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17.12: Signal Transduction in Evolution

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    89018
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    We saw that signal transduction typically requires a few signal molecules interacting with a few cell-surface receptors to amplify a response in a cascade of enzyme-catalyzed reactions (typically phosphorylations), which activate or inactivate target proteins. Amplification cascades can take a single effector-receptor interaction and magnify its effect in the cell by orders of magnitude, making the signaling systems rapid and highly efficient. The range of cellular and systemic (organismic) responses to the same chemical signal is broad and complex. Different cell types can have receptors for the same effector but may respond differently. For example, adrenalin targets cells of liver and blood vessels, among others, with different effects in each. As it happens, adrenalin is also a neurotransmitter.

    As organisms evolved, they must have responded to environmental imperatives by adapting and co-opting already existing signaling systems in the service of new pathways. Just as the same signal transduction event can lead to different pathways of response in different cells, evolution has allowed different signal transduction pathways to engage in crosstalk. This occurs when two different signal transduction pathways intersect in the same cells. In one example, the cAMP produced at the front end of the PKA signaling pathway can activate (or under the right circumstances, inhibit) enzymes in the MAP kinase pathway. These effects result in changes in the levels of active or inactive transcription factors and can therefore modulate the expression of a gene using two (or more) signals. We are only beginning to understand something that looks less like a linear pathway, and more like a web of signal transduction.


    This page titled 17.12: Signal Transduction in Evolution is shared under a not declared license and was authored, remixed, and/or curated by Gerald Bergtrom.

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