Second messengers and specific metabolic events

[EmmaNemma]

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Just curious how specific metabolic process are activated when there are very few second messengers. I would logically think that you would need to have a specific second messenger created for a specific metabolic process. Can someone straighten me out on this? Thanks.

 

[icaruswalks]

Just curious how specific metabolic process are activated when there are very few second messengers. I would logically think that you would need to have a specific second messenger created for a specific metabolic process. Can someone straighten me out on this? Thanks.

I think in the cases of cAMP and PIP2/IP3 you wouldn't run out... since they come from essential cellular compartments. cAMP from ATP which would be necessary to sustain the life of the cell and PIP comes from the cellular membrane.

That molecular cell biology major is paying off!

 

[ensuii]

I think in the cases of cAMP and PIP2/IP3 you wouldn't run out... since they come from essential cellular compartments. cAMP from ATP which would be necessary to sustain the life of the cell and PIP comes from the cellular membrane.

That molecular cell biology major is paying off!

Apparently not...I think OP was asking how a certain second messenger system can trigger a specific response in one cell whereas another cell elsewhere in the body would have an entire different response.

My guess, OP, (which might not be so great given my background as an econ major and grade school teacher) is that each cell has different enzymes and enzyme concentrations in the cytosol. For example, beta cells in the pancreas are going to have enzymes and transport systems that trigger the release of insulin once its beta2 receptor is activated. Conversely, hepatocytes have an entirely different framework of cytosolic enzymes so they carry on a different task.

Just my (un)educated guess 😛

 

[Vagus08]

I'm obviously not a regular poster here, but I came across this topic and it's one that definitely interests me. I think the mechanism whereby different cells are able to carry out vastly different functions using the same common pool of second messengers likely has a lot to with small changes at the level of gene transcription; that, and the fact that many integral 2nd messengers, and cellular enzymes have a number of different isoforms which vary in their concentrations by cell localization and cell type -- in order to meet differing needs. So, my understanding is not so much that different cells and different messengers altogether, but rather, that they have different isoforms of the same messengers/enzymes and/or versions of the same molecules that have been rendered more (or less) active at the level of gene transcription.

 

[SeekerOfTheTree]

Just curious how specific metabolic process are activated when there are very few second messengers. I would logically think that you would need to have a specific second messenger created for a specific metabolic process. Can someone straighten me out on this? Thanks.

So if I get this straight you are asking how is it that if for example you have the GOAT acronym (GNRH, Oxytocin, ADH, TRH) how is it that a specific pathway is activated when the second messenger for all of these is IP3 or PKC?
I believe this is the question you are asking, correct me if I am wrong. Based on this assumption I will answer. The first event to occur is the binding of the primary signal on the cell membrane. So first GNRH or TRH will bind to the membrane receptor. Since it binds at a specifiic receptor that is unique for that pathway it will activate the second messenger. Granted the second messenger is the same for all four of these pathways but the selection process occured when the primary messenger was bound to the membrane. So now when IP3/PKC are activated, they will go through the process of activating the second messenger pathway for that signal.
Now if your question goes even one step further in asking why is it when the IP3/PKC pathway is activated for the specific messenger, why doesn't it go ahead and activate it for the rest in the GOAT acronym, I cannot help you. I would just believe it and move on with life. Better things to worry about.

 

[EmmaNemma]

Apparently not...I think OP was asking how a certain second messenger system can trigger a specific response in one cell whereas another cell elsewhere in the body would have an entire different response.

My guess, OP, (which might not be so great given my background as an econ major and grade school teacher) is that each cell has different enzymes and enzyme concentrations in the cytosol. For example, beta cells in the pancreas are going to have enzymes and transport systems that trigger the release of insulin once its beta2 receptor is activated. Conversely, hepatocytes have an entirely different framework of cytosolic enzymes so they carry on a different task.

Just my (un)educated guess 😛

Your answer would explain my question. Can anyone confirm that this is how it works? Thanks.

 

[dozitgetchahi]

I was thinking about this, and there must be at least a few mechanisms -

1) The types of cells capable of executing x, y, and z processes caused by the increase of the same second messenger are generally (but not always) segregated by receptor type. To use the previous GOAT example, how many cells have GnRH AND TSH AND ADH receptors? I'd wager not many. Likewise, while most cells have insulin receptors, relatively few have GH or prolactin receptors.

2) Spatial/temporal mechanisms likely further separate the cells capable of responding to > 1 receptor type.

Now, granted, things get a lot more messy in places like the brain where you have a multitude of receptor subtypes capable of responding to the same 1st messenger (i.e., serotonin and its half-dozen or more receptor subtypes) and many different varieties of receptor use the same 2nd messenger etc. I suspect that's a long way from being sorted out completely.

 

[icaruswalks]

Apparently not...I think OP was asking how a certain second messenger system can trigger a specific response in one cell whereas another cell elsewhere in the body would have an entire different response.

My guess, OP, (which might not be so great given my background as an econ major and grade school teacher) is that each cell has different enzymes and enzyme concentrations in the cytosol. For example, beta cells in the pancreas are going to have enzymes and transport systems that trigger the release of insulin once its beta2 receptor is activated. Conversely, hepatocytes have an entirely different framework of cytosolic enzymes so they carry on a different task.

Just my (un)educated guess 😛

Wow dude, not my fault at answering the question posed. No need to put somebody down for answering the question and not "guessing" at what the OP wanted.

Anyways, the answer lies in the differential expression of genes, in this case specific receptors during development, regeneration of the tissue in question that are specific to the certain cell line. So yeah my molecular background does pay off jerk.

 

[iamcool]

Cells are huge when you compare them from a molecular perspective. If something is triggered in New York, it is not going to induce response in Dallas. Key proteins for a specific signal transductions tend to be close together. Secondary messengers are also degraded very fast so they do not travel far and induce something else.

This is my take on it and I am not in medical school so take this as a grain of salt.

 

[tco]

If you can think of the most complex possible explanation for why different second messengers cause different responses in different cell types, it's probably the correct one. Seriously.