Strain-dependent differences in coordination of yeast signalling networks

被引:2
|
作者
Scott, Taylor D. D. [1 ]
Xu, Ping [2 ]
McClean, Megan N. N. [1 ,2 ,3 ]
机构
[1] Univ Wisconsin Madison, Dept Biomed Engn, Engn Ctr Bldg 3156, 1550 Engn Dr, Madison, WI 53706 USA
[2] Princeton Univ, Lewis Sigler Inst Integrat Biol, Princeton, NJ USA
[3] Univ Wisconsin, Sch Med & Publ Hlth, Carbone Canc Ctr, Madison, WI USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
crosstalk; HOG; MAPK signalling; mating; signal transduction; ACTIVATED PROTEIN-KINASE; POLYMERASE EXTENSION CLONING; SACCHAROMYCES-CEREVISIAE; MAP KINASE; TRANSCRIPTIONAL RESPONSE; MATING-PHEROMONE; BINDING DOMAIN; CROSS-TALK; SPECIFICITY; PATHWAY;
D O I
10.1111/febs.16689
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The yeast mitogen-activated protein kinase pathways serve as a model system for understanding how network interactions affect the way in which cells coordinate the response to multiple signals. We have quantitatively compared two yeast strain backgrounds YPH499 and sigma 1278b (both of which have previously been used to study these pathways) and found several important differences in how they coordinate the interaction between the high osmolarity glycerol (HOG) and mating pathways. In the sigma 1278b background, in response to simultaneous stimulus, mating pathway activation is dampened and delayed in a dose-dependent manner. In the YPH499 background, only dampening is dose-dependent. Furthermore, leakage from the HOG pathway into the mating pathway (crosstalk) occurs during osmostress alone in the sigma 1278b background only. The mitogen-activated protein kinase Hog1p suppresses crosstalk late in an induction time course in both strains but does not affect the early crosstalk seen in the sigma 1278b background. Finally, the kinase Rck2p plays a greater role suppressing late crosstalk in the sigma 1278b background than in the YPH499 background. Our results demonstrate that comparisons between laboratory yeast strains provide an important resource for understanding how signalling network interactions are tuned by genetic variation without significant alteration to network structure.
引用
收藏
页码:2097 / 2114
页数:18
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