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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-07
    Description: Biofilms are formed by the aggregation of microorganisms into multicellular structures that adhere to surfaces. Here we show that bakers' yeast Saccharomyces cerevisiae can initiate biofilm formation. When grown in low-glucose medium, the yeast cells adhered avidly to a number of plastic surfaces. On semi-solid (0.3% agar) medium they formed "mats": complex multicellular structures composed of yeast-form cells. Both attachment to plastic and mat formation require Flo11p, a member of a large family of fungal cell surface glycoproteins involved in adherence. The ability to study biofilm formation in a tractable genetic system may facilitate the identification of new targets for antifungal therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, T B -- Fink, G R -- 5 RO1 GM40266/GM/NIGMS NIH HHS/ -- GM20565/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Feb 2;291(5505):878-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11157168" target="_blank"〉PubMed〈/a〉
    Keywords: Agar ; Biofilms/*growth & development ; Cell Adhesion ; Culture Media ; Fungal Proteins/genetics/physiology ; Genes, Fungal ; Glucose ; Lipoproteins/physiology ; MAP Kinase Signaling System/genetics/physiology ; Membrane Glycoproteins ; Membrane Proteins/genetics/physiology ; *Nuclear Proteins ; Peptides/physiology ; Pheromones ; Plastics ; Ploidies ; Saccharomyces cerevisiae/genetics/growth & development/*physiology ; *Saccharomyces cerevisiae Proteins ; Trans-Activators/genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2012-09-18
    Description: The dimorphic switch from a single-cell budding yeast to a filamentous form enables Saccharomyces cerevisiae to forage for nutrients and the opportunistic pathogen Candida albicans to invade human tissues and evade the immune system. We constructed a genome-wide set of targeted deletion alleles and introduced them into a filamentous S. cerevisiae strain, Sigma1278b. We identified genes involved in morphologically distinct forms of filamentation: haploid invasive growth, biofilm formation, and diploid pseudohyphal growth. Unique genes appear to underlie each program, but we also found core genes with general roles in filamentous growth, including MFG1 (YDL233w), whose product binds two morphogenetic transcription factors, Flo8 and Mss11, and functions as a critical transcriptional regulator of filamentous growth in both S. cerevisiae and C. albicans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Owen -- Shapiro, Rebecca S -- Kurat, Christoph F -- Mayhew, David -- Baryshnikova, Anastasia -- Chin, Brian -- Lin, Zhen-Yuan -- Cox, Michael J -- Vizeacoumar, Frederick -- Cheung, Doris -- Bahr, Sondra -- Tsui, Kyle -- Tebbji, Faiza -- Sellam, Adnane -- Istel, Fabian -- Schwarzmuller, Tobias -- Reynolds, Todd B -- Kuchler, Karl -- Gifford, David K -- Whiteway, Malcolm -- Giaever, Guri -- Nislow, Corey -- Costanzo, Michael -- Gingras, Anne-Claude -- Mitra, Robi David -- Andrews, Brenda -- Fink, Gerald R -- Cowen, Leah E -- Boone, Charles -- 42516-4/Canadian Institutes of Health Research/Canada -- GM035010/GM/NIGMS NIH HHS/ -- GM40266/GM/NIGMS NIH HHS/ -- MOP-97939/Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1353-6. doi: 10.1126/science.1224339.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, University of Toronto, Toronto, ON M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984072" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Biofilms/growth & development ; Candida albicans/cytology/*genetics/*growth & development ; DNA Mutational Analysis ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Hyphae/genetics/growth & development ; Nuclear Proteins/genetics ; Saccharomyces cerevisiae/cytology/*genetics/*growth & development ; Saccharomyces cerevisiae Proteins/genetics ; Trans-Activators/genetics ; Transcription Factors/genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-02-20
    Description: Saccharomyces cerevisiae strains of the 1278b background generate biofilms, referred to as mats, on low-density agar (0.3%) plates made with rich media (YPD). Mat formation involves adhesion of yeast cells to the surface of the agar substrate and each other as the biofilm matures, resulting in elaborate water channels that create filigreed patterns of cells. The cell wall adhesion protein Flo11p is required for mat formation; however, genetic data indicate that other unknown effectors are also required. For example, mutations in vacuolar protein sorting genes that affect the multivesicular body pathway, such as vps27 , cause mat formation defects independently of Flo11p , presumably by affecting an unidentified signaling pathway. A cell wall signaling protein, Wsc1p , found at the plasma membrane is affected for localization and function by vps27 . We found that a wsc1 mutation disrupted mat formation in a Flo11p -independent manner. Wsc1p appears to impact mat formation through the Rom2p - Rho1p signaling module, by which Wsc1p also regulates the cell wall. The Bck1p , Mkk1 / Mkk2 , Mpk1p MAP kinase signaling cascade is known to regulate the cell wall downstream of Wsc1p - Rom2p - Rho1p but, surprisingly, these kinases do not affect mat formation. In contrast, Wsc1p may impact mat formation by affecting Skn7p instead. Skn7p can also receive signaling inputs from the Sln1p histidine kinase; however, mutational analysis of specific histidine kinase receiver residues in Skn7p indicate that Sln1p does not play an important role in mat formation, suggesting that Skn7p primarily acts downstream of Wsc1p to regulate mat formation.
    Electronic ISSN: 2160-1836
    Topics: Biology
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