Abstract
The transition between a unicellular yeast form to multicellular filaments is crucial for budding yeast foraging and the pathogenesis of many fungal pathogens such as Candida albicans. Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation. Overexpression of either ECM22 or UPC2 leads to increased filamentation, whereas cells lacking both ECM22 and UPC2 do not exhibit filamentous growth. Ecm22 and Upc2 positively control the expression of FHN1, NPR1, PRR2 and sterol biosynthesis genes. These genes all play a positive role in filamentous growth, and their expression is upregulated during filamentation in an Ecm22/Upc2-dependent manner. Furthermore, ergosterol content increases during filamentous growth. UPC2 expression also increases during filamentation and is inhibited by the transcription factors Sut1 and Sut2. The expression of SUT1 and SUT2 in turn is under negative control of the transcription factor Ste12. We suggest that during filamentation Ste12 becomes activated and reduces SUT1/SUT2 expression levels. This would result in increased UPC2 levels and as a consequence to transcriptional activation of FHN1, NPR1, PRR2 and sterol biosynthesis genes. Higher ergosterol levels in combination with the proteins Fhn1, Npr1 and Prr2 would then mediate the transition to filamentous growth.
Highlights
Many fungal species form filaments in response to extracellular stimuli such as nutrient deprivation (Cullen and Sprague, 2012)
We further show that UPC2 transcription is regulated by Sut1 and Sut2 and that UPC2 levels increase during filamentation
We have previously shown that the zinc cluster protein Sut1 regulates filamentous growth (Foster et al, 2013)
Summary
Many fungal species form filaments in response to extracellular stimuli such as nutrient deprivation (Cullen and Sprague, 2012). Filamentous growth is called pseudohyphal growth and can be induced by low nitrogen levels (Gimeno et al, 1992) Under these conditions, round yeast cells become more elongated and do not separate following cytokinesis. Several signalling cascades are critical for filamentous growth including a mitogen-activated protein kinase (MAPK) pathway, the cAMP-dependent protein kinase A pathway and the target of rapamycin (TOR) pathway (Cullen and Sprague, 2012). These signalling pathways regulate a complex network of transcription factors that includes Flo, Mga, Phd, Sok, Ste and Tec (Borneman et al, 2006). These transcription factors alter the gene expression pattern which drives the transition to filamentous growth
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