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Yeast. 2005 Oct 30;22(14):1143-53.

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

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  • 1Department of Medical Biochemistry and Genetics, Texas A&M University System, Health Science Center, 428 Reynolds Medical Building, College Station, TX 77843-1114, USA.


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 HU-induced 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.

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