Calcium Inhibits Coral Growth

[mojoreef]

Another foot long post eh?? and you stayed up until what time to write it?? hehe
Ok I dont have a ton of time here to reply properly as I have to leave town for a couple of days, so when I return I will put up a better post. BUT their is still time to stir it up a bit!!!!:evil:

I have never seen such data on soft tissue growth of x mass / cm^ 2 vs high rate of growth of x mass /c m^2. I'm one that wants to see data and or measurements

When I come back I will dig for ya.

Nope, high calcium has shown time and time again not to increase coral growth, as the surrounding water is already supersaturate at NSW levels. Meaning, they can not take bring about more precip. So, if the Ca++ is 360 ppm to 500+ ppm ( or higher) they grow at the same rate. Chris Jury has shown this in the lab. What accelerates coral growth of hard the skeleton is increasing the Alk and pH. However, the higher Ca++ *may produce less tissue growth and the coral may expend energy more, thus less soft tissue development by dealing with the high outside Ca++ gradient or expel the Ca++ out of the tissue, which would use up needed energy budget for soft tissue growth.

Ok this one we need to talk about a little more Theri are some variables missing in this logic. Just the increase of calcium will not produce the effect as calcium level increase is not the driver. Ok we understand that Ca2 is continually pumped from the surface gradient of the coral to the calcifying site (skeliton) and thus decreases the concentration of calcium in the calicoblastic cells and also in the coelenteron. And as a result it increases calcium concentration at the skeliton area or zone. So you have Ca-ATPase transporting Ca2 to the skeliton in exchange for H+, so the expression is Ca2 +CO2 +H2O = CaCo3 +2H+ (god I hate chemistry!!) Soooo the only way the equalibruim is shifted towards calcification is by the removal of protons, which is where the enzyme Ca-ATPase comes into play. Right? So the enzyme is the true driver as it not only creates this transport mechanism through the cells but also controls the ph levels between the calicoblastic layer and the skeliton. I believe the that at a NSw ph of 8.2 the ATPase raises the PH in that level to 9.3?? and thus creates a enviroment for rapid percipatation.
Which again brings me back to the whole energy thing. With the ATPase being the main player in this game and with the fact that it can only be created by the coral mean that the coral must expend x amount of energy in order to create it thus taking away from its overall energy budget for the sake of nothing??..really? And the coral must maintain this equalbrium with in the different layers of its form in order to complete the basic function of cell growth which is cell division.

OK Disclaimer: Its way to damm early in the morning and I am doing this post with only one cup of coffie and one smoke. So I have no idea if I am translating stuff from my head to this post in any way shape or form!!!!

Anyway got to head out of town for a couple of days, have a good one.


Mojo

 

[Boomer]

Ok this one we need to talk about a little more Theri are some variables missing in this logic. Just the increase of calcium will not produce the effect as calcium level increase is not the driver. Ok we understand that Ca2 is continually pumped from the surface gradient of the coral to the calcifying site (skeliton) and thus decreases the concentration of calcium in the calicoblastic cells and also in the coelenteron. And as a result it increases calcium concentration at the skeliton area or zone. So you have Ca-ATPase transporting Ca2 to the skeliton in exchange for H+, so the expression is Ca2 +CO2 +H2O = CaCo3 +2H+ (god I hate chemistry!!)

Ca2 +CO2 +H2O = CaCo3 +2H+ .........No, no You can not make CaCO3 by adding Ca++ + CO2 + H20

Ca++ + HCO3- ==> CaCO3 + H+
or

Ca++ + HCO3- + CO2 ==> Ca(HCO3)2 ==> CaCO3 +CO2 + H2O

or

Ca++ + CO3-- ===> CaCO3



Lets go Dick & Jane

What you posted is general biology but are still missing the chemistry. I'll try to explain it different. Your "logic", is if Mojo has a pipe filled with water (Calcium) that holds 8 oz of water (Calcium) it is full, no air space and you are saying you can add more to the pipe. When the water is super saturated the coral is super saturated, it is like that pipe. The coral can not take in any more, the "pipe" is full. You can not change the size of the pipe and you can not change how much water fills the pipe but we can change the pressure and flow of the pipe by increasing the Alk and/or pH. It is these that control coral growth mostly not how much Calcium there is. At the same Alk and pH if the Ca++ is 360 ppm or higher the growth rate is about the same.

The story is if you have a tank that is 500 ppm Ca++, Alk 2.25 meq/l @ 8.15 pH and I have a tank 400 ppm Ca++, Alk 3.5 meq/ l @ 8.0 pH my coral will grow faster than yours. Why ? I have plenty of Calcium but have a higher Alk which means I have crap loads more of HCO3- than you and since the corals kind pump up the pH my corals will precip faster. Even if you raise the Alk and pH to mine yours will not grow faster as the pipe is still full. They will grow at about the same rates as mine more or less.

From Chris

Physiological data and models of coral calcification indicate that corals utilize a combination of seawater bicarbonate and (mainly) respiratory CO2 for calcification, not seawater carbonate. However, a number of investigators are attributing observed negative effects of experimental seawater acidification by CO2 or hydrochloric acid additions to a reduction in seawater carbonate ion concentration and thus aragonite saturation state. Thus, there is a discrepancy between the physiological and geochemical views of coral biomineralization. Furthermore, not all calcifying organisms respond negatively to decreased pH or saturation state. Together,these discrepancies suggest that other physiological mechanisms, such as a direct effect of reduced pH on calcium or bicarbonate ion transport and/or variable ability to regulate internal pH, are responsible for the variability in reported experimental effects of acidification on calcification. To distinguish the effects of pH, carbonate concentration and bicarbonate concentration on coral calcification, incubations were performed with the coral Madracis auretenra (= Madracis mirabilis sensu Wells, 1973) in modified seawater chemistries. Carbonate parameters were manipulated to isolate the effects of each parameter more effectively than in previous studies, with a total of six different chemistries. Among treatment differences were highly significant. The corals responded strongly to variation in bicarbonate concentration, but not consistently to carbonate concentration, aragonite saturation (= Calcium levels) state or pH. Corals calcified at normal or elevated rates under low pH (7.6–7.8) when the seawater bicarbonate concentrations were above 1800 lM. Conversely, corals incubated at normal pH had low calcification rates if the bicarbonate concentration was lowered. These results demonstrate that coral responses to ocean acidification are more diverse than currently thought, and question the reliability of using carbonate concentration or aragonite saturation state as the sole predictor of the effects of ocean acidification on coral calcification.

Now if you go dig you will find this:

Effect of calcium carbonate saturation of seawater on coral calcification

J. -P. Gattuso , M. Frankignoulle I. Bourge, S. Romaine and R. W. Buddemeier

Abstract

The carbonate chemistry of seawater is usually not considered to be an important factor influencing calcium-carbonate-precipitation by corals because surface seawater is supersaturated with respect to aragonite. Recent reports, however, suggest that it could play a major role in the evolution and biogeography of recent corals. We investigated the calcification rates of five colonies of the zooxanthellate coral Stylophora pistillata in synthetic seawater using the alkalinity anomaly technique. Changes in aragonite saturation from 98% to 585% were obtained by manipulating the calcium concentration. The results show a nonlinear increase in calcification rate as a function of aragonite saturation level. Calcification increases nearly 3-fold when aragonite saturation increases from 98% to 390%, i.e., close to the typical present saturation state of tropical seawater. There is no further increase of calcification at saturation values above this threshold. Preliminary data suggest that another coral species, Acropora sp., displays a similar behaviour. These experimental results suggest: (1) that the rate of calcification does not change significantly within the range of saturation levels corresponding to the last glacial-interglacial cycle, and (2) that it may decrease significantly in the future as a result of the decrease in the saturation level due to anthropogenic release of CO2 into the atmosphere. Experimental studies that control environmental conditions and seawater composition provide unique opportunities to unravel the response of corals to global environmental changes.

This is what Chris tore apart due to the methods and procedures they used to manipulate growth by raising the Calcium levels.


OK, have funny see you later buddy

 

[NWDiver]

Thanks much Boomer!
So what we want is stable Ca >360 and stable pH >8.
Higher Ca >400 would add no benefit to the coral?
To accelerate growth, an increase in alk would be the ticket. I assume that the typical 9-11dkh is still the range to go for?

-Todd

 

[Boomer]

NSW @ ~ 410 ppm is fine or 420 ppm . The issue is there is no reason to have it any higher. It accomplishes nothing. NSW Alk is nowhere near 9-11 dKH but ts 6.5 dKH. I have no issue boosting it about a bit to say 8, due to acid and the need for more buffer. I not to kine and neither is Mojo on to rapid coral growth, as we worry about potential tissue and skeletal density issues. It is common in tank corals that grow to fast to have low density skeletons which are quite fragile and break easy. There is also what some term Alkalinity Burning of the tissue when the Alk is to high. That is a poor term to use as high Alk does no burn things. The term is used as that is just what it looks like or more of a melting away like from burning. We have no clue as of yet what actually causes that effect, as others do not see it. But is a common occurrence. At more normal Alk this does not seem to happen at all. At much lower levels of 360 ppm Ca++ or so they probably have to work harder. If one wants to run lower Ca++ that is fine but then the Salinity should follow also to a lower level. It is pretty easy to figure out

NSW Std 35 ppt Ca++ 410 ppm

410 / 35 = 11.7

Ca++ X = ppt x 11.7

Ca++ X = 31 ppt x 11.7 = ~ 365 ppt

Most Ocean reefs are 32 ppt - 37 ppt. That means the Ca++ is 375 ppm - 433 ppm .

In the balance scheme for Alk, Mg++ and Ca++ it is we start at 360 ppm Ca++ = 0 Alk

For each 1 meq / l rise in Alk we add 20 ppm to 360 ppm

420 ppm Ca++ - 360 = 60

60 / 20 = 3

3 x 1 = 3 meq / l @ 420 ppm Ca++



Mg ++X = ppt x 36.8

Mg ++X = 31 ppt x 36.8 = 1140 ppm Ca++

 

[mojoreef]

Yea I tried to copy and paste that chemical expression and it came out like that, Whats up with that??

Anyway I agree with you Boomer coming from the chemistry side of the equation the addtion of high levels of calcium will not have a noticable effect on calcification. But that only of side of the equation, their is a whole other side that shows its negative effect on the coral. Let me see if I can make it a bit clearer.

So first a little picture so everyone can see what we are talking about. The picture is a result of a micro sensor test with in various layers of a corals tissue.

It is understood that corals (tissue) can not produce cellular division with the presence of calcium with in their cell structure itself. The coral has created a means by which it actively transports Ca2+ from the seawater to the skeliton. When you compare Ca2+ concentrations in seawater, (on the polyp surface) and inside the coelenteron shows a downward gradient of Ca2+ between seawater and the coelenteron. This concentration gradient drives Ca2+ diffusion from seawater to the coelenteron. Thus active transport of Ca2+ must take place to transport the ion against its concentration gradient to the skeleton. Sooo the way they do it is by the use of Ca-ATPase (an enzyme) which transports the Ca++ to the skeliton site in exchange for H+. So yes they can actually shift the equalibrium towards calcification by removing the protons.

So in other words, The enzyme transports Ca2+ to the site of calcification at the same time it removes protons away from it, thereby driving the reaction of calcification towards CaCO3 formation. The aragonite saturation state under the calicoblastic layer increases from ca. 3.2 in dark to ca. 25 in light compared with ca. 4 in seawater. This change in the aragonite saturation state drives calcification at the skeleton.

Ok so a couple of things are known.
1. Basic biology, corals can not cellularly divide with the presence of calcium with in their cell structure. (Barnes and Chalker 1990); did a pretty comprehensive study on this and it is concidered the norm.
2. Corals can absorb calcium (yes along with othe elements) through thier cell structure and concentrate it at the skelital area, and yes they can do it with out the calcium levels changing in the surrounding SW. They also drive the formation of CaCO3 by exchanging the Ca2+ for protons which they move away from that area. This process basically changes the saturation state and then precipatates to the skeliton. This process is done by the coral (with no manipulation of the calcium level in the surrounding water) by the creation and use of an enzyme called ATPase.

Ok so now to the point I was trying to make, about 3 pages back or so, lol At normal SW conditions that coral must donate a portions of its FINITE energy budget for the processes listed above. The energy budget is limited on the input side (as in 8 hours of light and normal nutrient absorbsion daily) so it takes this energy budget and must divide it amongst the various things it needs to do, among them are growth, conversion of carbohydrates, creation of a organic matrixes, creation of material for slime net capture, defencive tactics and so on and so on. A big list for a small thing.
If you create a situation where you elevate the level of calcium in the tank water, you are forcing the coral to create more of the enzyme in order to maintain its normal parameters with in the coral. Since ALOT of energy is needed to create this enzyme and the energy budget is limited in the first place, the only place to get the extra energy required is to STEAL it from one of the other REQUIRED processes. Thus putting the coral into a weakened state. for nothing

Anyway, I need more coffie now

MOJO

 

[user 2204]

Makes sense seeing all the chemisrty equations and the such. Very good job Boomer and Mojo for the detailed explanations.

Cheers,
Alex

 

[Herefishyfishy]

Nobody brought up the fact that the energy to deposit Ca comes from light and thus more light is a bigger factor in REAL growth than Ca and that carbonates which do not inhibit reproduction helps in the precipitation of the aragonite from the cells. Thus simple NSW with either water changes or suplimentation if depletion with Excellent lighting in the absence of "polution" is the goal.

"Formation of the calcareous exoskeleton involves deposition of the mineral aragonite by the polyps from calcium and carbonate ions they acquire from seawater. The rate of deposition, while varying greatly across species and environmental conditions, can be as much as 10 g / m² of polyp / day (0.3 ounce / sq yd / day). This is light dependent, with night-time production 90% lower than that during the middle of the day."

I have seen more coral display systems killed by Dosing/CaRx/Kalk errors than any ammount of lighting or water change mistakes. Best to Keep it simple...

 

[Boomer]

OK, here we go again Devil's advocate :lol:

If you create a situation where you elevate the level of calcium in the tank water, you are forcing the coral to create more of the enzyme in order to maintain its normal parameters with in the coral. Since ALOT of energy is needed to create this enzyme and the energy budget is limited in the first place, the only place to get the extra energy required is to STEAL it from one of the other REQUIRED processes.


Issue #1
At what level does this Energy Budget loss for to much Calcium take place the gives us a unhealthy coral tissue ? We seem to be forgetting something here, that many Acropora coral species that live in the Indian Ocean and Pacific are also found in the Red Sea, where the Ca++ is ~ 460 ppm. So, where should we put that limit, i.e, 475 ppm ? So, is it really to high a Calcium level or is it really to high an Alk that is stressing corals, taxing their EB ? I will add that corals can also control the carbonate/bicarbonate/ CO2 they take in. We do know that tha people have had corals with to thin a coral tissue or low to low skeletal density but we still do not know from what other than it is environmental.

Issue # 2
Randy goes into great detail about coral calcification rates and controls. Meaning, the corals more or less have a "control valve" on that "pipe" that only lets in the proper amount of Calcium. Meaning, the coral can control the diffusion rates of the Calcium into the coral form surrounding seawater. Although it is no known who it really works. Second, is the ECF ( Extracytoplasmic Calcifying Fluid), which lies under the Calcioblastic Layer. About nothing is known about this fluid and how it does or does not coral coral growth.



Nobody brought up the fact that the energy to deposit Ca comes from light and thus more light is a bigger factor in REAL growth than Ca and that carbonates which do not inhibit reproduction helps in the precipitation of the aragonite from the cells.

True for photosynthetic corals but many corals grow more less in the dark or are non-photosynthetic. So, throwing in light has no bearing on ALL hard corals and the Calcium issue of being to high.

In conclusion, we know that corals are taxed on their EB but not how or by what. So, the moral of the story is to keep levels at or near NSW ion parameters, at x Salinity and Temperature. Until someday, somebody, finds out what it really is.

I will now throw this into the ****-pile

Morphological studies of the soft tissues involved in skeletal dissolution in the coral Fungia fungites

Yamashiro, H.; Yamazato, K.
Coral Reefs, Volume 15, Issue 3, pp.177-180

Light and transmission electron microscopy were used to study mechanisms involved in the separation of the disc from the stalk in juvenile Fungia fungites (Scleractinia, Fungiidae). Separation occurs because the skeleton is weakened by dissolution across a distinct plane at the junction of the stalk and disc. The tissue layer adjacent to the skeleton in the stalk was composed of typical, squamose, calicoblastic cells. In contrast, calicoblastic cells in the region of skeletal dissolution were tall and columnar. They contained many microvilli, abundant mitochondria and several different types of vesicles. It is assumed that these calicoblastic cells are actively involved in skeletal dissolution.​

Determinate growth and the scaling of photosynthetic energy intake in the solitary coral Fungia concinna (Verrill)




Robin Elahib and Peter J. Edmundsa

Abstract

For many marine invertebrates, the maximum size of an individual is influenced heavily by environmental factors and may be limited by energetic constraints. In this study, an energetic model developed originally for anemones was applied to the free-living scleractinian Fungia concinna (Verrill) from Moorea (French Polynesia) to test the hypothesis that energetic constraints limit the size of this solitary coral. The modified model assumed that photosynthesis was the primary source of metabolic energy, and that metabolic costs were represented by aerobic respiration; these sources and sinks of energy were compared using daily energy budgets that were analyzed using double logarithmic regressions of energy against coral size. With this approach, energy limitation is characterized by a scaling exponent for energetic cost (bcost) that is larger than the scaling exponent for energy intake (bintake). For the size range of F. concinna studied, bintake = 0.73 ± 0.09 and bcost = 0.46 ± 0.10, thereby demonstrating that large individuals accumulated an energetic surplus, even when the expenditure associated with host tissue and symbiont growth was included in the model. The surplus of energy that this coral acquires as it grows appears to be driven by the scaling of traits associated functionally with the scaling of respiration and photosynthesis. Specifically, tissue biomass displayed a strong positive allometry with respect to surface area (i.e., b > 1), and this constraint on surface area may be the mechanistic basis of the low scaling exponent for metabolic cost. In contrast, the capacity for autotrophy – defined indirectly as Symbiodinium population density and chlorophyll content – increased isometrically with surface area, and likely contributed to the higher scaling exponent for intake relative to cost. Our results suggest that growth in F. concinna is not limited strictly by energy, but instead maximum size must be determined by alternative physiological or ecological constraints.

Allometry

For those that do not know, it is a differential growth rate between x vs. y, i.e, the growth rate of the length of a branch vs the growth rate of the diameter of that branch.

Similar to Mojo's but with more detail and not a "Deep Six" article.

How Reefs Grow
http://www.coralscience.org/main/articles/biochemistry-2/how-reefs-grow

 

[mojoreef]

Issue #1
At what level does this Energy Budget loss for to much Calcium take place the gives us a unhealthy coral tissue ? We seem to be forgetting something here, that many Acropora coral species that live in the Indian Ocean and Pacific are also found in the Red Sea, where the Ca++ is ~ 460 ppm. So, where should we put that limit, i.e, 475 ppm ? So, is it really to high a Calcium level or is it really to high an Alk that is stressing corals, taxing their EB ? I will add that corals can also control the carbonate/bicarbonate/ CO2 they take in. We do know that tha people have had corals with to thin a coral tissue or low to low skeletal density but we still do not know from what other than it is environmental

Really??? thats your Devils advocate?? Your going to make me work for that?? lol

In taking two seperate locations like that and all that differs between the two, to just take calcium out and look at it seems a little extreme, nes pas??
A corals energy budget is set by a number of factors, light clairity, co2 levels, available nutrients, and so on and so on. So in one area it is X and in the other area it is Y and it doesnt change that much. The same could be applied in anyones tank, the sum or total of the corals energy budget is based on the surrounding abundance of the above. The bottom line is that the energy budget intake is relatively fixed. From that you start to take away processes with in the coral, 26% is used for animal respiration and growth, 22% for zooxanthellae respiration and growth, then their is reproduction, mucus formations and then even just loss. Anyway betting a dead horse here. Thier isnt a hard fast number and you know that, but in the same breathe you rob Peter to pay Paul then peter has less to pay his bills, and then something gets turned off

Issue # 2
Randy goes into great detail about coral calcification rates and controls. Meaning, the corals more or less have a "control valve" on that "pipe" that only lets in the proper amount of Calcium. Meaning, the coral can control the diffusion rates of the Calcium into the coral form surrounding seawater. Although it is no known who it really works. Second, is the ECF ( Extracytoplasmic Calcifying Fluid), which lies under the Calcioblastic Layer. About nothing is known about this fluid and how it does or does not coral coral growth.

I have not seen anything that a coral has that only lets in the proper amount of calcium. On the Extracytoplasmic Calcifying Fluid theirs a bunch of info if you dig, From what is written is that it contains protiens, polysaccharides, electrolites, dic, and protons. Basically an exchange fluid that gives up protons H+ for calcium and dic.

Ok tired now


Mojo

 

[Boomer]

corals energy budget is set by a number of factors, light clairity, co2 levels, available nutrients, and so on and so on

I said that here more or less
In conclusion, we know that corals are taxed on their EB but not how or by what. So, the moral of the story is to keep levels at or near NSW ion parameters, at x Salinity and Temperature. Until someday, somebody, finds out what it really is.

The issue has been is high Ca++ taxing the EB and there is no evidence that going from 400 ppm Ca++ to 500 ppm Ca++ in the same tank will affect the EB at all. I would be much more worried about high Alk. BUT that high Ca++ is part of the whole picture. Therefore try to get things with in reason of NSW.

Extracytoplasmic Calcifying Fluid ........proteins, polysaccharides, electrolites, dic, and protons.

Means much of nothing , it is the pH, Alk, Ca++ of that fluid that really counts. As that can affect the rate of calcification or even dissolution.


I have not seen anything that a coral has that only lets in the proper amount of calcium

Have you looked

Entry of Calcium into the Calicoblastic Epithelium​

The next question to answer is how the calcium enters the calicoblastic epithelium. Clearly, it does not just freely flow from the coelenteron because that space is largely in equilibrium with the external fluid (at least with respect to calcium in seawater; 10 mM calcium). If calcium did enter freely, the cell contents would also be at 10 mM calcium. While this might seem like an efficient process, cells do not survive well at 10 mM calcium, and need to keep the free concentration substantially lower as calcium plays a critical role in numerous cell processes and cannot be permitted to be unusually high.

​

Nevertheless, huge amounts of calcium are flowing across the calicoblastic epithelium, and somehow the inflow of calcium must be gated. In fact, there is a calcium channel that regulates the flow of calcium into the cell. This voltage dependent channel has been characterized, and a portion of it has even been cloned.

See:
Cloning of a calcium channel a1 subunit from the reef-building coral, Stylophora pistillata. Zoccola, Didier; Tambutte, Eric; Senegas-Balas, Francoise; Michiels, Jean-Francois; Failla, Jean-Pierre; Jaubert, Jean; Allemand, Denis. Observatoire Oceanologique Europeen, Centre Scientifique de Monaco, Monaco, Monaco. Gene (1999), 227(2), 157-167.


This calcium channel does not pump calcium, but only allows it to flow in the direction of the concentration gradient (which is from the coelenteron into the calicoblastic epithelium. What it does do is open and close this calcium pathway in response to the voltage across the cell membrane. Such voltage dependent channels are very common in creatures of every type, but how they work on a molecular level is beyond the scope of this article. In short, however, the cell must change its surface electrical potential in response to its internal calcium concentration somehow, and this voltage change opens or closes the calcium channels.
The evidence that this channel is important in calcification is substantial. Chemical inhibitors specific to these types of channels inhibit calcification in corals such as Galaxea fascicularis and Stylophora pistillata. Immunohistochemistry has also been used to localize the cloned portion of the channel to the calicoblastic epithelium (as well as the oral ectoderm).


See


A compartmental approach to the mechanism of calcification in hermatypic corals. Tambutte, E. Allemand, D. Mueller, E. and Jaubert, J. (1996) J. Exp. Biol. 199, 1029-1041.

Calcification in hermatypic and ahermatypic corals. Marshall, A. T.. School Zool., LaTrobe Univ., Melbourne, Australia. Science (Washington, D. C.) (1996), 271(5249), 637-9.

 

[mojoreef]

The issue has been is high Ca++ taxing the EB and there is no evidence that going from 400 ppm Ca++ to 500 ppm Ca++ in the same tank will affect the EB at all. I would be much more worried about high Alk. BUT that high Ca++ is part of the whole picture. Therefore try to get things with in reason of NSW.

It would be pretty easy to assume that what ever ammount Ca went over natural would have an incremental effect on the the EB. But I guess we could turn a blind eye

Have you looked

Always looking brother I would think it might be a bit of a reach to say that calcium induction is controled by voltage across the cells membrane. Entry into this chamber is done by two pathways, one being the a calcium channel which is L-type of voltage dependant (could even call it an antiporter). The second is specialized protiens/enzymes, now both are required to mediate Ca2+ entry across the lipid bilayer of the aboral ectoderm. but in saying that they both dont have to be running at the same time.
On the cloning thing, They have no idea for sure as to what the L-type is, I believe they had like a 85% similarity to an amino acid sequence of rabbit a lC subunit. Once inside the calicoblastic cells, Ca2+ ions must be sequestered in vesicles or organelles
and/or bound to Ca2+-binding proteins in order to maintain a low free intracellular
concentration.

Anyway facinating stuff but I would say not a carved in stone process and we getting to deep again, lol

Mojo

 

[Boomer]

You need to read this, it was posted here

I would think it might be a bit of a reach to say that calcium induction is controled by voltage across the cells membrane

How is that ? It is a common known biochemical fact


Such voltage dependent channels are very common in creatures of every type, but how they work on a molecular level is beyond the scope of this article. In short, however, the cell must change its surface electrical potential in response to its internal calcium concentration somehow, and this voltage change opens or closes the calcium channels.



The Chemical and Biochemical Mechanisms of Calcification
http://www.advancedaquarist.com/issues/apr2002/chem.htm




A pyridinium derivative from Red Sea soft corals inhibited voltage-activated potassium conductances and increased excitability of rat cultured sensory neurones.

Temraz TA, Houssen WE, Jaspars M, Woolley DR, Wease KN, Davies SN, Scott RH.


A pyridinium derivative from Red Sea soft corals i... [BMC Pharmacol. 2006] - PubMed result


Cloning of a calcium channel alpha1 subunit from the reef-building coral, Stylophora pistillata.

Zoccola D, Tambutté E, Sénégas-Balas F, Michiels JF, Failla JP, Jaubert J, Allemand D.
Observatoire Océanologique Européen, Centre Scientifique de Monaco, Avenue Saint Martin, MC-98000, Monaco, Monaco.


Abstract

While the mechanisms of cellular Ca2+ entry associated with cell activation are well characterized, the pathway of continuous uptake of the large amount of Ca2+ needed in the biomineralization process remains largely unknown. Scleractinian corals are one of the major calcifying groups of organisms. Recent studies have suggested that a voltage-dependent Ca2+ channel is involved in the transepithelial transport of Ca2+ used for coral calcification. We report here the cloning and sequencing of a cDNA coding a coral alpha1 subunit Ca2+ channel. This channel is closely related to the L-type family found in vertebrates and invertebrates. Immunohistochemical analysis shows that this channel is present within the calicoblastic ectoderm, the site involved in calcium carbonate precipitation. These data and previous results provide molecular evidence that voltage-dependent Ca2+ channels are involved in calcification. Cnidarians are the most primitive organisms in which a Ca2+ channel has been cloned up to now; evolutionary perspectives on Ca2+ channel diversity are discussed.


Structure of three high voltage-activated calcium channels


Abstract

Voltage-gated calcium (Ca#+) channels contribute to impulse propagation in excitable cells and also regulate intracellular levels of Ca#+. High voltage-activated (HVA) Ca#+ channels are heteromultimeric membrane proteins. The pore-forming, voltage-sensing subunit is the a" subunit. We have cloned 3 HVA Ca#+ channel a" subunit cDNAs from Schistosoma mansoni. One of these sequences most closely resembles the L-type class of HVA a" subunits. The other two sequences are most closely related to non L-type a" subunits. These schistosome a" subunits have many of the features common to HVA Ca#+ channels, but also have distinct structural motifs. Analysis of the structural and functional properties of schistosome Ca#+ channel subunits may provide information about these critical components of excitable cell.

 

[ReefLogic]

This has been a very education thread thus far. Interesting disputes, not to mention I think most are under the impression that dosing calcium is good....even though I have never dosed anything in my tank and have always had very good growth.

 

[mojoreef]

This has been a very education thread thus far. Interesting disputes, not to mention I think most are under the impression that dosing calcium is good....even though I have never dosed anything in my tank and have always had very good growth.

No one is saying that dosing calcium is a bad thing reeflogic, we all do it as calcium is constantly being depleted. What we are saying is that raising ones levels of calcium to levels that are way higher then normal sea water level, are not good and could ultimately hurt the coral from stripping away from its energy budget.

On this me and the Boomister are in agreement, the rest is just me and him talking about mechanisms the corals use.

mojo

 

[ReefLogic]

I understand that....and I was serious....I don't dose anything....at all....I have zoa's and SPS in my tank and all grows well. Now this is somewhat of a moot point as I have unloaded all but 10 frags or so from my tank. But for the past 3 years I have had LPS, Zoa's, softies, and SPS all in my tank with zero dosing....I don't even use RO much less RO\DI

 

[mojoreef]

How is that ? It is a common known biochemical fact

Yes, even though how they exactly work is not totaly known, we know that they are their, BUT they are only ONE of TWO primary methods a coral uses to transport calcium into that cell layer. SO even if the coral had control over the L-type (which is not known for sure) their is still another fully functioning pathway?? right?

Mojo

 

[Aquanaut]

Man my head hurts...complexity of all this...then why do synthetic salts promote and carry CA as high as 450 and PH 8.6? This sounds detrimental to those of us who bi-weekly change out 20%. Makes some sense as to why my monti cap nearly crashed w/trying to maintain the initial mixes params. When I backed-off, the monti recovered.

 

[ReefLogic]

Thought I should add that I am doing frequent water changes now with the sharks....what I mentioned above was when I had coral

Sent from my D2 using Swype and Tk

 

[mojoreef]

Man my head hurts...complexity of all this...then why do synthetic salts promote and carry CA as high as 450 and PH 8.6? This sounds detrimental to those of us who bi-weekly change out 20%.

Your head hurts?? try writing down all this stuff

The concept of salt mixes having higher levels of Calcium and so on are to help us replace the elements in our tank that have been depleted. As we run our tanks Calcium is taken up by corals, algae and is just percipatated out (on our heaters and so on). So it is an element that requires us to replenish it based on our bioload uptake.

To be honest 450 is not that big a deal and could be concidered a fairly safe level. The reason I strated this is that their seemed to be alot of folks that consistantly run calcium levels from 475 to over 500 which I would concider wasteful from a water chemistry side and harmful from a biological side.

Mojo

 

[ReefLogic]

Dang Mojo....between you, Boomer, and the others here you guys are like a library of knowledge....we are lucky to have such educated people here.