If the human atlanto-axial joint is pivotal only, what accounts for the craniums additional degrees of freedom? The atlanto-axial joint is supposedly a pivot joint. I assumed it would be considered a ball-and-socket joint, based on a) the physical shape of the dens, and b) the degrees of motion of the cranium relative to the spinal column.

A pivot joint is distinct from a typical ball-and-socket joint because it only allows for a single degree of freedom; yaw - to rotate about it's own axis or diameter, like a spindle. A typical ball-and-socket joint allows at least one additional plane of limited movement.

I can think of (or observe) at least three degrees of freedom of the cranium, relative to the spinal column; pitch & roll. Pitch allows you to direct your gaze from the ceiling, to the floor. Roll allows lateral movement in a similar manner, so you can point your left ear to the ground, and then your right.

The additional degrees of freedom are provided by the entire cervical spine, rather than the atlantoaxial joint alone, which is the joint between C1 and C2. What you're describing as roll (when you point one ear to the ground), is provided by contraction of the sternocleidomastoid. The sternocleidomastoid muscle pulls the mastoid process (behind the ear) down and in, toward the fixed clavicle and sternum.  The joint that provides lateral flexion in response is the entire cervical spine.

Here you can see the sternocleidomastoid muscle (the SCM):

And here, a drawing with a reasonable approximation of the way the cervical spine responds to lateral flexion (due to contraction of the SCM). I can't find a good c-spine film at the moment to demonstrate it in a human person, rather than an artists imagination. But this drawing is accurate to my recollection. You can see the space between C1 and C2 on the right is quite limited (that atlas and the axis are in close apposition). C2 and C3, as well as the other cervical vertebrae, have more space between them on the right:


How does the light-independent stage of photosynthesis get H+ ions? From what I understand from my grade 11 biology:
During the light-dependent stage of photosynthesis, water molecules split, producing hydrogen and oxygen atoms. The oxygen atoms are basically “waste products” — used by mitochondria for respiration after being inhaled. These H+ ions are then taken by a hydrogen carrier (i.e. NADP+) to form NADPH (which is necessary for the light-independent stage). Where do these H+ ions suddenly just come from?
From what I’ve understood so far, the H+ ions are now “in” the NADPH.
I’m confused as to how in the light-independent stage, the carbon dioxide (CO2 molecules) can combine with the H+ ions to form glucose. I thought that these H+ ions had already got “converted” to form NADPH? Or is it something like only some of the H+ ions are necessary for NADP+ to form NADPH?

Summary
The question shows confusion about the purpose of the splitting of water in photosynthesis. Quoting from Berg et al., in the light reactions of photosynthesis

“Light is absorbed and the energy is used to drive electrons from
water to generate NADPH and to drive protons across a membrane. These
protons return through ATP synthase to make ATP.”

The useful product of splitting water is energy.
There is no problem in the provision of hydrogen ions for biochemical reactions as such — they are available from the dissociation of water.
Explanation

The diagram above, summarizing the light reactions may be helpful, although it conceals detail and introduces the complexity of energy generation. It shows the (thalkaloid) membrane separating the location of the reduction of NADP+ (outside) from where water is split (inside).

The important product of the reaction of light photons with water is excited electrons. The chemical products are relatively unimportant — certainly for oxygen, and the only importance of the hydrogen ions produced is their location within the thalkaloid, lowering the pH.

The initial fate of the hydrogen atom is complex, and there a many intermediates to which the excited electron is transferred before, ultimately to NADP+:

NADP+ + H+ + 2e– → NADPH

It is important to realize that the energy is used to reduce NAD to NADPH, that NADPH can be regarded as a special type of ‘high-energy compound’ — not a general one like ATP, but one that can specifically drive the reduction of carbon backbones needed in synthesis.
The misapprehension is that there the hydrogen ions for the above reaction are those produced in the splitting of water, or that there is in general any problem in obtaining hydrogen ions for biochemical reactions. Biology exists in an aqueous environment, and water dissociates into hydrogen and hydroxyl ions.

H2O ⇌ H+ + OH–

So hydrogen ions are irrelevant to the reduction reactions involved in the conversion of carbon dioxide to carbohydrates in the light-independent reactions of photosynthesis (they are actually produced in NADPH reductions.). It is NADPH that is supplying the hydrogen component of the carbohydrates.
ATP
The diagram also brings in a complexity that needs a book chapter to explain: the hydrogen ion gradient generated between the inside and outside of the thalkaloid space provides the energy to phosphorylate ADP to ATP. The ATP is relevant to the light-independent reactions of photosynthesis in that it ultimately provides the energy for formation of the carbon–carbon bonds.


What is the 'job' of the byproduct water in the Electron Transport Chain? I understand what happens in the Electron Transport Cycle, but I fail to understand that after Oxygen has accepted an electron, it forms water, but why? what happens to the water? I can take an educated guess but again its a guess.

Does it then react with ADP?

Thanks in advance! I'm doing an animal welfare course and as part of it I need to study basic biology.

Thanks for your question.
One reason is, if this chemical reaction does not happen so there will be a lot of electrons in mitochondria in a short time consequently the environment inside the mitochondria will be charged in negative and as we know the environment inside the all parts of cells should not change during the time
and on the other hand, these extra electrons may carry out some chemical reactions which result in producing some materials which are not good for cell, for ex H2O2, as we know it is a poisonous material for cell.
But maybe you ask why H2O and not another product? because H2O exists in cell, in a large amount, it is solvent for many materials, it is not poisonous for cell, and many other reasons.


What photoreceptors are necessary to permit infrared vision? Humans have red green and blue photoreceptors allowing them to sense colours in the spectrum of about 400-700nm. Certain proteins allow for the extending of wavelength range in the RGB receptors, this however is only perceived as more shades of the colour in question. Additional photoreceptors are necessary to sense a new colour, explicitly separate from RGB.

Organisms such as mantis shrimp can sense infrared light as they have 12-16 cones, allowing them to see into the infrared spectrum.

The issue is that there seems to be no information detailing the the structure of mantis shrimp eyes, specifically regarding the the aspects of which are responsible for vision into the near infrared spectrum (roughly 700-1000nm).

What would the cones of an organism that saw exclusively in infrared look like? (assuming the organism had eyes like a human)

Would they be differently coloured or structurally different to our own?

The photoreceptors of the mantis shrimp (Fig. 1) are quite different from that of the human retina (Fig. 2).

Importantly, when light enters the units in the shrimp's eye, it must first pass through a crystalline cone, which lies over the receptors. These crystalline cones contain frequency-specific light-blocking substances called MAAs (mycosporine-like amino acids). These filters help to filter the spectrum and this means that less different opsins are necessary tod etect different wavelengths. In other words, a mantis shrimp does not feature 16 different opsins. Instead it utilizes the same opsins for various wavelengths by putting a filter on top of the cone (source: National Geographic).

Fig. 1. Mantis shrimp photoreceptors. source: Physiologizing

Fig. 2. Human cone cell. source: Wikipedia


Why are primary sensory cells considered neurons but muscle cells are not? The rough picture of cells involved in neural processing looks like this:

I wonder, why primary sensory (receptor) cells (like rods, cones, hair cells, Merkel cells) are consensually considered neurons (accidently having no synaptic input, but synaptic output), while muscle cells are not (even though they have synaptic input, but accidently no synaptic output).

The last cells that are unequivocally neurons are the motor neurons. Curiously, the first cells that are unequivocally neurons are mostly called "ganglion cells", not "ganglion neurons".

Is it all just a manner of speaking/matter of parlance and words? I believe not.

I received an interesting answer from Quora:

  "Muscle cells are derived from mesoderm, sensory cells (like all
  neurons) are derived from ectoderm."

But is this all that is to say? What’s the “deeper” source of this asymmetry? In the beginning there was only one type of cell, which was both sensory and muscle?

The quote from Quora has the correct answer; the distinction between neuronal and non-neuronal is an embryological rather than functional definition. Along those same lines, some of the other receptors you listed are considered sensory epithelia rather than neuronal. The retina is of neuronal origin, but hair cells in the cochlea are often not considered to be neuronal, despite the diagram you provided, nor are Merkel cells. The distinctions between epithelial and nervous tissue are often more difficult to identify because both derive from the same preceding embryonic tissues, whereas muscle is entirely separate.

In the end, these distinctions don't matter much unless you are interested in development or trivia (though I don't mean to discount the importance of development there, I just recommend that you don't worry too much about the distinctions if you are thinking only about final functions).


Is there a correlation between muscle fibers and body types? I have been told the number of muscle fibers a particular muscle has varies from person to person. Unfortunately, the person who told me this did not know much more than this. Initial searching on the web did not reveal much detail on this; some random sources suggested there was a correlation but they weren't referenced.

Is there a general correlation between the number of muscle fibers and body type (mesomorph, endomorph, ectomorph)?

What about a correlation between muscle fiber type (Type I/Type IIa/Type IIx/Type IIb) and body type?

A recent paper called 'Genetic Influences in Sport and Physical Performance'[1] states:

  "Muscle fibre type determination is complex. Whilst initial composition is likely to be strongly influenced by genetic factors, training has significant effects on fibre shifts."

They also go onto say that:

  "However, the role of genetic variation in determining psychological state and responses remains poorly understood; only recently have specific genes been implicated in motivational behaviour and maintenance of exercise."

Finally:

  "With the current state of knowledge, the field of genetic influences on sports performance remains in its infancy, despite over a decade of research."

An older paper which also examined fiber types stated that:

  "These results reveal the existence of large interindividual variability and gender differences in the most common characteristics of the human skeletal muscle."[4].

Another study hypothesises that there may be racial differences in muscle fibre types.[2]. It's also said that a large variation in fiber composition of skeletal muscle within subgroups of athletic ability. This suggests that factors other than fiber-type composition contribute to performance.[3].

A small study carried out in the Croatian Navy found that ectomorphs had a better ability to sprint than endomorphs.[5]. They also found a positive correlation between calf girth and sprinting ability.

The information is a bit disjointed and sparse. However, to finally come around to the question at hand, it seems that although there may be differences according to body type initially (which obviously also has a genetic basis), training and physical activity contributes significantly to what number and types of fibres individuals possess.

There are lots of sport-specific research papers examining individuals' performance and suitability on body types.

A note on somatotyping: I guess it might also be handy note that somatotyping (endomorph, ectomorph and mesomorph) is just one theory on measuring an individual and it does have critics. The theory was initially developed in an attempt to link body type to behaviour.

It's been suggested that measurements like BMI are much more objective and useful.[6]. Another point made was that bodies change according to a number of environmental variables, nutrition etc.[7]. For example, one study suggested that intense labour during adolescence may affect somatotype (there are a few similar studies).[8]. So perhaps while using somatotypes to identify a person at one point in time is useful, it has limits in use as a long term classification.

This point probably has more relevance to the question at hand since with training and physical activity, a person can potentially change their somatotype at least to some extent; and also the number and types of muscle fibers (which evidence supports).

Puthucheary Z, et al. Genetic influences in sport and physical performance. Sports Med. 2011. 41:845-59.
Nielsen J. Glucose intolerance in the West African Diaspora: a skeletal muscle fibre type distribution hypothesis. Acta Physiol. 2011. 202(4):605-16.
DeLee: DeLee and Drez's Orthopaedic Sports Medicine. 3rd ed. Saunders.
Simoneau, et al. Human variation in skeletal muscle fiber-type proportion and enzyme activities. AJP - Endo. 1989. 257(4):567-572.
Sporis G. Impact of body composition on performance in fitness tests among personnel of the Croatian navy. Coll Antropol. 2011. 35(2):335-9.
Maddan, et al. The BMI as a somatotypic measure of physique: A rejoinder to Jeremy E.C. Genovese. The Social Science Journal. 2009. 46:394–401.
Parnell. Simplified somatotypes Original Research Article. Journal of Psychosomatic Research. 1964. 8(3):311-315.
Ozener, et al. The effect of labour on somatotype of males during the adolescent growth period. Homo. 2008. 59(2):161-72.


Are there any bacteria, virus or mold that can withstand ozone? Ozonation is often promoted as one of the most effective disinfection procedures. There are numerous reports on how ozone effectively kills bacteria and molds, and disarms viruses within seconds due to its exceptional oxidative activity and small size.

Still, there are examples of thermophilic bacteria existing in volcanoes, as well as viruses in arctic ice, so they both can adapt to extreme conditions. Are there any examples of bacteria, viruses or molds (not necessarily pathogens) that cannot be killed by ozone, or at least show significantly higher resistance to oxidation?

Bacteria resistant to ionizing  radiation (e.g., Deinobacterium chartae, Deinococcus spp., Desertibacter roseus, Geodermatophilus dictyosporus, Hymenobacter actinosclerus, Kineococcus radiotolerans, Methylobacterium radiotolerans, Microbacterium radiodurans, Paenibacillus darwinianus, Pseudomonas radiora, Rubrobacter radiotolerans, Spirosoma radiotolerans, Streptomyces radiopugnans; for links to the paper describing these species, see: Bacteria I. Names), can be expected to withstand higher doses of ozone compared to bacteria sensitive to ionizing radiation.

The sensitivity to ozone of different strains of the same bacterial species can differ markedly if the strains differ in the efficiency of DNA repair mechanisms.

Brinkman et al. (1964) Radiomimetic toxicity of ozonised air. Lancet 1: 133-136.

https://www.ncbi.nlm.nih.gov/pubmed/14074479

Hamelin & Chung (1976) Rapid test for assay of ozone sensitivity in Escherichia coli. Mol Gen Genet 145: 191-194.

  ozone resistance is probably involved with DNA repair mechanism

https://www.ncbi.nlm.nih.gov/pubmed/778585


What is the difference between a "semi-contracted" muscle and a "contracted" muscle? I read on http://www.spine-health.com/glossary/muscle-tension:

  Muscle tension refers to the condition in which muscles of the body remain semi-contracted for an extended period.

What is the difference between a "semi-contracted" muscle and a "contracted" muscle?

If you consider the length of a muscle can vary from resting length to shortest length, my guess is that semi-contracted is somewhere in between. I believe that spine-health.com isn't being entirely clear with their definitions.


Is this modification of Livak's 2-delta delta CT method valid? I have done a modification to include qPCR efficiency in the calculations:

In a given gene I calculate the fold changes relative to an arbitrary sample. That sample will be one and the rest will vary according to 2-dCT (equation 13 in Livaks paper). The efficiency comes into play when 2 becomes 1+efficiency (e.g. 1.9 when efficiency is 90%).
The gene of interest will be normalized by the reference gene:
$$\frac{(1+\text{efficiency})^{-\Delta CT_\text{GOI}}}{(1+\text{efficiency})^{-\Delta CT_\text{ref.}}}$$

This makes sense to me more because it includes PCR efficiency and keeps the all groups in the calculations. But I can't tell if I am missing somethng, since no one has descirbed this approach before.

What do you think?

PCR efficiency is not usually expressed as percentage (or per-unit). Its bounds are [0 2] i.e the maximum efficiency is 2 and the minimum is 0. (Ruijter et al. 2009; also see this post for calculation of efficiency.)

However, I just noticed that some people do express efficiency as percentage or per-unit. In that case your formula would be correct. I realize that there may be a confusion within the community; so you should know what you are calculating. For avoiding confusion lets just call this measure as amplification factor (denoted by E), which would be 1 + per-unit efficiency (as you mentioned).

When the primers have different efficiencies then you can't really use the $\Delta\Delta CT$ method. You'll end up with this formula (pretty much similar to what you have mentioned):

$$\large\text{Fold Change}=\frac{\left[E_\text{GOI}^{-CT^\text{condition}_\text{GOI}}\right]\bigg/\left[E_\text{Ref}^{-CT^\text{condition}_\text{Ref}}\right]} {\left[E_\text{GOI}^{-CT^\text{control}_\text{GOI}}\right]\bigg/\left[E_\text{Ref}^{-CT^\text{control}_\text{Ref}}\right]}=\frac{E_\text{GOI}^{-\Delta CT}}{E_\text{Ref}^{-\Delta CT}}$$

Where:

$CT^\text{condition}_\text{GOI}$ means CT value of the gene of interest (GOI) in a given condition (other than control), and $E_\text{GOI}$ means the efficiency of the primers for your GOI.  Similarly for the reference (Ref).

See this post too.


Can animals also get Down syndrome? I heard that animals cannot get Down syndrome or trisomy. Is that true and why can't they get it? They also have chromosomes.

Animals can be generated with genetic defects similar to Down Syndrome, but not that exact condition, except in the case of great apes.

Down Syndrome is a kind of defect called a chromosomal abnormality, meaning that either there is an extra chromosome or an excessive repetition of the same genes on a particular chromosome. In the case of Down Syndrome, that repetition in on a region of the 21st chromosome. Similar abnormalities in other chromosomes are possible, such as the abnormality which causes Klinefelter Syndrome.

Although animals do have chromosomes, they have different chromosomes than human beings do. For example, a horse has 32 chromosomes whereas a human has 23. Apes are most similar to humans, having 24 chromosomes. Therefore, if trisomy is to be found, apes would be most likely to have it. Researchers have attempted to answer this exact question and there is a paper on the subject entitled "Conservation of the Down syndrome critical region in humans and great apes".

The result of this study was that the area on chromosome 21 in humans that is responsible for trisomy is found analogously on chromosome 22 in apes and that apes can, indeed, get Down Syndrome, if they have duplication of this region. There do appear to be apes that suffer from this condition. The band diagram for both chromosomes is shown below:

where "H" indicates human and "C" indicates chimpanzee.


Role of microvilli in cell volume regulation Does the presence of microvilli on a cell's surface ensure that it's more resistant to cell swelling or lysis in a hypotonic solution, as compared to a normal cell?

Microvilli, are cellular protrusions on the membrane and hence they increase the total surface area of the cell in context.

If we evaluate the characteristics of microvilli and the structural appearance, we know that; they have many small folds; strengthened and lined by the protein filament actin; bedded in a terminal web of alpha-actinin and keratin. All of these characteristics, work in harmony to support its ability, for it to do its function. That being, to allow greater diffusion whilst controlling the cells integrity. Evidently, the microvilli do help resist the hydrostatic pressure within a cell as a result to the distribution of pressure and the microfilaments present.

Most animal cells have microvilli so, there is a huge excess of factual evidence to support what happens to them in under specific conditions. Knowing this, it confuses me why you even asked this question. It just takes a simple comparison.

I'm presuming, a normal cell is a cuboidal cell, too. So, yes, if they were both placed in a variable hypotonic solutions, with gradual increases in concentrations for comparison, the cuboidal cell would rupture much earlier rather, the cell with the microvilli would be still standing at a further stage (concentration). However, the cell with the microvilli will nearly all of the time still lyse despite it's additions. Microvilli don't sorround the entire cell, if they did, the integrity of the cell in greater hypotonic solutions would be more applaudable vs a plant cell (cell wall containing pectin).

Yes

References:

**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'keratin is a type intermediate filament in cells' [...] 'The nucleation of actin fibers occurs as a response to external stimuli, allowing a cell to alter its shape to suit a particular situation.'

**
http://www.westfield.ma.edu/personalpages/draker/edcom/final/webprojects/sp10/cell/Ross44.jpg; 'A hypotonic solution has decreased solute concentration, and a net movement of water inside the cell, causing swelling or breakage.'

**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'Intermediate filaments are inserted into desmosomes at cell-cell junctions, and help to maintain cell-cell connectivity, as well as the structural integrity of the cell itself.'

P.s. Most of the answer was achieved by the application of knowledge so, direct references cannot be found!


Trying to understand the big picture behind DNA sequencing, alignment and searching I'm about to start a bioinformatics research project but I haven't any biological background.

I know my project is in regards to a performance analysis of DNA sequencing and searching "weapons" like Hadoop, Apache Spark and Apache Flink - so I've spent the last couple of days trying to put together the "DNA picture" before I get started with the programming stuff.

My understanding of the situation is that:

Next-generation sequencing (NGS) techniques are used to efficiently provide reads of DNA (conversions from real, physical DNA to something that can be read and analysed), however today's most practical methods provide reads that are short and in disorder.
Reads tell us which nucleotides, labeled one of ACGT, occur in sequence. Different nucleotides or values to take their place may exist, like N or X. Reads could range from 50 to 1000s of nucleotides in length depending on the method of sequencing.
You can find historical raw read data in various places online, including the Sequence Read Archive (SRA). The same website contains lots of other DNA/bio related information. Reads are commonly stored in .fasta files which follow a simple and practical standard. A single file could contain a very small or very large read or sequence.
Reads are then provided to DNA alignment programs like bowtie which will place them back in the correct order. The algorithms could use a template sequence to align them, or run "de novo" (without a template). The result of these alignments have also been indexed online however for the purpose of my studies I'll probably be aligning them myself.
Once aligned (or maybe during alignment), nucleotide differences from a template sequence can be programmatically found or searched for, with crossbow for instance. Note that many other tasks can too be performed - not only this search. If a particular substitution occurs in more than 1% of a what I think is called a "genome's" population, then it is called a Single-nucleotide Polymorphism (SNP or snip). Most SNPs have two alleles, or two different recorded nucleotides (like either G or C), but more than two is possible.
SNPs can be studied and mapped to various conditions or characteristics. A particular nucleotide could be responsible for part of one's emotional tendencies, reaction to particular medicines, or maybe anything, so a particular SNP could make a big difference.

What am I missing/what did I get wrong?

Here's a quick summary of a few mis-hits in your otherwise good analysis:

Not many bioinformatics applications use Hadoop, Apache Spark or Apache Flink. In fact, I have never heard of the Apache Spark and Flink tools, and I've seen only 2 people use Hadoop to process alignment files.

Reads are not "converted" real, physical DNA. They are representations of the signals from the molecules making up the DNA, as read by sequencing machines.
A,T,C,G are molecules making up DNA. N refers to "any of A,T,C,G", which translates to either unknown or ambiguous.
Reads are stored in FASTQ files. Sequences are stored in FASTA files. Reads include sequence as well as quality information, so, FASTA+QUAL=FASTQ
Re-ordering is a crude but approximate way to think about it. Remember, this process involves overlaps while reordering seldom does. Overlaps are crucial to the process of assembly/alignment. You are correct about the alignment to reference sequence and de novo assembly parts.
This is correct, though statistical models are applied to account for differences that are not necessarily significant variants (such as for sequencing errors)
Yes, variants, which include SNPs, can be correlated to differences in phenotype (traits). Emotional tendencies is something a bit too advanced, think of something more basic like diabetes or eye color.

The picture you have here is of a regular NGS analysis pipeline. This involves alignment/assembly, variant calling and biological analysis with relevant hypotheses. The assembly/alignment is the most computationally expensive part, and we use either HPC clusters or scalable cloud services such as AWS to get this done.

You should definitely talk to a biologist that has some computational experience to gain insight into the reason behind our analyses. Once you understand the motivations, your contribution will be more relevant and helpful to the community.


Could I use spiders to catch unwanted insects? I was wondering if its possible to catch spiders and place them in my greenhouse in order to kill unwanted insect that feast on my plants? I don't really mind presence of spiders since then are not dangerous in my country (Czech republic).

Common species that live outside are Araneus diadematus, we got many that live in presence of human like Tegenaria domestica, but I read that they are type that live at human build constructions and can't really survive outside.

What you describe is called biological pest control. Lacewings and earwigs are more common, but there are ways to use spiders.

http://unossc1.undp.org/GSSDAcademy/SIE/Docs/Vol4/Rearing_spiders.pdf

http://www.annualreviews.org/doi/abs/10.1146/annurev.en.29.010184.001503?journalCode=ento


Since Darwinian times, has there been any striking/notable effects of evolution on humans? I understand that evolution is constant process that acts on a population in successive generations. Thus, it is obvious that evolution is happening. However, I'm curious as to the  stricking examples of evolution that have occurred since Darwin's publication of the theory.

Essentially, how different are we now from the humans at the time at which evolution was conceived?

Well, "On the origin of species" was published in 1859. If we assume that for humans a generation is approximately 20 years, that means that there have been between seven and eight generations since 1859. That is nowehere near enough time to observe evolutionary changes.

So, in answer to your question, not very different at all.

EDIT:

I think I need to clarify my answer. When we talk about a species evolving or a species being different today than it was X years ago, we are referring to the species as a whole. Of course evolution is an ongoing process, selective pressures are shaping our gene pool constantly. However, in order to say that humans are different today to those of 1859, we would need to show that the prevalence of particular genotypes has changed. That a specific trait (a gene or a mutation in a gene) has become "fixed", or, at the very least, that it has spread to a significant percentage of the population.

@niallhaslam's answer gives a link to a wired.com article about genetic resistance to HIV. This is not something that has recently evolved in response to HIV but is the result of an ancestral mutation. The article itself states that:

  Using formulas that estimate how long genetic mutations have been
  around, researchers have discovered that the mutation dates to the
  Middle Ages.

Granted, this could be a good example of selection in action. If, after many, many more generations, this mutation has spread to the majority, or a significant percentage, of the population, we could point to it as an example of how humans have changed under the selective pressure of HIV infection. In order for this to happen, HIV will have to become common enough that having a resistance to is beneficial to a very large subset of humanity. I would expect to see such selective pressure in, for example, countries like South Africa where 12% of the population is HIV positive. Such pressure, however, will be negligible in countries with lower infection rates. In the US, for example, a recent study found HIV incidence among persons aged 13 years and older to be 42,200–54,000. Since the US has ~312 million people, 54,000 represents ~0.02% of the population. This will not provide enough of a selective pressure to observe differences in the short term evolutionary scale.

We do not, in fact, "evolve quickly in response to parasites viruses etc". Pathogens may apply selective pressure yes. But this is not a quick process. In any case, we do not evolve in response to them. Mutations occur, randomly usually, and if they confer an advantage they may be selected for. Said advantage may be because they confer resistance to disease but even then, the original mutation was not "in response" to the pathogen, However, such selection happens over many successive generations and will spread relatively slowly (quickly by evolutionary standards perhaps, but still slow for us, and certainly slower than 7 generations) across the population. The same holds true of epigenetic changes. Even if they can (as now seems likely) be transmitted down the generations, any selective advantage they confer will still act at the generational level.

So, while we are, of course, constantly evolving, there are no significant differences between the humans of today and those of Darwin's times. Sure, some genotypes may exist today that did not then and vice versa. These, however, are not representative of the species' genome. They may become so after many generations but, even if they exist, they have not had time to propagate through the gene pool and cannot be taken as evidence that H. sapiens as a species is "different" today.


What exactly does 'reverse use-dependence' mean? I understand 'use-dependence' related to a drug, for instance, more angiotensin2 effects in a hypertensive more prominent is the action of angiotensin2 receptor blockers. But I do not get the term, 'Reverse use-dependence'.

https://en.m.wikipedia.org/wiki/Potassium_channel_blocker
In this site, in Medical Uses, the term is mentioned.

Reverse use dependence is the reduction of a drug's efficacy with the repeated use of the target. This contrasts with ordinary use dependence, for instance with $\mathrm{Na}^+$ blocking local anaesthetics, where they exert more block after tissue use. Reverse use dependence is particularly (but not exclusively) seen with channel blockers such as quinidine.

Quinidine is a $\mathrm{Na}^+/\mathrm{K}^+$ blocker that can slow heart rates, and does so more effectively when the heart rate is already slow. Increased use of the tissue, with a raised heart rate, reduces the effectiveness of the drug. So, strangely, quinidine exerts less block when the target is in use. This is shown in figure 4 from (Breithardt et al., 1995). As the tissue is used less (cardiac cycle length increases), the effect of the drug becomes stronger (action potential duration prolongation increases).

The reverse use dependence of quinidine can be demonstrated on a molecular level with application of quinidine to a voltage-clamped channel with an $\mathrm{i}_\mathrm{Ks}$ current. We see better block when short electrical pulses are given than when longer ones are. The mechanism behind use- and reverse use dependence is by state-dependent affinities, e.g. the drug can bind more easily to the channel in open/closed state. For example, a channel blocker whose binding site becomes occluded when the channel is opened could exhibit use dependent block.

But be warned: reverse use dependent drugs may also exhibit normal use dependence. Quinidine is not just reverse use dependent, but also use dependent
as a $\mathrm{Na}^+$ blocker. The type of tissue and its state change the effect of the drug and must be taken into account.

See (Breithardt et al., 1995) for a review of the topic:

  In 1990 Hondeghem and Snyders introduced the concept of reverse use dependence as being a drug effect which is less marked with increased use. Specifically
  quinidine, N-acetyl-procainamide and sotalol lengthened action potential
  duration markedly at slow heart rates but much less or not at all at fast heart rates
  (Fig. 4 [27)). Frequently, reverse use dependence has become equated with reverse
  use-dependent block of ion channels. Although reverse use-dependent block of ion
  channels can lead to a reverse use-dependent drug effect, this does not need to be
  the case. Worse, reverse use-dependent drug effect does not require reverse use dependent block of channels.

References:

Breithardt, G., Borggrefe, M., Camm, A., Shenasa, M., Haverkamp, W. and Hindricks, G. (1995). Antiarrhythmic Drugs. pp.97-98.


Is the SHC014 chimeric coronavirus "eerily similar" to Covid-19 in anything but a journalistic sense? Gulf News writes:

In the virology community, their project is known as "chimeric coronavirus", eerily similar to COVID-19. This chimera is created in a petridish, reportedly with the "surface spike protein (S protein) of a coronavirus found in horseshoe bats, called SHC014, and the backbone of a SARS virus that could be grown in mice".
Here's the scary bit: In the lab (we don't know which one), this new coronavirus was found so potent it could infect and replicate in human airway cells naturally. It also infected mice lung cells. It's one of the experiments which prompted Prof Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, to warn that such research is "misleading" and "irrational", stating thus: “The consequence of any accident would be anywhere from a handful of infections to a catastrophic pandemic.”

Is this SHC014 chimeric coronavirus "eerily similar to COVID-19" in a scientific (not just journalistic) sense? Have any scientific publications drawn a parallel between the two viruses?
(I know that SARS-CoV-2 is most closely similar to RaTG13 at whole genome level and at RBD level [most likely] to Pangolin-CoV. I'm asking what if any scientific relevance does SHC014 have to Covid-19.)

The "similarity" of this specific chimera was addressed in a recent paper concerning the lack of evidence that SARS-CoV-2 is lab-grown:

  Another claim in Chinese social media points to a Nature Medicine paper published in 2015 [7], which reports the construction of a chimeric CoV with a bat CoV S gene (SHC014) in the backbone of a SARS CoV that has adapted to infect mice (MA15) and is capable of infecting human cells [8]. However, this claim lacks any scientific basis and must be discounted because of significant divergence in the genetic sequence of this construct with the new SARS-CoV-2 (>5,000 nucleotides).

Liu, S. L., Saif, L. J., Weiss, S. R., & Su, L. (2020). No credible evidence supporting claims of the laboratory engineering of SARS-CoV-2. Emerging Microbes & Infections, 9(1), 505-507.

The "eerily similar" nature seems at most to be something well recognized by virologists, particularly in the wake of SARS: coronaviruses circulating in bats could become dangerous to humans if mutations occur in key parts of their genome or recombinations occur with other coronaviruses in bats or intermediate hosts. That's more or less what happened with the first SARS and more or less what happened with SARS-CoV-2, as best as can be told right now.

I'd also take a bit of umbrage at the language used in that article:

  this new coronavirus was found so potent it could infect and replicate in human airway cells naturally

seems like a bit of fear-mongering. Any virus that affects humans can "naturally replicate" in human cells: the author could have merely written that instead of calling it "so potent".


Could the denaturation of protein during cooking could generate a prion, by any chance? It may sound silly, but it appeared to me as a theoretical possibility; not a practical fear.

On a healthy and correctly folded protein if cooking process is applied (that includes heating and mixing with various other things), is there by any chance a possibility to develop a prion?

Just my speculation here. Prions seem to need some sort of template to guide their folding as well as the cooperation of chaperone proteins. https://en.wikipedia.org/wiki/Prion  I would suspect that denaturing, and potential re-folding, of proteins during cooking would be rather random. So even if one, or very few, copies of a potential prion happened to be produced, the high temperatures, rapid pace of denaturation and the lack of chaperone proteins would not allow the formation of meaningful amount of potential prions to cause disease. Add to that the doubtful chance a prion would be produced in the first place, due to the lack of the usual physiological conditions and participants, feel free to eat cooked food!


Did not understand a small excerpt from a research paper Was going through this paper, among multiple things that i did not understand, I came across this part:

  Each amino acid residue of a single
  window was encoded into a unitary bit string of length 20, where a
  bit was set (value = 1) if its position in the string corresponds to the position of the amino acid residue and zero otherwise

Did not understand this line. Someone please explain what position they are talking about

The paper's description is poor, but they seem to be describing an encoding where each of 20 possible amino acids are associated with a position within a string of 20 bits, e.g. alanine with offset 0, cysteine with offset 1, etc.  With that representation, one amino acid residue within a window is encoded by a string of 20 bits, 19 of them being 0 and the other a 1; the single 1 bit occurring in the place corresponding to the residue.

This interpretation is supported by the paper's citation of  Qian N, Sejnowski TJ (1998) "Predicting the secondary structure of globular
proteins using neural network models." J Mol Biol 202: 865–884.  Qian's paper says:

  Each group has 21 units, each unit representing 1 of the amino acids (or spacer). For a local encoding of the input sequence, 1 and only 1 input unit in each group, corresponding to the appropriate amino acid at each position, is given a value 1, and the rest are set to 0.


What does the term "relay competent" mean? I was reading the article of Dallon & Othmer (2010) which deals with cell aggregation in Dictyostelium discoideum. In the introduction of the paper it is said that cells becomes "relay competent". I googled for the term but could not find a good explanation for it.

  After a period of starvation they become chemotactically sensitive to cyclic adenosine 3 , 5- monophosphate (cAMP), as well as relay competent.

Can someone help me understand this term?

If you read the lines immediately following your quoted line (on p.391, left column, last paragraph in the linked article) it becomes clear what relay competent means (and I quote):

  As a result, the cells sense and move toward a source of cAMP, and they relay the signal as well by secreting cAMP. [..] After about 8 h of starvation randomly located cells, called pacemakers, begin to emit cAMP periodically (Raman et al. 1976), the chemotactically competent cells move toward these pacemakers, and eventually the entire population forms a mound-shaped aggregate of up to 105 cells.

In other words, starvation makes cells move toward cAMP by chemotaxis, and  makes them secrete cAMP as well, which factually relays the cAMP signal back to other cells that are also attracted to cAMP due to starvation.


Why would a 2019-nCoV protein sequence in the NCBI database match a protein submitted in 2018? There seems to be a bit of a conspiracy theory brewing over some data in the NCBI database, and I don't have the necessary knowledge to make sense of it.

It basically goes like this:

Go to NCBI BLAST
Click on the big Protein BLAST button
Enter AVP78033 in the main search box and click BLAST
Click on the first result that shows a 100% match and click "See 5 more title(s)" in the first entry

This shows that the search is a complete match for a Bat SARS-like coronavirus protein from a 2018 research paper, for Wuhan seafood market pneumonia virus (which the NCIS site indicates is an alias for 2019-nCoV), and for Bat coronavirus from 29 Jan 2020.

My question is - why would a protein from Bat SARS-like coronavirus and 2019-nCoV be showing up as a perfect match for one another? Does this mean that 2019-nCoV might actually be a previously-discovered coronavirus that very recently started infecting humans? Or could it be that a recently collected sample from Wuhan was mis-identified as 2019-nCoV when it is actually the same coronavirus from the 2018 submission?

Clicking around the links on that site seem to bring up dozens of similar but different pages that I don't have the knowledge to distinguish, but the Accession column from the search results described above contains a link to this page, which says that it is a provisional refseq and acknowledges that it is identical to the bat coronavirus:

  PROVISIONAL REFSEQ: This record has not yet been subject to final
              NCBI review. The reference sequence is identical to QHD43418.
              Annotation was added using homology to SARSr-CoV NC_004718.3.

Can somebody who actually understands these things please make sense of this?

2019-nCoV is a virus that originated from the bat (at least this is the current hypothesis). It shows 96% squence similarity to the BatCoV RaTG13 sequence (see reference 1), showing its origin.

It still is 87,99% identical to the "Bat SARS-like coronavirus", which explains the hit you found and is not unexpected, as these viruses are very closely related (see reference 2).

These viruses are closely related, so I wouldn't expect too many differences at all. Then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. Additionally, due to the redundancy caused by the codon degeneracy, not every mutation in the genomic material translates into changes in the protein.

References:

Full-genome evolutionary analysis of the novel corona virus
(2019-nCoV) rejects the hypothesis of emergence as a result of a
recent recombination event
Genomic characterisation and epidemiology of 2019 novel coronavirus:
implications for virus origins and receptor binding


Name of this kind of stain on fruits and how do they form Last year I made some photos with avocados touched by some stains. They were even more delicious than the regular ones.

What's the name of such stains and how do they form? My guess is that they form because the fruit was hurt but maybe that's just me.

Later edit: A farmer told me it's a disease. Then I've found that it looks quite similar with apple scabs. Is it correct to call this "Avocado scab"? Is it made by the "Sphaceloma perseae" fungus?

Here are the photos:

You never visited the avocado blemish identification fanpage? do you use google? it's quite good.

http://ipm.ucanr.edu/PMG/C008/m008fpfrtdmg.html
Causes of avocado Damage

Avocado thrips

Anthracnose

Caterpillars

Branch canker and dieback

Fruit and stem-end rots

Genetic mutations

Greenhouse thrips

Latania scale
Mechanical injury

Nutritional disorders

Off-season fruiting

Persea mite

Phytophthora fruit rot

Sooty mold

Sunblotch

Sunburn

Vertebrates

Weather extremes

Wildland fire

mosty they are insects, funghi, viruses, mechanical forces, and sometimes, like the woody avocado, the cause is unknown:

referenced.


Pharmacological inhibition of Ras I was reading this review and came by this:

  Direct pharmacologic inhibition of RAS has been a major challenge.
  Interference with the nucleotide-binding pocket of the protein seems
  to be far more difficult than interfering with the analogous
  ATP-binding pocket in kinases. This is presumably due to the much
  higher (picomolar) affinity of RAS for GTP.

What is meant by affinity? How do inhibitors work (in this context)?
Kindly help me as to what does this mean, I am new to biochemistry.

Protein binding interactions are usually referred to by how easily the binding partner can be displaced by something other than the preferred substrate. Usually, this is in reference to the concentration of the binding partner required such that the average occupancy of the protein (in this case RAS) to the binding partner is ~ 50%.

If the affinity protein for a given binding partner is in the picomolar range, that means that it binds so tightly that very very little substrate is needed to achieve 50% occupancy. In order to interfere with RAS's preference for GTP, you would have to design something that RAS likes to bind to with even greater preference that would be able to displace GTP. This has proven quite challenging.

Other kinases, whose affinity for their substrate is not nearly as high, have been easier to design molecules that displace their endogenous ligands and hence interfere with their function.

I know it is Wiki, but the activation/deactivation section of this Page provides some insight into how RAS binds GTP and turned on, how GAP functions to help RAS hydrolyze GTP->GDP, resulting in turning off RAS downstream signalling. RAS signalling is actually a balance between Guanine nucleotide exchange factors causing RAS to drop GDP for GTP (turning RAS on) and GTPase activating proteins mentioned above (GAP).

Mutated RAS in cancer often involves a coding change such that the ability to hydrolyze GTP->GDP is mitigated, thus leaving RAS in the ON state.

For your initial question of inhibitors (and more general). Cellular signalling involves the interaction of proteins with other proteins and/or signalling molecules and/or DNA/RNA. Very generically, inhibitors interfere with this interaction.

Example: Kinases add a phosphate group to another protein, that can among other things change the affinity of that protein for its binding partners, and thus set off a downstream signalling cascade. If kinase A phosphorylates protein 1, and you inhibit kinase A from doing this, you have inhibited downstream effects from protein 1's signalling cascade.

Take a look at this picture:  The two drugs in red interfere with downstream signalling cascades in B-cell receptor signalling by preventing endogenous binding/signalling events.


How does Darwinian Evolution work? Let me explain... A friend and I read some articles, part of a Biology book, and watched a video on evolution. We then tried to explain what Evolution is to each other.

My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

So is the DNA mutation process random or is mutation directed to make an organism that is suited to survive its environment?

None of my friends are Biology students, so I can't ask then which explanation is correct (or at least more valid).

I'd prefer you don't answer: "None of these explanations are correct," but to say which one is more valid and correct misconceptions or add more that is missing (of course these are only summaries of our discussion). But of course, you can answer that neither of our explanations is correct...

I accidentally wrote a lot!

I first discuss the term Darwinian evolution. I then describe the main evolutionary processes insisting on the two elements of interest in your question, that is mutations and natural selection. In the end, I directly address your two statements and bring a few more complications into the subjects.

Did you say Darwinian evolution?

Evolution is more than Darwinian evolution

The expression "Darwinian evolution" easily yield to misunderstandings. Darwin was probably the most important scientist and one of the first (if not the first) to develop the theory of evolution but evolutionary biology today is so much more than Darwin's theory of evolution.

Examples of very basic things Darwin did not know

We discovered the structure of DNA in the 1950s-1960s only with Miesher, Chargaff and most renowned Watson and Crick (history of the discovery). Darwin had no idea of the existence of DNA and had not even hypothesized about the existence of such a molecule (which came first by Erwin Schrödinger).
Darwin was not aware either that inheritance was through the transmission of "particles/atomic" and not through the inheritance of some kind of "fluid/continuum". In other words, Darwin did not know the Law of Segregation by Gregor Mendel (even if they lived in the same epoch).
Darwin had no idea about Evo-Devo, that is he had no idea about the similitudes in developmental processes among related (even distantly related) organisms.
Globally speaking, while Darwin managed to touch a little bit about many of the subjects of modern evolutionary biology (which is very impressive), he only manages to mention them and failed to provide any prediction. This is a large part because no one had no concept in genetics at that time.

Evolution is more than natural selection and mutations

Evolution is not only about natural selection. Even C. Darwin knew that evolution is way more than natural selection. It is for example very important to consider random events. One of them is mutation, another is genetic drift (I am not trying to list every process that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment. Evolutionary biology is a big field of knowledge and there is a lot to know about evolutionary processes.

Natural Selection and Mutations explained by the Lewontin Recipe

The Lewontin's recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin's recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.

Natural Selection

Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.

Mutations

In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.

Genetic drift

If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo a more random change in frequency of their genes than are big population.

Considering your opposing statements

Hopefully, the following is clear from the above discussion but I would like to directly address your statements.

  My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

You are right that your friend is wrong!

It indeed sounds more or less Lamarkian. In any case, it is very wrong, as you said. Mutations are not caused deterministically under the pressure of natural selection to do specific things.

Are mutations completely random?

See Are mutations random?.

I do not want to go into too many complications. The sentence "mutations are random" is unclear. Does it mean that the mutation rate is random? Does it mean that the effect of a new mutation is random? And also the concept of randomness only make sense if we consider a set of a priori knowledge. So it is a little hard to fully answer this question and the easy, close-enough approximation for a starter in evolutionary biology is just to say that mutations are random (whatever that means). A slightly better approximation of reality is that mutation rate is an adaptive trait and can vary depending on the environment where the individual is found (adaptively or not). However, the effect of new mutations is really not deterministic.

The mutation rate varies with the type of sequence considered. For example, a microsatellite sequence is a sequence or repeated DNA. For example AATAATAATAATAATAATAAT etc.. (note that the genetic code is written with 4 letters, A, T, C and G). Such sequences are highly mutable. So a mutation is more likely to occur in this region than in the middle of a coding region. And it is more likely for a mutation occurring in a coding region to affect fitness than for a mutation occurring in a microsatellite (it is possible that a mutation occurring in a microsatellite will affect fitness).

Depending on the level of stress some organisms (plants mostly to my knowledge) can change their mutation rate. Consider for example an individual that is maladapted to its environment. If it mutates little, then the offspring will likely be as maladapted and in the long run, the lineage will disappear. If the individual is mutating a lot then, most offspring will have a very low fitness but eventually one will receive a beneficial mutation that will make it very strong and by itself, this offspring may save the lineage. This is what is called a bet-hedging strategy. The concept of bet-hedging can be summarized with the expression "Don't put all your eggs in the same basket".

You will note that the mutation rate is an evolving feature of an organism. This yield observation such as what is now called Drake's rule (original paper). Drake's rule indicates that the genome-wide mutation rate is always at the order of 1 (there is quite a bit of variation but it is a good approximation).

  I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

Sounds quite right!

You pretty much nailed it. Mutation adds genetic variation and natural selection selects from the available genetic variation. Your wording is a little uncommon though :). For example, an individual, it is incorrect to say that an individual has fitness or not. Each individual has a fitness, that is some value that encompasses both its fertility and survival probability. In a simple model, fitness is simply the expected number of offspring.

Note also, that the majority of mutations that affect the fitness of the individuals are not so much dependent on the details of the environment. Many mutations are just bad wherever you are. Think about a mutation that would reduce the efficiency of energy production (ATP in mitochondria). Such a mutation will be deleterious regardless of whether the weather is hot or cold for example.

Introductory course to evolutionary biology

You probably want to have a look at an introductory course to evolutionary biology such as Understanding Evolution.


What are the molecular mechanisms behind tachyphylaxis (downregulation of receptors in response to an agonist?) Anyone know of a good source which explains this?  Or is this still an open question?  This wikipedia article describes some molecular biology behind morphine tolerance, but it sounds like its newer research, and isn't fully understood. http://en.wikipedia.org/wiki/Drug_tolerance

I would have thought that something like this would be very well understood.

There are many mechanisms of receptor down-regulation, including internalisation and degradation e.g for the epidermal growth factor receptor and uncoupling via post-translational modifcation e.g. for G protein-coupled receptors.

In the case of opioid receptors there is emerging evidence that down-regulation is achieved, at least in part, by post-transcriptional regulation by a microRNA. Presumably this could also accompanied by inactivation of existing receptors, but if the adaptation/desenitisation is long-term then normal receptor turnover may be sufficient.


Evolution, What would the first plants have been like? I am curious what the first plants are thought to have been like, what they may have evolved from, and how much earlier (or later) than animals they are thought to have moved to land, if they even started in water like animal-life?

You can have a look to the most basal branches and you may get a pretty good idea of what those early plants looked like.

What we call plants is what we call plantae or Archaeplastida in Latin. This clade contains the red algae and the green algae. Within the green algae are the land plants. In the land plants are the embryophyta which contain all what you think of when talking about plants. Below are a bunch of pictures so that you can get an idea of what the basal branches look like.

(Basal Plantae) Red algae

(Basal Green Algae) Green Algae

(Basal embryophyta) Green Algae > Embryophyta > Hornworts

(Basal embryophyta) Green Algae > Embryophyta > Mosses

You can explore the tree of life by yourself by going on tolweb.org. You can try to find the apple tree, the ladybug of the human by clicking on the links. It is fun and it is good to learn a bit how the tree of life looks like.


Which of these components has C-H and COOH groups A) Amino acids and triglycerides that have a carbon-carbon double bond

or

B) proteins and fatty acids

I think they are both true, but I should choose only one
I think that because since amino acids have COOH and C-H group, proteins do too and fatty acids have these groups too just like triglycerides with a double bond. But since I have to choose one I would choose B. Am I right?

Answer A is wrong because triglycerides are esters not carboxylic acids so they have -COOR group, not -COOH. Amino acids and fatty acids have -COOH groups and proteins too - on C-termini and in side chains.


Why do Lapidaria margaretae look like stones? Previous Research

I stumbled across a trending reddit post "Lapidaria margaretae looks like stones" (as of 3rd Februrary 2015); but I could not find discussions as to reasons behind why.

Question/s

Why do Lapidaria margaretae look like stones? I am interested in both the morphological/physiological reasons, as well as possible evolutionary mechanisms.
Or perhaps I am asking the wrong question, then what should it be?

"Teleology is like a mistress to a biologist: he cannot live without her but he's unwilling to be seen with her in public." - J.B.S. Haldane (1892 - 1964)

I can't tell you why Lapidaria margaretae looks like 'stones'. But I can deduce something from the way this plant looks.

First and foremost, I can say this plant probably evolved in an arid region, possibly a desert (less than 10 inches of water per year), because it is a succulent, with a shape that comes pretty close to minimizing it's surface to volume area (decreased evaporation, decreased transpiration). Seeing as it's a dwarf and shaped as it is, I might hazard that it's windy and sandy where this plant evolved, also because of it's shape - low to the ground, sturdy, low surface area, able to resist the wind. Finally, the light color of the plant suggests a lot of bright sun (reflects sunlight more than some darker colors).

None of that is foolproof, but in this case, it turns out to be right; the plant comes from southern Namibia, and is commonly called the "Karoo rose".

This is one image of the Karoo region:

Stones come in all kinds of shapes and sizes, also influenced by water, wind and other environmental influences. That this plant looks like stones is mostly coincidental.


Why can't people talk while inhaling? Why do we have to exhale in order to talk? From looking on Wikipedia, it seems like it has something to do with the glottis, but I'm not clear on the mechanism that makes speech sound so different when air is coming in.

Via deep scientific analysis (i.e. trying it myself 5 seconds ago), I have determined that you can in fact speak while breathing in, it just sounds funny.

Think of the vocal chords as being like the body of a flute. As air passes by them, they vibrate and make sounds. Through careful modulation of their shape, specific sounds can be reproducibly made (this is equivalent to opening and closing the stops on the metaphorical flute). The way the pressure in your throat changes when you inspire (breathe in) is very different from the way in which the pressure changes when you expire (breathe out). These pressure differences are a large part of the reason why you sound different when you speak during inspiration as opposed to expiration, just like breathing into a flute differently would produce different sounds (although potentially the same notes).

Other physiological, neurological, etc. effects probably also cause differences in the vocal cords during expiration/inspiration and thus also contribute somewhat to the differences in the sound.


High protein turnover rate and protease inhibitors? I work with mice, and I want to see what happens to some specific proteins in the mouse brain after IL-1b injection (intracerebroventricular).

I have a problem: when I measure the mRNA and protein levels, I see that there are some differences between them.

It can be like:  mRNA (upregulated)  Protein (no difference)

Is it possible that these proteins have a high turnover rate? If so, how can I prevent that?

Can I (if it is possible) inject (intracerebroventricular) IL-1b mixed with protease inhibitors?

Scientists are recently finding (or coming to accept the notion) that, at least in eukaryotes, mRNA expression is poorly correlated to protein expression. There are several factors influencing translation regulation, such as siRNA or microRNAs, sequestering mRNAs while they are transported to various cell compartments, and others.  Even after the protein is made, there can be factors interfering with your expression reporter.  And as you mention, it may be degraded faster than you expect.  Cells try to keep proteins at certain expression levels, so if IL-1b is promoting expression without inhibiting the degradation pathway, degradation might kick into overdrive to bring the levels back down to normal.

Trying some protease inhibitors is worth a shot, since it's pretty simple by itself.  It should also increase your protein expression regardless of whether protein degradation is your limiting factor. If this doesn't work, or if it's prohibitively expensive to be sacrificing mice while you're working out a protocol (and is usually is), then I would turn to cell cultures and try and discern where you're getting blocked.  That kind of information will generally make a decent PNAS paper by itself.


Insect identification - Possible grasshopper or grass beetle We found a small insect on our window and we cannot decide whether it is a type of grasshopper or grass beetle. It doesn't seem to want to fly, but was on a first floor bedroom window, and walks slowly and has a strong grip on the window and petri dish. We live on the outskirts of a town in Essex, UK and it could have come from a field, but they are on the other side of the house. It is a small brown insect (the main body is approximately 2cm long) with 6 legs, and the back 2 legs seem to bigger than the others.

Neither beetle nor grasshopper, it is a hemipteran, Coreidae. Leptoglossus occidentalis or
Western Conifer Seed Bug.  https://www.britishbugs.org.uk/heteroptera/Coreidae/leptoglossus_occidentalis.html


Where does the mass come from when you grow plants in water? How do plants like green onions seem to grow forever when put in jar of water?  I understand that plants get a lot of their carbon from the air (as per this question) but surely they need more than just carbon to grow new leaves.

The answer in the linked question mentions that plants in general get their mass from sources like water and nutrients like nitrogen and phosphorous, and ions.

However, if a plant is growing directly in [distilled] water where will it get those nutrients (like phosphorous and the ions) from?

Where does that extra mass come from?

Short answer
Plants with storage compartments can grow for extended periods on water alone.

Background
It indeed seems the question is indeed different from the suspected dupe after all.

According to Turesson (2014)

  Seeds, tubers and roots are the most common sites for [...] energy storage and the forms in which energy is stored are predominantly oil, starch and sugars. Underground storage organs mainly store starch and sugars, while seeds from different plant varieties accumulate high levels of starch and also oils and proteins.

So storage compounds like "seeds, tubers and roots" can sustain prolonged growth in the absence of pretty much anything, except water; just consider the familiar seedlings of cress on cotton wool (Fig. 1). There's basically nothing there, just water.

Fig. 1. Cress grown on cotton wool and water. source:Dreamstime

Reference
 - Turesson,  Carbon Allocation in Underground Storage Organs, Doctoral Doctoral Thesis (2014), Swedish University of Agricultural Sciences
Alnarp


How does the molecular machinery choose where to cut a chromosome for recombination? I'm wondering about a few technicalities of crossover in meiosis. The point of crossover is to create new chromosomes that don't have the same allele combinations as the original two chromosomes. Usually, the chromosomes are cut at the same place on both chromosomes, and each piece is then stitched to that place on the other. This is to avoid unequal recombination, a scenario in which one chromosome has several instances of a gene and the other no instance at all. I'm wondering how the molecular machinery knows where to cut.

So here's my question: How does the molecular machinery choose where to cut a chromosome for recombination?

This question has two parts: At what type of place does it occur (does the machinery choose a completely random place, regardless of where genes start and end, does it just cut at the start of genes, or does it do something else)? Given that it happens at this type of place (e.g. start of a gene), how does it decide that it will cut here (the start of this gene) and not there (the start of that gene)?

In humans and mice anyway ,a lot of it boils down to the recognition of a specific sequence that marks recombination hotspots by PRDM9.
http://www.sciencemag.org/content/327/5967/836

Edit - I'm expanding in response to the comment below...

Meiotic recombination occurs at vastly greater frequencies in some locations in the genome than others and these are called Recombination Hotspots. For example, the figure here, sourced from http://www.sciencemag.org/content/327/5967/876/F1.large.jpg

shows the recombination rate at the hotspot and further away from it for Chimps and Humans.

These hotspots are recognised by the cutting machinery thanks to the binding of PRDM9, a zinc finger protein, to a DNA sequence that it specifically recognises and is present at hotspots. The DNA sequence varies from species to species (as does the sequence and the function of PRDM9) but in humans is a well-characterised motif 13 base pairs long and of the sequence CCNCCNTNNCCNC (where N is any one of the 4 bases in DNA) , and accounts for the activity of nearly 40% of known hotspots.

The first link I posted has evidence to suggest that variation in composition of PRDM9 is a determinant of which hotspots get used. PRDM9, it appears, stimulates the formation of a specific histone modification - H3k4me3 (DNA is wrapped around histones, there are five histones - H1, H2A, H2B, H3, H4, and each of them has a tail that can be chemically modified, and eight of these (2 of H2A, 2 of H2B, 2 of H3 and 2 of H4) form a nucleosome - in this case the fourth lysine residue of the tail of Histone H3 is trimethylated as regulated by PRDM9, and facilitates crossing over and recombination initiation.
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Can wood frogs who have frozen and thawed remember their past lives? Wood frogs (Rana sylvaticus) can survive being frozen for up to 7 months at temperatures as low as -16 °C. Their breathing stops, their heart stops and all signs of life disappear. (Source)

I have looked for research that shows that when these frogs thaw in spring, they retain memories from before they became frozen, but I haven't found any. Can anyone give me any insights?

Note: This research shows how butterflies can remember experiences they had as caterpillars, before their metamorphosis. Perhaps something similar can be done or has been done with wood frogs?

Wood frogs are highly philopatric to their breeding ponds. And the fact that they return to the same pond after multiple winters, would indicate that, at the very least, they must retain at least some spatial memory after freezing.
It is worth noting that a frozen wood frog is not nearly the same scenario as a butterfly metamorphing. Butterfly metamorphosis involves complex reintegration of all bodily systems, whereas frog brains do not reform during the winter--they just cease neurological activity. Even frog metamorphosis is less complex since much of the chondocranium and brain morphology is retained from tadpole to frog.
I know it wasn't the original question, but it is relevant to note that tadpoles seem to retain their personality through metamorphosis (see Wilson & Krause, 2012; Koenig & Ousterhout, 2018), which also seems to indicate that they have neurological stability.
References:
Wilson, A. D. M., & Krause, J. (2012). Personality and metamorphosis: is behavioral variation consistent across ontogenetic niche shifts? Behavioral Ecology: Official Journal of the International Society for Behavioral Ecology, 23(6), 1316–1323.
Koenig, A. M., & Ousterhout, B. H. (2018). Behavioral syndrome persists over metamorphosis in a pond-breeding amphibian. Behavioral Ecology and Sociobiology, 72(12), 184.


Immunology Book Suggestion Which book will give a brief account about B-cell development so that it covers two questions about the following cells:

Plasmablast
Plasma cell
Memory B cell
Marginal zone (MZ) B cell
B-1 cell
B-2 cell
Regulatory B (Breg) cell

Where do they lie in the course of B-cell development and differentiation?
What are their functions (outline)?

P.S. I need to know the development part in details rather than the functions.

The best immunology book hands down is Janeway's Immunobiology. There is no debate among the immunology community.  The middle section is devoted to B cell development.


Ear ossicles a part of Skull? Is there anything special about not considering ear ossicles as a part of skull?

I could not understand the reasoning behind such  classification.

The justification is simple.

The bones of the ear [ear ossicles] do not articulate with any other bone of the skull hence it is not considered as a part of the skull, similar is the case with the hyoid which is attached to the tongue.These bones have been placed under the group of associated bones.


How is centriole number maintained during meiosis? I've found a website (Pearson's BioCoach) that claims centrioles duplicate in Prophase II. Is this accurate? Does it depend on the species in question?

Looking at three textbook illustrations of meiosis, none of their illustrations are consistent. All depict the movement and number of centrioles through Telophase I the same way: centrioles replicate in S of Interphase, then do their thing through Meiosis I. We end up at Telophase I with 2 centrosomes, each with 2 centrioles. There is one centrosome at either pole of the cell.

After that, the diagrams are unclear:

One text (general biology) seems to indicate either centrioles or entire centrosomes replicate after Telophase I, because Prophase II is shows both cells with 2 centrosomes, each with 2 centrioles.

Another (basic genetics) illustrates 2 daughter cells of Meiosis I inherit one centrosome each following Telophase I. In Prophase I, the centrioles in this centrosome splits, with one centriole going to either pole. Cytokinesis after Meiosis II results in 4 daughter cells, each with one centriole.

A third (more thorough genetics) stops depicting centrioles after Telophase I, instead showing the spindles growing in an aster formation from an empty space, the space where there were 2 centrioles up until Telophase I.

When a cell enters the cell cycle and passes through S phase, each centriole is duplicated. A "daughter" centriole grows out of the side of each parent ("mother") centriole. Thus centriole replication — like DNA replication (which is occurring at the same time) — is semiconservative.


Function of papain in papaya I know that papain is a proteolytic enzyme present in papaya. It is often used to tenderise meat.  What is the function of papain in papaya?  Is papain sweet? Does it function as an antibiotic?

Papain is a cysteine protease, for which Wikipedia should be sufficient:

  Cysteine proteases play multi-faceted roles, virtually in every aspect of physiology and development in plants such as in growth and development, in senescence and apoptosis (programmed cell death), in accumulation and mobilization of storage proteins such as in seeds. In addition, they are involved in signalling pathways and in the response to biotic and abiotic stresses. In humans they are responsible for apoptosis, MHC class II immune responses, prohormone processing, and extracellular matrix remodeling important to bone development.


What came first? The DNA or the DNA polymerases? I know this sounds a lot like chicken and egg question and while the latter has an answer, I am intrigued about the former.

A modified form of the question would be, in the course of abiogenesis, what formed first? The DNA or the proteins (hence enzymes and DNA polymerases)?

The principle behind it is that the DNA needs an enzyme to replicate.(DNA pol)

But DNA pol itself, being a protein, needs a DNA pol A/B/C gene on the DNA! (Transcription and translation) Not to mention all the other proteins required for transcription and translation.

Same is the case for RNA and RNA pol.

If the DNA/RNA formed first, how did it replicate without a protein?
If Protein formed first, then how did it came to existence without DNA/RNA?

Let's make a big assumption and say that nucleic acid formed for the first time and replicated without proteins. Is it possible for nucleic acids replicate without proteins? For example, a abiogenetically formed DNA sequence just randomly attracted its complementary strand and whatever could fit, fitted and somehow the phosphodiester bonds were sealed sans proteins. That sounds too implausible.

Would love if somebody provides sources with evidences of DNA/protein abiotically forming de novo sans enzymes, genes.

The straight forward answer is: we don't know. We don't have any direct evidence for what happened at that time nor any completely developed and coherent theories for how it worked.

The widely believed hypothesis is the "RNA World" hypothesis. RNA, unlike DNA, is capable of spontaneously folding to form catalytic molecules and thus avoids the needs for translation and transcription by proteins since it can bootstrap it's own synthesis. The idea is that, over time, the RNA developed the means to synthesize proteins and then started using DNA as a more stable storage molecule. The earlier RNA-based RNA polymerases were supplanted by higher fidelity protein polymerases over evolutionary time so we no longer see them in modern cells.


Does cooking or ripening reduce the concentration of solanine in nightshade? I recall a story from one of my Botany professors where he encountered a woman picking Solanum dulcamara (nightshade) berries. When he asked her what she was doing with them, she responded that her husband had her make a pie from them every year.

As her husband was presumably still alive, and since I regard this particular professor as reliable, what would have removed enough solanine from the berries to avoid ill effects? Does the concentration decrease upon ripening, or would cooking destroy the toxin? Would that also be why we fry green tomatoes?

(As a disclaimer, no-one should eat plants that are known to be poisonous. Even though some people don't react to poison ivy, it is still a bad idea to rub it all over your body.)

If you ask Dr. Duke's phytochemical database, by far the most solanine is found in green potatoe fruits (their skin), with much less in leaves and tissues. Similar values are seen in green tomatoes, with dozens of mg per 100g fruit. There is no value for Solanum dulcamara (doesn't mean there is nothing in it) but it appears to have small quantities of atropine. Furthermore, Wikipedia gives for solanine a minimum toxically effective dose for humans of 200 mg---that's where dizzyness and dispnoe starts---, and gives for children a lethal amount of S. dulcamara of 30-40 unripe berries or less. The amount of solanine increases (in potato) when temperature goes up, because it is produced by plants as an antifungal against rot. Ripening in S. dulcamara and, as we know all ourselves, potato and tomato, destroys solanine, so fully ripe berries seem to be okay. Solanine does not degrade when cooked but is lost with the cooking water. For an account of solanine poisoning from potatoes see e.g. this free paper. Newer potato varieties have much less solanine than those from former times.

http://www.ars-grin.gov/duke/

http://de.wikipedia.org/wiki/Solanin

Know your databases!


what is “a group of living things that can interbreed and produce full interfertile offspring”? lets call this term "collection" Example: group of humans.

what is not a "collection" horses and donkey: can't produce full interfertile offspring, lions and tigers: can't produce full interfertile offspring, Camels and Lama: can't produce full interfertile offspring.

And no this is not "species". Polar bear is a species grizzly bear is a species they can produce interfertile offspring, they are of the same "collection"
Two species can belong to the same "collection". Two different "collections" can't be of the same species.

And no this is not a homework question.

Why is this not defined in biology?

Why is this down-voted? I know what ring species is. First and last generation do not interbreed naturally. But it does not say they can not interbreed at all or can not produce full interfertile offspring.
The question is about having the ability of intebreeding and producing full interfertile offspring.

I will add more details:
The term species is a fuzzy term and makes a lot of confusion. I'm not asking about it.
There is a clean cut for all living things that intebreed and produce. For a given group of living things they either can intebreed and produce full interfertile offspring or not. There are many example.
Why is this clean cut not have a term in biology?

Again. This is not a "species" and from my point of view the term species should not be used in biology. Anything is a species... Homo sapiens, Neanderthals two different species although they had interbred and produced full interfertile offspring.....

Different dogs "races" are sometimes called different speices although they can intebreed and produce full interfertile offspring.

I already know about the fly experiment where the author claims that he got two different "species" of flies after some year of combination of sexual isolation and interbreeding. But no, all flies during the whole experiment of the same "collection" even if the author says they are different "species". The author did not make sure that they intebreed, he let them naturally decided whether they want to interbreed or not. They did not because they are not attacted to each other, but this does not mean they can not interbreed and produce full interfertile offspring.

Based on the biological species concept, you're referring to two different species that experience ecological isolation (also called "habitat isolation") as a prezygotic reproductive isolating mechanism.

See here for a simple explanation of various concepts regarding species.

This, of course, is just one of the many reasons (see here for more) why we have multiple species concepts. Some might argue that these organisms are the same species based on their ability to produce interfertile offspring. If said researcher wanted to do so, they would define these organisms using a different concept.

Recognize that “species” is an artificial construct to allow conceptualization and organization of an incredibly complex, dynamic, and otherwise continuously variable genetic world.

We have not found a perfect way to "cut up" the world neatly/consistently into describable and functionally useful units, and --in fact -- we likely never will. Why? Because the lives of these organisms do not care about our cataloging and description systems -- these concepts are strictly for humankind to functionally relate to and react to their presence. The concept chosen almost inherently relies on the underlying motivation of the describer for naming the organism in the first place.


Criteria for the numbering of human chromosomes What were the criteria devised for the numbering convention employed in human chromosomes? When was it fixed?

Correct me if I am wrong; it appears that chromosome pairs 1 to 22 were originally ordered in terms of perceived structural size, which ended up fitting neatly with the quantity of base pairs (but not with the quantity of genes).

The sex chromosomes in turn were arbitrarily assigned as "pair 23".

Is this sound?

Thanks in advance.

Why do you think it was "fixed?"  Here's a nice review of the history of human cytogenetics, which included not only the original image from 1956 but points out a report which comments on the standardization of chromosome number.  The autosomes were indeed numbered by length, and the sex chromosomes are traditionally put at the end as they are "numbered" 23 but clearly function quite differently.  Gene content was decades away from being known at the time, and honestly isn't even known now.  It's also just as arbitrary; simple size is easy enough and makes for rather nice pictures.


why has evolution favored sexual reproduction using two mates over sexual reproduction using three mates? Many animals species require two members — a male and a female — to sexually reproduce. Why has nature (or the process of evolution) chosen to favor the form of sexual reproduction which requires two members? Why didn't nature encourage the form of sexual reproduction which involved three members?

The reason for sexual reproduction being a better choice over asexual reproduction is justified by saying that sexual reproduction involves mixing of genetic information from two living beings and hence if one set of them had an error, the other would compensate for it. With the same kind of reasoning, we can argue that sexual reproduction involving more than two organisms coming together would cause better genetic variation, shuffling of mutations, etc. and thereby produce a better offspring.

However, most of the organisms as we see today have evolved to reproduce sexually using two beings of the same species.

Consider an animal species which has 24 pairs of chromosomes.

Sexual Reproduction Type 1:

There are two sexes: male and female. During the event of sexual reproduction, the male transfers 24 chromosomes to the female where the chromosomes from both the sexes are mixed to produce an offspring.

Sexual Reproduction Type 2:

There are three sexes: male, female and [insert word]. During the event of sexual reproduction, each member transfers 16 chromosomes to the female where it gets mixed to produce an offspring.

We don't observe sexual reproduction of type 2 (or it is rare). Doesn't the type-2 form of sexual reproduction cause better mixing of genetic information than type-1 form of sexual reproduction? Despite the aforementioned advantage, nature has chosen to encourage the type-1 form of sexual reproduction. Why is the type-1 form of sexual reproduction more common than the type-2 form of sexual reproduction?

This question can be extended to "Why has evolution favored sexual reproduction involving two mates than sexual reproduction involving $n \space (n > 2)$ mates?

Let's break it down: The chance that two individuals of distinct gender meet at one location in space time is tremendously higher than for three. We could do some math here (assuming biased random walks of points in three classes on a 2d surface etc.) but that is not necessary I guess. As far as we know sexual reproduction evolved long before complex sensory systems and/or brains (namely 1250 million years versus 500 million years) that allow for active search behavior beyond chemotaxis. Therefore a random walk would be a reasonable first approximation for organism behavior to simulate the situation back then. Having two genders seemed to have been a good trade-off between the chance to meet and advantages in terms of mixing the genetic information. Note that this answer might not be valid for organisms being able to reproduce in both ways, sexual as well as asexual.


Are fishes evolving? As far as I know, Fishing has been one of the important occupation since early ages, and infinite number of fishes have already been captured.

As the time passes, they must've developed some sort of knowledge about the fish-nets, and should've figured out a way to escape from them. But, still now, we are able to capture them at the same rate(I guess)

So, Are they developing any sort of hereditary memory to escape from us?

P.S. I'm not sure whether this is the right SE to ask.

Fish are definitely evolving to avoid fishing pressure. For example, largemouth bass evolve toward avoiding hooks.  More broadly, since fishing selectively removes larger fish from the population, there's selection toward fish evolving smaller size.  A brief review, linking to many studies demonstrating this, is Evolutionary impacts of fishing: overfishing's ‘Darwinian debt’.


How much of a DNA difference is between Chicken of the Woods, and Hen of the Woods? I've noticed that when a COW is touching the ground it turns a gray color, but when on a log/tree it's bright orange. Is there a correlation between the DNA, and where it grows?

I will assume from your comment that your question is

  Is a chicken of the woods just a hen of the woods growing on the side of a tree?

, which is very similar to me to

  Is a chicken of the woods and a hen of the woods the same species?

No, they are not the same species. Chicken of the woods is the common name of a number of species of the genus Laetiporus. Hen of the woods is the common name of the species Grifola frondosa. In fact, Grifola and Laetiporus don't even belong to the same family but only to the same order (order Polyporales).

According to the wikipedia links posted above, Grifola frondosa is indeed usually found at the base of the tree while Laetiporus is generally found in the wound of trees (mainly oak trees).


Favored Conditions of Bacterial Growth I have read that bacteria "thrive" in warm places. Naturally, I am very interested in why this is the case. Humans for instance thrive also in relatively warm conditions if it's too cold or too warm we die. However why would this also apply to bacteria?

The idea that bacteria thrive in warm places is mostly biased from a human perspective. Human researchers will tend to care more about bacteria that cause human disease. These pathogenic bacteria can replicate in/on humans at ~37 °C (which is warm). As Dexter points out, bacteria can grow at other temperatures.

But I'd go deeper and consider proteins (and other macromolecules) in the cell. For example, the enzymes that carry out many important processes for the bacteria (such as DNA polymerases that build the DNA) are most active at certain temperatures: in E. coli or humans or dogs that's ~37 °C; for a thermophile it's warmer. See below:


How hard would it be to create a protein "by chance"? I just read an article about David Gelernter, who was arguing against Darwin's theory of Natural Selection. He said one particular thing which stood out to me:

"...how hard it would be to create just one new protein by chance — the odds are so astronomical that there are fewer atoms in the entire universe in comparison: “The odds bury you. It can’t be done.”

I'm wondering how one could back up this idea. My back of the envelope (not being a biologist...) would go something like this:

Protiens are made of amino acids. Amino acids are essentially made up of four things, C, H, O, and N. In order to "make" amino acids, I just gotta give these things the right energy so they can strip some electrons and hook up to each other. If want to make all amino acids with say 20 molecules, I get four choices for each of twenty things, or $4^{20}\sim 10^{12}$ possible amino acids. Wikipedia tells me "most proteins are built from up to 20 different amino acids", so how many proteins are there made up to 20 amino acids?

$$(10^{12})^{20}\sim 10^{240}$$

So ignoring overcounting and how stupid this estimate is, that's a big number. And indeed, that's bigger then the number of atoms in the universe (like $10^{80}$ by some estimates).

Can someone confirm that's how he arrived at that estimate?

NOTE: Careful, I am not trying to get into an argument about Darwin - I only want to know how people who use this argument, make this argument.

In the original column for The Claremont Review of Books, David Gelertner does not suggest starting from atoms, but from amino acids. This changes the calculation slightly:

  The total count of possible 150-link chains, where each link is chosen separately from 20 amino acids, is 20^150. In other words, many. 20^150 roughly equals 10^195, and there are only 10^80 atoms in the universe.

In any case, these kinds of estimates are purely theoretical and are not hugely useful. We do not know how early proteins evolved, but they did not have to just assemble from scratch.

As mentioned in the comments, this kind of argument for creationism (or 'Intelligent Design') is like a card trick - you start by dazzling with vast numbers, and use them to conceal the logical sleight of hand.

The premise of his argument is simple - there are a vast number of possible sequences, only a small fraction of those can fold into functional proteins, and there have not been enough mutations to make up the difference.

There is this strange argument:

  But what does generating new forms of life entail? Many biologists agree that generating a new shape of protein is the essence of it

I'm not sure who these 'many biologists' are, but the relationship between novel folds and new species is not clear to me, at least.

Anyway, the second part of his argument relies on the work by Douglas Axe on estimating the fraction of functional folds (see this paper for example). Although he describes him a bit oddly ("Axe is a distinguished biologist with five-star breeding") it's reasonable to make this kind of estimate.

  He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

So here is the very small number to contrast with the very large one of the first step. Now for the 'bridge' - the large number of attempts that would be necessary to make a very rare event (a folded, functional protein) possible.

  Suppose, then, that every bacterium that has ever lived contributes one mutation before its demise to the history of life. This is a generous assumption; most bacteria pass on their genetic information unchanged, unmutated. Mutations are the exception. In any case, there have evidently been, in the whole history of life, around 10^40 bacteria—yielding around 1040 mutations under Axe’s assumptions.

So the argument - roughly - is that 10^-77 * 10^40 is still very small. That is, mutations are not frequent enough to overcome the extreme rarity of functional sequences.

The sleight of hand, I think, is to confuse abiogenesis and mutation. When talking about the entire 'landscape' of possible sequences we are talking about abiogenesis - randomly picking 150 amino acids (say) from an alphabet of 20. When talking about bacteria we are obviously talking about mutation.

We really have no idea how the first primordial proteins formed, or what their properties were. They could have used a smaller set of amino acids (although this does not change the numbers much), or could have assembled from multiple smaller peptides, or even been partially folded.

On the other hand, mutation of existing proteins necessarily happens on sequences that can already fold. Moving to a sequence that is a neighbour in fold space is very different to picking a completely new point in that space.

So really, the numbers do not tell us anything because they relate to separate questions.