Department of Biology, University of Copenhagen, Copenhagen, Denmark.
PLoS One. 2012;7(7):e41272. doi: 10.1371/journal.pone.0041272. Epub 2012 Jul 26.
Amino acids can induce yeast cell adhesion but how amino acids are sensed and signal the modulation of the FLO adhesion genes is not clear. We discovered that the budding yeast Saccharomyces cerevisiae CEN.PK evolved invasive growth ability under prolonged nitrogen limitation. Such invasive mutants were used to identify amino acid transporters as regulators of FLO11 and invasive growth. One invasive mutant had elevated levels of FLO11 mRNA and a Q320STOP mutation in the SFL1 gene that encodes a protein kinase A pathway regulated repressor of FLO11. Glutamine-transporter genes DIP5 and GNP1 were essential for FLO11 expression, invasive growth and biofilm formation in this mutant. Invasive growth relied on known regulators of FLO11 and the Ssy1-Ptr3-Ssy5 complex that controls DIP5 and GNP1, suggesting that Dip5 and Gnp1 operates downstream of the Ssy1-Ptr3-Ssy5 complex for regulation of FLO11 expression in a protein kinase A dependent manner. The role of Dip5 and Gnp1 appears to be conserved in the S. cerevisiae strain ∑1278b since the dip5 gnp1 ∑1278b mutant showed no invasive phenotype. Secondly, the amino acid transporter gene GAP1 was found to influence invasive growth through FLO11 as well as other FLO genes. Cells carrying a dominant loss-of-function PTR3(647::CWNKNPLSSIN) allele had increased transcription of the adhesion genes FLO1, 5, 9, 10, 11 and the amino acid transporter gene GAP1. Deletion of GAP1 caused loss of FLO11 expression and invasive growth. However, deletions of FLO11 and genes encoding components of the mitogen-activated protein kinase pathway or the protein kinase A pathway were not sufficient to abolish invasive growth, suggesting involvement of other FLO genes and alternative pathways. Increased intracellular amino acid pools in the PTR3(647::CWNKNPLSSIN)-containing strain opens the possibility that Gap1 regulates the FLO genes through alteration of the amino acid pool sizes.
氨基酸可以诱导酵母细胞黏附,但氨基酸是如何被感知的,以及信号如何调节 FLO 黏附基因的表达尚不清楚。我们发现,在长时间氮限制下,出芽酵母酿酒酵母 CEN.PK 进化出了侵袭性生长能力。利用这些侵袭性突变体来鉴定氨基酸转运体作为 FLO11 和侵袭性生长的调控因子。一个侵袭性突变体中 FLO11 mRNA 水平升高,并且 SFL1 基因(编码 FLO11 的蛋白激酶 A 途径调节抑制子)中的 Q320STOP 突变。在这个突变体中,谷氨酰胺转运体基因 DIP5 和 GNP1 对于 FLO11 的表达、侵袭性生长和生物膜形成是必需的。侵袭性生长依赖于 FLO11 的已知调控因子以及 Ssy1-Ptr3-Ssy5 复合物,该复合物控制 DIP5 和 GNP1,这表明 Dip5 和 Gnp1 作为 Ssy1-Ptr3-Ssy5 复合物的下游,以蛋白激酶 A 依赖的方式调节 FLO11 的表达。Dip5 和 Gnp1 的作用似乎在酿酒酵母菌株∑1278b 中是保守的,因为 dip5 gnp1∑1278b 突变体没有侵袭表型。其次,发现氨基酸转运体基因 GAP1 通过 FLO11 以及其他 FLO 基因影响侵袭性生长。携带显性失活功能 PTR3(647::CWNKNPLSSIN)等位基因的细胞中,黏附基因 FLO1、5、9、10、11 和氨基酸转运体基因 GAP1 的转录增加。GAP1 的缺失导致 FLO11 表达和侵袭性生长的丧失。然而,FLO11 和编码丝裂原激活蛋白激酶途径或蛋白激酶 A 途径成分的基因的缺失不足以消除侵袭性生长,这表明涉及其他 FLO 基因和替代途径。含有 PTR3(647::CWNKNPLSSIN)的菌株中细胞内氨基酸池的增加,使得 Gap1 通过改变氨基酸池的大小来调节 FLO 基因成为可能。