Faculty Opinions recommendation of New Aspects of Invasive Growth Regulation Identified by Functional Profiling of MAPK Pathway Targets in Saccharomyces cerevisiae.

2020 ◽  
Author(s):  
Mark Johnston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Growth Regulation ◽  
Mapk Pathway ◽  
Invasive Growth ◽  
Functional Profiling

scholarly journals New Aspects of Invasive Growth Regulation Identified by Functional Profiling of MAPK Pathway Targets in Saccharomyces cerevisiae

Genetics ◽  
2020 ◽  
Vol 216 (1) ◽  
pp. 95-116 ◽  
Author(s):  
Matthew D. Vandermeulen ◽  
Paul J. Cullen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Adhesion ◽  
Stress Responses ◽  
Cellular Response ◽  
Growth Regulation ◽  
Mapk Pathway ◽  
Filamentous Growth ◽  
Invasive Growth ◽  
Link Type ◽  
Mapk Pathways

MAPK pathways are drivers of morphogenesis and stress responses in eukaryotes. A major function of MAPK pathways is the transcriptional induction of target genes, which produce proteins that collectively generate a cellular response. One approach to comprehensively understand how MAPK pathways regulate cellular responses is to characterize the individual functions of their transcriptional targets. Here, by examining uncharacterized targets of the MAPK pathway that positively regulates filamentous growth in Saccharomyces cerevisiae (fMAPK pathway), we identified a new role for the pathway in negatively regulating invasive growth. Specifically, four targets were identified that had an inhibitory role in invasive growth: RPI1, RGD2, TIP1, and NFG1/YLR042c. NFG1 was a highly induced unknown open reading frame that negatively regulated the filamentous growth MAPK pathway. We also identified SFG1, which encodes a transcription factor, as a target of the fMAPK pathway. Sfg1p promoted cell adhesion independently from the fMAPK pathway target and major cell adhesion flocculin Flo11p, by repressing genes encoding presumptive cell-wall-degrading enzymes. Sfg1p also contributed to FLO11 expression. Sfg1p and Flo11p regulated different aspects of cell adhesion, and their roles varied based on the environment. Sfg1p also induced an elongated cell morphology, presumably through a cell-cycle delay. Thus, the fMAPK pathway coordinates positive and negative regulatory proteins to fine-tune filamentous growth resulting in a nuanced response. Functional analysis of other pathways’ targets may lead to a more comprehensive understanding of how signaling cascades generate biological responses.

Cellular Differentiation in Response to Nutrient Availability: The Repressor of Meiosis, Rme1p, Positively Regulates Invasive Growth in Saccharomyces cerevisiae

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1045-1058
Author(s):  
Dewald van Dyk ◽  
Guy Hansson ◽  
Isak S Pretorius ◽  
Florian F Bauer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cellular Differentiation ◽  
Promoter Sequence ◽  
Quiescent State ◽  
Invasive Growth ◽  
Limited Growth ◽  
Yeast Saccharomyces Cerevisiae ◽  
A Cell ◽  
Signaling Modules ◽  
Differentiation Pathways

Abstract In the yeast Saccharomyces cerevisiae, the transition from a nutrient-rich to a nutrient-limited growth medium typically leads to the implementation of a cellular adaptation program that results in invasive growth and/or the formation of pseudohyphae. Complete depletion of essential nutrients, on the other hand, leads either to entry into a nonbudding, metabolically quiescent state referred to as G0 in haploid strains or to meiosis and sporulation in diploids. Entry into meiosis is repressed by the transcriptional regulator Rme1p, a zinc-finger-containing DNA-binding protein. In this article, we show that Rme1p positively regulates invasive growth and starch metabolism in both haploid and diploid strains by directly modifying the transcription of the FLO11 (also known as MUC1) and STA2 genes, which encode a cell wall-associated protein essential for invasive growth and a starch-degrading glucoamylase, respectively. Genetic evidence suggests that Rme1p functions independently of identified signaling modules that regulate invasive growth and of other transcription factors that regulate FLO11 and that the activation of FLO11 is dependent on the presence of a promoter sequence that shows significant homology to identified Rme1p response elements (RREs). The data suggest that Rme1p functions as a central switch between different cellular differentiation pathways.

scholarly journals Urmylation: A Ubiquitin-like Pathway that Functions during Invasive Growth and Budding in Yeast

2003 ◽  
Vol 14 (11) ◽  
pp. 4329-4341 ◽  
Author(s):  
April S. Goehring ◽  
David M. Rivers ◽  
George F. Sprague
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Growth ◽  
Genetic Interaction ◽  
Nutrient Sensing ◽  
Genetic Interactions ◽  
Invasive Growth ◽  
Tor Pathway ◽  
Molecular Functions ◽  
Simultaneous Loss ◽  
P21 Activated Kinase

Ubiquitin is a small modifier protein that is conjugated to substrates to target them for degradation. Recently, a surprising number of ubiquitin-like proteins have been identified that also can be attached to proteins. Herein, we identify two molecular functions for the posttranslational protein modifier from Saccharomyces cerevisiae, Urm1p. Simultaneous loss of Urm1p and Cla4p, a p21-activated kinase that functions in budding, is lethal. This result suggests a role for the urmylation pathway in budding. Furthermore, loss of the urmylation pathway causes defects in invasive growth and confers sensitivity to rapamycin. Our results indicate that the sensitivity to rapamycin is due to a genetic interaction with the TOR pathway, which is important for regulation of cell growth in response to nutrients. We have found that Urm1p can be attached to a number of proteins. Loss of five genes that are also essential in a cla4Δ strain, NCS2, NCS6, ELP2, ELP6, and URE2, affect the level of at least one Urm1p conjugate. Moreover, these five genes have a role in invasive growth and display genetic interactions with the TOR pathway. In summary, our results suggest the urmylation pathway is involved in nutrient sensing and budding.

scholarly journals Regulation of Mat Responses by a Differentiation MAPK Pathway in Saccharomyces cerevisiae

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e32294 ◽  
Author(s):  
Sheelarani Karunanithi ◽  
Jyoti Joshi ◽  
Colin Chavel ◽  
Barbara Birkaya ◽  
Laura Grell ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mapk Pathway

Phosphatidylinositol 4,5-bisphosphate is required for invasive growth in Saccharomyces cerevisiae

2013 ◽  
Vol 126 (16) ◽  
pp. 3602-3614 ◽  
Author(s):  
I. Guillas ◽  
A. Vernay ◽  
J.-J. Vitagliano ◽  
R. A. Arkowitz
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Invasive Growth

The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1

Microbiology ◽  
2004 ◽  
Vol 150 (7) ◽  
pp. 2197-2208 ◽  
Author(s):  
Marcus E. Marvin ◽  
Robert P. Mason ◽  
Annette M. Cashmore
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Iron Uptake ◽  
Invasive Growth ◽  
Hostile Environment ◽  
Null Mutant ◽  
Copper Uptake ◽  
Similar System ◽  
Copper Transporter ◽  
High Affinity ◽  
Null Strain

The ability of Candida albicans to acquire iron from the hostile environment of the host is known to be necessary for virulence and appears to be achieved using a similar system to that described for Saccharomyces cerevisiae. In S. cerevisiae, high-affinity iron uptake is dependent upon the acquisition of copper. The authors have previously identified a C. albicans gene (CaCTR1) that encodes a copper transporter. Deletion of this gene results in a mutant strain that grows predominantly as pseudohyphae and displays aberrant morphology in low-copper conditions. This paper demonstrates that invasive growth by C. albicans is induced by low-copper conditions and that this is augmented in a Cactr1-null strain. It also shows that deletion of CaCTR1 results in defective iron uptake. In S. cerevisiae, genes that facilitate high-affinity copper uptake are controlled by a copper-sensing transactivator, ScMac1p. The authors have now identified a C. albicans gene (CaMAC1) that encodes a copper-sensing transactivator. A Camac1-null mutant displays phenotypes similar to those of a Cactr1-null mutant and has no detectable CaCTR1 transcripts in low-copper conditions. It is proposed that high-affinity copper uptake by C. albicans is necessary for reductive iron uptake and is transcriptionally controlled by CaMac1p in a similar manner to that in S. cerevisiae.

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