I watched it once and didn’t see anything objectively false. I’m sure it’s there. I doubt it matters.
Everything and nothing.
That’s a childish question. An animation is just a kind of visualization, no different in principle from a graph or a schematic. None of those things should be “substituted” for evidence but to single out animation is pretty silly and to even ask the question is to treat an audience like a child. I’ll grant that there are people who post at PS who behave and think like children but that question is embarrassingly dumb.
The importance of crowding in protein folding is of particular interest in biophysics. Here, the crowding effect can accelerate the folding process, since a compact folded protein will occupy less volume than an unfolded protein chain. However, crowding can reduce the yield of correctly folded protein by increasing protein aggregation. Crowding may also increase the effectiveness of chaperone proteins such as GroEL in the cell, which could counteract this reduction in folding efficiency. It has also been shown that macromolecular crowding affects protein-folding dynamics as well as overall protein shape where distinct conformational changes are accompanied by secondary structure alterations implying that crowding-induced shape changes may be important for protein function and malfunction in vivo.
This phenomenon is very important to undrestand the evolution of protein-protein binding and interfaces. It turns out that in the extremely crowded intracellular space, proteins are effectively squeezed up against each other all the time, so that any given protein will always exhibit some weak level of association with it’s neighbors. The effect of the phenomenon is so strong that there is actually evidence that many proteins show signs of negative selection against these intrinsic aggregation propensities:
Proteins are central components of almost all biological processes, being involved in a variety of complex interactions in the crowded cellular environment . The establishment of non-functional protein–protein interactions has a detrimental impact on cell fitness, both because these contacts sequester proteins into inactive complexes  and because it can lead to the aggregation or co-aggregation of proteins into toxic soluble and insoluble assemblies . Importantly, it is increasingly evident that, instead of being an unusual feature of a reduced set of proteins, aggregation is a generic property of many polypeptides . Accordingly, hundreds of unrelated proteins have been reported to aggregate under stress or during ageing [5,6,7]. It has been suggested that this intrinsic propensity to establish anomalous interactions and aggregate is encoded in the amino acid sequence [8,9,10] and, therefore, a variety of complementary methods have been developed to predict those propensities from the linear sequence . Large-scale analysis using these algorithms has led to the hypothesis that proteins have evolved sequence adaptations to counteract their natural propensity to aggregate [12,13,14]. Because in these studies aggregation is analysed along sequences, they mostly measure the aggregation potential of the unfolded state; indeed, the aggregation-prone regions (APRs) that these algorithms identify and evaluate are blocked in properly folded proteins, either because they are buried inside the hydrophobic core or engaged in the series of cooperative non-covalent interactions that sustain the secondary and tertiary protein structure . These sticky sequences might, however, become accessible in case the protein fails to fold due to translational errors. Accordingly, prevention of mistranslation-induced protein misfolding is thought to constraint the evolution of sequences [16,17]. However, it is worth to point out that protein aggregation is not always deleterious and different organisms have exploited the structural/mechanical properties of protein aggregates for functional purposes [18,19].
This unique attribute of the intracellular space largely turns the whole issue of the evolution of protein-protein binding around on it’s head. Rather than developing strong and specific associations between different proteins constituting some sort of difficult barrier to evolution, the whole system seems to exhibit some tendency for protein-protein associations between proteins to be the default state of affairs.
When it comes to correctly depicting some intracellular process in terms of an animation, I don’t really think animators have much of a choice. If they were to try to accurately animate what is going on inside a cell, we wouldn’t be able to see what they are trying to show, it would all be just a thick soup of macromolecules in solution obscuring our view of whatever it is animators want us to see.
IMO, nothing serious, at least for teaching about the dynamics of the protein.
The kinesin protein appears to move like regular human machines. If an ID supporter sees this, he/she says, oh wow that’s beautifully designed. But when they see an animation of a tumor cell or HIV particle doing it wonders, with the same level of apparent purposefulness, most of them don’t come to the conclusion that they were intelligently designed.
Animations are just visualization tools. They are excellent for teaching, but too much should not be read into them, as they do not always fully reflect the actual systems they model.
How could you have an informed opinion if you don’t know?
The experiments demonstrating the falsehood of this representation tended to be lead articles in Nature, and they formed a major part of the work that earned a Lasker for two of the field’s leaders. The missing attribute is literally the 4-word title of a Nature News and Views article.
So I guess some people don’t agree with you and did not doubt that it matters. I find it odd that this would not interest someone with an interest, however ill-defined, in design.
Back in 2006, the folks at Uncommon Descent touted the animation itself as evidence of design. Bill Dembski got in legal trouble for using it without permission.
At Telic Thoughts, a couple of commenters who pointed out this problem were shouted down, including a flat-out lie that the omitted phenomenon never happens.
I would say that in principle, animations have much more potential for convincing and misleading laypeople. This animation became a staple of Dembski’s talks.
Yet I’m sure that many here would answer it affirmatively.
You’d have to know what’s wrong with it to make an informed judgment.
That’s a problem too, but the more fundamental problem with the animation I posted is about how these motors work, which is in turn consistent with their evolutionary origin.
It’s not at all intuitive.
In the case of crowding, yes. In the video I linked to, that wouldn’t apply at all to the most important of the missing attributes. It would have required mere seconds to include.
I’d say that if you started from the assumption that this animation correctly depicts the dynamics, you would never have conceived of the experiments that show the assumption to be false.
I agree–like a designed machine. The biophysical data indicate that it does not, and those data fit beautifully with its ancestry.
Hey, I once saw an animation that depicted intracellular transport literally using little spaceships shuttling “building blocks” around to be consumed by actual man-made factories that had prototypical robotic arms.
Can’t find the video now but it basically looked like this:
This is Fig. 6D from this report, showing the density of ribosomes in E. coli. The situation is similar in eukaryotic cells (if anything, even more crowded, what with ribosomes and many different phase-separated “organelles” and other compartments).
You did not understand my comment. I wasn’t arguing that cancer disproves intelligent design, I was arguing that the way tumor cells operate makes it appear like they are intelligently designed, but ID proponents don’t arrive at that conclusion. In contrast, when they see (the discredited) animation of kinesin, they immediately conclude it was designed. This is ironic considering that tumorigenesis is way more complex than the molecular mechanism of kinesin action.
What about HIV, was it designed? If you say no, please indicate how you can tell apart what is designed from what is not designed. Also note that if you affirm that HIV is not intelligently designed, then you have conceded to the claim that natural processes can fashion complex systems (like HIV and it’s life cycle).
Skimming through the ENV article you linked, I saw certain points I disagreed with, and I think @swamidass has responded to it.
Have you seen them quoted denying the design of cancer?
I think this confuses function and design. I can design a chair, but if books are set on it, or a leg breaks, it is still designed, even if it now is functioning like a table or has lost its function all together.
Yes, it is designed. Separate questions are - why was it designed, what was its original design, and has its function changed from the original design? Those questions may or may not be able to be answered by science. Science probably cannot answer the first one. Science can obviously confirm its function in the present.
If Wells is representative of the ID community on this, then its obvious they don’t regard cancer as being intelligently designed, but a perversion of existing design.
We have to ask how you and other ID proponents know that cancer wasn’t intelligently designed by the mysterious designer? What if cancer is a kill switch mechanism put in multicellular organisms by this designer? How can you rule out these claims?
Chairs and tables are consciously designed by humans to carry weights, whether those weights comes from a person or pile of books, so if a table or chair breaks, we know its original function has been compromised.
We have no example of conscious design in biology. Its all blind and unguided. The burden of proof is on you to pick any biological system and tell us how you know its current function was set by a designer, otherwise you will be making baseless claims.
Again how do you know?
This questions are irrelevant until you determine if HIV was intelligently designed.
Sorry science says its had no default function, because there is no evidence to even think it had any in the first place. In addition, HIV isn’t like a table or chair, it’s a quasi-organism. AFAIK, organisms don’t have any pre-specified function, or do you think lions and cheetahs had original functions too? If yes, what were they and how do you know?
It is somewhat nonsensical to believe organisms come with pre-specified functions, but if you believe HIV had an ancient function which got distorted, you must tell us how you know it had that original function in the first place? Failure to demonstrate this would place you in the same category as homeopaths who can’t demonstrate water has memory.
I recall this animation and the controversy it stirred when someone in ID plagiarized it. What is false is the manner it is presented, with almost anthropomorphic “walking” forwards. A more realistic animation (and there is one, somewhere) shows a much more random progression.
Extremely useful. Picturing the flow of electrons through the electron transport chain from the static images in my biochemistry textbook was quite difficult, until I saw this cool animation of the process.
Thanks to John though, I now realize one has to be a bit skeptical about what the animation presents until you are sure it’s evidence-based.
If you go deeper into these motors, you’ll see that the more accurate metaphor is that they are ratchets that harness Brownian motion.
If you apply this to the metaphor of human walking, it would be as if you are only capable of lifting your foot off the ground, then only making it somewhat more likely that the wind will blow your foot in the direction you intend to go.
Sure. Kinesins, myosins, and G proteins all have a common ancestor. The ATP hydrolysis nonintuitively causes the motor domain to release from the substrate. This is completely bonkers if you’re thinking of human-designed motors in which burning the fuel produces the force to move forward.
Both hydrolysis and the release of the product ADP induce conformational changes in the motor domain, which to show that all metaphors eventually fail, is called a head but looks more like a foot in these animations. The neck and tail is basically a long lever added to that ATPase core.
What that conformational change does is merely create a bias that makes the next step more likely to be forward than backward. The ratio of forward to backward steps is altered by changing the load on the motor–the cargoes in these animations and in vivo, or a laser trap in the lab.
The product of bombardment by Brownian motion coupled with this bias is a step. That’s the source of the incredible energy efficiency of these motors, which is, of course, load dependent.