Ca2+ Inside the Cell: Reason?

[justadream]

What's the point of having Ca2+ inside the mitochondria and inside the ER? I ask because there are Ca2+ pumps that pump Ca2+ from the cytosol into these two locations.

I mean I get that Ca2+ is involved in muscle regulation but what about for non-muscle cells? And even for smooth muscle cells, for example, I think the main source of Ca2+ for muscle contraction comes from the outside (not from the inside of the cell)?

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[Czarcasm]

What's the point of having Ca2+ inside the mitochondria and inside the ER? I ask because there are Ca2+ pumps that pump Ca2+ from the cytosol into these two locations.

I mean I get that Ca2+ is involved in muscle regulation but what about for non-muscle cells? And even for smooth muscle cells, for example, I think the main source of Ca2+ for muscle contraction comes from the outside (not from the inside of the cell)?

In addition to assisting with muscle contraction as an intracellular reserve of calcium (as you mentioned), it also plays roles in other physiological process. The other day we spoke about the cortical reaction and how the release of calcium influenced the exocytosis of storage vesicles containing a soup of enzymes that block sperm from entering. More important however, calcium is an important second messenger and helps to amplify signals from the outside of cell when a signal is encountered. In neurons, calcium plays an important role in exocytosis of synaptic vesicles. There's still others, but these are the main ones.

 

[justadream]

@Czarcasm

I can see how the ER might be used as a reservoir to hold Ca2+ for the functions you mentioned. But as far as you know, does the mitochondria serve a similar purpose (to store Ca2+)?

 

[Czarcasm]

@Czarcasm

I can see how the ER might be used as a reservoir to hold Ca2+ for the functions you mentioned. But as far as you know, does the mitochondria serve a similar purpose (to store Ca2+)?

Honestly, I don't know. That knowledge is not something commonly taught in introductory classes (even higher level courses I've taken). Whenever I think of mitochondria function, I think of the endosymbiotic theory of origin because their function is closely tied to bacteria (even sharing the same ribosomes as prokaryotes). I do know mitochondria have their own DNA (including multiple chromosome copies), their own enzymes and replication machinery, etc. I also know that in humans, mitochondria is maternally inherited from the mother's ovum (because only the sperm nucleus contributes to the zygote); probably of interest if a passage is discussing a mitochondrial disorder. I'd suspect it may have something to do with enzyme function since some enzymes require calcium to function properly (clotting factors for instance). Anything else would be specified in a passage.

 

[The Brown Knight]

Ca plays an ENORMOUS role as a second messenger in signal transduction pathways.
Binding of some hormone (or any primary messenger) will release a membrane chemical that induces the smooth ER to release Ca2+ which subsequently binds to calmodulin just as in smooth muscle, but in non-muscle cells this complex initiates a cascade (similar to the cAMP second messenger cascade) that activates other kinases and enzymes necessary for desired function.
As for mitochondria, I would like to know myself.

 

[justadream]

@The Brown Knight

How much should we know for MCAT about calmodulin?

Is it bad that I treat it as a black box ("some mechanism by which muscle contraction in smooth muscle is initiated")?

 

[Mad Jack]

Ca plays an ENORMOUS role as a second messenger in signal transduction pathways.
Binding of some hormone (or any primary messenger) will release a membrane chemical that induces the smooth ER to release Ca2+ which subsequently binds to calmodulin just as in smooth muscle, but in non-muscle cells this complex initiates a cascade (similar to the cAMP second messenger cascade) that activates other kinases and enzymes necessary for desired function.
As for mitochondria, I would like to know myself.

Pretty much this. Mitochondria serve as both calcium buffers and as secondary calcium reservoirs for replenishing of the second messenger system. Calcium might also have a role in the maintenance of mitochondrial membrane potentials. Finally, excess calcium triggers a sort of self destruct pathway in mitochondria (and cells in general). Calcium is super important in every single cell of the body, basically.

 

[The Brown Knight]

@The Brown Knight

How much should we know for MCAT about calmodulin?

Is it bad that I treat it as a black box ("some mechanism by which muscle contraction in smooth muscle is initiated")?

I think it's definitely important to know that smooth muscle employs calmodulin instead of troponin/tropomyosin. I wouldn't think it's much more important for MCAT purposes.
As for the black box thing, maybe be familiar with calmodulin's connection to myosin light chain kinase?

 

[justadream]

@The Brown Knight

Care to enlighten me about calmodulin's connection to myosin light chain kinase?

 

[Lighthill-FFT]

It is hard to justify why things are the way they are a posteriori. The best we can do is offer up guesses.

That being said, there are a few reasons why calcium ions should be trapped inside compartments as opposed to out of them. First, some background.

The reason why calcium ions are trapped in different concentrations at all is to generate a gradient of energy that can be harvested by the cell for use. The gradient created in this case is a gradient of charge. A lot of different ions are used in different parts of the body, but usually they are ions because they are small and easier to manage. Examples would be the hydrogen gradient or pH gradient found in Mitochondria and Chloroplasts.

How do we create charge the fastest? We use more highly charged ions. For cells that have high energy demands, multiple charged ions create a gradient faster per unit pumped. However, we also have to consider the design of the system. It takes a lot more calcium to build up a high concentration of calcium (or whatever charge carrier we want to use) in the cytoplasm than the little organelle because there is more cytoplasm as measured by volume. It would also wreak havoc on secondary messengers and a variety of other things, but from a purely energetic standpoint it makes no sense to keep so much calcium in the cytoplasm when the same gradient can be established with much less calcium by keeping it on the inside of the organelle. Hence things tend to pump in rather than out.

Of course, we are only justifying after the fact. There is no way we can ever really know why things are the way they are. We can just justify why they are the way they are.

 

[The Brown Knight]

@The Brown Knight

Care to enlighten me about calmodulin's connection to myosin light chain kinase?

Simple: the Ca-calmodulin complex ACTIVATES myosin light chain kinase which eventually promotes myosin binding to actin whereas in other muscle Ca binding to the troponin/tropomyosin complex eventually promotes myosin-actin binding.

Some details:
Smooth muscle: release of intracellular Ca --> Ca binds to calmodulin --> Ca-calmodulin complex activates MLCK --> MLCK is a KINASE so it phosphorylates (this is a way of activation) whatever's in its name (i.e. myosin light chain) --> activated MLC will form cross-bridge to the free actin filaments floating around in cell (they are NOT organized into sarcomeres in smooth muscle)

Skeletal/cardiac: Ca released --> goes inside myofibrils (i wanna know myself how it gets in there) --> binds to troponin C --> tropomyosin undergoes configurational change to open up binding sites for myosin on actin filaments --> cross bridge forms --> then the sliding filament model

Key is to realize the DIFFERENCES between both pathways; most of the details i have shown are irrelevant.