scholarly journals Signalling of abscisic acid to regulate plant growth

1998 ◽  
Vol 353 (1374) ◽  
pp. 1439-1444 ◽  
Author(s):  
Axel Himmelbach ◽  
Monika Iten ◽  
Erwin Grill
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Mammalian Cells ◽  
Growth Control ◽  
Signal Transduction Pathway ◽  
Negative Control ◽  
Transduction Pathway ◽  
Aba Signal Transduction ◽  
Experimental Approaches ◽  
Main Components

Abscisic acid (ABA) mediated growth control is a fundamental response of plants to adverse environmental cues. The linkage between ABA perception and growth control is currently being unravelled by using different experimental approaches such as mutant analysis and microinjection experiments. So far, two protein phosphatases, ABI1 and ABI2, cADPR, pH and Ca 2+ have been identified as main components of the ABA signalling pathway. Here, the ABA signal transduction pathway is compared to signalling cascades from yeast and mammalian cells. A model for a bifurcated ABA signal transduction pathway exerting a positive and negative control mechanism is proposed.

Characterization of the ABA signal transduction pathway in Vitis vinifera

Plant Science ◽  
2012 ◽  
Vol 187 ◽  
pp. 89-96 ◽  
Author(s):  
Uri Boneh ◽  
Iris Biton ◽  
Amnon Schwartz ◽  
Giora Ben-Ari
Keyword(s):  
Signal Transduction ◽  
Vitis Vinifera ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Aba Signal Transduction

CK2 Is Acting Upstream of MEK3/6 as a Part of the Signal Control of ERK1/2 and p38 MAPK during Keratinocytes Autocrine Differentiation

2011 ◽  
Vol 66 (1-2) ◽  
pp. 83-86 ◽  
Author(s):  
Antonia R. Isaeva ◽  
Vanio I. Mitev
Keyword(s):  
Signal Transduction ◽  
P38 Mapk ◽  
Mammalian Cells ◽  
Protein Kinase Ck2 ◽  
Cell Signalling ◽  
Signal Transduction Pathway ◽  
Signal Control ◽  
Transduction Pathway ◽  
Protein Levels ◽  
Kinase Ck2

Protein kinase CK2 (formerly termed “casein kinase II”) is a ubiquitously in mammalian cells distributed Ser/Thr kinase, with global role in cell regulation. Although, the involvement of CK2 in cell signalling is vast-investigated, virtually nothing is known about its contribution to signal control of keratinocytes differentiation. Here we show that, in autocrine differentiating keratinocytes, inhibition of the CK2 activity induced by 4,5,6,7-tetrabromobenzotriazole (TBB) causes reciprocal changes in the activities of major signal transduction regulators of keratinocytes differentiation, i.e. ERK1/2 and p38 MAPK, without affecting their protein levels. The ERK1/2 activity is strongly suppressed, while the activity of p38 is increased. We have also found that the activity of upstream and specifi c for p38 MAPK kinase MEK3/6 is also stimulated by TBB. These original results clearly demonstrate the participation of CK2 in the signal transduction pathway controlling MEK3/6, p38 MAPK, and ERK1/2 in the used model system.

An osmosensing signal transduction pathway in mammalian cells

Science ◽  
1994 ◽  
Vol 265 (5173) ◽  
pp. 806-808 ◽  
Author(s):  
Z Galcheva-Gargova ◽  
B Derijard ◽  
I. Wu ◽  
R. Davis
Keyword(s):  
Signal Transduction ◽  
Mammalian Cells ◽  
Signal Transduction Pathway ◽  
Transduction Pathway

Reduced embryo sensitivity to abscisic acid in a sprouting-susceptible sorghum (Sorghum bicolor) variety is associated with altered ABA signalling

2007 ◽  
Vol 17 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Nicolás Gualano ◽  
Fernando Carrari ◽  
María Verónica Rodríguez ◽  
Laura Pérez-Flores ◽  
Rodolfo Sánchez ◽  
...  
Keyword(s):  
Abscisic Acid ◽  
Sorghum Bicolor ◽  
Developmental Stages ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Aba Signal Transduction ◽  
Aba Sensitivity ◽  
Two Stages ◽  
Aba Content ◽  
Endogenous Aba

AbstractIn the work reported in this paper, we attempted to elucidate the nature of the different abscisic acid (ABA) sensitivities presented by developing embryos from sorghum [Sorghum bicolor (L.) Moench] lines with contrasting pre-harvest sprouting (PHS) behaviour (Redland B2, susceptible; IS 9530, resistant). We explored two different hypotheses for a possible mechanism: (1) a different functionality of the ABA signalling pathway, and (2) a different rate of ABA degradation/conjugation in the apoplast of embryos from these genotypes. To assess the first possibility, we used an ABA-responsive gene (Rab17) as a reporter of changes in endogenous ABA content, which were artificially induced in embryos from both genotypes by means of fluridone application immediately after anthesis, to reduce ABA content, and embryo incubation in the presence of ABA. A defect in ABA signalling should be seen as a level of Rab17 expression that is independent of endogenous ABA content. For testing the second possibility at two stages of development, embryos from both lines were isolated and incubated in water for different periods. ABA concentrations in embryos and the incubation media were quantified through radioimmunoassay. In contrast to our findings for the resistant IS 9530 line, Rab17 expression did not respond to changes in ABA levels in sensitive Redland B2 embryos. The ABA degradation/conjugation rates in embryos and incubation media did not show clear differences between sorghum lines for any of the developmental stages analysed. These results suggest that a disruption in the ABA signal transduction pathway in Redland B2 underlies the low ABA sensitivity shown by embryos from this line.

scholarly journals Effects of expression of mammalian G alpha and hybrid mammalian-yeast G alpha proteins on the yeast pheromone response signal transduction pathway

1990 ◽  
Vol 10 (6) ◽  
pp. 2582-2590
Author(s):  
Y S Kang ◽  
J Kane ◽  
J Kurjan ◽  
J M Stadel ◽  
D J Tipper
Keyword(s):  
Signal Transduction ◽  
Mammalian Cells ◽  
Short Form ◽  
Signal Transduction Pathway ◽  
Inhibitory Effect ◽  
Negative Control ◽  
Growth Defect ◽  
Pheromone Response ◽  
Long Form ◽  
Similar Inhibitory Effect

Scg1, the product of the Saccharomyces cerevisiae SCG1 (also called GPA1) gene, is homologous to the alpha subunits of G proteins involved in signal transduction in mammalian cells. Scg1 negatively controls the pheromone response pathway in haploid cells. Either pheromonal activation or an scg1 null mutation relieves the negative control and leads to an arrest of cell growth in the G1 phase of the cell cycle. Expression of rat G alpha s was previously shown to complement the growth defect of scg1 null mutants while not allowing mating. We have extended this analysis to examine the effects of the short form of G alpha s (which lacks 15 amino acids present in the long form), G alpha i2, G alpha o, and Scg1-mammalian G alpha hybrids. In addition, we have found that constructs able to complement scg1 are also able to inhibit the response to pheromone and mating when expressed in a wild-type SCG1 strain. Overexpression of Scg1 has a similar inhibitory effect. These results are consistent with a model proposed for the action of Scg1 as the alpha component of a heterotrimeric G protein in which the beta gamma component (Ste4/Ste18) activates the pheromone response after dissociation from Scg1. They suggest that the G alpha constructs able to complement scg1 can interact with beta gamma to prevent activation of the pathway but are unable to interact with pheromone receptors to activate the pathway.

scholarly journals Effects of expression of mammalian G alpha and hybrid mammalian-yeast G alpha proteins on the yeast pheromone response signal transduction pathway.

1990 ◽  
Vol 10 (6) ◽  
pp. 2582-2590 ◽  
Author(s):  
Y S Kang ◽  
J Kane ◽  
J Kurjan ◽  
J M Stadel ◽  
D J Tipper
Keyword(s):  
Signal Transduction ◽  
Mammalian Cells ◽  
Short Form ◽  
Signal Transduction Pathway ◽  
Inhibitory Effect ◽  
Negative Control ◽  
Growth Defect ◽  
Pheromone Response ◽  
Long Form ◽  
Similar Inhibitory Effect

Scg1, the product of the Saccharomyces cerevisiae SCG1 (also called GPA1) gene, is homologous to the alpha subunits of G proteins involved in signal transduction in mammalian cells. Scg1 negatively controls the pheromone response pathway in haploid cells. Either pheromonal activation or an scg1 null mutation relieves the negative control and leads to an arrest of cell growth in the G1 phase of the cell cycle. Expression of rat G alpha s was previously shown to complement the growth defect of scg1 null mutants while not allowing mating. We have extended this analysis to examine the effects of the short form of G alpha s (which lacks 15 amino acids present in the long form), G alpha i2, G alpha o, and Scg1-mammalian G alpha hybrids. In addition, we have found that constructs able to complement scg1 are also able to inhibit the response to pheromone and mating when expressed in a wild-type SCG1 strain. Overexpression of Scg1 has a similar inhibitory effect. These results are consistent with a model proposed for the action of Scg1 as the alpha component of a heterotrimeric G protein in which the beta gamma component (Ste4/Ste18) activates the pheromone response after dissociation from Scg1. They suggest that the G alpha constructs able to complement scg1 can interact with beta gamma to prevent activation of the pathway but are unable to interact with pheromone receptors to activate the pathway.

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