death stimuli, it also enhances virulence in an insect model. C. albicans shows altered cell and colony morphology on Lee’s medium. Evidence is presented to suggest that these functions appear to be dependent upon active mitochondria. In this study it has also been shown that key caspase substrates may be conserved between humans and the yeasts Saccharomyces cerevisiae and Candida albicans. Many substrates, particularly those which are essential, have retained their caspase cleavage motifs. 14 protease mutants displayed altered activity against caspase 1, 3, 6 or 8 substrates during acetic acid-induced PCD and caspase 1-like activity appeared to be particularly associated with PCD. Using a novel bioinformatic analysis of experimental LC-MS/MS data, changes in the degradation patterns of the proteome (destructome) following acetic acid-induced cell death have been investigated in wild-type yeast. In addition, potential native substrates of the yeast Mca1 have also been identified. The future challenge is to characterise the destructome of different proteases under a range of cell death conditions. In this way it may be possible to identify key components of the cell death machinery and their substrates and so reveal the most promising targets for future therapeutics.

Published
2011

37. Stage-by-stage exploration of normal embryonic development in the Arabian killifish, Aphanius dispar.

Author

Alsakran A, Minhas R, Hamied AS, Wilson RW, Ramsdale M, and Kudoh T

Abstract

Background: Arabian killifish, Aphanius dispar, lives in marine coastal areas of the Middle East, as well as in streams that experience a wide range of salinities and temperatures. It has been used as a mosquito control agent and for studying the toxicities of environmental pollutants. A. dispar's eggshell (chorion) and embryos are highly transparent and are suitable for high resolution microscopic observations, offering excellent visibility of live tissues., Results: In this study, the staging of normal embryonic development of A. dispar was described and investigated at different temperatures. Embryonic development was then examined under different thermal environments from 26 to 34°C. Our data suggest that temperature has a significant effect on embryonic development, with accelerated development at higher temperatures., Conclusion: A. dispar exhibits broad thermal tolerance and extended independent feeding capabilities, making it a promising model organism for toxicology and pathogenesis studies conducted over an extended period of time (12 days post-fertilization)., (© 2024 The Author(s). Developmental Dynamics published by Wiley Periodicals LLC on behalf of American Association for Anatomy.)

Published
2024
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