Signalling models and the valuation of new issues: An examination of IPOs in Singapore

1997 ◽  
Vol 5 (5) ◽  
pp. 511-526 ◽  
Author(s):  
Michael Firth ◽  
Chee Keng Liau-Tan
Keyword(s):  
Development ◽  
1997 ◽  
Vol 124 (20) ◽  
pp. 4053-4063 ◽  
Author(s):  
S.S. Blair ◽  
A. Ralston

It is thought that the posterior expression of the ‘selector’ genes engrailed and invected control the subdivision of the growing wing imaginal disc of Drosophila into anterior and posterior lineage compartments. At present, the cellular mechanisms by which separate lineage compartments are maintained are not known. Most models have assumed that the presence or absence of selector gene expression autonomously drives the expression of compartment-specific adhesion or recognition molecules that inhibit intermixing between compartments. However, our present understanding of Hedgehog signalling from posterior to anterior cells raises some interesting alternative models based on a cell's response to signalling. We show here that anterior cells that lack smoothened, and thus the ability to receive the Hedgehog signal, no longer obey a lineage restriction in the normal position of the anterior-posterior boundary. Rather these clones extend into anatomically posterior territory, without any changes in engrailed/invected gene expression. We have also examined clones lacking both en and inv; these too show complex behaviors near the normal site of the compartment boundary, and do not always cross entirely into anatomically anterior territory. Our results suggest that compartmentalization is a complex process involving intercompartmental signalling; models based on changes in affinity or growth will be discussed.


2013 ◽  
Vol 10 (87) ◽  
pp. 20130469 ◽  
Author(s):  
Frazer Meacham ◽  
Aaron Perlmutter ◽  
Carl T. Bergstrom

Costly signalling theory is commonly invoked as an explanation for how honest communication can be stable when interests conflict. However, the signal costs predicted by costly signalling models often turn out to be unrealistically high. These models generally assume that signal cost is determinate. Here, we consider the case where signal cost is instead stochastic. We examine both discrete and continuous signalling games and show that, under reasonable assumptions, stochasticity in signal costs can decrease the average cost at equilibrium for all individuals. This effect of stochasticity for decreasing signal costs is a fundamental mechanism that probably acts in a wide variety of circumstances.


2000 ◽  
Vol 355 (1403) ◽  
pp. 1581-1591 ◽  
Author(s):  
H. C. J. Godfray ◽  
R. A. Johnstone

The evolution of biological signalling in the face of evolutionary conflicts of interest is an active area of evolutionary ecology, and one to which Maynard Smith has made important contributions. We explore the major theoretical challenges in the field, concentrating largely on how offspring signal to their parents when there is the potential for parent–offspring conflict. Costly offspring solicitation (begging etc.) has been interpreted in terms of a Zahavi–Grafen honest handicap signal, but this has been challenged on the grounds of the costs of signalling. We review this controversy and also explore the issue of pooling versus separating signalling equilibrium. An alternative explanation for costly begging is that it is due to sibling competition, and we discuss the relationship between these ideas and signalling models in families with more than one offspring. Finally we consider signal uncertainty, how signalling models can be made dynamic, and briefly how they may be tested experimentally.


2010 ◽  
Vol 262 (3) ◽  
pp. 452-470 ◽  
Author(s):  
Nick D.L. Owens ◽  
Jon Timmis ◽  
Andrew Greensted ◽  
Andy Tyrrell

2021 ◽  
Vol 17 (11) ◽  
pp. e1009515
Author(s):  
Mathurin Dorel ◽  
Bertram Klinger ◽  
Tommaso Mari ◽  
Joern Toedling ◽  
Eric Blanc ◽  
...  

Very high risk neuroblastoma is characterised by increased MAPK signalling, and targeting MAPK signalling is a promising therapeutic strategy. We used a deeply characterised panel of neuroblastoma cell lines and found that the sensitivity to MEK inhibitors varied drastically between these cell lines. By generating quantitative perturbation data and mathematical modelling, we determined potential resistance mechanisms. We found that negative feedbacks within MAPK signalling and via the IGF receptor mediate re-activation of MAPK signalling upon treatment in resistant cell lines. By using cell-line specific models, we predict that combinations of MEK inhibitors with RAF or IGFR inhibitors can overcome resistance, and tested these predictions experimentally. In addition, phospho-proteomic profiling confirmed the cell-specific feedback effects and synergy of MEK and IGFR targeted treatment. Our study shows that a quantitative understanding of signalling and feedback mechanisms facilitated by models can help to develop and optimise therapeutic strategies. Our findings should be considered for the planning of future clinical trials introducing MEKi in the treatment of neuroblastoma.


2017 ◽  
Author(s):  
Katherine H Fisher ◽  
David Strutt ◽  
Alexander G Fletcher

SummaryIn developing tissues, sheets of cells become planar polarised, enabling coordination of cell behaviours. It has been suggested that ‘signalling’ of polarity information between cells may occur either bidirectionally or monodirectionally between the molecules Frizzled (Fz) and Van Gogh (Vang). Using computational modelling we find that both bidirectional and monodirectional signalling models reproduce known non-autonomous phenotypes derived from patches of mutant tissue of key molecules, but predict different phenotypes from double mutant tissue, which have previously given conflicting experimental results. Consequently, we re-examine experimental phenotypes in the Drosophila wing, concluding that signalling is most likely bidirectional. Our modelling suggests that bidirectional signalling can be mediated either indirectly via bidirectional feedbacks between asymmetric intercellular protein complexes, or directly via different affinities for protein binding in intercellular complexes, suggesting future avenues for investigation. Our findings offer insight into mechanisms of juxtacrine cell signalling and how tissue-scale properties emerge from individual cell behaviours.


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