Cell Trends
- Thread starter bob b
- Start date
stipe said:
http://www.creationsafaris.com/crev200610.htm
The opening page lists the back issue years by month. I go through each month in turn and cut and paste the ones on the "cell" to a Word file, from which I select some interesting ones to post here.
For example:
Cells Squeeze Out Their Dead 12/13/2001
Cells die, and if left in place in tissues, they would shrivel, rot and leave a hole. Something must be done, and the cellular machinery is built to handle every contingency. At the American Society for Cell Biology meeting this week, the process was described by London biologists, reports Science Now. Early in its death throes, the dying cell sends out a warning to neighboring cells, who produce extra motor proteins actin and myosin. These go into action retracting the healthy cells around it into a contractile ring, as if saying Heave ho on cue, squeezing the dead cell out like toothpaste, then reforming the intact tissue. The scientists switched the proteins on and off in skin epithelial tissue to test their hypothesis.
There are thousands of things like this going on in our bodies that we take for granted, but are necessary. Even cell death (apoptosis) and tissue regeneration requires the motor vehicles we described in last week’s headline. A cell has been likened to a city; this story takes a look at the morgue.
Cellular Motor Vehicles Souped Up for Speed 12/06/2001
The awe is palpable in Susan Gilbert’s News and Views entry in the Dec. 6 issue of Nature, “Cell biology: High-performance fungal motors.” Reviewing recent findings, she introduces the subject matter:
Motor proteins are tiny vehicles that move molecular cargoes around inside cells. These minute cellular machines come in three broad families, the kinesins, the myosins and the dyneins. There are over 250 kinesin-like proteins, and they are involved in processes as diverse as the movement of chromosomes and the dynamics of cell membranes. They all have a similar catalytic portion, known as the motor domain, but beyond this they are astonishingly varied - in their location within cells, their structural organization, and the movement they generate.
She spends time especially on the “Ferrari” of these motor vehicles, a kinesin from the fungus Neurospora crassa, that can move along its microtubule tracks at 2.5 microns per second, five times faster than other similar kinesins (if this molecule were the size of a car, it would top 1200 mph). Describing three possible means of achieving such speeds, she suggests ways microbiologists might learn more about “these splendid molecular machines.”
Two other papers (1), (2) in the same issue discuss ATPase or ATP synthase, the molecular motor of exquisite precision and function discussed earlier in Creation-Evolution Headlines. The second describes how it is involved in helping stomata (openings) in a plant leaf open and close to exchange gases. Apparently ATPase creates an electrical potential that works with other proteins that are responsive to blue light.
These motor vehicles (80 times smaller than a wavelength of light) and the microtubule tracks they run on have been likened to a nanotrain or intracellular railroad system in the cell.
Molecular motors in all living cells: think of it! And there are not just one or two, but hundreds of them, each finely crafted, each enormously more efficient than any motors man has ever produced (ATP synthase approaches 100% efficiency). This is all recent discovery; it is big news; it’s one of the hottest areas of research right now, and engineers are actively studying molecular motors as models for nanotechnology. But who is asking the obvious question of how these motors could originate, without a Designer? The motor Gibson describes operates in a fungus! Do you know any engineering fungus among us, any mushrooms that are masters of nanotechnology?
The science of biochemical motors fits intelligent design theory to a T, but is a major headache for evolution. It is not necessary to mention God, Genesis, creation, or the identity of the Creator to observe the obvious, that these are wonderfully crafted machines. You don’t have to know the manufacturer to look at a Ferrari and conclude it was designed, and designed well. Just do good observation, measurement, and reporting, and leave the obvious conclusion to the reader instead of stretching credibility to come up with a story about how they designed themselves.
The awe is palpable in Susan Gilbert’s News and Views entry in the Dec. 6 issue of Nature, “Cell biology: High-performance fungal motors.” Reviewing recent findings, she introduces the subject matter:
Motor proteins are tiny vehicles that move molecular cargoes around inside cells. These minute cellular machines come in three broad families, the kinesins, the myosins and the dyneins. There are over 250 kinesin-like proteins, and they are involved in processes as diverse as the movement of chromosomes and the dynamics of cell membranes. They all have a similar catalytic portion, known as the motor domain, but beyond this they are astonishingly varied - in their location within cells, their structural organization, and the movement they generate.
She spends time especially on the “Ferrari” of these motor vehicles, a kinesin from the fungus Neurospora crassa, that can move along its microtubule tracks at 2.5 microns per second, five times faster than other similar kinesins (if this molecule were the size of a car, it would top 1200 mph). Describing three possible means of achieving such speeds, she suggests ways microbiologists might learn more about “these splendid molecular machines.”
Two other papers (1), (2) in the same issue discuss ATPase or ATP synthase, the molecular motor of exquisite precision and function discussed earlier in Creation-Evolution Headlines. The second describes how it is involved in helping stomata (openings) in a plant leaf open and close to exchange gases. Apparently ATPase creates an electrical potential that works with other proteins that are responsive to blue light.
These motor vehicles (80 times smaller than a wavelength of light) and the microtubule tracks they run on have been likened to a nanotrain or intracellular railroad system in the cell.
Molecular motors in all living cells: think of it! And there are not just one or two, but hundreds of them, each finely crafted, each enormously more efficient than any motors man has ever produced (ATP synthase approaches 100% efficiency). This is all recent discovery; it is big news; it’s one of the hottest areas of research right now, and engineers are actively studying molecular motors as models for nanotechnology. But who is asking the obvious question of how these motors could originate, without a Designer? The motor Gibson describes operates in a fungus! Do you know any engineering fungus among us, any mushrooms that are masters of nanotechnology?
The science of biochemical motors fits intelligent design theory to a T, but is a major headache for evolution. It is not necessary to mention God, Genesis, creation, or the identity of the Creator to observe the obvious, that these are wonderfully crafted machines. You don’t have to know the manufacturer to look at a Ferrari and conclude it was designed, and designed well. Just do good observation, measurement, and reporting, and leave the obvious conclusion to the reader instead of stretching credibility to come up with a story about how they designed themselves.
aharvey
New member
Hey, if you happen to find a paper, anywhere, that actually demonstrates (even defines!) cellular specified complexity, now that would be worth reporting! Or are you assuming that all cellular complexity is specified complexity?bob b said:Apparently you did not read the initial posting on this thread which stated that ALL of the sources I would be using for my postings would be from creationsafaris.com, which in turn summarize and reference information from articles in the mainline scientific journals..
I started with the earliest one they had back in late 2000 and am gradually working my way up to the present. We are now at December 2001.
Lots more cellular specified complexity to go!!!
From Bob b's OP:
1) What is the author’s intent in identifying these as “brainless, sightless molecules” since every molecule in existence, no matter what it’s function is “brainless and sightless”?
2) Can you seriously say that you do not know how a “cell (could ) survive that didn't have these (repair) capabilities from the start?”
Bob b – you are not a biologist, nor am I. So I will ask you, as a fellow non-biologist, consider (from the OP) “How do brainless, sightless molecules perform first aid?”
1) What is the author’s intent in identifying these as “brainless, sightless molecules” since every molecule in existence, no matter what it’s function is “brainless and sightless”?
2) Can you seriously say that you do not know how a “cell (could ) survive that didn't have these (repair) capabilities from the start?”
ThePhy said:
I am sure you can speculate as well as I can regarding the author's intent.
I believe that the reason for doubting that cells would be able to survive without a repair mechanism is called error castastrophe, meaning that a certain degree of fidelity in DNA replication is required and normal replication without a repair mechanism is apparently
not adequate. I'm afraid that you would have to look it up to get any more detail.
BTW, I good example of error catastrophe seems to be my failing memory, because my wife asked me a few minutes ago to look something up on the internet for her, but after finishing my last posting I completely forgot and now she has returned and is asking me again. So I better go off and do it for her before I completely forget once again.
It just sounded to me like a simplistic appeal showing that ID must have been involved. But as I already mentioned, the brainless sightless nonsense is pure silliness.bob b said:
Your quote in the OP made no distinction about what cells are being discussed. It made no mention of the fidelity of DNA replication, other than saying that when mistakes are made, they might be amenable to repair.
Based on several years of experience with you, I probably shouldn’t introduce real math, but who knows, maybe you will show you can really do it this time. Specific example - if a fatal folding error occurs in 25% of some type of cells, but one healthy cell is successful in splitting into two cells, which then each split into two more cells, etc, what is the chance that the lineage will be terminated due to the occurrence of the error? (I will venture to guess that 25% fatal errors in protein folding in a cell is wildly more frequent than is the norm in most living cells.)
ThePhy said:
I do not see the point of your request. Are you saying that there is a 25% probability of error in a single protein or does this apply to all the proteins in the cell involved in the "splitting" of the cell into two cells? If the latter then considering that there may be several thousand proteins involved in a cell then only a 25% probability that just one of them will sustain some type of folding malfunction would seem to be a fairly high level of fidelity in replication.
In any case I have no idea how one would approach an answer to such a problem, since not all folding problems are necessarily fatal to the organism, just as the loss of a single protein is not necessarily fatal either.
However, I think that it is clear that at some level of breakdown of fidelity in the "splitting" process of cell replication that extinction of the line will occur.
Mature Muscle Stem Cells Can Make Blood 12/11/2001
Nature Science Update is reporting that mature muscle cells in mice have stem cells that can migrate to form blood cells, then come back and make more muscle, an “amazing thing,” according to the University of Pittsburgh researchers who reported to the American Society for Cell Biology. They weren’t even looking for stem cells in the muscle tissue. Helen Blau at Stanford says, “It shows that cells can go in many different directions given the right environment.” She believes the traditional view that stem cells permanently lose their ability to produce other cell types is changing. Others argue that research on embryonic stem cells should continue.
More and more discoveries are taking the wind out of the sails of those who advocate tinkering with human embryos for medical progress. This is a highly charged ethical drama worth watching. If embryonic stem cell researchers can no longer claim it’s the only way to get the totipotent cells, will they have a case for continuing at all?
Nature Science Update is reporting that mature muscle cells in mice have stem cells that can migrate to form blood cells, then come back and make more muscle, an “amazing thing,” according to the University of Pittsburgh researchers who reported to the American Society for Cell Biology. They weren’t even looking for stem cells in the muscle tissue. Helen Blau at Stanford says, “It shows that cells can go in many different directions given the right environment.” She believes the traditional view that stem cells permanently lose their ability to produce other cell types is changing. Others argue that research on embryonic stem cells should continue.
More and more discoveries are taking the wind out of the sails of those who advocate tinkering with human embryos for medical progress. This is a highly charged ethical drama worth watching. If embryonic stem cell researchers can no longer claim it’s the only way to get the totipotent cells, will they have a case for continuing at all?
25% chance that of all the proteins in the cell, one critical protein will misfold, killing the cell.bob b said:
Keep it simple – assume that that chance of a fatal protein (fatal to the cell) fold error in any one of the cells in question is 25%.
But that is the point. You are finding it necessary to impose a condition the original article never imposed, that there is a high enough breakdown of fidelity that the cells will all die out. The article never made any such stipulation, instead it carefully planted the idea in the mind of the casual reader that cells without repair abilities could not last.
Just use the 25% chance that a cell will be killed by a misfolded protein. You may not know how to work out the exact odds of the extinction of the cell line. So change it to this mathematically similar problem. Go to Las Vegas with $1. Bet, it with the return being a sure $2, except each of those 2 one-dollar bills has a 1 in 4 chance of being counterfeit, and you have to throw it away. The genuine ones you play again. Is it likely that you are going broke? I would seriously question the mathematical competence of any engineer involved in orbital mechanics who couldn’t at least qualitatively handle this question. Come on Bob, you can do it.
I am trying to see if there is a rational answer to the question in your OP:
I claim it is perfectly possible for many types of cells to multiply sans such a mechanism. If over the evolutionary history of a cell it developed folding repair mechanisms, then natural selection would select for the retention of such mechanisms. Sounds like classic evolution to me.
On a broader note, having just taken the time to read carefully a few more of your posts in this thread, I find them kind of interesting. It seems each on is started by a brief unbiased description of an interesting aspect of cell biology, but then each one is supplemented by a couple of lines of typical creationist spin-doctoring drivel – just like the identification of molecules as brainless and blind. But it plays well to ignorant folk.
And the sum total of the proof you have offered under direct questions – is for you to (once again) run like a scared jackrabbit from the simple math. Aerospace systems engineer? Hah, bad, really bad joke.bob b said:
I gave you the specific scenario to address the claim. You are the one who is too cowardly (or incompetent) to give answer to it.Go ahead and support your claim, if you can.
So now the status of the creationist claims in his OP – 1) Childish silliness in portraying molecules a brainless and blind, and 2) Broad claims about the viability of cells that didn’t have protein repair mechanisms, claims that the bob b can’t defend without adding new conditions to, an then resorts to his oft-used tactic of ignoring everything that was said that he can’t handle.
Maybe we should go back to vectors and Joshua’s long day. Bob b has had a year or so to learn what vectors are, maybe he can defend that thread now.
Why is it that Bob b is primarily active in commenting on evolution - a field in which he has no technical or educational experience, and even there he limits himself to the safety of “Nobody in their right mind would believe that” type generalities? I just wish he would wander more often into the world of astronomy and physics. I need to play with him too.