Mss11, a Transcriptional Activator, Is Required for Hyphal Development in
            <i>Candida albicans</i>

Su, Chang; Li, Yandong; Lü, Yang; Chen, Jiangye

doi:10.1128/ec.00190-09

Cited by 29 publications

(29 citation statements)

References 55 publications

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“…From previously published genetic epistasis studies, Mss11p may be acted upon by many filamentous growth factors, including the transcriptional regulators PHD1, NRG1/2, and FLO8 itself (68); thus, in S. cerevisiae, Mss11p is thought to act downstream of Flo8p. In C. albicans, however, Flo8p and Mss11p physically interact with each other and may cooperatively bind target gene promoters (75). Similar results have been found in Saccharomyces diastaticus, where Mss11p and Flo8p bind cooperatively to the sequence TTTGCnGCAAA (n ϭ 97) in the STA1 promoter (76).…”

Section: Pun1 Is Essential For Filamentous Growth and Is An Importantsupporting

confidence: 66%

A Profile of Differentially Abundant Proteins at the Yeast Cell Periphery during Pseudohyphal Growth

Shively

Jin

et al. 2010

Journal of Biological Chemistry

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Yeast filamentous growth is a stress response to conditions of nitrogen deprivation, wherein yeast colonies form pseudohyphal filaments of elongated and connected cells. As proteins mediating adhesion and transport are required for this growth transition, we expect that the protein complement at the yeast cell periphery plays a critical and tightly regulated role in pseudohyphal filamentation. To identify proteins differentially abundant at the yeast cell periphery during pseudohyphal growth, we generated quantitative proteomic profiles of plasma membrane protein preparations under conditions of vegetative growth and filamentation. By isobaric tags for relative and absolute quantification chemistry and two-dimensional liquid chromatography-tandem mass spectrometry, we profiled 2463 peptides and 356 proteins, identifying 11 differentially abundant proteins that localize to the yeast cell periphery. This protein set includes Ylr414cp, herein renamed Pun1p, a previously uncharacterized protein localized to the plasma membrane compartment of Can1. Pun1p abundance is doubled under conditions of nitrogen stress, and deletion of PUN1 abolishes filamentous growth in haploids and diploids; pun1⌬ mutants are noninvasive, lack surface-spread filamentation, grow slowly, and exhibit impaired cell adhesion. Conversely, overexpression of PUN1 results in exaggerated cell elongation under conditions of nitrogen stress. PUN1 contributes to yeast nitrogen signaling, as pun1⌬ mutants misregulate amino acid biosynthetic genes during nitrogen stress. By chromatin immunoprecipitation and reverse transcription-PCR, we find that the filamentous growth factor Mss11p directly binds the PUN1 promoter and regulates its transcription. In total, this study provides the first profile of differential protein abundance during pseudohyphal growth, identifying a previously uncharacterized membrane compartment of Can1 protein required for wild-type nitrogen signaling and filamentous growth.Under conditions of nitrogen stress, certain strains of Saccharomyces cerevisiae implement a dramatic change in growth form characterized by the development of multicellular pseudohyphal filaments (1-4). During pseudohyphal growth, yeast cells delay in G 2 /M, resulting in an extended period of apically polarized growth and an elongated cell morphology (5-7). The yeast cells also exhibit an altered pattern of budding in which daughter cells emerge from mother cells predominantly opposite the birth end, as opposed to the bipolar pattern of bud emergence observed in diploid cells under conditions of vegetative growth (8). Perhaps most strikingly, filamentous yeast cells remain physically connected after cell division (1). The resulting pseudohyphal filaments adhere to and invade growth substrates, such as agar (9 -11). Thought to be a foraging mechanism, yeast filamentous growth has been studied extensively as a model for related hyphal growth transitions in the opportunistic human pathogen Candida albicans, wherein these growth transitions are required for virulen...

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Section: Pun1 Is Essential For Filamentous Growth and Is An Importantsupporting

confidence: 66%

A Profile of Differentially Abundant Proteins at the Yeast Cell Periphery during Pseudohyphal Growth

Shively

Jin

et al. 2010

Journal of Biological Chemistry

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“…Firstly, Sfl2 was named by Spiering et al (2009) according to its sequence similarity to Sfl1; we present the evidence for the functional correlation between Sfl2 and Sfl1 by a complementation test in S. cerevisiae (Fig. This expression pattern implies a positive role of Sfl2 in morphogenesis, considering that body temperature (37 1C) serves as a hyphal inducer and that several positive regulators of filamentation, such as TEC1, UME6, and MSS11, have been shown to be induced by morphogenetic stimuli (Schweizer et al, 2000;Su et al, 2009;Zeidler et al, 2009). Secondly, Spiering et al (2009) suggested that SFL2 transcription is upregulated by the environmental culture conditions in the RHE infection model; we show here that high temperature (37 1C) has a major impact on induction of SFL2 at both transcriptional and translational levels.…”

Section: Discussionmentioning

confidence: 93%

Candida albicans Sfl2, a temperature-induced transcriptional regulator, is required for virulence in a murine gastrointestinal infection model

Song

Wang

Chen

2011

FEMS Yeast Research

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Many transcriptional regulators play roles in morphogenesis of the human pathogen Candida albicans. Recently, Sfl2, a sequence homolog of C. albicans Sfl1, has been shown to be required for hyphal development. In this report, we show that, like Sfl1, Sfl2 could complement the phenotypes of the Saccharomyces cerevisiae sfl1 mutant, and green fluorescent protein-tagged Sfl2 localized in the nuclei of both yeast and hyphal cells in C. albicans, reflecting its role as a transcriptional regulator. In C. albicans, SFL2 expression was induced at a high growth temperature (37 °C) at both transcriptional and translational levels. The deletion of SFL2 impaired filamentation at a high temperature, whereas the overexpression of SFL2 promoted filamentous growth at a low temperature. Sfl2-activated hyphal development needs the existence of Efg1 and Flo8 under aerobic conditions. Thus, in contrast to Sfl1, which represses filamentation, Sfl2 acts as an activator of filamentous growth in C. albicans. Functional analysis of chimeric Sfl proteins demonstrated that the opposite actions of C. albicans Sfl1 and Sfl2 were mainly mediated by their heat shock factor domains. Furthermore, the deletion of SFL2 attenuated virulence in a mouse model of gastrointestinal colonization and dissemination, indicating that Sfl2 is important for virulence in the gastrointestinal model of candidiasis. Our results provide new insights into Sfl2 functions in C. albicans morphogenesis and pathogenesis.

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“…Flo8 interacts with Efg1 in yeast and hyphal cells, and Flo8 regulates a subset of genes controlled by Efg1 (92). Recently, the transcriptional activator Mss11 was shown to interact with Flo8 and influence C. albicans morphogenesis (568). The overexpression of MSS11 enhances filamentation, while the homozygous deletion of MSS11 blocks filamentation under many conditions (568).…”

Section: Major Morphogenetic Signaling Cascadesmentioning

confidence: 99%

“…Recently, the transcriptional activator Mss11 was shown to interact with Flo8 and influence C. albicans morphogenesis (568). The overexpression of MSS11 enhances filamentation, while the homozygous deletion of MSS11 blocks filamentation under many conditions (568). Another transcription factor thought to act downstream of PKA is Sfl1.…”

Section: Major Morphogenetic Signaling Cascadesmentioning

confidence: 99%

Regulatory Circuitry Governing Fungal Development, Drug Resistance, and Disease

Shapiro

Robbins

Cowen

2011

Microbiol Mol Biol Rev

499

547

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SUMMARY Pathogenic fungi have become a leading cause of human mortality due to the increasing frequency of fungal infections in immunocompromised populations and the limited armamentarium of clinically useful antifungal drugs. Candida albicans , Cryptococcus neoformans , and Aspergillus fumigatus are the leading causes of opportunistic fungal infections. In these diverse pathogenic fungi, complex signal transduction cascades are critical for sensing environmental changes and mediating appropriate cellular responses. For C. albicans , several environmental cues regulate a morphogenetic switch from yeast to filamentous growth, a reversible transition important for virulence. Many of the signaling cascades regulating morphogenesis are also required for cells to adapt and survive the cellular stresses imposed by antifungal drugs. Many of these signaling networks are conserved in C. neoformans and A. fumigatus , which undergo distinct morphogenetic programs during specific phases of their life cycles. Furthermore, the key mechanisms of fungal drug resistance, including alterations of the drug target, overexpression of drug efflux transporters, and alteration of cellular stress responses, are conserved between these species. This review focuses on the circuitry regulating fungal morphogenesis and drug resistance and the impact of these pathways on virulence. Although the three human-pathogenic fungi highlighted in this review are those most frequently encountered in the clinic, they represent a minute fraction of fungal diversity. Exploration of the conservation and divergence of core signal transduction pathways across C. albicans , C. neoformans , and A. fumigatus provides a foundation for the study of a broader diversity of pathogenic fungi and a platform for the development of new therapeutic strategies for fungal disease.

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Mss11, a Transcriptional Activator, Is Required for Hyphal Development in Candida albicans

Cited by 29 publications

References 55 publications

A Profile of Differentially Abundant Proteins at the Yeast Cell Periphery during Pseudohyphal Growth

A Profile of Differentially Abundant Proteins at the Yeast Cell Periphery during Pseudohyphal Growth

Candida albicans Sfl2, a temperature-induced transcriptional regulator, is required for virulence in a murine gastrointestinal infection model

Regulatory Circuitry Governing Fungal Development, Drug Resistance, and Disease

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