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Developmentally regulated MAPK pathways modulate heterochromatin in Saccharomyces cerevisiae.

Mazor Y, Kupiec M - Nucleic Acids Res. (2009)

Bottom Line: The expression state of genes placed near telomeres shows a variegated pattern of inheritance due to heterochromatin formation, a phenomenon that is called telomere position effect (TPE).We provide new evidence that link MAPK signaling and heterochromatin formation in yeast.Our results show that the same components that regulate gene expression states in euchromatic regions regulate heterochromatic expression states and that stress can play a part in turning on or off genes placed in heterochromatic regions.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel.

ABSTRACT
Variegated expression of genes contributes to phenotypic variation within populations of genetically identical cells. Such variation plays a role in development and host pathogen interaction and can be important in adaptation to harsh environments. The expression state of genes placed near telomeres shows a variegated pattern of inheritance due to heterochromatin formation, a phenomenon that is called telomere position effect (TPE). We show that in budding yeast, TPE is controlled by the a1/alpha2 developmental repressor, which dictates developmental decisions in response to environmental changes. Two a1/alpha2 repressed genes, STE5, a MAPK scaffold and HOG1, a stress-activated MAPK, are the targets of this heterochromatin regulation pathway. We provide new evidence that link MAPK signaling and heterochromatin formation in yeast. Our results show that the same components that regulate gene expression states in euchromatic regions regulate heterochromatic expression states and that stress can play a part in turning on or off genes placed in heterochromatic regions.

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MAPK pathways regulate heterochromatin: All strains contain a telomere-proximal URA3 gene. Strains were 5-fold serially diluted and plated on YPD plates to assess growth and on SD-URA plates to assess the extent of telomeric silencing. (A) Effect of mutations in two scaffold proteins, Ste5 and Pbs2. (B) Effect of mutations in Ste4 and Ste18, components of the trimeric G protein, in combination with hog1. (C) Effect of mutation in Ste7, the MAPK kinase, combined with either hog1 or pbs2.
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Figure 5: MAPK pathways regulate heterochromatin: All strains contain a telomere-proximal URA3 gene. Strains were 5-fold serially diluted and plated on YPD plates to assess growth and on SD-URA plates to assess the extent of telomeric silencing. (A) Effect of mutations in two scaffold proteins, Ste5 and Pbs2. (B) Effect of mutations in Ste4 and Ste18, components of the trimeric G protein, in combination with hog1. (C) Effect of mutation in Ste7, the MAPK kinase, combined with either hog1 or pbs2.

Mentions: We have already established that Hog1 activation is necessary in order to reduce TPE (Figure 2D). This suggests that the entire Hog1 and pheromone response pathways participate in heterochromatin regulation. To examine this hypothesis we created single and double mutants of various pathway components. As seen in Figure 5A, deleting pbs2, the HOG pathway MAPKK, recapitulates both the phenotype of hog1 and its relationship with ste5 with regard to telomeric silencing, showing that indeed we are looking at pathway interactions. We further created combinations of both ste7 (the pheromone response MAPKK) and ste18 (the G protein gamma subunit of the pheromone response pathway) with either hog1 or pbs2 and found similar patterns of interactions (Figure 5B and C). In summary, our results show that both MAPK-signaling pathways contribute to heterochromatin regulation via separate mechanisms.Figure 5.


Developmentally regulated MAPK pathways modulate heterochromatin in Saccharomyces cerevisiae.

Mazor Y, Kupiec M - Nucleic Acids Res. (2009)

MAPK pathways regulate heterochromatin: All strains contain a telomere-proximal URA3 gene. Strains were 5-fold serially diluted and plated on YPD plates to assess growth and on SD-URA plates to assess the extent of telomeric silencing. (A) Effect of mutations in two scaffold proteins, Ste5 and Pbs2. (B) Effect of mutations in Ste4 and Ste18, components of the trimeric G protein, in combination with hog1. (C) Effect of mutation in Ste7, the MAPK kinase, combined with either hog1 or pbs2.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2724302&req=5

Figure 5: MAPK pathways regulate heterochromatin: All strains contain a telomere-proximal URA3 gene. Strains were 5-fold serially diluted and plated on YPD plates to assess growth and on SD-URA plates to assess the extent of telomeric silencing. (A) Effect of mutations in two scaffold proteins, Ste5 and Pbs2. (B) Effect of mutations in Ste4 and Ste18, components of the trimeric G protein, in combination with hog1. (C) Effect of mutation in Ste7, the MAPK kinase, combined with either hog1 or pbs2.
Mentions: We have already established that Hog1 activation is necessary in order to reduce TPE (Figure 2D). This suggests that the entire Hog1 and pheromone response pathways participate in heterochromatin regulation. To examine this hypothesis we created single and double mutants of various pathway components. As seen in Figure 5A, deleting pbs2, the HOG pathway MAPKK, recapitulates both the phenotype of hog1 and its relationship with ste5 with regard to telomeric silencing, showing that indeed we are looking at pathway interactions. We further created combinations of both ste7 (the pheromone response MAPKK) and ste18 (the G protein gamma subunit of the pheromone response pathway) with either hog1 or pbs2 and found similar patterns of interactions (Figure 5B and C). In summary, our results show that both MAPK-signaling pathways contribute to heterochromatin regulation via separate mechanisms.Figure 5.

Bottom Line: The expression state of genes placed near telomeres shows a variegated pattern of inheritance due to heterochromatin formation, a phenomenon that is called telomere position effect (TPE).We provide new evidence that link MAPK signaling and heterochromatin formation in yeast.Our results show that the same components that regulate gene expression states in euchromatic regions regulate heterochromatic expression states and that stress can play a part in turning on or off genes placed in heterochromatic regions.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel.

ABSTRACT
Variegated expression of genes contributes to phenotypic variation within populations of genetically identical cells. Such variation plays a role in development and host pathogen interaction and can be important in adaptation to harsh environments. The expression state of genes placed near telomeres shows a variegated pattern of inheritance due to heterochromatin formation, a phenomenon that is called telomere position effect (TPE). We show that in budding yeast, TPE is controlled by the a1/alpha2 developmental repressor, which dictates developmental decisions in response to environmental changes. Two a1/alpha2 repressed genes, STE5, a MAPK scaffold and HOG1, a stress-activated MAPK, are the targets of this heterochromatin regulation pathway. We provide new evidence that link MAPK signaling and heterochromatin formation in yeast. Our results show that the same components that regulate gene expression states in euchromatic regions regulate heterochromatic expression states and that stress can play a part in turning on or off genes placed in heterochromatic regions.

Show MeSH