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Boolean modeling of transcriptome data reveals novel modes of heterotrimeric G-protein action.

Pandey S, Wang RS, Wilson L, Li S, Zhao Z, Gookin TE, Assmann SM, Albert R - Mol. Syst. Biol. (2010)

Bottom Line: Although G-protein control of the transcriptome has received little attention to date in any system, transcriptome analysis allows us to search for potentially uncommon yet significant signaling mechanisms.We find that (1) classical mechanisms of G-protein signaling are well represented.Our method holds significant promise for analyzing analogous 'switch-like' signal transduction events in any organism.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Pennsylvania State University, University Park, PA 16802, USA.

ABSTRACT
Heterotrimeric G-proteins mediate crucial and diverse signaling pathways in eukaryotes. Here, we generate and analyze microarray data from guard cells and leaves of G-protein subunit mutants of the model plant Arabidopsis thaliana, with or without treatment with the stress hormone, abscisic acid. Although G-protein control of the transcriptome has received little attention to date in any system, transcriptome analysis allows us to search for potentially uncommon yet significant signaling mechanisms. We describe the theoretical Boolean mechanisms of G-protein x hormone regulation, and then apply a pattern matching approach to associate gene expression profiles with Boolean models. We find that (1) classical mechanisms of G-protein signaling are well represented. Conversely, some theoretical regulatory modes of the G-protein are not supported; (2) a new mechanism of G-protein signaling is revealed, in which Gbeta regulates gene expression identically in the presence or absence of Galpha; (3) guard cells and leaves favor different G-protein modes in transcriptome regulation, supporting system specificity of G-protein signaling. Our method holds significant promise for analyzing analogous 'switch-like' signal transduction events in any organism.

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Gene expression patterns illustrating the classical II G-protein regulatory mode coupled with regulation by ABA (A), or independent of ABA (B) in guard cells. The heat map is generated with the matrix2png software (Pavlidis and Noble, 2003). The rows of each pattern correspond to genes, and the columns correspond to conditions, that is four genotypes, agb1 gpa1 double mutant (db), gpa1 mutant, agb1 mutant, wild type (wt), without or with ABA treatment. The header of each group of patterns indicates the Boolean rule and the idealized expression pattern associated with the group. The expression level for each gene is extracted from the original expression profiles by subtracting CABA (if relevant), then averaging over the three replicates and normalizing across the samples such that the mean is 0 and the s.d. is 1. TAIR (http://www.arabidopsis.org/) derived accession numbers and a brief description of the genes are shown next to the heat map.
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f4: Gene expression patterns illustrating the classical II G-protein regulatory mode coupled with regulation by ABA (A), or independent of ABA (B) in guard cells. The heat map is generated with the matrix2png software (Pavlidis and Noble, 2003). The rows of each pattern correspond to genes, and the columns correspond to conditions, that is four genotypes, agb1 gpa1 double mutant (db), gpa1 mutant, agb1 mutant, wild type (wt), without or with ABA treatment. The header of each group of patterns indicates the Boolean rule and the idealized expression pattern associated with the group. The expression level for each gene is extracted from the original expression profiles by subtracting CABA (if relevant), then averaging over the three replicates and normalizing across the samples such that the mean is 0 and the s.d. is 1. TAIR (http://www.arabidopsis.org/) derived accession numbers and a brief description of the genes are shown next to the heat map.

Mentions: We observe that in guard cells, A5 (and/or A12)-related regulatory modes are the most representative: B12(ABA, A5)=ABA or not (not GPA1 and AGB1)=ABA or not A5, B15(ABA, A5)=not ABA or not A5, and B5(ABA, A5)=not ABA and A5. These co-regulatory modes of the G-protein and ABA are consistent with Figure 1D where the mediator M1 is regulated by the classical II G-protein regulatory mechanism dependent on the Gβγ subunit on its release from Gα, and the mediator M2 is combinatorially regulated by ABA and M1. Figure 4A uses the commonly used ‘heat map' portrayal to illustrate one of these well-supported classical II modes, B12(ABA, A5), in which the absence of Gα frees Gβγ to downregulate downstream genes, in this instance with the effect of Gα knockout on gene expression dependent on the absence or presence of ABA. In guard cells, G-protein-only signaling and G-protein–ABA additive regulation, where the relative effect of subunit knockout is the same regardless of the presence or absence of ABA, are also possible. The classical II mode B11(ABA, A5)=not (not GPA1 and AGB1) (Figure 4B) and the non-classical mode B6(ABA, A6)=AGB1 (Figure 5) are the two most supported G-protein-only/G-protein–ABA additive regulatory modes.


Boolean modeling of transcriptome data reveals novel modes of heterotrimeric G-protein action.

Pandey S, Wang RS, Wilson L, Li S, Zhao Z, Gookin TE, Assmann SM, Albert R - Mol. Syst. Biol. (2010)

Gene expression patterns illustrating the classical II G-protein regulatory mode coupled with regulation by ABA (A), or independent of ABA (B) in guard cells. The heat map is generated with the matrix2png software (Pavlidis and Noble, 2003). The rows of each pattern correspond to genes, and the columns correspond to conditions, that is four genotypes, agb1 gpa1 double mutant (db), gpa1 mutant, agb1 mutant, wild type (wt), without or with ABA treatment. The header of each group of patterns indicates the Boolean rule and the idealized expression pattern associated with the group. The expression level for each gene is extracted from the original expression profiles by subtracting CABA (if relevant), then averaging over the three replicates and normalizing across the samples such that the mean is 0 and the s.d. is 1. TAIR (http://www.arabidopsis.org/) derived accession numbers and a brief description of the genes are shown next to the heat map.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2913393&req=5

f4: Gene expression patterns illustrating the classical II G-protein regulatory mode coupled with regulation by ABA (A), or independent of ABA (B) in guard cells. The heat map is generated with the matrix2png software (Pavlidis and Noble, 2003). The rows of each pattern correspond to genes, and the columns correspond to conditions, that is four genotypes, agb1 gpa1 double mutant (db), gpa1 mutant, agb1 mutant, wild type (wt), without or with ABA treatment. The header of each group of patterns indicates the Boolean rule and the idealized expression pattern associated with the group. The expression level for each gene is extracted from the original expression profiles by subtracting CABA (if relevant), then averaging over the three replicates and normalizing across the samples such that the mean is 0 and the s.d. is 1. TAIR (http://www.arabidopsis.org/) derived accession numbers and a brief description of the genes are shown next to the heat map.
Mentions: We observe that in guard cells, A5 (and/or A12)-related regulatory modes are the most representative: B12(ABA, A5)=ABA or not (not GPA1 and AGB1)=ABA or not A5, B15(ABA, A5)=not ABA or not A5, and B5(ABA, A5)=not ABA and A5. These co-regulatory modes of the G-protein and ABA are consistent with Figure 1D where the mediator M1 is regulated by the classical II G-protein regulatory mechanism dependent on the Gβγ subunit on its release from Gα, and the mediator M2 is combinatorially regulated by ABA and M1. Figure 4A uses the commonly used ‘heat map' portrayal to illustrate one of these well-supported classical II modes, B12(ABA, A5), in which the absence of Gα frees Gβγ to downregulate downstream genes, in this instance with the effect of Gα knockout on gene expression dependent on the absence or presence of ABA. In guard cells, G-protein-only signaling and G-protein–ABA additive regulation, where the relative effect of subunit knockout is the same regardless of the presence or absence of ABA, are also possible. The classical II mode B11(ABA, A5)=not (not GPA1 and AGB1) (Figure 4B) and the non-classical mode B6(ABA, A6)=AGB1 (Figure 5) are the two most supported G-protein-only/G-protein–ABA additive regulatory modes.

Bottom Line: Although G-protein control of the transcriptome has received little attention to date in any system, transcriptome analysis allows us to search for potentially uncommon yet significant signaling mechanisms.We find that (1) classical mechanisms of G-protein signaling are well represented.Our method holds significant promise for analyzing analogous 'switch-like' signal transduction events in any organism.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Pennsylvania State University, University Park, PA 16802, USA.

ABSTRACT
Heterotrimeric G-proteins mediate crucial and diverse signaling pathways in eukaryotes. Here, we generate and analyze microarray data from guard cells and leaves of G-protein subunit mutants of the model plant Arabidopsis thaliana, with or without treatment with the stress hormone, abscisic acid. Although G-protein control of the transcriptome has received little attention to date in any system, transcriptome analysis allows us to search for potentially uncommon yet significant signaling mechanisms. We describe the theoretical Boolean mechanisms of G-protein x hormone regulation, and then apply a pattern matching approach to associate gene expression profiles with Boolean models. We find that (1) classical mechanisms of G-protein signaling are well represented. Conversely, some theoretical regulatory modes of the G-protein are not supported; (2) a new mechanism of G-protein signaling is revealed, in which Gbeta regulates gene expression identically in the presence or absence of Galpha; (3) guard cells and leaves favor different G-protein modes in transcriptome regulation, supporting system specificity of G-protein signaling. Our method holds significant promise for analyzing analogous 'switch-like' signal transduction events in any organism.

Show MeSH
Related in: MedlinePlus