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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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Numbers of genes in each G-protein regulatory mode specified by an A(GPA1, AGB1) function in the four data sets. Blue and red bars correspond to the number of genes regulated in guard cells in the absence and presence of ABA, respectively. Yellow and green bars correspond to the number of genes regulated in leaves in the absence and presence of ABA, respectively. Idealized expression patterns for each mode are indicated below each A(GPA1, AGB1) function; each idealized expression pattern consists of four connected segments corresponding to genotypes; genotype order is as in Figure 2. The inset shows the number of genes in merged regulatory modes, each including an A(GPA1, AGB1) function and its logical negation.
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f3: Numbers of genes in each G-protein regulatory mode specified by an A(GPA1, AGB1) function in the four data sets. Blue and red bars correspond to the number of genes regulated in guard cells in the absence and presence of ABA, respectively. Yellow and green bars correspond to the number of genes regulated in leaves in the absence and presence of ABA, respectively. Idealized expression patterns for each mode are indicated below each A(GPA1, AGB1) function; each idealized expression pattern consists of four connected segments corresponding to genotypes; genotype order is as in Figure 2. The inset shows the number of genes in merged regulatory modes, each including an A(GPA1, AGB1) function and its logical negation.

Mentions: We observe a number of G-protein-regulated genes in the absence of ABA in both guard cells and leaves, indicating that the G-protein has regulatory activity independent of ABA treatment. Only the two knocked-out genes, GPA1 and AGB1, are common to the G-protein-regulated gene sets in guard cells and leaves in either of the two ABA conditions, suggesting system specificity of G-protein action. The distribution of genes in each G-protein regulatory mode in guard cells and leaves, with and without ABA treatment, is given in Figure 3. Note that it is possible that the genes in Ai and A17-i are regulated by the G-protein through the same signaling pathway, for example for A2 and A15, GPA1 and AGB1 could synergistically regulate a mediator (e.g. a transcription factor or other regulator of gene expression such as a microRNA), which activates the genes in A2 and inhibits the genes in A15. To gain insight into the overall abundance of possible G-protein regulatory mechanisms, we plot the cumulative number of genes in each G-protein regulatory group by merging the genes present in A17-i with those in Ai, as shown in the inset of Figure 3 (see also Supplementary information 9 for the interpretation of the relationship between an A(GPA1, AGB1) function and its negation).


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)

Numbers of genes in each G-protein regulatory mode specified by an A(GPA1, AGB1) function in the four data sets. Blue and red bars correspond to the number of genes regulated in guard cells in the absence and presence of ABA, respectively. Yellow and green bars correspond to the number of genes regulated in leaves in the absence and presence of ABA, respectively. Idealized expression patterns for each mode are indicated below each A(GPA1, AGB1) function; each idealized expression pattern consists of four connected segments corresponding to genotypes; genotype order is as in Figure 2. The inset shows the number of genes in merged regulatory modes, each including an A(GPA1, AGB1) function and its logical negation.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f3: Numbers of genes in each G-protein regulatory mode specified by an A(GPA1, AGB1) function in the four data sets. Blue and red bars correspond to the number of genes regulated in guard cells in the absence and presence of ABA, respectively. Yellow and green bars correspond to the number of genes regulated in leaves in the absence and presence of ABA, respectively. Idealized expression patterns for each mode are indicated below each A(GPA1, AGB1) function; each idealized expression pattern consists of four connected segments corresponding to genotypes; genotype order is as in Figure 2. The inset shows the number of genes in merged regulatory modes, each including an A(GPA1, AGB1) function and its logical negation.
Mentions: We observe a number of G-protein-regulated genes in the absence of ABA in both guard cells and leaves, indicating that the G-protein has regulatory activity independent of ABA treatment. Only the two knocked-out genes, GPA1 and AGB1, are common to the G-protein-regulated gene sets in guard cells and leaves in either of the two ABA conditions, suggesting system specificity of G-protein action. The distribution of genes in each G-protein regulatory mode in guard cells and leaves, with and without ABA treatment, is given in Figure 3. Note that it is possible that the genes in Ai and A17-i are regulated by the G-protein through the same signaling pathway, for example for A2 and A15, GPA1 and AGB1 could synergistically regulate a mediator (e.g. a transcription factor or other regulator of gene expression such as a microRNA), which activates the genes in A2 and inhibits the genes in A15. To gain insight into the overall abundance of possible G-protein regulatory mechanisms, we plot the cumulative number of genes in each G-protein regulatory group by merging the genes present in A17-i with those in Ai, as shown in the inset of Figure 3 (see also Supplementary information 9 for the interpretation of the relationship between an A(GPA1, AGB1) function and its negation).

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