Asymmetrically localized Bud8p and Bud9p proteins control yeast cell polarity and development

Taheri, Naimeh; Köhler, Tim; Braus, Gerhard H.; Mösch, Hans‐Ulrich

doi:10.1093/emboj/19.24.6686

Cited by 63 publications

(78 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The snowflake clusters are distinct from S. cerevisiae pseudohyphal phenotypes, which have filamentous elongate cells and arise under conditions of nutrient stress (26). Clustering in snowflakephenotype yeast is independent of pseudohyphal growth, as the snowflake phenotype is stable under both high-and low-nutrient conditions.…”

Section: Resultsmentioning

confidence: 93%

Experimental evolution of multicellularity

Ratcliff

Denison²,

Borrello³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

469

619

View full text Add to dashboard Cite

Multicellularity was one of the most significant innovations in the history of life, but its initial evolution remains poorly understood. Using experimental evolution, we show that key steps in this transition could have occurred quickly. We subjected the unicellular yeast Saccharomyces cerevisiae to an environment in which we expected multicellularity to be adaptive. We observed the rapid evolution of clustering genotypes that display a novel multicellular life history characterized by reproduction via multicellular propagules, a juvenile phase, and determinate growth. The multicellular clusters are uniclonal, minimizing within-cluster genetic conflicts of interest. Simple among-cell division of labor rapidly evolved. Early multicellular strains were composed of physiologically similar cells, but these subsequently evolved higher rates of programmed cell death (apoptosis), an adaptation that increases propagule production. These results show that key aspects of multicellular complexity, a subject of central importance to biology, can readily evolve from unicellular eukaryotes.T he evolution of multicellularity was transformative for life on earth (1). In addition to larger size, multicellularity increased biological complexity through the formation of new biological structures. For example, multicellular organisms have evolved sophisticated, higher-level functionality via cooperation among component cells with complementary behaviors (2, 3). However, dissolution and death of multicellular individuals occurs when cooperation breaks down, cancer being a prime example (4). There are multiple mechanisms to help ensure cooperation of component cells in most extant multicellular species (5-8), but the origin and the maintenance of multicellularity are two distinct evolutionary problems. Component cells in a nascent multicellular organism would appear to have frequent opportunities to pursue noncooperative reproductive strategies at a cost to the reproduction of the multicellular individual. How, then, does the transition to multicellularity occur?Understanding the evolution of complex multicellular individuals from unicellular ancestors has been extremely challenging, largely because the first steps in this process occurred in the deep past (>200 million years ago) (9, 10). As a result, transitional forms have been lost to extinction, and little is known about the physiology, ecology, and evolutionary processes of incipient multicellularity (11). Nonetheless, several key steps have been identified for this transition. Because multicellular organisms are composed of multiple cells, the first step in this transition was likely the evolution of genotypes that form simple cellular clusters (1, 3, 12-16). It is not known whether this occurs more readily through aggregation of genetically distinct cells, as in biofilms, or by mother-daughter cell adhesion after division. Once simple clusters have evolved, selection among multicelled clusters must predominate over selection among single cells within clusters (1,15,17,18). T...

show abstract

Section: Resultsmentioning

confidence: 93%

Experimental evolution of multicellularity

Ratcliff

Denison²,

Borrello³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

469

619

View full text Add to dashboard Cite

show abstract

“…In S. cerevisiae, Bud1 is required for pseudohyphal growth (11,40), as this G protein is necessary for unipolar budding and therefore filament formation. Although CaBUD1 is not essential for invasive hyphal growth, its reduced expression resulted in a decrease in hyphal growth and pathogenicity, a finding consistent with a previous report in which a ⌬bud1/⌬bud1 C. albicans strain exhibited modest defects in the yeast-to-hyphal transition and virulence (44).…”

Section: Vol 2 2003mentioning

confidence: 99%

Cdc24, the GDP-GTP Exchange Factor for Cdc42, Is Required for Invasive Hyphal Growth of Candida albicans

Bassilana¹,

Blyth

Arkowitz³

2003

Eukaryot Cell

117

134

View full text Add to dashboard Cite

Candida albicans, the most common human fungal pathogen, is particularly problematic for immunocompromised individuals. The reversible transition of this fungal pathogen to a filamentous form that invades host tissue is important for its virulence. Although different signaling pathways such as a mitogen-activated protein kinase and a protein kinase A cascade are critical for this morphological transition, the function of polarity establishment proteins in this process has not been determined. We examined the role of four different polarity establishment proteins in C. albicans invasive growth and virulence by using strains in which one copy of each gene was deleted and the other copy expressed behind the regulatable promoter MET3. Strikingly, mutants with ectopic expression of either the Rho G-protein Cdc42 or its exchange factor Cdc24 are unable to form invasive hyphal filaments and germ tubes in response to serum or elevated temperature and yet grow normally as a budding yeast. Furthermore, these mutants are avirulent in a mouse model for systemic infection. This function of the Cdc42 GTPase module is not simply a general feature of polarity establishment proteins. Mutants with ectopic expression of the SH3 domain containing protein Bem1 or the Ras-like G-protein Bud1 can grow in an invasive fashion and are virulent in mice, albeit with reduced efficiency. These results indicate that a specific regulation of Cdc24/Cdc42 activity is required for invasive hyphal growth and suggest that these proteins are required for pathogenicity of C. albicans.

show abstract

“…Unipolar distal budding in classic nitrogen starvation or short-chain alcohol-induced filamentous growth also require Bud8 (Mosch and Fink, 1997;Lorenz et al, 2000;Erdman and Snyder, 2001;Cullen and Sprague, 2002). Homozygous bud8 diploids undergo unipolar proximal budding with or without nitrogen starvation (Taheri et al, 2000). However, in bud8 homozygous strains we observed near normal HU-induced filamentous growth with a predominantly unipolar distal budding pattern.…”

Section: Introductionmentioning

confidence: 73%

“…A haploid yeast-form cell undergoes axial or proximal budding (relative to the birth site), while diploid yeast-form cells undergo bipolar budding (Casamayor and Snyder, 2002). The distal budding in diploid bipolar budding requires Bud8, a membrane-bound protein that functions as a distal landmark (Zahner et al, 1996;Taheri et al, 2000;Harkins et al, 2001;Ni and Snyder, 2001). The budding pattern in filamentous growth is unipolar distal.…”

Section: Introductionmentioning

confidence: 99%

Genetic/genomic evidence for a key role of polarized endocytosis in filamentous differentiation of S. cerevisiae

Wu¹,

Jiang²

2005

Yeast

View full text Add to dashboard Cite

Unicellular S. cerevisiae cells switch from the yeast form to pseudohyphal or filamentous form in response to environmental cues. We report that wild-type BY diploids (in which yeast ORFs have been systematically deleted) undergo normal HUinduced filamentous growth and discernable nitrogen starvation-induced filamentous growth, despite their perceived filamentation-deficient S288C genetic background. This finding allowed us to perform a genome-wide survey for non-essential genes that are required for filamentous growth with the homozygous deletion strains. We report that genes involved in endocytosis are required for both HU-induced and nitrogen starvation-induced filamentous growth. Surprisingly, no known genes involved in exocytosis are required. Despite the fact that polarized growth involves transport of vesicles to the site of growth, we failed to obtain genetic/genomic evidence that exocytosis plays an essential role in filamentous growth. A possible key role of polarized endocytosis (from the growth tip) is consistent with the proposed biological function of filamentous growth as a foraging behaviour. In addition, BUD8 that encodes the distal landmark in yeast-form bipolar budding is required for nitrogen starvation-induced but not HU-induced filamentous growth. Moreover, BUD5, SPA2, PEA2 and BUD6 that regulate bipolar bud site selection do not regulate the unipolar distal budding pattern in HU-induced filamentous growth.

show abstract

Asymmetrically localized Bud8p and Bud9p proteins control yeast cell polarity and development

Cited by 63 publications

References 37 publications

Experimental evolution of multicellularity

Experimental evolution of multicellularity

Cdc24, the GDP-GTP Exchange Factor for Cdc42, Is Required for Invasive Hyphal Growth of Candida albicans

Genetic/genomic evidence for a key role of polarized endocytosis in filamentous differentiation of S. cerevisiae

Contact Info

Product

Resources

About