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What are the lifetimes of cellular components on organelle or molecular level?
I was thinking that even though I know how generally the cell works, I don't really have a feeling of how volatile it is.
I want to know what is the lifetime/turnover rate of different constituents of the cell.
On the molecular level what are the lifetimes for various proteins, for ribosome, lipids, carbohydrates, DNA and RNA. What about aminoacids, nucleotides?
On the organelle level what are the lifetimes of the mitochondria, golgi apparatus. Does nucleus or ER ever change if not during meiosis.
I understand that the lifetime depends on the context. For example, for DNA, cells that replicate, half-life is about one replication as a whole new strand is generated. In neurons, that don't replicate for decades it's not the case. But the DNA can't just sit there. It is constantly unraveled, transcribed, damaged and repaired. So it has a different time constant.
I am still very interested to know any specific numbers.

Your question has several parts to it so I will attempt to address them one-by-one.
In terms of protein stability and turnover, this is a nice paper describing how human cell (HeLa) line, although this is a cancerous cell line, is used to measure the turnover of proteins (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316722/?report=classic). They have used labelled amino acid technique and mass spectrometry (SILAC) to make measurements of protein turnover. It is concluded that on average the turnover is 20 hours, which is correct in my experience when doing gene knockdowns in Drosophila (S2) cells using RNAis as we incubate the RNAi with cells for 72 hours to ensure most proteins that we targeting are degraded and we can see the desired effects in cells.
Now getting to your questions regarding organelle turnover, you have to consider that cellular organells are very precious to the cells as most of them consume a lot of energy to build hence they are maintained unless they suffer critical damage, and they would become detrimental to the cellular integrity. In that case organells such as mitochondria undergo a specific type of degradation called mitophagy, which is a subtype of autophagy. Now I'm sure there are specific average times for the so called turn-over of cellular organelle under "normal" conditions but thats a slightly misleading view since the turnover can be tipped through reactive oxygen species (ROS) or ageing leading to less efficient cellular maintenance and buildup of toxic aggregated proteins or ROS.
Now just to clarify the use of the word half-life in you last paragraph, half-life normally refers to the time it takes for half the molecules in a given system to degrade (or to be more correct Half-life is the amount of time required for a quantity to fall to half its value as measured at the beginning of the time period) so I do not agree with your use of the word half-life in the last paragraph of above question although human DNA does have a replication limit (Hayflick limit) of roughly 40-60 due to telomer shortening and afterwards the cells (due to the DNA) that no longer replicates will enter senescence and eventually die.
Now getting to non-replicating, highly differentiated cells such as neurons, it still remains a mystery as to how neuronal DNA remains so highly stable (although DNA is a highly stable molecule (compared to RNA) and its further stabilised through histones), while undergoing many dynamic processes such as transcription (since if anything goes wrong the cells cannot be replaced at least in CNS) and how axons of some neurone that can reach over a meter in length are maintained so well for decades. There is a lively argument amongst the scientific community about this, which you can find out about if you simply search for axonal maintenance in a search engine.
Hope this answers some of your questions.

I agree that the DNA doesn't degrade per se, so in that sense half-life is the wrong word. What I meant was some temporal metric of its change from the original. If we look on one DNA, during replication it looses one half and a new one is attached. In that sense half of the DNA is no longer the same. So half of it has changed in one replication. After the second replication we will either with probability one half exchange the second old half, or the new one. I have calculated and on average it takes 3 divisions for the DNA to change.

In PCR based plasmid replication it is different, and more in line with your description, since primers are used and after annealing and amplification, you get denaturation, and the cycle continues so the original strand gets matched against new ones many times so you get a dilution effect of the original stand v.s the newly synthesised strands.

I am pretty confused now. http://en.wikipedia.org/wiki/DNA_replication#mediaviewer/File:DNA_replication_en.svg             Doesn't this show that DNA stays with its new strand?

Apologies, my bad. You are correct, it is a semi-conservative replication in cells so I see your point!

I was thinking of RNA pol and I confused myself and you. Sorry.


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How are individual neuron firing rates characterized?
I'm reading this paper that the Human Brain Project published in Cell and I'm confused how they recorded the firing rates shown in the firing below:

In the publication, they mention that they use the Petilla convention. However, upon reviewing that publication, I was unable to determine the procedure of characterising neuronal firing rates. How are they able to isolate a neuron's firing behaviour away from the network it is usually contained in? Where do they measure the outputted firing rate?
I am aware that usually to characterize a neuron in a network, Spike Sorting or single-neuron recording can be used, however this doesn't seem like a valid way to characterize the physiological properties of an individual neuron.
If you consult the experimental procedures section of the paper, you can find that they used methods previously established in three papers. However, upon reviewing these papers, it appears that the neurons were stimulated while still inside the tissue, but after the tissue had been sliced. However, this seems so absurd that I must be misreading it.
How were the electrophysiological properties of these neurons characterised?

However, upon reviewing these papers, it appears that the neurons were
  stimulated while still inside the tissue, but after the tissue had
  been sliced. However, this seems so absurd that I must be misreading
  it.

You're not misreading it. I can't access the paper you refer to, but this is a standard way to measure the electrophysiological properties of individual neurons, and has been for more than 25 years. (I'm really curious what you find "so absurd" about this).
I'll take an educated guess (since I can't read the methods online) that these recordings are from rats (or possibly mice), using whole cell patch clamp technique in thin slices of the young rat neocortex. Briefly put: the animal is sacrificed, the brain is removed, it is sliced into about 400 micron thin slices using a vibrating razor blade, and the slices are kept in a artificial cerebrospinal solution that allows the neurons to remain functional for a day's worth of experiments. Then individual neurons are imaged under a microscope and "patched onto" with a glass micropipette that contains a silver wire. Electrical events in the neuron can thereby be recorded into one's computer and plotted as shown in the figure you provided.
In this case, what's shown are what are known as current clamp recordings, in which current is injected into a neuron and the resulting voltage changes are recorded. Here, they are injecting a depolarizing current to make the neurons spike (have action potentials) and seeing that the neurons they sampled vary in their spiking properties. Some are fast spiking, some are slower spiking, some have different spike waveforms or patterns of spiking.

"absurd" was a bit of a strong word. I really just meant to say that if the measurements are taken while the neuron is still connected to other neurons, how do they know the spiking pattern is due to the neurophysiological properties of the neuron and not because of the neuron's placement in the network?

Also, why are you unable to read the methods online? I think all the papers are free.

@Seanny123 1st question: they could do these recordings in a pharmacological blockade of excitatory synaptic transmission to eliminate any spontaneous excitatory drive from the network (Did they?). 2nd question: No, it's behind a paywall for me ("To view the full text, please login as a subscribed user or purchase a subscription."). Maybe you're accessing it from on a campus that has a subscription to Science Direct, or something like that?

Could you email me or tweet me so I can send you the papers?

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Correlation between genetic distance and birth defects
It is folk knowledge that in-breeding causes birth defects due to similarity of genetics between parents. Consequently, is there a similar correlation between genetic distance of parents and probability of birth defects?
The best reference I can find of this is this handout by the Australian Centre for Genetics Education which says:

If parents are unrelated, their chance of having a child with a birth
  defect or disability is between 2% and 3%.
If parents are first cousins, the chance is a little higher at 5% to
  6%. This is due to the increased chance that they will both carry the
  same autosomal recessive mutation, passed down through the family.

However this doesn't talk about genetic distance in particular.
This question is really just a more specific version focused on a single metric (genetic distance) and outcome (birth defects) of two previously answered questions:

Genetic pros or consequences of children born to parents of mixed nationalities?
Does it make sense to classify all humans in a single species?

Are you looking for any evidence of the effect of inbreeding on fitness? Are you specifically interested in humans? What is your goal? Are you trying to estimate something specific such as the number of lethal equivalents of inbreeding for example, or are you just looking for any reference showing evidence of inbreeding depression to cite?

@Remi.b yes, I am specifically interested in humans, as per the tag. I'm looking for any evidence that can show a correlation between genetic distance and "inbreeding depression". Although, I must admit I had not heard of the term "inbreeding depression" until now and am embarrassed by this.

It depends how much the source populations share the same defects. If chinese and euro villages parents both had high prevalence of clubfoot, they would have worse outcome than close source parents. ... besides, an Italian village of 400 people genetics was studied because they have the lowest heart problem percentage in europe. They found that nearly all the village was inbred from 2 ancestors. they were all similar and healthy. Secondly, another study found that cousins breeding is about as troubled as late motherhood at the age of 38 onwards, i.e. having one after 38 is as good as a cuzin.

For humans the closest argument may come from observational studies (since experiments aren't possible due to ethical reasons).
One example for the correlation of genetic distance and "defects" comes from a recent study of Chagnon et al. PNAS, 2017 http://www.pnas.org/content/114/13/E2590.full . Rather than asking for birth defects directly they however survey the number of children, and survival of children to age 15 (which would be one example of the term "inbreeding depression" that is more general than "birth defects")
Note that their study also sheds some light on the underlying big question, why certain types of kin relationships can be common despite their effect on the creation of healthy offspring - and why certain types of cousin relations are different from others.

I was hoping to extend the level of observation to an even larger dataset/population. Is there reasons why this dataset wouldn't exist?

Suggestions, if want to look for large dataset: check Danish statistics, as Denmark has good records for several generations and is thus a model system for population-wide studies of health (note: kin relations will be unusual - nowadays). Since question relates to a phenomenon that isn't that exciting to contemporary research, but would seem to fit the 20ies-60ies, and large scale studies tend to get many citations: Look for old reference in the paper mentioned above. Search for reference in google scholar, select citing paper with most citations -> look at oldest reference --> iterate

Legit. Currently don't have the motivation to make the time to do that, but that's my problem.

ad larger dataset/population: Being able to observe something within a small population makes an even stronger argument than something that is only seen in large populations (since it effect size must be relatively large)

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Evolutionary reasoning behind redundancy of CST and RuST
According to my neuro-anatomy class, both the Corsticospinal Tract (CST) and the Rubrospinal Tract (RuST) control upper limb movement. What the evolutionary reasoning behind this redundancy and the fact that the RuST is much more important in non-human primates when compared to humans?

@Susan thanks for the suggestion, I've edited my question


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How well does the event-driven DVS sensor approximate the rods of the retina?
There is a neuromorphic vision sensor that is generating some interesting research these days that is called the Dynamic Vision Sensor. One of the claims of this sensor is good approximation of the conventional retina. However, there's no detail on the website in what way this is true or to what degree this is true.
It does not detect colour, so obviously it isn't an accurate approximation of the cones found in the retina. Additionally, the function of the cornea is fulfilled by the lens of the camera, so this input isn't totally approximated. Consequently, the only significant component that remains to be evaluated is the rods of the retina?
What are the similarities and differences between a retina and the DVS sensor?
First, let me save you some reading by explaining how the DVS sensor is different from a typical camera. Instead of synchronously sending frames with data about every pixel, the DVS is event driven. That means, when a light intensity change occurs, an event is fired with the address of that change, a time-stamp and whether the pixel observed an increase or a decrease.
Do rods also encode changes in light intensity in the same manner? If not, what is the difference?


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Trade-offs between phage and yeast displays?
If you wanted to test a peptide you designed, you can do a phage display or a yeast display experiment to assess binding affinity.
What are the trade-offs between these two methods?
I've heard anecdotally that yeast display is more sensitive and closer to human cells?

According to Creative Biolabs, the primary differences are:

In the screening/panning step, yeast display is suitable for Fluorescence Activated Cell Sorting (FACS), allowing to sort out antibodies with desired binding properties
precisely. However, the affinity of antibodies to antigens in phage
display can only be roughly stratified (sorted into categories of goodness) by adjusting the washing buffer
compositions.

Owing to its eukaryotic expression system, yeast displayed antibodies can be correctly folded and modified, such as [...] to be closer to their native structure in mammals
compared to the antibodies expressed by E.coli in phage display.

The diversity of yeast displayed antibodies may be lower than phage (107-109 for yeast, up to 1011 for phage), due to the low
transformation efficiency of yeast.

Due to the many more copies of antibody on yeast surface (104-105) than phage, it is possible to select out low affinity antibodies
according to antibody avidity with yeast display system.

Anecdotally, phage display is also cheaper.

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Soma-soma paired neurons
I'm reading this paper about how neurons can connect. Wikipedia says, typically neurons connect via axon (transmitter) and dendrites (receiver) but there are also special cases where dendrites connect with dendrites, axons with with another axon, neurons with no axon etc.
Now in the paper they refer to the soma-soma paired neurons and their strength of their cholinergic synapse.
Does that now mean that they neurons do directly interact via their soma? If so, how much different is that process to the generic axon->dendrite pathway?

Just for completeness: not all neurons connect to another neuron :)

Yep, the soma-soma synapse in that paper appears to be a chemical synapse between two cell bodies. There are no axons or dendrites in that preparation so the synapse must be between the somas. They are using two snail neurons that are far from each other (in different ganglia) in vivo, but which are known to synapse. This in vivo synapse is long-range and so must be mediated by an axon. In the dish, they can encourage the  synapse to form even without encouraging axons and dendrites to grow.
Note that this is an artificial in vitro preparation and they are, in some sense, forcing a synapse to occur in an unusual way in a cell culture dish. They do this because it makes it easy to study certain aspects of the signalling mechanisms for generating synapses. In your paper, they appear to be using it as an easy preparation for a proof of principle for the interface between a biological neuron and a non-biological semiconductor substrate.
The paper you cited references this paper that outlines the soma-soma preparation with a pretty picture to make things clear: http://www.jneurosci.org/content/19/21/9306

With 'preparation' you mean something like the 'setup'? So they prepare the cells in that manner?
Thanks for the answer, will read that paper! Cheers

Exactly right, they prepare (or setup) the cells in a particular way so that they can study them later. For instance, here they are removing the neurons from the snail and putting them together in a dish. Then they add a solution that encourages the synapse to form. As you might imagine, any given preparation will be good for investigating some things but bad for other things. A major part of experimental design in biology is choosing the right "preparation."


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How do we know that everybody's DNA fingerprint is unique?
How do we know that everybody's DNA fingerprint is unique?
I know, I know, everybody's DNA is unique.
But when we do DNA fingerprinting, we're looking at very specific regions of high variability.
How do we know that just by chance, two people's DNA could be the exact same in the spot(s) we're observing.
With real fingerprints, uniqueness is (almost) guaranteed (I believe it's a 1 in 64 billion chance) because they are developed by physical stresses on the fetus in the womb.
Is there any similar mechanism/affect that acts on these non-coding/highly variable sections of DNA?
Thanks!
evamvid

Yes, the fact that they are highly variable. I don't have the numbers at hand but while it is theoretically possible for two DNA fingerprints to be identical, I would expect a similar or smaller probability of this than for "real" (let's call them digital) fingerprints.

@terdon one meaning of the word digit is finger :)

@user13107 yes, that's why I used it.

Essentially, for the same reason we "know" that no one is going to be struck by lightning 100 times. It is possible but highly unlikely.

First, remember that identical twins actually have the same genotype. So its not exactly true that everyone has a unique genome.
But to get at the heart of it, you're asking how I can be sure that I have a different genome than you, or even than say my brother. And moreover you're asking how these differences are obvious enough that they can be detected without whole genome sequencing.
The answer is that there is no mechanism to ensure differences, but that the differences arise from the enormous variability of our genome. Look at the major histocompatibility complex, or MHC, a cluster of genes that affect our immune system.
Just to simplify things, lets focus in on four genes in this cluster: HLA-A, HLA-B, HLA-C and HLA-DRB1. According to this site there are 2579, 3285, 2133 and 1411 alleles for each, respectively. If we make a naive assumption that each of us received a random assortment of these genes, that makes 2579 x 3285 x 2133 x 1411 = 25,549,791,000,000 possible combinations. The chance that we both have the same combination is then about 1 in 25 trillion, just considering 4 genes.
But wait, you say, surely some of these genes are not equally likely and surely they segregate together, making this chance much smaller. You would be right. But this consideration stops mattering very much when you account for the rest of the variable regions. They combine multiplicatively, so considering a fifth gene with only 2 possible alleles brings the possible combinations to 50 trillion.
If you consider just a few more genes, the numbers get unthinkably high. This pretty much ensures that, even considering a small sequence, we can be sure that the genetic fingerprint is unique.

That said, you would need to compare one very large number to another to evaluate overall uniqueness. For example, although there are only 6 or so billion people in the world (i.e., approximately 10^9), The relevant divisor for overall uniqueness would be the number of possible pairwise comparisons between people (e.g., around 10^17; which is much larger than a trillion).

Identical twins don't have identical genotypes.  They have very similar genotypes, but there will typically be a few dozen base pairs that differ due to mutations.  These usually won't be in the regions used for DNA fingerprinting, though, and will require full-genome sequencing to spot.  A complicating factor is that the error rate for sequencing is similar to the mutation rate, so you 'll need to sequence multiple times to be sure you're seeing the actual mutations.

Thats not true. Twins do not have exactly the same genotype, since they occured some individual variations. Its possible though, that the standards used for genetic fingerprinting in crime scenes is not precise enough to differentiate twins. This has happened in Germany and led to the release of a subject from prison as he couldn't be distinguished from his twin brother. With more test points (which was not allowed at this time) the differentiation woud have been possible.

Possibly partly offtopic, but I'd like to add that when using dna fingerprint as evidence of identity in a legal investigation, the odds become smaller due to combination of human factors and reduced accuracy. There is the twin issue already mentioned, but in addition there are laboratory errors and the possibility of contamination with other evidence. Samples may be damaged in other ways as well, and dna samples can be planted.
In the analysis done by Jonathan Koehler, it was found that around 1.2% of tests used in this context gave out an incorrect match. Additionally, in this other study by him it was found that the way results are presented has a considerable impact as well.


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Bacterial Conjugation/Horizontal Gene Transfer -- how does the plasmid exchange work?
So according to a PPT I'm reading, bacterial conjugation works by the two bacteria joining pili and exchanging plasmids. So how exactly do the plasmids get across the gap? If I understand this correctly, the pili are little hair-like things on the outside of the bacteria -- so unless the plasmids were actually able to somehow be pushed through the pili, there would be gap. Right?
The only other possibility I can think of would be that the membranes fused or something like that. But that comes with it's own whole set of problems.
How does this work?
Thanks!
evamvid

The donor cell retracts it pilus upon contact with another cell and both cells form a pore between the two cells, which allows the transfer of DNA.
Take a look at the image, I think this makes it clearer (from the Wikipedia article on Pili):

This has even be seen in an electron microscope:


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Is it impossible for a retrovirus to be lysogenic?
Is it impossible for retroviruses to be lysogenic? In the lysogenic cycle, the viral genetic material is incorporated into the host cell's DNA. Because retroviruses have RNA, it would be impossible for their genetic material to be incorporated into the host cell's DNA, unless the RNA is reverse-transcribed or something.
Is this the case? How does this work?
Thanks!
evamvid

Sorry! I phrased the question completely wrong -- I managed to confuse myself with my own question!

Both things are not exclusive of each other. Retroviruses are RNA-based viruses which need to reverse transcribe their RNA genome into DNA before they can multiply. This is done by the reverse transcriptase enzyme, which is part of the virus and is incorporated into the cell.
Once the reverse transcriptase has been active and made the DNA, this DNA can also be incorporated into the hosts genome. If you look into the Wikipedia article on Bacteriophages, you will find a list of different bacteriophages, with all kind of genomes, among them as well a number of RNA-based viruses.
RNA-based viruses which enter the lysogenic pathway are obviously either pretty rare or they haven't been discovered yet in bigger numbers. Two examples are the phages F2 and MS2 (which are closely related).

Are there any RNA phages that exhibit lysogeny?

Yes, there are a few. I added two references.


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Systematic anticoagulant injection after a CVA
Since most of the cerebrovascular accident are ischemic ones, would it be usefull to have anticoagulant everywhere (we already have  AEDs everywhere) so that everytime someone would have symptoms of a CVA we would be able to destroy the blood clot before any permanent damage to occur ?
On the other hand may it make the case of ruptured aneurysm getting worse ?
So what are the potential negative and positive effect of such a policy ?

I think it would be useful to rephrase this to ask for the potential positive and negative effects of anticoagulants. Right now the question is close to primarily opinion-based.


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How can TMS induce enough depolarization to cause an action potential?
Creating an action potential needs at least tens of mV potential difference across the membrane to occur.
But the membrane is really thin, surely less then 0.01µm (some reference give 25A).
Then the potential gradient, that is to say the electric field E, must be very strong :
The order of magnitude of the needed electric field is much greater than 10mV/0.01µm = $10^{6}$ V/m
But TMS produces E of the order of 200 V/m on the scalp, which is even less inside the brain. Then how can TMS induces neurons depolarization ?

Do you have a reference for those TMS numbers? I found here that computed field is even less, on the order of 1 V/m

http://cntrics.ucdavis.edu/c2meeting1/talks/Lisanby.pdf

my guess is that TMS is used to depolarize myelinated axons (white matter). They are thicker (up to 20um) so that required field is on order of 100s $V/m$, not $10^6V/m$. And here TMS fields are noted at 500V/m level

That would make sense

And by "depolarize" I mean that you don't explicitly cause action potential to fire (like cortical electrodes do), but rather increase excitability of the region. Does that make sense?

No I wanted to say depolarize enough to provoke an action potential

In fact I'm not sure the myelin explanation can work since an action potential can only be created at Ranvier nodes

I think my mistake was to believe that the electric field has to be somewhat perpendicular to the membrane, so that it can directly apply a voltage difference across the membrane, and that the resistance inside and outside the axon was the same, so that a tangential field was useless.
In fact these are false : depolarization and action potential creation happen where the axon is parallel to the electric field and where the gradient of the tangent field is the bigger.
Here you have a complete explanation but I think we can make a simplified one :
http://stbb.nichd.nih.gov/pdf/Nerve_Fiber_Stimulation_Model.pdf
Let's look at a membrane model (Hodgkin-Huxley) :

As we said if we try to apply an electric field $\vec{E}$ along $\vec{y}$ , it should be incredibly strong to produce a trans-membrane potential $V$ strong enough to create an action potential.
In between the inside an the outside of the membrane you have all the channels and the capacitance of the membrane. but I think the crux of the matter here are the resistances inside and outside : the small surface of a section of axon limits the conductivity, whereas the outside is supposed to be bigger so that its resistance is negligible.
As a result if you apply a gradient $\frac{dE_{x}}{dx}$ you can create trans-membrane current and potential:
because of the gradient, the fields $E_{1} = E(x)$ and $E_{2} = E(x+\Delta x)$ are different : $E_{2} = E_{1} + \frac{dE_{x}}{dx}\Delta x$.
Then using electricity laws :
$$i_{m} = I_{1} - I_{2}$$
$$i_{1} = -\frac{ E_{1} \Delta x}{R}$$
$$i_{2} = -\frac{ E_{2} \Delta x}{R}$$
then :
$$i_{m} = \frac{\Delta x}{R} (E_{2}-E_{1}) = \frac{\Delta^{2} x}{R} \frac{dE_{x}}{dx}$$
This trans-membrane current will produce a potential across the membrane which will be proportional to $\frac{dE_{x}}{dx}$, electromagnetic stimulations shows that TMS can easily produce gradients strong enough to create actions potential.

authors: Юрий Вольский


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Are there enzymes found in nature or the man made world that can help break down metals?
The title says it all.
Do natural or human engineered enzymes exist that can speed up the break down kitchen utensils, aluminum cans, wires, etc. into small particles or powders?
To be clear I am not talking about chemical transformation (e.g. iron turning to rust).

what do you mean by breakdown of metals ?

Can you clarify your question - what do you mean by breakdown?

I've attempted to clarify my question. Sorry for not being clear enough.

there are no such enzymes..

So you are asking about physical breakdown into particles and not chemical transformation, e.g. iron to rust?

I would say transformation of iron to rust makes the things more fragile and so they more easily break into particles.

@Barbara Sure, but the poster seems to (?) be asking for breakdown of the original substance. Iron -> rust involves a transformation into a different substance.

@fileunderwater yes I am talking about the break down into particles.

+1 for inspiring me.. just think of the economic implications in e.g. recycling-industries.

There are bacteria, which can assist the proces of rust.
"Some sulfate-reducing bacteria produce hydrogen sulfide, which can cause sulfide stress cracking. Acidithiobacillus bacteria produce sulfuric acid; Acidothiobacillus thiooxidans frequently damages sewer pipes. Ferrobacillus ferrooxidans directly oxidizes iron to iron oxides and iron hydroxides; the rusticles forming on RMS Titanic wreck are caused by bacterial activity. Other bacteria produce various acids, both organic and mineral, or ammonia." (http://en.wikipedia.org/wiki/Microbial_corrosion)
As you see, many of these active ingredients, like hydrogen sulfide, sulfuric acid, other acids or ammonia are not enzymes per se, although they are produced by enzymatic processes in bacteria.
Closer to your specification is Ferrobacillus ferrooxidans (synonyms: Acidithiobacillus ferrooxidans, Thiobacillus ferrooxidans, Ferrobacillus sulfooxidans), which directly acts on iron by enzymes associated with the cell membrane:
Valid XHTML http://c431376.r76.cf2.rackcdn.com/18185/fmicb-03-00096-HTML/image_m/fmicb-03-00096-g001.jpg.
Figure 1. Schematic representation of ferrous iron oxidation by the Gram-negative autotrophic acidophile, At. ferrooxidans. Controlled influx of protons is used to generate ATP via the membrane-bound ATP synthetase complex (ATPase). Iron oxidation is mediated by a cytochrome located on the outer membrane and electrons transferred via periplasmic cytochromes and rusticyanin either to a terminal oxidase (“downhill pathway,” indicated in brown text and by **) where they are used to reduce oxygen, or used to reduce NAD+ (“uphill pathway,” indicated red text and by *) in a reaction also driven by the proton motive force across the inner membrane (Bonnefoy and Holmes, 2011). Source: Johnson et al. 2012.

I am actually speaking of just breaking a metal object down into finer particles (powder). Thank you though.

Non-oxidized metals are rarely substrates for enzymes, although they can be used as electron donors in some reactions.
But you are asking about enzymes capable of cleaving metallic bonds without oxidation, and neither can I recall something of this kind, nor can imagine a biological role for such a reaction.

Ok but is it theoretically possible? Could such an enzyme theoretically be engineered?

No, I don't think it's even theoretically possible, because metallic bonds are very strong. Or, otherwise you need an oxidating enzyme to dissolve the metal (this step is difficult, if you want the metal to be direct substrate of the enzyme) and then a reducing enzyme. Such a system is potentially engineerable. May be, someone has a more realistic opinion.

@max, what do you really need to do with your metallic powder ? Or what was the exact argument which induced you to post this question ? The corrosion, even partial, would make metal easier to break into small pieces. That is the way nature will deal with your kitchen utensils, when they are disposed of as waste.

@Barbara I am just simply curious as to what is possible and what is not. The only way I have seen metal break down is via oxidization and I find that quite ugly. Metal powders can be used to create new metal objects. I guess I just want to see if a new technique can be developed to break metal down in a new more elegant way. Do you think it is possible to engineer a new set of enzymes that can achieve this?

I do not feel competent to predict what is possible in principle. I certainly never heard of such biotechnology you are looking for.

@har-wradim you need to think outside the box. Imagine a waste yard of cars.

Yes TMOTTM, exactly


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How does the creative process of Biological Evolution work?
In order for nature to go from microbes to man, there needs to be new information. Where does this new information come from?
It is understood that Evolution basically involves three elements. Natural selection, genetic mutation, and time. The problem for Evolution, is that none of those three elements are creative. Natural selection is basically just a pruning process. It selects from what is there and advantageous, and prunes off what is deleterious to the organism as far as its fitness.
Genetic mutation is just errors in replication. So it creates nothing. It simply degrades. We have no new information, just an erroneous replication, and degradation of what was there before.
That is still true of gene duplication. We have an error that repeats the same information/genes. So we have two copies of something but there is still no new information.
This brings us to the second problem. What mechanism or process of nature/Evolution, carries out the instructions. What I mean by this, is that it essentially has to work like a computer. If I want my computer to have a more advanced program, I need to input new information, and its often codified in the form of say a disk, or installation file.
What is the equivalent of this installation file for Evolution?
For example. Say I'm a cephalopod. And I'm getting environmental pressure from predators and I want, or need, to advance my defenses, so I want to built some spikes on a hard outer shell. Where does the cephalopod get the new information, or rather, instructions, to know how to do this new feature?

Please do not downvote questions because they disagree with our views. This is a fair question, despite being a little bit to close to a rant. The arguments presented are wrong, yes, but that is a reason to answer, and explain to the OP using arguments, not to downvote. We should welcome this type of question and do our best to answer it well.

The last comment was not directed at you, but to the regulars of the site. However, you might be interested in these: How does the modern theory of evolution solve these apparent problems?, How does evolution produce complex organs and Human evolution: Where *exactly* did the first human come from, whose parents were not? among other Q&As on the site.

But this question is not simply misconceived- it is not even wrong! I'd make the argument that this question is not well formed, nor do I see the possibility for a constructive outcome because OPs premise is wildly ignorant. Check OP's other questions- every one is a a variation on the same theme. None are useful and none are resolved. This is question is simply persistent noise.

@adamwong246 that's irrelevant. Remember that the SE sites are wikis and the information we give should not be aimed at the OP alone. The basic misconceptions here can be addressed, I've tried to do so in my answer. As I'm sure you know creationist and ID arguments tend to be ridiculously easy to shoot down, just like this one is. We should welcome the chance to do so in the hope that we might increase the understanding, if not of the OP, then of the next poor misguided soul who has fallen under the influence of pseudoscience.

Perhaps this should be moved to a meta-discussion but is there really a hope that OP will ever select one of the following answers as correct? I'm not optimistic.

@adamwong246 again, that's completely besides the point. The Q&As here are not only for the OP and this is the same for all sites on the SE network. We aim to be a repository of useful information.

@terdon I don't see a problem with downvoting this Q, but it should clearly not be done because of disagreement. However, this Q completely lacks background research (both from BioSE and basic biology), is mostly phrased as a personal trail-of-thought, and the poster has clearly not bothered to look up the basics of evolutionary theory - also see How do I ask a good question. I don't think the Q should be closed, but it is still not a good Q.

Creationism is off-topic on Biology SE.

@fileunderwater yes, that is a very good point. I commented when this question was at -2 with 1) no explanation of why people downvoted 2) no attempts to edit it into shape (I have now tried to do so) 3) no suggestions on how to improve. Had this been on another subject, we would have done all three. I just don't want us to downvote only because we disagree with the views expressed. I feel that one of the most important things this site can accomplish is to refute pseudoscience and any creationist/ID advocate who's willing to post here deserves a  good answer. Shoved down their throats.

opened chat for further comments/discussion: http://chat.stackexchange.com/rooms/13789/how-does-the-creative-process-of-biological-evolution-work

@JackAidley I'm not sure that it is and I'm very sure that it shouldn't be. There are conflicting views, see Creationist "canard" refutation type questions? and Are questions about creationism or intelligent design on-topic here? and Just how (un)welcome is creationism here?. Please weigh in on one of these meta posts, I don't think there's true consensus yet. I think we should welcome such questions (as long as they are Good Questions®) and just shoot the

@Jack Aidley "Creationism is off-topic on Biology SE" Your comment is very ignorant and troubling. It's ignorant because the question was ABOUT Evolution, not about Creationism. And your comment is troubling because it comes off as you treating Evolution as a religion, such that you get your defenses up if anyone questions or criticizes your religion of Evolution.

Adam Wong, reading your comments up there, you need to calm down. You're a little too aggressive and out of pocket over a biology question.

@TERDON "if not of the OP, then of the next poor misguided soul who has fallen under the influence of pseudoscience." Silly and unnecessary. Even more silly since I am an Evolutionist. This video is making me question that position: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology You may want to give details of the specific times in that video that are relevant. Its an hour long and has a lot of propaganda in it. It also has serious problems with the things it claims to accept. For example saying that "small mutations between generations is called breading and simply remixes existing genes" at 16:00. This is obviously wrong, twice, and brings into question how much research was done on this video. There are creationist arguments which are well reasoned (although they are rare), this is not one of them.

@LotusBiology Whatever your own positions are, the arguments you are presenting in this answer are based on several assumptions that are quite frankly wrong. Whether you believe them or not is another matter but they are classic examples of the type of question that arises when people have been influenced by the kind of pseudoscience of which the video you linked is an example. I'm not about to watch an hour of that drivel, but for example, evolution does not attempt to give an answer to how life originated, only to what happens after it has arisen.

@LotusBiology: When you rock up repeating a bunch of creationist misinformation using creationist language I'm going to assume you're a creationist. Trotting out "religion of evolution" in your response doesn't make me think this is any less likely.

@LotusBiology I recommend that you take some time and have a look at Understanding Evolution by UC Berkeley. It is fast and very introductory and you will learn a lot faster

Your basic problem is indeed a fundamental misunderstanding of how DNA and by extension its evolution works. First of all, there is no such thing as "correct" or "error", there are only changes, some of them are better for the individual and some are worse. You also have a basic misunderstanding of the concept of information. An error does not decrease the amount of information, it just alters that information. For example, consider this sentence:

The book is read

Say I make a simple error when I transcribe it:

The book is red

The two statements contain the same amount of information. Nothing has been lost, only changed. But that change created new information. Now what if I try a different change:

The book is rled

Now, this one is nonsensical, indeed, but how does that translate into DNA?
The computer analogy is a bad one. Programming languages have a very specific set of rules and anything outside those rules results in an error. For example, while this is a perfectly valid statement in many scripting languages:
print "Hello World"

This one is not:
priint "Hello World"

That, however, is not the way that DNA works. DNA is read in words of three characters, the codons. Every single possible
combination of those characters actually has a meaning. Therefore, a mutation like that above which would decrease the information content of the sentence (here, the gene) is not possible. Let's quantify. The DNA sequence consists of a long series of chemicals, commonly known as A, C, T and G. Since these are read in "words" of three "letters", this means you have:
$$4^{3} = 64$$
64 possible combinations. Of these 64, 61 are words with a specific meaning and 3, the STOP codons, are punctuation marks, full stops if you will. In other words, all possible combinations of letters have meaning in DNA.
Because all possible 3-letter combinations have meaning, no change will affect the information content of the "sentence". All it can do is change it. Now, changing the information can indeed result in "sentences" that make no sense. In the DNA world, this most often results in what are known as deleterious mutations. These happen all the time, but the result is usually a dead individual. Those with such mutations are not even born (speaking of mammals).
However, other mutations, such as the change from read to red that I mentioned before, can give rise to a change of meaning, this change, if it turns out that it makes the individual carrying it more likely to reproduce, will spread across the population and will be selected for. That is how new traits can arise.
In closing, another point that you have misunderstood is that evolution is not a path from the least to the most complex. In many ways it is the inverse. In fact, by any measure that counts, bacteria are far more "evolved" than humans for the very simple reason that the only way you can measure evolution is in terms of numbers of generations. Think of evolution as happening every time a species reproduces, this means that bacteria have had orders of magnitude more time to evolve than mammals have. Still, this is a useless comparison which is why nobody compares species by how "evolved" they are. For a discussion on that, have a look here.

The computer analogy might work better if you look at machine code. Every combination of zeros and ones means something. Change one bit, and maybe a bit of data changes, maybe something gets stored in a different register, or maybe a different instruction gets called. It might end up doing that makes no sense, it might throw an error, or, just maybe, it does something that means meaningful. Still not a perfect analogy by a long shot though, and it's certainly not how genetic programming is generally implemented.

Nice answer. I would like to add that the last remark "Say I'm a cephalopod..." contains two further erroneous assumptions. First, it seems assume that individuals evolve - only lineages/populations evolve. Second, it is implying "guided" evolution (I have this problem; with what instructions can that be solved?), ignoring that evolution is a trial and error process.

@TERDON "First of all, there is no such thing as "correct" or "error"," That's interesting you say this, cause MCV said below that Mutation introduces random errors. So  you say there is no such thing as error, and MCV is saying that mutations are errors, or at least introduces random errors.

@LotusBiology so? We are two different people giving different answers, what's your point? Anyway, while there are errors at the cellular level, where the copied DNA is not identical to the template, there are no "errors" in the evolutionary level. The term carries a certain implication and it was that implication I wanted to avoid. As far as evolution is concerned, there are no errors, only changes.

It is worth mentioning duplications are fairly common mutations, which can add quite a bit of code.

Your question, I'm afraid, betrays a deep misunderstanding of evolution.

Genetic mutation is just errors in replication. So it creates nothing. It simply degrades.

This is patently false. The vast majority of mutations are "errors", in that they produce a less fit organism. But once in a while, a mutation will confer an advantage, rather than an disadvantage. This, I suppose, is where "new information" comes from, though I would not use those terms. Your metaphor with software is not very accurate. If you want to "evolve" a piece of software through evolution, you do not insert new functionality into the source code. Instead, you would make a number of copies of the source code, each with a small, random alteration. Then you make the software available to all. The version that is most highly used on the market is then taken and the process is repeated. But good software is not developed in this way, for reasons that I hope are obvious.
I would highly recommend reading "The Selfish Gene" or "The Extended Phenotype" by Richard Dawkins.

The Blind Watchmaker would be a good book to read, probably better than The Selfish Gene.  In any case, skip The Extended Phenotype until you are well acquainted with biology and evolution.

"a mutation will confer an advantage, rather than an disadvantage." Sure. But it will only confer an advantage in a horizontal way. In other words, it's just a variation on what was already there, not a new trait or morphology that will advance us from microbes to man. Which is what I was looking for as far as explanation. Also, what is the physical process that reads, understands and implements these changes and additions of new abilities? What is evolution's central processing unit?

This is no such thing as a "horizontal" advantage. Every mutation is a subtle tweak which may or may not have benefits. The evolutionary process is a steady procession of such small changes. There is no single process which can be said to comprehend evolutionary changes, other than the ordinary processing of DNA within the cell. And evolution certainly has no CPU. Evolution is a distributed, emergent phenomenon. In no way is the process analogous to a computer.
I highly suggest you step back, do some real research and reevaluate your premises.

Consider also The Magic of Reality. It is an introduction to science itself. http://www.amazon.com/The-Magic-Reality-Whats-Really/dp/1451675046

@AdamWong Let me explain what horizontal means there. It's known as horizontal evolution, where you have evolution that happens with breeding. To get from microbes to man, we need vertical evolution. Where we advance up in complexity and changes in kinds of species, rather than variation within kinds.

"In no way is the process analogous to a computer". Well, I don't know how else to explain what I'm looking for. When you build something, it works like a computer. You have an input, processing, then output. To get our vertical evolution, you need an input of new instructions, physical mechanisms to understand the instruction and PHYSICALLY implement it, and output the new ability or morphology. How is that done in evolution? Where does the new information come from, and what in nature physically implements this new information?

@ADAMWONG Let me give you another example besides the computer. To build something you need an Input/Output system. Take ants. When they want to build an ant mound for the queen. They already have this knowledge of how to build it, its innate. They then set out physically implementing this knowledge by gathering dirt and transporting it to the mound site. Eventually the mound is build which is the finished output. How does Evolution do that with organisms? New information, what reads it, and tells the genes 10 spikes, 1 inch apart, 5 inches up, and physically implements this morphology?

To answer your first question, your notion of horizontal vs vertical evolution is unfounded. There is no such thing- mutations are small, though their effects may be outstanding. But very large changes, (ie microbes to men) are merely the accumulation of smaller changes.

To answer your second question, I suppose the new information could said to be in the form of mutations and I suppose evolution can be said to implement that information in DNA. But that is projecting agency into a system which has none, so I would not use those terms.

To answer your 3rd comment, the mapping of genotypes (information) to phenotypes (characteristics) is complicated. Genes are not instructions like "Make the flamingo this precise shade of pink." Genes are instructions for creating proteins which eventually define the characteristics of the organism. (This explanation of gene expression is greatly simplified) In the same way, ants do not "know" how to build ant hills. They are parts within a larger machine (the ant colony) from which complicated behavior (ant hill building) emerge.
Read this: emergence

@LotusBiology: I almost wrote the same as adamwong246 just now. But one very accessible area (and I think quite amazing/beautiful) to help understand your question is introductions to Hox genes: see http://en.wikipedia.org/wiki/Hox_gene

"Genes are not instructions like "Make the flamingo this precise shade of pink." What does do that then?

@LotusBiology The shade of pink or the ant hill is emergent behaviour; simple rules leading to a complex outcome. Much like evolution itself

It's seems to me you forget something pretty important about evolution : it has nothing to do with improvement. All living organisms have the exact same time of evolution as they all derive from a common ancestor. They simply evolved through different paths, that's what explain the biodiversity we can observe today and no organism is better than others, not even human.
New functions are not created just like that, because a species need it. To take your cephalopod's example : if there's pressure from predators, they won't simply grow spikes in order to protect themselves. However, if mutations (one or many) appear in the DNA sequence that make spikes instead of, say, skin, then this particular cephalopod will have better chances of surviving than others and so, better chances to reproduce and pass his new genes.
Mutations do not necessarily imply degradation -just as the los of one function is not necessarily a degradation. Every organs appeared thanks to mutations and / or duplications. For example, the humans' ability to see colors is due to 3 types of pigments (blue, red, green) named opsine S (blue), opsine M (green), opsine L (red). You add rhodopsine which is sensible to light to see clearly. If you study a mouse's eye, you'll only find 2 opsines + rhodophsine. Scientists have been able to recreate evolution's story : you start with an ancestral gene for opsine. The gene is duplicated and the copy is translocated on another chromosome. You now have 2 copies of the gene on 2 different chromosomes. They both mutate as mutations occur all of the time. You end up with 2 new genes. Then, duplication will happen again (no particular reason). You now have 4 genes, identical two by two. Three genes stay where they are, one of them is translocated on another chromosome and they'll all mutate. You finally get 4 genes on 3 different chromosomes (opsine M, L, S and rhodopsine). New genes and new ability appeared thanks to mutation, duplication and translocation. It just took millions of years of evolution and probably an impressive amount of tests.
As Shigeta wrote, everything potentially exists. Some of the possibilities have been discovered, some have not. Evolution applies on hundreds millions of years and billions of living organisms and it process accidents after accidents. If what appears is selected, it stays, if not, it disappears.

"and no organism is better thant others, not even human." Are you seriously trying to tell me that a human is no better than a virus? Are you serious? You are seriously trying to tell me there's no advance in complexity or ability between a bacteria and a lion?

By "better", evolutionist mean "well suited to their environment." Many very simple organisms can be very successful within a specific domain. For instance, the eyeless fish that live in completely dark caves. In this instance, eyes are a waste of the creatures resources. Thus, over time they adapt to their environment and lose their eyes, though most people would say that fish with eyes are "better." Crocodiles and sharks are another example of an organism so well-adapted, they have hardly changed at all in the past few million years.

She was still wrong. Clearly some organisms are better than others, even under that undrstanding of better. Which is why some organisms survive, and others go extinct. Because some are better than others. I.E. MORE FIT.

I'm not. Check history : most extinctions occured due to big climate changes or geological catastrophes and very important selection pressures. A simple example -the one with "dinosaurs" and mammals : the second ones survived not because they were better but because environmental pressures were way not as important as it was for dinosaurs. You really don't seem to get that evolution does not imply any notion of superiority. Being more complex does not mean being better in a superior way. It means being different.

@LotusBiology while it is true that some organisms outcompete their peers, the word better is a moral construct and has no bearing here. More efficient is the best you can say.

"Being more complex does not mean being better in a superior way"  Oh, absolutely it does. That way you are higher on the food chain. The superiority in evolution is at the very least, the one that survives. Survival of the fittest. So clearly, complex animals that are high on the food chain, like SHARKS, are much superior in evolutionary terms, than say the plankton or fish they feed off of. Humans are WAY MORE superior than bison or cows.

I still havent gotten my questions answered. Where does the new information come from since natural selection and mutations are not creative, and what are the physical mechanisms that implement these new blueprints/information?

We cannot answer your question because it is not well-formed. The questions you have asked do not make sense in light of what is known about evolution. You might as well be asking "What is the square root of a purple?"

@LotusBiology doesn't your food chain analogy suggest that viruses/bacteria are "better" than humans?

Whilst being higher on the food chain may make an organism "superior" in our eyes, evolution doesn't care about that. In fact, top predators are often more vulnerable to extinction (look at large predatory dinosaurs, or indeed modern examples like big cats), as their survival depends on what happens lower down in the food chain. Sabre-toothed cats may seem superior to algae, but algae is still here, and sabre-toothed cats are not.

@LotusBiology "Better because higher on the food chain" is a value judgement that you attach to a certain property. Humans like compexity, being high on the food chain, and generally feeling important, but from an evolutionary perspective, the only thing that matters is survival for you and your offspring. Bacteria are evolutionary unbelievably successful. They live everywhere (deep underground, in your gut), and there's far more of them than of more complex organisms. Fortunately for us, there's also a niche for more complex organisms.

"I still havent gotten my questions answered. Where does the new information come from since natural selection and mutations are not creative" : we answered that part of your question at least.

@LotusBiology I think a key issue here is that you are assuming that evolution has some "plan", or is going from less complex to more complex. It isn't, it's going in random directions; more complex (as in more DNA, not necessarily better DNA), less complex, dead, better at surving, worse at surving. Natural selection then cuts off all the directions that make an animal "less fit" - by killing it. You are saying "more information" but what I think you mean is "more useful-information", more information is ridiculusly easy; just tack some noise on the end

"doesn't your food chain analogy suggest that viruses/bacteria are "better" than humans" No. Because viruss and bacteria are not higher on the food chain than us. They also generally do not eat us, but rather, in the cause of viruses, use our machinery to help their replication, and in the case of bacteria, make us sick, but many times, it's a symbiotic relationship. Also, unlike plankton and fish, we can fight back and kill bacteria and viruses in return.

@Richard Tingle "it's going in random directions;" Yeah, and that's the problem. To think that a random process can create so much complexity, variation and purposeful looking design, make me doubt Evolution. Take a look at this video. This is where i got the crux of this question from: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology You accept that random mutation can create small amounts of new information and that natural selection can remove those changes that are in some sense "bad"? Having accepted that it is simply a matter of time, huge huge amounts of time. Remember if we represented the entirity of human civilisation (12,000 years) on a 24 hour clock reprensing the entire history of life (3.5 billion years) then our civilisation has existed for 1/5th of a second. Huge amounts of time are involved here

Where does the information come from?
From the environment, and the previous history of interactions in that environment. The process of evolution can be viewed as an undirected search for "good" solutions (i.e. those that better support replication) to problems presented by the environment.
There is a large amount of information (in the information-theory sense) in a differentiated environment.
Note that information content of the whole system is preserved when this happens. Partly the misunderstanding of "information is being created" is not seeing what a huge resource of information (in the same sense used with information theory that says it may not be created or destroyed) is available from the environment. It is many many orders of magnitude greater than anything stored in genetic codes.

+1 Short and to the point.  The other answers does a decent job of explaining evolution, but this answers OP's question.

So what in the environment, tells the organism to make a new innovation like compound eyes, or superposition eyes? And again, what is Evolution's central processing unit. I.E. what physically deploys these new adaptations and abilities into the organism or population as a whole? Also, if you have the time, can you answer this video if you have a Youtube account. This is where I got these objections: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology: The pattern of light distribution is the information that "tells" the organism to create eyes (or more accurately rewards organisms that better sense light). The feasible and likely process from no eyes to complex eyes is well-studied, and indications are that this process has happened multiple times in the history of creatures. As for "central processing unit" there is no need for such a thing. Genes and proteins do not need a "CPU"

@NEIL SLATER Cool. If you have the time and a Youtube account, can you answer this video by Mark Champneys. This is where I got the crux of these questions: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology: In my opinion, the "scientific objections" raised in the video are actually a thin veil over desire for the end result (evolution being "wrong"). That is because it protects a cherished world view, and not due to any rigour in the arguments raised. Which means debating with someone who has published a video and has a lot of face to lose (and a lot of like-minded followers) is a waste of time. That's probably how you feel logging into biology.stackexchange and trying to challenge scientific consensus. But I have no desire to reciprocate.

It is understood that Evolution basically involves three elements. Natural selection, genetic mutation, and time. The problem for Evolution, is that none of those three elements are creative.

They absolutely are creative in that they create something new. Mutation introduces random errors, some of which may never have existed before in that combination of genes. Now usually errors are bad, and natural selection prunes the result, but every once in a while, you accidentally stumble upon something new that provides an advantage, and now natural selection means it gets kept and passed on to the next generation.
So on their own, it might seem that mutation doesn't add information and natural selection doesn't create anything new, but together, natural selection adds information to the randomness of mutation: it selects what works and what doesn't.
Imagine you're rolling a die (warning! simplified analogies don't accurately reflect the complexities of evolution). What are the chances of you rolling 10 sixes in a row? Vanishingly small of course. But that's not what evolution does. What it does is in every phase (generation), it rolls 10 dice, and only keeps the sixes. What is the chance of getting a six in every phase now? Quite a lot bigger. All through randomness and selection.
(In fact, have you ever played Yahtzee? How can you get the right patterns there if you're just rolling dice and selecting some of them?)
Take your analogy with the sentence "Make an eye that is compound". A mutation might turn that into "Make an eyye that is compound" which is useless. But another mutation might turn it into "Bake an eye that is compound" which is grammatically correct though nonsensical. Yet another mutation might create "Make an eyr that is compound", and if that one happens to survive a generation, you might get "Make an ear that is compound".
Thing is, there are a lot of mutations. Really a lot. Most of them have no measurable effect. Of the remainder, the vast majority breaks something, which means they automatically get weeded out by natural selection. A tiny fraction accidentally adds something useful. If you look at any single mutation, it's impossible to imagine how that could ever result in anything useful, but there's a lot of them. Every generation again, over thousands and millions of years, and eventually, those very few positive mutations start to add up.
It's impossible to fully grasp how evolution can introduce totally new species without first grasping the enormous time scale on which evolution works. And we humans are limited beings and bad at truly understanding such enormous scales. But it clearly works. We can see the results all around us. We can run simulations on computers that show that the process really does work. I consider it one of God's greatest miracles (warning! personal opinion might not reflect those of others).

I think this is a little like writing a book.  The most common advice is for aspiring writers to write every day and write a decent amount.
Evolution creates by testing everything against its fitness - its ability to survive and reproduce.  If something is advantageous, it stays in the corpus of genes and genetic solutions to problems.  If something is not working well or even not as well, it may be lost and forgotten - dropped out of the gene pool.
So just as a writer may throw out 90% of their writing to get to their published novel, 90+% of biological experiments are thrown out and don't have long lasting repercussions in the biosphere.  its probably more like 99.9999999% really.
The creation of information you are talking about are all inherent in the physical universe.  Just as every computer program is potentially existant in the laws of logic and mathematics, all the potential mechanical and informational and configurational advantages of living things are embedded in the physical laws in which they operate.  It is not an event of creation, but an event of discovery when a new biological function appears.

evolution means unrolling http://www.etymonline.com/index.php?term=evolution
Now if you imagine a tree with one root then the stem rolls out, branches roll out twigs and leaves roll out etc. Same with the roots on the other and to balance it out.
And that's it. Evolution does not happen in a vacuum. It happens in and together with an environment. If the environment changes and you have unrolled something that helps you cope with that change then you can continue to procreate so that your offspring also have a chance to test any eventual new unrollings in the constantly changing environment. If they die then the branch or twig that was unrolled is cut off and might unroll again later and be cut off again until maybe, just maybe some sunlight will reach it and it can survive. Until night falls again.

Another important point about evolution is, that rhere are many, many small steps - not huge leaps.
E.g. going from a bacteria to something with four legs in one step will not happen - that is simply too much change at once, and it's probabillity is close to zero.
But small steps happen all the time - if we take your example with a cephalopod: Imagine that there are some individual cephalopods who have a harder skin. Without predatory pressure this is next to useless: the cephalopod are investing energy on something which brings no benefit. So they are less fit and will probably have fewer offspring than the original ones. Now a predator kill many soft-skinned cephalopods but sometimes fails to eat their harder skinned brethren. The hard-skin variant will producre more offspring and theier genes spread. Then the next round happens: cephalopods with the hard skin might have another mutation which hardens the shell even more - or the predators might get better teeth.
But be aware that this most not happen: maybe no variant with harder skin exists or the genetic error is not present at the time and the whole race simply dies - this happens a lot. Look at dinosaurs or the polar bear (is under pressure because the polar ice melts) etc.
Some fun fact: since each step is random and has a low probabillity, you willl never get the same reult twice. If you start the evoluation again, the world would look completely different because the steps would look different.

From bacteria to something with 4 legs probably close to zero? Just going from bacteria to single celled eukariotes took a billion years. That may have been the hardest and most fundamental step in our evolution. The chance of that happening in a single generation is as zero as quantum mechanics allows.

@mcv That should qualify as close to zero ;)
Acutally, the probabillity is even lower, because you need them twice (male and female), otherwise it will get lost at once.

@ChristianSauer Male and female is somewhat of a specialisation of sexual reproduction, things can be simultaneously male and female or it can be N/A. Even bacteria have sexual reproduction without the concept of gender. In the presence of individuals who are mixedgender becoming purely male isn't a disadvantage

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why are these allium (ornamental onion) cells green?
Can you help tell me why these three images of allium (ornamental onion) slides are appearing as green, even though there is no chloroplast in onions? Thank you.

Welcome Tomma. This doesn't appear to be a species ID question so I've submitted an edit to remove the tag. Tell us, where did you get the pictures, did you take them? How had the samples been prepared? Had any stain been used (Aldehyde Fuchsin, Alcian Blue, Movat's Pentachrome Stain for example)?

Also - have you adjusted the white balance on your camera? what sort of optical set-up are you using?

Just to clarify, you should [edit] the question with the additional information requested.

I would bet strongly it is the by product of the stains or fixative agents used in slide preparation.  A type of stain called malachite green is sometimes used to stain cellulose and lignin in plant cell walls, and to make cell structures more visible by creating contrast.  In some concentrations, it can even take on a bluish-green color.  Fast green is used in a similar fashion.  Without knowing the exact staining protocol used, it's impossible to know for certain, but one of these is my best bet for the reason why your cells appear greenish.


text:
Insect Identification please
Location Kothrud, Pune
This was found on Sonchafa plant.

About a centimetre wide in the middle?

It could be a Yellow-spotted stink bug Erthesina fullo
https://www.padil.gov.au/pests-and-diseases/pest/main/136074/772

EDIT:
more frequently found in India is Erthesina acuminata
http://insecta.pro/taxonomy/1037721
For more information, read the excellent answer on this question:
Can anyone identify this grey spotted insect -- is it a tree bug species?


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Actual definition of cardiac output
Is cardiac output the amount of blood pumped by both ventricles in 1 minute or only by the left ventricle in 1 minute?

Cardiac output is the amount of blood pumped only by the left ventricle, per minute.

Cardiac output (CO) has also been defined as the amount of blood pumped out by each ventricle in one minute. I've seen it both ways. Maybe a source would be good.


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What`s this? (Found among circulating tumor cells)

I filter circulating tumor cells out of patients blood with metastatic breast cancer using track-etched membrane. I've stumbled upon this... cluster(?) of cells and can`t get what it is. "Greenish" circles are the pores of the membrane of size ~6,5 - 7 um.

The cells you're asking about are neutrophils in varying stages of maturity. Neutrophils are the most abundant of leukocytes, and frequently found in cancerous tissue. Note first that they are all about the same size and stain similarly.
The most segmented of the cells are Polymorphonuclear neutrophils (PMN), of which I count two, and a third that's almost there. There is one band cell (a stage before becoming segmented), one precursor that is starting to become a band (a metamyelocyte), and the immature forms, the myelocytes (two of them). There's also some damaged cells that I won't try to identify.

The photograph is from Cornell University's ECLINPATH page.
See also this page.
If you google neutrophils and cancer, you'll see how they come to be present.
Histology!!! I love it! Always have, always will.

Aren't there four myelocytes in the main cluster? (Perhaps the ones that you called damaged)

@Hedgehog - Probably, but as it's damaged, I'd rather not consider it. If it were critical, I might, but it's not (I presume!).

It`s ... semi-critical - we are trying to determine whether they are circulating tumor cells or not (without immunofluorescent staining)...


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What's the exact mechanism of oral tolerance?
I have mainly two matters of confusion need to be clarified.
First question:

The immune system does not necessarily kill everything hat has PAMPS, the bacteria living in the gut, have PAMPS (Pathogen-associated molecular pattern) in their surface, but they are not harmful to the body

Is this proposition correct?
and the second question is about my confusion of the following statement

the mechanism by which the immune system tolerates the presence of the bacteria that live in the gut is not fully understood

So I am wondering, is there some textbooks or reference particularly talk about oral tolerance?
Moreover, I am especially curious about the fact that, since PAMPS trigger innate immune first rather than adaptive immune system, How can oral tolerance even avoid innate immune? is there some resources about that particular topic?

Please define acronyms that you use. And I wouldn't use chatGPT to study things....

@Bryan Krause Sorry about that, I just make the first citation  also a susceptible question which needs references, thank you!


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Mites on ginger root
I was just looking at some mouldy ginger found in the fridge under the microscope and was horrified/delighted to find (what looked to be) mites growing in it. I have searched the web and can only find references to red spider mites which these are certainly not. They were clear white and under 40x zoom about less than a mm across - does anyone know what they could be? Furthermore, what are they feeding on (ginger root is only ~15% carbohydrates - is that enough?) and has a minimal (~1%) amount of protein.
Here is a picture (sorry for the quality but the white thing looks to be a mite).

LOL "horrified/delighted to find..."

Pictures? Or, lacking that, can you tell how many body segments they have?

@Oreotrephes Have fished piece of ginger out of bin and added pic

Saw a bbc program the other day which talked about mites on cheese, they are (deliberately) all over the rind of some cheeses! I'll try to find it, might (or mite) inspire you to look at other things in your fridge too!

Does this look like the same bug to you ?
.
This one is a bulb mite, Rhizoglyphus robini, see here.

Yes - I think that's it! I'ts amazing how you can be both fascinated and disgusted at once ;) (It does seem to be harmless though nonetheless)

I share your feelings :-)

This is very interesting. We think about microbes (micrometer) and insects (centimeter) as main plant pathogens, but know very few about what fills the gap between these 2 different sizes. At least I learned a lot about medical microbiology, and I know a few plant pathogens as well, but I know nothing about mites. :-)


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Pharmacodynamics of Ethinyl estradiol + Drospirenone and interactions with istotertinoin
Does pharmacodynamics of Ethinyl estradiol + Drospirenone in OCP pills like (Yaz, Yasminelle etc.) while using isotretinoin (Axotret, Roaccutane etc.) is changed? Does isotretinoin weakens the OCP pill by any means in any situation?
I know about interaction towards incrase of lipids. The only info I have found is this: https://www.ncbi.nlm.nih.gov/pubmed/15116059 and results could be translated: we discovered nothing.

I'll give it another look tonight, thanks for editing the advice portion out of the picture

@jonsca Thank you very much. I will be waiting for your reply.


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Question about Autosomal Recessive Alleles
I had a homework question that I could not figure out.
It states:

A woman has cystic fibrosis in her family and did not want to have a
  child that suffered from the disease. She and her spouse went for
  genetic testing and counselling. She tested positive as a carrier and
  her spouse tested negative, and their first child was born with cystic
  fibrosis. Explain how this could happen.

This doesn't make sense because the punnet square would be:
$$
\begin{array}{c|c|c}
  & A  & A  \\
\hline
A & AA & AA \\
\hline
a & Aa & Aa
\end{array}
$$
This says there are no two recessive alleles which can cause  cystic fibrosis.

Well, if the question is perfectly correct, than as per my opinion the only alternative left is MUTATION.

I asked my Biology teacher and she said that the if the father is not a carrier, he must have the disease. So the father is aa.

You should tell your teacher that's a terribly worded question then - "negative" definitely doesn't mean they have the disease! Not your error at all.

The question came from the book we use, and she also said it was a bad question.

Well, this answer does not answer your question! It answers it assuming that the real meaning of the question was different than what was actually written! So, I am not quite sure this should be accepted as an answer and not flagged, although I agree that most likely your textbook did not expect you to perform probabilistic calculations and it actually was a very simple terribly poorly written question.

I copied the question right out of the book, and its only Grade 11 Biology. We didn't learn any calculations.

If really cystic fibrose is expressed only in homozygotes, then here are some possible explanations:

Mutation

very improbable

Autofecundation

very improbable

False Negative when testing the father

Because of the test False Negative Rate. @kmm made a very interesting comment below. He said that according to this article 75% of the mutations coding for disease correspond to one pattern (3 base pair deletion). The other 25% of the mutations coding for disease might not be detected in the standard test. If so, it is very likely that a the test conducting on the father was a false negative. It would be worth further investigate the test that are usually performed to confirm this.
Because of human error. The laboratory operator might accidentally switch two samples or accidentally introduce stranger DNA before PCR (assuming the test is performed through sequencing)
I have no idea concerning the probability for such thing to occur!

trisomy

The assumes that a trisomic that have two recessive allele coding for disease and on dominant allele coding for health yield to a individual expressing the disease!
The gene for cystic fibrose is on chromosom 7. Trisomy 7 is extremely rare if I'm not mistaken.

The father is not the father!

According to different studies between 5% and 20% of the people are not fathered by the man they think is their dad.
According to this source the frequency of the disease is 1/2500 in UK. Assuming Hardy-Weinberg equilibrium the frequency of the allele coding for disease should be $p=0.02$.
The probability that the baby comes from another man and that the baby express the disease is $$a \cdot \left(\frac{2\cdot p\cdot (1-p)}{4} + \frac{p^2}{2}\right)$$, where $a$ is the probability that the baby was fathered by another man (let's say 10%) and $p$ is the frequency of the allele coding for the disease (0.02). The division by 2 and 4 are due to the probability that the (real) father and the mother transmit both the alleles coding for the disease.  This probability equals $$0.1 \cdot \left(\frac{2\cdot 0.2\cdot (1-0.2)}{4} + \frac{0.2^2}{2}\right) = 0.01$$ This seems to be from far the most likely explanation! Note: this assumes that the mother is heterozygote (does not express the disease) otherwise, the probability would be 0.02.

I would also add "human error" to the list, a person changing the outcome, e.g. by contaminating the sample or a spelling error while transcribing the result. This might be surprisingly likely - somebody overly tired, or having a bad day.

Yes, I kinda incorporated "human error" within the False Negative point. I'll make it more clear

It's probably the false negatives. According to http://www.ncbi.nlm.nih.gov/pubmed/2014829, 75% of carriers have the standard pattern. They are probably not routinely testing the other 25% (which might constitute lots of different patterns).


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Is Natural Selection like a Copy Editor?
I am stuck on a Homework Question. It says:

Evaluate the following statement: “Natural selection works like a copy
  editor; it works only with
  what is already present in a population.” (Note: Copy editors check
  written material before it is set into type, to correct errors in
  spelling, grammar, usage, and style.)

I thick that Natural Selection is not like a Copy editor because:
Natural Selection has no set direction, which means it does not decide on anything. A weak organism might be able to survive by luck. While a copy editor knows the mistakes and eliminates them instantly.
Can I get some help on this. Thanks!

If I had to compare natural selection to a job in the publishing industry, I'd say it's more like a commissioning editor -- that is, the guy who decides what to accept and what to throw in the garbage bin.

Thats good but its not answering the question. Is natural selection like a copy editor or not?

It not my question. Its part of my Homework.

Since this is a homework question, regardless of wheteher its a good one or not, you're supposed to give some indication that you have tried to answer it on your own. Maybe you should list how you think it is similar and how you think it is different.

Is natural selection like a copy editor?

Is a railway car like a weasel?
Honestly, I don't think that's a very good question.  The only reasonable answer is, put briefly, "In some ways it is, and in some ways it isn't."
It also doesn't really help that the "statement" the homework exercise asks you to to evaluate is actually two statements, and they're not really equivalent.  (Real copy editors don't just "work only with what is already present," at least not in the same sense as natural selection does.)  Sorry if that seems unhelpful, but that's how I see it.

OK, let me expand on that a bit:
Evolution, in the Darwinian sense, can be broadly described as the interaction of three processes: inheritance, mutation and selection.
Of those three processes, mutation is the one that produces novel innovation, by occasionally producing new alleles that did not exist in the parent population.  It is, however, a blind innovator — the novel genotypes produced by mutation are essentially random, and no more likely to be advantageous to the organisms carrying them than one would expect by change (i.e. not very likely at all).
Selection, whether natural or artificial, is what happens when the organisms carrying the diverse genomes produced by mutation end up competing for survival and reproductive opportunities against each other and against their environment.  It acts on the diversity generated and replenished by mutation, favoring those mutations that happen to confer a survival advantage.
Finally, inheritance ensures that the beneficial alleles generated by mutation and filtered by selection get passed on to successive generations, allowing them to spread in the population and to be further modified by successive mutations.  In a sense, inheritance and mutation can be seen as opposite sides of the same coin: the more faithfully genes are inherited, the less mutations there are.  Yet both are necessary for evolution; an organism that never mutates obviously could not evolve, but neither could one that mutated so much that all of its genes were totally scrambled in each generation.
Of course, this whole process is stochastic in nature — even the best adapted individual may die without offspring due to simple bad luck, just as even a maladapted individual may get lucky and prosper.  But over generations, there is nonetheless a statistical tendency for individuals carrying certain alleles, or combinations of them, to be more fecund than others, and those will be the alleles that will eventually come to dominate the population (assuming they're not it turn displaced by even more successful mutants).
Thus, I would personally say that, of these three components of evolution, (natural) selection indeed "works only with what is already present in a population."  However, it's not really like a copy editor, since it does not seek to "correct errors" in the genome; it's more akin to a slush reader, who just sorts the incoming texts into ones to keep and ones to throw away.


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Maintaining purebred pedigrees and how to lessen chance of getting disease?
Many breeds of dogs are known for a high incidence of genetic disorders. German shepherd and Saint Bernard dogs are predisposed to developing a crippling condition called hip dysplasia.
Q: What advice would you give to dog breeders who want to maintain their dogs' purebred pedigrees, but also want their dogs to be as healthy as possible?

Interesting question. I assume that "natural"/"ancient" dog breeds like huskies have fewer problems with inbreeding, but still maintain their traits; but I don't know that that's true, or why it would be the case.

choose mates from as far away in the breed by pedigree as possible.  I don't think there is anything that can stop the inbreeding problem for breeds like bulldogs who are so far along and come from a small progenitor group.  Ultimately you have to allow genes to come in from the greater pool.

heard about the same problem being faced in the breeding of white tigers in India. http://en.wikipedia.org/wiki/White_tiger

Outbreed your dog every couple of generations with a bloodline that is slightly different or at the very least a similar looking breed.

Many races of dogs are relatively new with most of them appearing (were bred) in the last few hundred years. These variations are caused by small mutations in certain genes and this is also the problem. To keep a race pure, it has to be interbred to maintain the special set of mutations. And this makes the dogs vulnerable to collect more damaging mutations, especially when the number of animals used for breeding are too small. This is the same problem, that animal conservation projects face in zoos.
A good example for that is the Dalmatian dog. Its characteristic spotted pattern is caused by genes, that can also cause sensineural deafness. To avoid this, deaf dogs are excluded from the breeding and a backcross project was started.


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People say the cardiac cycle depends on blood pressure? How so?
I know what the cardiac cycle is. There are two phases diastole and systole. One is the relaxed, and the other is the contracted form of the heart. The diastole is where blood is pumped to the ventricles and systole is when blood goes to the aorta, and lungs. But what is the connection to blood pressure?

In the title, by heart pressure do you mean blood pressure ?

yes, blood pressure

"People say..." - What people? Who? https://en.wikipedia.org/wiki/Weasel_word

There are two levels to take your question at.  The first is simpler but I'm not sure if it is what you are looking for:
If you imagine the heart and all the blood vessels in your body as a closed plumbing system with no leaks (not entirely accurate) then when the heart contracts and squeezes the blood from the ventricles the total surface area the blood is pushing against has decreased - there is more blood in a smaller space.  This means that the pressure on the arteries from the blood has to increase when the heart contracts - in systole blood pressure is much higher than in diastole.
The second level is a little more in depth:
Cardiac output (a measure of how much blood is being pumped around the body to the organs where it is needed) is defined as the product of stroke volume and heart rate.
$$CO = SV \times HR$$

Heart rate is the number of times the heart beats per unit time
Stroke volume is the amount of blood that is pumped out of the heart in one beat. It is this that is related to blood pressure.

The relation of stroke volume to blood pressure is defined by Starling's Law.  This states that the more blood that is in the heart, the more its walls are stretched.  The more the walls are stretched, the harder the heart contracts in response.  This increases blood pressure as again more blood is displaced from the heart.


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Relationship between small and large fast-twitch motor units
When large fast-twitch motor units are temporarily fatigued, non-fatigue small motor units in the same muscle are impaired for small delicate tasks. Why?
When impulses from the brain comes down, the impulses from interneuron goes to small diameter motor neuron, which are associated with non-fatigue motor units, and large diameter motor neurons, which are associated with fast-twitch motor units. More impulse is necessary to activate the fast twitch-muscles because the larger neurons have higher leak current and capacitance. Thus, we have an ascending activation of muscle units, from least forceful units to most forceful. Now my question is, if the fast-twitch muscle units are fatigued, why cant we perform delicate movement/ task?
Fatigue is mainly caused when the motor unit runs out of ATP. So, is that the bridge between these to things, or is it something else?
Or, is it related to how motor units are used is a fixed ascending order for completing tasks? If so, how?
Thanks for all the help!

I am finding it difficult to understand what exactly you are trying to ask here.

When impulses from the brain comes down, the impulses from interneuron goes to small diameter motor neuron, which are associated with non-fatigue motor units, and large diameter motor neurons, which are associated with fast-twitch motor units. More impulse is necessary to activate the fast twitch-muscles because the larger neurons have higher leak current and capacitance. Thus, we have an ascending activation of muscle units, from least forceful units to most forceful. Now my question is, if the fast-twitch muscle units are fatigued, why cant we perform delicate movement/ task?