TCGA data, and bioinformatics design questions for SNP/ mirna analysis It's my first time posting to this forum but was looking for some help on the data aspects of this project.

My tools of choice would be in python/R .

Goal: I'm looking to create a disease specific profile of just SNPs and SNPs in miRNAs and miRNA target sites.

PART 1: TCGA
My first step is using TCGA data which lists a ton of harmful mutations in a LOH .txt format. I'd like to be able to map those mutations to SNPs or genes or miRNAs  (whatever entities they belong to). The TCGA datasheet is here.
Example data is here. for breast cancer. I guess I can use this miRNA and mRNA data as well.

Questions here:

How to decipher the LOH data to figure out if it's meaningful and where it maps?
Which Tools to use for mapping and what formats for final data ? Fasta ?

miRNA/Targets and SNPs
Next up is getting cancer specific miRNAs and mRNAs and mapping SNPs to them?
I'm assuming using dbSNP or Sanger miRNA databases to get miRNA/targets and seed sequences.

I'm a bit lost as how to combine all these pieces of information, what formats to use for output (linked to individual pieces) and which tools if any to use to gather all this data using python. This tool is useful tool mirdsnp.

You can take a look at this tutorial to understand TCGA MAF files. And you can find a list of TCGA MAF files containing mutations mapped to genes and miRNA at https://www.synapse.org/#!Search:syn1710680


What counts as a 'breach of the skin' for infections(like rabies) that spread via wounds? I've been looking at several sources on how the virus spreads and they all mention that the skin has to be broken, but does it mean broken to the naked eye?

A minor scratch where the skin appears unbroken and there was no bleeding could still have microscopic breaks of the skin, therefore it seems risky to rely on the naked eye.

I believe that your books refer to 'broken' not necessarily meaning broken to the naked eye, but as in any broken epidermis.

The outer layer of your skin that protects you against infection is the epidermis. It's a water-tight layer mostly composed of keratinocytes joined together by adherens junctions. Logically, even if you can't see a breach in your skin (epidermis), there may still be one. While the chance of getting an infection from a non-visible break is less than the chance of infection from a visible scratch, it's still possible.


How are neural networks encoded in the DNA? The central nervous systems as well as the brain->muscles and sensory cells->brain nervous pathways, need to be precisely wired for life to be possible. Moreover they are wired almost exactly the same way for the individuals of a same species (animal, man, insects, etc.).

This information, must therefore be somehow encoded in the DNA.

I have never heard of any study or theory on how this would be possible - only about how proteins are encoded, and I couldn't find any bit of information on this topic (I am not a biologist though).

I would like to have a broad idea of what is currently know about the construction of such networks, i.e. not detailed explanation but rather takeaways facts and references.

How is information about neural connections encoded in the DNA?

e.g. are there any genes linked with neurons (e.g. coding for neurotransmitters)? Do the DNA code for precise neural connections? Can development of specific parts of the brain be linked to specific parts of the DNA? How does a neuron knows from the DNA to which neurotransmitter be sensitive?

How are connections between specific neurons established?

e.g. how an axon does know where to establish deliver a potential? How can the end of an axon move to the correct place?

Here's at least one paper describing some of what is known about development of neural network in Caenorhabditis elegans

http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1001044

It mentions at least one relevant gene

" There is evidence showing that several guidance molecules like Netrin and Nerfin-1 are expressed in the early stages of development. Netrin is a protein involved in axonal guidance in vertebrates as well as in invertebrates [21], [22], [23] and is specifically known to influence early path-finding events [23], [24], [25]. Nerfin-1 belonging to a highly conserved family of Zn-finger proteins, is found transiently expressed in neuron precursors and plays a role in early path finding. Studies involving pioneering neurons in the central nervous system of Drosophila melanogaster have shown that Nerfin-1, whose expression is spatially and temporally regulated [25], is essential in early axonal guidance. "

You can also have a lot at the Wikipedia article called  "Development_of_the_nervous_system_in_humans"

One interesting fact is that C. elegans has 20 000 genes, 302 neurons and about 5000 chemical synapses, 2000 neuromuscular junctions and some 500 gap junctions. In humans there are an estimated 20 000-25 000 genes in humans, about 85 billion neurons and 100 trillion synapses.

This excerpt from http://www.tandfonline.com/doi/full/10.3109/0954898X.2011.638968 explains this seeming paradox though

"studies in a range of species suggest that fundamental similarities, in spatial and topological features as well as in developmental mechanisms for network formation, are retained across evolution. ‘Small-world’ topology and highly connected regions (hubs) are prevalent across the evolutionary scale, ensuring efficient processing and resilience to internal (e.g. lesions) and external (e.g. environment) changes. Furthermore, in most species, even the establishment of hubs, long-range connections linking distant components, and a modular organization, relies on similar mechanisms."


Why is cartilage replaced by bones in a vertebrate adult? Why is cartilage present in a vertebrate embryo replaced by bones in an vertebrate adult even though cartilage can also provide me the structural framework like as in Chondrichthyes and they seem to do well with it as Sharks are members of Chondrichthyes which are some of the most fearsome creatures of the world.

Bones are complex organs, made of more than just a structural element. Cartilage is just a tissue, usually devoid of nerves and blood vessels.

Chondrichythes live in water (ἰχθύς ichthys is Greek for 'fish'); the difference in specific gravity and buoyancy is considerable, and cartilage is not robust enough to mechanically support your body out of the water.

Vertebrates have evolved to have a bone marrow, which is part of the bone. If the structural element of the bone (the dense mineral matrix) was replaced by cartilage only, then the hollow structure would make things even worse.

Additionally, cartilage has about the same density as water (Pan et al, 2016) whereas dense bone is 60-90% more dense, which means extra weight pulling aquatic animals down.


Why does the HLA show a high degree of polymorphism? I know how the HLA undergoes high degree of polymorphism (random genetic rearrangements), but I have not understood why it undergoes rearrangements. What is the advantage offered when HLA shows a high degree of polymorphism? What would have happen if all individuals had the same HLA?

There are multiple explanations for the enormous polymorphism in major histocompatibility complex (MHC -- the general term for the equivalent of HLA in all species) proteins. In general they reflect resistance to infectious disease, with the details being mildly debated, and usually not mutually exclusive -- multiple reasons probably apply.

The overall phenomenon is called balancing selection (Wikipedia link), and the most common explanations for the phenomenon in MHC are heterozygote advantage (which is not quite the same as overdominance), frequency-dependent selection, disease-specific selection, sexual selection, maternal-fetal interactions, and drift.

Simplistically, since MHC molecules are involved in protection against infectious disease, if there was only one MHC type then infectious agents that developed resistance to that type would be able to spread throughout the entire population readily. That means you as an individual are better off if your MHC is different from your neighbors', since you're likely to be more resistant to whatever pathogen is infecting them.

Many years ago I wrote a series of blog posts discussing the various evolutionary explanations in some detail, including dozens of references. The posts include:

Evolution of MHC: Elimination round
SEX! (… and MHC diversity)
Heavyweight championship: Overdominance vs. frequency-dependent selection
Testing overdominance in MHC: Can it be done?


Sodium potassium balance in a cell In a resting cell at steady state, is sodium influx or potassium efflux higher according to the concentration gradients and permeability, and given that the sodium potassium ATPase is active?

If potassium ions were alone inside and outside of the cell, they would be tended to diffuse along out of the cell due to high gradient inside. Because of potassium ions have positive charge, potassium lose would cause negativity inside. Within a few seconds, potential loss would rise enough to be able to stop potassium exit out of the cell. Because against decreasing concentration gradient, there would be reverse direction electrical gradient increase so these forces have to be balanced somewhere. For a large mammal nerve cell , needed potential gradient is about-94 millivolts.

We can assume similar concepts for sodium ions also. This time direction will be outer to inner side of cell. And this makes a positive potential (about +61 millivolts) due to gaining positive ions .

When we calculate total diffusion potential for only one ion, Nernst equation is used. For ions more than one we have to use Goldman equation, which is more complicated , instead.
Goldman equation consists of three factors:

Electrical charge for each ions.
Permeability for each ions.
Concentrations inside and outside of the cell for each ions.

Major factor on this resting potential is membrane permeability. For potassium ions, membrane permeability is about 100 times more than sodium ions. Because potassium leakage channels makes potassium leakage more easier than sodium. When we put this factor on Golman equation, we find resting potential about-86 millivoltes which is closer to potassium diffusion potential.
(source:Wikipedia)
(source:KhanAcademy)


Are there any websites offering graphs for the light absorption of different enzymes? I have found graphs for the light absorption of water, haemoglobin, lipids, melanin, etc., but I am having a hard time finding graphs about enzymes.

Are there any websites or other reference sources for this type of information?

It is not typical to investigate spectral absorption of compounds that are not useful for light absorption qualities, such as the compounds you've listed. Enzymes in particular will have less information because of the changes in binding partners our physical conformation to be enzymatically active. If you think there should be known info then I would try Google Scholar, Pubmed and a google search, in that order.

Edit:
The intended meaning of the question is related to spectroscopy and quantification of protein concentration. There are two common ways to determine protein concentration using optical methods (spectroscopy). The methods use colorimetric assays (colour intensity is proportional to protein concentration) or light absorbance at a reference wavelength. Both methods rely on light absorbance at a specific wavelength, but the former relies on an reagent that changes colour in response to protein quantity, and the latter depends on direct UV light absorbance. Here's a quick breakdown of each.

For both of these assays, to determine the quantity of a specific protein, they require a source of purified protein.

Colorimetric Assays:

These are traditional biochemical assays, of which the most widely used are the: Bradford, BCA and Lowry protein assays. These assays rely on reduction-oxidation reactions between the key assay reagent (Bradford's reagent, bicinchonic acid, or Lowry's reagent) and protein. For example, the BCA reagent is reduced in the presence of protein, causing a chelated copper ion, Cu(II), to be reduced to Cu(I), and effecting a purple colour. This purple colour intensity, which read at a specific wavelength (~520 nm) will indicate the amount of protein.

Near-UV Absorbance:

This method relies on 280 nm (near-UV) absorbance. Usually absorbance at 260 nm is also used for a correction factor. Specifically, amino acids with aromatic rings (eg, tryptophan) cause absorption at 280 nm. Peptide bonds absorb at 200 nm, and various other bonds, pH, ionic conditions, all influence and absorb at various wavelengths.

These methods cannot be used with a protein sample alone, because there are a number of conditions that can affect readings. To correct for this, a protein standard is also used. A protein standard uses a series of known concentrations of a known protein. The common protein concentrations can range from 20-2000 µg/mL; the common protein standards are bovine serum albumin, chicken ovalbumin or purified IgG. The protein standard acts as a reference for protein concentrations that are valid for that experiment, under those specific conditions. A curve is fit to the readings of the protein standard, and the sample concentrations can be read off the standard curve by using the absorbance readings.


What is the difference between SOLiD, 454, and Illumina next-gen sequencing? I've started teaching myself about next-generation sequencing in preparation for a new job, and I'm wondering what the main differences are between the 454, SOLiD, and Illumina/Solexa machines, in terms of sample/library preparation and chemistry. How difficult is it for a protein veteran but next-gen newbie to get high-quality useful reads? I'm mainly going to be looking at antibody diversity, but consider this in general terms for any next-gen project.

I understand the basic theory of fluorescent chain-termination sequencing, but it's been a number of years since I last did it, and my career is now taking me back into the DNA realm.

Here is a short summary of the sequencing technologies you listed. Illumina is the most frequently used one.

Roche/454 FLX Pyrosequencer technology is based on pyrosequencing method, which utilizes the use of the enzymes ATP sulfurylase and luciferase. After the incorporation of each nucleotide by DNA polymerase, a pyrophosphate is released, which further takes part in downstream light-producing reactions. The amount of light is proportional to the incorporated number of nucleotides. The DNA is fragmented and adapters are ligated at both ends. The fragments are mixed with agarose beads, which carry adapters complementary to the library adapters, and thus each bead is associated with a unique DNA fragment. The beads and DNA fragments are isolated in individual micelles, where emulsion PCR takes place and million copies of the single fragments are amplified  onto the surface of each bead. Each bead is placed in a well of picotiter plate (PTP), as the wells have dimensions such that only one bead can fit per well. Enzymes are added to the beads and pure nucleotide solutions are added with an immediate imaging step. On one side of the array a CCD (charge-optic device) camera records the light emitted from each bead. The first four nucleotides (TCGA) are the same as the start of the adapter, which allows for the emitted light to be calibrated according to the type of nucleotide added. The major disadvantage of this method is the misinterpretation of homopolymers (consecutive nucleotides, e.g. AAA or CCC). Such areas are prone to insertions or deletions, as the length of the stretch can be inferred only by the intensity of the light emitted. On the other hand, substitution errors are very unlikely. The 454 FLX instrument generates ~400 000 reads per instrument-run, as the reads are 200-400bp. The greatest advantage of this platform is the read length, which is the longest of all second generation technologies. Although sequencing on 454 platform is more expensive than sequencing on Illumina platform (40USD per Mega base versus 2USD per Mega base), it could still be the best choice for de novo assembly or metagenomics applications. (Mardis, E., 2008, Shendure, J. and Ji, H., 2008).

Illumina is the most frequently used one. The DNA to be sequenced is fragmented into about 200 base strands. Adapters are ligated onto the ends of the fragments and one of these adapters is hybridized on a flow cell. Illumina essentially utilizes a unique "bridged" amplification reaction that occurs on the surface of the flow cell. Localized PCR reaction is performed, and each of the hybridized pieces of DNA will get locally amplified to generate clusters which will have the exact same molecule. Subsequently, the DNA sequence is determined by adding a primer on one of the ends of the molecule. A mixture of modified nucleotides is added. Each one of them carries a base-specific fluorescent label attached to it. Also, each one has the 3' OH group blocked which ensures the incorporation of one nucleotide at a time.  The flow cell is placed under a microscope and when light is shined on its fluorescence, the emission light shows which base was incorporated on each one of those clusters. The Illumina read length is approximately 35 bases, but over billion reads are generated at a time. The major error type is substitution, rather than deletion or insertion (Mardis, E., 2008, Shendure, J. and Ji, H., 2008).

The SOLiD platform utilizes the use of DNA fragmented library, which is flanked by ligated adapters. The fragments are attached to small paramagnetic beads and emulsion PCR is performed to amplify the fragments. In contrast to the other sequencing platforms, sequencing by synthesis is performed by utilizing DNA ligase, rather than polymerase. Each cycle of sequencing involves the ligation of a degenerate population of fluorescently labeled universal octamer primers. A specific position of the octamer (e.g., base 5) carries a fluorescent label. After ligation, images are acquired in four channels, followed by cleavage of the octamer between positions 5 and 6, removing the fluorescent label. After several rounds of octamer ligation, which enable sequencing of every 5th base (e.g., bases 5, 10, 15, and 20), the extended primer is denatured. Different primers can be used to examine the previous or next positions (e.g., base 3 or 6).  The platform can use primers which carry two adjacent correlated with label bases. This approach involves the examination of the bases twice in a cycle, which decreases the error rates. SOLiD read lengths are 25-35 bp, and each sequencing run yields 2–4 Gb of DNA sequence data (Mardis, E., 2008, Shendure, J. and Ji, H., 2008).

References:

Mardis, E., Next generation DNA sequencing methods. Ann. Rev. Genomics Hum. Genet, 9: 387-402 (2008). DOI 10.1146/annurev.genom.9.081307.164359
Shendure, J. and Ji, H., Next-generation DNA sequencing. Nat. Biotechnol., 26: 1135-1145 (2008). DOI 10.1038/nbt1486


How long can Legionella survive at 60°C? I'm coding some stuff for water heaters and one of the functions is anti-Legionella.

Anyway, I've read on wikipedia that 90% Legionella dies in first two minutes if the water temperature is 60°C, but I'm interested in how long should the temperature be 60°C for 99.99999% of Legionella to die? (I guess I can never get to 100%)

Follow-up question: On what intervals should this be done so that the water isn't contained? Should it be one week, two weeks, several days?

Final question: If the water in a water heater has 60°C for 30 minutes every 2 weeks, would the water be safe?

Usually cell death would follow first order kinetics.

$$X=X_0e^{-kt}$$

where $X$ is the number of cells at time $t$, $X_0$ is the initial number of cells and $k$ is the death rate constant. You can get the constant by solving for 90% reduction in 2 minutes. Then just substitute and get the time required for 99.99999% reduction — 10 minutes.

For your follow up questions, see the same wikipedia article.

  Moist heat sterilization (superheating to 140 °F (60 °C) and flushing)
  is a nonchemical treatment that typically must be repeated every 3–5
  weeks.

It also depends on how much is the bacterial load in the input.

Other sources (Farhat et al. 2012; Whiley et al., 2017) suggest 70°C treatment for 30 minutes.

However, Legionella has been shown to survive heat treatment of 70°C/30min (reviewed by Whiley et al., 2017). Legionella can also be "protected" by other micro-organisms such as certain types of Amoeba, in the water.

So, probably multiple levels of disinfection is needed.


Is there any research on how accurately people can follow a beat? I'm currently helping develop a rhythm game, and as part of the scoring system, I'd like to make scores and ranks based more on accurate pattern recognition rather than hitting notes very exactly on time as is the case for many games of this variety.

In many cases, the margin of error for the best judgment in rhythm games is so small that it seems to be a matter of chance more than skill that a certain judgment is counted between "excellent" and "good" (for example, one game has the margin as small as ±0.011 s).

Of course, some people are better at hitting notes accurately than others either naturally or through practice, but I would like to find some actual research into what the base neurological limitations to rhythmic precision are and to what degree practice can actually improve it.

As a baseline benchmark for the best judgment, I was thinking of looking for some research into how accurately people can follow the tick of a metronome - for example, by measuring the average deviation of somebody tapping a button to a regular beat after about 100 beats or so when they've gotten used to it.

A Google search didn't return anything useful, probably because the search terms draw up so much other, irrelevant content. Is there any prior research on this subject? If so, where can I find it? If not, how could I conduct such an experiment myself?

You might begin your search with the characteristics of Parkinson's disease. This degenerative disorder is precipitated by the death of neurons in the substantia niagra. This brain structure is composed of multiple neurological nuclei. Its function is to connect cortical regions and nuclei together, most significantly with the basal ganglia. The difference between nuclei and cortical brain circuits is important to your question.

The symptoms of Parkinson's are directly correlated with the function of nuclei in central nervous system: the integration of information. It's the integration of conscious thought, muscle memory, sensory-motor pathways that makes voluntary movement possible. Disruption of this network in Parkinson's degrades one's ability to voluntarily execute a movement.

The cerebellum also controls voluntary movement. As a cortical structure, it is involved more with the formation and maintenance of muscle memory than information integration. Damage here results in the loss of fine motor control as opposed to gross motor control in Parkinson's.

This problem has a sensory and motor component. It might be difficult to tackle your problem as a whole. Perhaps breaking it down into smaller pieces would shed some light on what you're looking for.

Here are 2 articles I found relating motor control with the cerebellum and substantia niagra.

Relating cerebellar damage with learning sequence information

Relating the substantia niagra with interval timing


Metatranscriptomics Extraction I am attempting to perform metatranscriptomics analysis of a cleanroom. The DNA input is known to be rather low (<1pg). Despite this, I want to still attempt to try it. I am thinking it might be best to perform extraction trials before hand where certain parameters are manipulated. I can then determine from these extraction trials which values for which parameters are best.

As an example, I am reading a peer-reviewed paper called "Validation of picogram- and femtogram-input DNA libraries for microscale metagenomics" where they used the Illumina Nextera XT DNA library preparation kit on low biomass samples. Two of the parameters they manipulated were:

1) PCR cycle numbers (Values = 12, 14, 16, 18, 20)
2) ATM dilution (Values = undiluted, 1:5, 1:10, 1:20, 1:50)

I am hoping to use the same type of extraction trials to determine which combination of values from these two parameters is best for a clean room. My first question is: How can I determine which combination is best (as there are 25 combinations)? I have two ideas (but am open to others):

1) Check the amount of RNA derived
2) Check some quality metric on RNA

As I hope to do triplets of each of the 25 combinations, I will have 75 samples. I am hoping not to have to do sequencing as it is time consuming and possibly expensive in order to chose the best combination. Is there a way to chose which combination works best without having to sequence?

My second question is: Are there any other parameters in this workflow that I can also test for if I am not getting decent results in these low-biomass cleanrooms?

(As you can tell, I do not have too much direct molecular biology experience, so feel free to correct or question any of my post and/or "dumb down" your response). Thank you for sharing advice (for either question)!

Consider doing triplicates of just 4 combinations of cycle/dilution: low+low, low+high, high+ low, high+high.  Simpler.
Most important: prove you can extract DNA from a clean room.  If you extract from a real clean room and get no result from the PCR, maybe it is because you failed to collect anything or maybe nothing was there.   Idea - spray a known quantity of DNA into a room that will serve as your sham clean room.  Then do your extraction protocol.  You can test the cycle / dilution parameters with the sham clean room extraction and have those variables optimized for when you collect from a real "wild" clean room you did not dope with DNA.


Why are de novo genetic mutations usually NOT inherited? I am told de novo genetic mutations (germ mutations in either parent's sperm or egg cell, or the newly fertilised egg) are not usually inherited, and do not contribute to heritability.

It would seem to me that, intuitively, a de novo mutation would be passed from the affected individual (assuming they survive and are fertile) onto offspring, just like any other inherited mutation. But apparently not.

Why is this?

A germ line mutation will be passed to the offspring only if

the individual reproduces
the individual reproduces after the mutation has occurred in the germline. Indeed if the mutation appears in the testes 5 years after the individual has reproduced then the offspring will never carry this mutation. Note that female mammals make a big storage of ovules early in life while mammal males do not. As a consequence the number of new mutations transmitted to offspring is age-dependent in males but age-independent in females. See this post for more info
the gamete that is transmitted is descendent from the individual cell who had the mutation. There is of course many lineages of gametes and their pattern ancestry will affect what fraction of gametes carry a given mutation.
the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis). Of course, there is always segregation who decreases the probability of a new mutation to be transmitted by half.

Of course, there are also all the mutations occurring outside the germ lineages (somatic lineages) which won't be transmitted but you specifically asked for germ line mutations.


Is the DNA different in each type of cell? What DNA is passed to offspring? Our body contains many different types of cells and each of those cells have their own DNA (correct me if wrong) like skin cells their own DNA that makes them skin cells instead of muscle cells.

So my question is what DNA does a human pass down in a sperm or egg cell? Is it a specialised DNA imprint from which our whole body can be created?

Most cells in a human body contain a complete set of the genome, which is two sets of 23 chromosomes. Having two of each chromosome is called diploidy.

Within an individual human the DNA is approximately identical in every cell. Different cells are produced by differential use of that DNA: certain genes are more (or less) highly expressed etc. You can read more about that here.

You inherit one copy of each chromosome from each parent. Gametes (eggs and sperm) are a bit different from regular cells because they contain one copy of each chromosome; they are haploid. These gametes fuse to make the complete set of 23 pairs in the offspring. There are some exceptions such as cytoplasmic DNA and sex chromosomes.


Do nematodes have organ-level organisation? Some introductory biology books state that nematodes have a pseudocoelom. So, they have a false body cavity. So, does it also mean that they have organ level body organisation?

In Fig.1 is shown the body plan of a round worm:

Fig. 1. Nematode. source: University of Illinois

You ask whether there is an organization in terms of organs; an organ is:

  A group of tissues that perform a specific function or group of functions;

A tissue is:

  An aggregate of cells in an organism that have similar structure and function;

As you can see in Fig. 1, there are clearly organs present, including a mouth, pharynx, reproductive organs, among others. They fulfill different tasks and contain various tissues, each dedicated to specific functions. Hence, they fulfill the definitional requirement of being organs.


Picture of spider for identification Would like to get spiders identified . Specimens can be sent for detailed examination if required .

Spider seen on floor inside house - at Phoenix USA

White off color spider on twigs and flowers of oleander tree with white flower in backyard of house at phoenix USA  - seen dropping off on disturbance and camoflouging with. White flowers. Picture can be magnified spider sitting on green stalk  below brownish dried flowers.

The first is a male Theridiid, probably Parasteatoda tepidariorum (see below)

https://bugguide.net/node/view/1320395/bgimage.

The second is one of the "flower spiders" in the Misumena/Misumenops/Misumenoides/etc. group of Crab Spiders.  It would take a better photo to get closer than that, since this is a young female and isn't showing the color marks that make it easier to ID.  There's a hint of patterning on the abdomen, but it isn't clear enough to ring any bells with me.  In a comment below, I'll include a link to the Bug Guide page for these spiders so you can look at it - the relatively useful marks for field observation are the greenish bands (if any) on the sides of the cephalothorax, the 'mask' (if any) over the eyes, and the pattern (if any) on the abdomen.  Also, the reddish 'racing stripes' on the sides of the abdomen of fully adult females can be helpful in working out which spider it is.  I suspect that for most of us, most of the time, "Flower Spider" is going to be good enough.


Can DNA test of my grandparent's brother reveal my heritage from that branch of the family? I'm thinking about doing that DNA test on all my grandparents to know where their genes come from. They are getting very old and I don't want to let the opportunity pass to gather more knowledge about my heritage, something I find very interesting.

One of my grandparents died long ago, but he still has a brother and I was wondering if DNA testing him would reveal relevant information about my heritage from that branch of my family tree. Obviously all of his genes come from family of mine(his parents) but not all of his genes are the same as my grandparent's. Just how should I look at his tests to find information about my heritage?

By the way can I really trust these sort of tests?

As Rayoub's answer points, you are likely to share a random part of your genes with your grandparent's brother, and therefore analysing his DNA won't tell you where all your genes come from, since he has some genes you don't have and you have some genes he doesn't have.

However, I understand that you aren't that interested on your particular genes, but on what genetics can tell you on the history of your family - that is, to shed light on who were your ancestors and where they came from. Then, if your grandparent's brother was your grandparent's full brother, his ancestors are your grandparent's ancestors and therefore analysing his DNA can be as useful as analysing your grandparent's DNA.

In addition, since your grandparent and his brother doesn't share all the same DNA (likely just about 50% for full brothers) and each of them just have a 50% of each of their grandparent's DNA, if you could analyse DNA from both a grandparent and one or more siblings, you would be able to gather more information. In fact, you would be getting closer to get the same information you could have got from analysing your grandgrandparents'DNA.


What exactly is extreme heterozygosity and how does it work? What does the concept of "extreme heterozygosity" mean?
I first encountered this concept in "The Drunken Botanist". They describe that when planting a seed from, say, a 'red delicious' which was pollinated by another 'red delicious' does not guarantee growing another 'red delicious' tree. The author goes so far to say that the new tree may have almost none of its parent traits, and may barely resemble any other breed whatsoever. They argue this is caused by extreme heterozygosity.
I later found the concept of extreme heterozygosity the Wiki page for "apple"

This is because seedling apples are an example of "extreme heterozygotes", in that rather than inheriting DNA from their parents to create a new apple with those characteristics, they are instead significantly different from their parents.

On a PNAs article on Extreme genomic variation referencing extreme heterozygosity

We conclude that the extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.

My understanding of population genetics (allele frequencies and patterns of dominance)
I understand homozygous diploid pairs, like pp or PP, and heterozygous pairs like pP and Pp, and hetero/homozygous dominance and recession. I also found an interesting paper on sea squirts to work through later that suggests why extreme heterozygousity is popular in large population sizes.
What I can't seem to find is exactly how "extreme heterozygousity" works. How is this different than ordinary heterozygous? Is there an entirely different context I'm missing out on? The only way I can imagine a more "extreme" heterozygosity is with triploid mismatched pairs, which can't be right. So how does the process work and what exactly defines it?

Without reading the article, given the context that you have mentioned, I think extreme heterozygousity means that most of the individuals in the population are heterozygous (much higher than 50%). So there might be some kind of selection pressure that gives heterozygous individuals a reproductive benefit.


Does protein kinase A accelerate glycolysis or slow it down? In liver cells, the activity of PFK-1 is regulated by the PFK-2/FBP-2 complex, whose activity is in turn controlled by glucagon and insulin.

Glucagon activates protein kinase A.  Then protein kinase A phosphorylates the PFK-2/FBP-2 complex, so that the PFK-2/FBP-2 complex will make fructose-6P from fructose-2,6-bisP.  Since fructose-2,6-bisP activates PFK-1 (in liver cells), without it the process of glycolysis will slow down.

However I read from my notes that protein kinase A is dependent on cAMP (so that when the energy level is low, the increase in cAMP will cause protein kinase A to increase in activity).  It seems that protein kinase A should help increase glycolysis, so why does activating it by glucagon cause glycolysis to slow down instead?

There is a fallacy in your argument, which is the parenthetical statement:

  so that when energy level is low, the increase in cAMP will cause protein kinase A to increase in activity

The activity of adenyl cyclase (the enzyme catalysing the production oc cAMP) is not controlled by energy charge, but by hormones such as glucagon. That is how glucagon has its effect on protein kinase A (better thought of as cyclic AMP-dependent protein kinase to remind you of this fact). That is why cAMP is known as a ‘second messenger’ — the hormone being ‘first messenger’ (and the enzyme that becomes phosphorylated being the recipient of the message). See, for example, Figure 21.14 from Berg et al.

Therefore the explanation in the Wikipedia article on PFK2 is quite self-consistent:

  When glucose level is low, glucagon is released into the bloodstream, triggering a cAMP signal cascade. In the liver Protein kinase A inactivates the PFK-2 domain of the bifunctional enzyme via phosphorylation, however this does not occur in skeletal muscle. The F-2,6-BPase domain is then activated which lowers fructose 2,6-bisphosphate (F-2,6-BP) levels. Because F-2,6-BP normally stimulates phosphofructokinase-1(PFK1), the decrease in its concentration leads to the inhibition of glycolysis and the stimulation of gluconeogenesis.[8]

So the answer to the question posed in your title is: in liver cAMP causes the inhibition of glycolysis.


Can anyone identify this tall vine that has volunteered in our back yard? What is this 5-foot tall vine in Kentucky? It volunteered in our back yard.

I believe it is in the genus Dioscorea which is a wild yam.  There are several species native to the Eastern US.  A common species is Dioscorea villosa but you will have to look up details and compare to your specimen.


Open Reading Frames vs Coding Sequences (CDS), are they different? The two terms confuse me for a long time. What is the difference between ORF and CDS. Some people say ORF could contain intron and CDS does not. The wikipedia definition of ORF does not contains intron. Could someone define the two terms and point out their differences? Thanks!

I (mostly) like the definitions given on this page.

An ORF is a sequence of DNA that starts with start codon “ATG” (not always) and ends with any of the three termination codons (TAA, TAG, TGA). Depending on the starting point, there are six possible ways (three on forward strand and three on complementary strand) of translating any nucleotide sequence into amino acid sequence according to the genetic code. These are called reading frames.
The Coding Sequence (CDS) is the actual region of DNA that is translated to form proteins. While the ORF may contain introns as well, the CDS refers to those nucleotides (concatenated exons) that can be divided into codons which are actually translated into amino acids by the ribosomal translation machinery.

However, I do not entirely agree with this statement:

In Prokaryotes the ORF and the CDS are the same.

While it’s true that all CDSs are within ORFs, not all ORFs are CDSs. You can have ORFs that are transcribed as noncoding RNA elements, and ORFs that are not transcribed at all. CDS refers specifically to the ORFs whose post-transcriptional fate is to be translated.


Do antioxidants interfere with chemotherapy? Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.

However clinical trials are proving the opposite. Saying, antioxidants does not decrease chemotherapy efficacy but also make chemotherapy more effective, thus increase the survival rate.
http://www.ncbi.nlm.nih.gov/pubmed/17283738

The question is, why antioxidants do not interfere with chemo, while they are supposed to do ?

Since it's a very broad argument I'll try to summarize in a few sentences.

First of all the sentence:

  Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.

is a bit inaccurate as of today. The chemotherapy today uses the "classical" chemotherapy drugs which IN PART use the mechanism of free radical but there are a lot of mechanism such as microtubule damage and so on which do not depend on free radical toxicity. Today there are also a lot of biological drugs and inhibitors of tyrosine kinase inhibitor which use a completely different pathway.

You cite a paper from 2007, a bit dated, I cannot access full text because it's an abstract. It seems it's not performed in a systematic manner (it's a not a systematic review or meta-analysis) and is published in a journal of alternative medicine. Maybe there are more recent paper but unfortunately at the moment I cannot have the time to check.

Finally you are comparing the effects of a chemotherapy drug administered usually in high dosage to the use of antioxidant which I cannot recall are sold as drugs used regularly, so it's a potential interesting biological question but practically it's a bit difficult to compare the oxidative effect of a cancer drug with the effect of an antioxidant one in real patients since I don't think there are randomized controlled clinical trials comparing chemotherapy to antioxidant alone.


What evolutionary advantages does a longer muzzle have against a shorter muzzle and vice versa Basically I'm curious as to why when it comes to mammalian predators that some like say bears and canines tend to have longer muzzles than those like big cats.

aside from their ancestors/evolutionary line and such, what advantages or disadvantages do short muzzles and long muzzles have against each other and which is better?

Its mostly due to different forms of predation.

Longer jaws are deeper and can reach farther around a prey item, it also increases the chances of catching a moving target in the jaws becasue the area the jaw covers is larger, all things being equal it should always be favored but things are rarely equal, everything has a cost. It is common to see longer snouts in animals that hunt primarily with the jaws. There two ways to do this which depends on how big the pery to are after is, for predators going after relatively small prey they favor long thin snouts, is really noticable in aquatic predators like gharials, it makes for a very fast bite with a wide attack range. Alternatively if they are going after large prey they need to balance strength with speed so you see long, but not as long, more robust snouts. Think alligators, hyena, wolves. Whereas cats who attack with their forepaws can use a smaller head and jaw and favor a more precise bite, becasue they are moving with the prey becasue they have grabbed it, the arms are absorbing most of the stresses. Cats favor grabbing and strangulation for which a small short jaws works fine. Energy and material saved here can be used elsewhere. A longer snout would be weaker unless they add a lot more muscle to stabilize it. In terms of resources it is a lot of cost for little gain, whereas in wolves it is worth the cost becasue they need that strength anyway, becasue they jaw is where all the stress of the struggling prey is being transmitted.

You see the same thing in dinosaurs, predators that can attack with the claws have weaker bites/smaller heads. In the case of dinosaurs however snout length varies less because the small heads favor slashing bites, which favors a longer snout (thus a longer cutting row of teeth) there heads get narrower and weaker more than shorter.  Mammals can't use this strategy because they don't get replacement teeth, and they would quickly not have a tooth in their head, so instead you see strangulation favored instead.

Of course an animal can try to balance a range of strategies and there are all kinds of specialized forms like saber teeth, venoms, ect. Of course this is also simplified a lot of other things effect snout length as well, things like climate (long snouts cause less heat/water loss through breathing), sense of smell, or even vision.

https://www.cambridge.org/core/journals/paleobiology/article/dinosaurian-and-mammalian-predators-compared/BE3492DA7E0A103C6F6E77B9611D86A9

https://link.springer.com/chapter/10.1007/978-1-4615-0161-9_14

https://www.cambridge.org/core/journals/paleobiology/article/constraint-and-adaptation-in-the-evolution-of-carnivoran-skull-shape/77B1591461066F9D0E30F309F6C495C6

https://www.sciencedirect.com/science/article/pii/0034568770900757


Why didn't a concept like "pointers" in Computer Science evolve in the genome? I see that the genome contains large regions of repeating sequences called interspersed or dispersed elements. The long dispersed elements (LINES) such as LINE-1, can reach up to 6-8 kb in length.

I'm wondering, given the amount of repetition that takes place in these regions, wouldn't a system where a pointer (such as in computer programming) existed  be more efficient? For example, instead of including a LINE, include a unique 5 base pair sequence acting as a pointer to that LINE. A separate chromosome (containing one copy of each LINE) would then be read at the correct position once the pointer was read.

Do you think that given enough time in evolution, such a system would be more sustainable? Sort of like using a proper functional language instead of Assembler in computer programming, where f(x) can be defined once, and accessed via pointers, instead of being repeated many times?

Short answer: Pointers already exist within the genome, in terms of transcription elements (such as repressor/activator systems). These systems can remotely activate a specific gene for transcription based on concentrations of specific chemicals within the cell.

The problem with LINEs are that they are thought to be ancient retroviruses which lost their capacity to infect other cells, instead jumping around within the genome. They are therefore parasitic in nature, and they reproduce by inserting multiple copies of themselves into the genome. It makes more sense to think of LINEs as nearly inactivated retroviruses instead.


Location of nucleotide synthesis and transport I couldn't find this question directly asked so I thought I would ask it

In Fundamentals of Biochemistry 3e (Voet et al), it has a small small little comment about pyrimidine synthesis:
(In a diagram showing UMP synthesis)
"In the eukaryotic enzyme, which contains FMN and nonheme Fe, is located on the outer surface of the inner mitochondrial membrane where quinones supply its oxidizing power. The other five enzymes of pyrimidine biosynthesis are cytosolic in animal cells."

So it seems for the most part pyrimidine synthesis occurs in the cytosol??

When the book talks about purine synthesis no mention is made of where this is actually happening in the cell.

Also, if nucleotides are being made in the cytosol, I suspect there must be some kind of membrane protein that allows nucleotides to cross the nuclear and mitochondrial membranes... what are they??

I'm a visual person, and knowing where and how these things are happening in the cell helps me understand it better than just following what's happening after each synthesis step.

Thanks!

Correct, all but one step in pyrimidine synthesis occurs in the cytosol, and purine synthesis occurs in the cytosol only.

Nucleotides freely diffuse through nuclear pores but are actively transported through mitochondrial membranes via embedded membrane transport proteins (i.e. ATP-ADP translocators, GTP transporters, and pyrimidine nucleotide transporters).

http://themedicalbiochemistrypage.org/nucleotide-metabolism.php


Identification of an Insect (Hemiptera) I found a a few of these guys on my composter, so they could have easily been eating bugs or decaying organics (or both):

To me it looks like a stink bug with oversized legs, not like the ones I'm used to seeing. His body measures just under 3cm, and I haven't pulled on his legs to get a measurement (I haven't pulled on it at all).  The legs seem to be at least 1.5 times the body length as do the antenna.  The body is grayish brown and the antenna and parts of the leg seem reddish brown.

I'm a microbiologist, so things big enough to see in a jar are not really my specialty.  That said, here's info that I've been trying to use ID it:

Wingless Normal compound forelimbs (don't seem to have any kind of   prey modification)

Segments filiform antenna (I think)

2 Tarsomeres (I think)

In the middle of South East US

Have had (unusually) heavy rains

Underside of the limbs and antenna seem red, but to seems gray

I've never seen it before! (and I usually notice such things).

Update: Despite my 4 year old putting other bugs and some leaves in with it, the bug died.  I took the opportunity to get some much better photos, and low and behold when I started manipulating it I was able to pull out a substantial rostrum that I missed!  These guys are good at hiding those.  So going back to assassin bugs, can anyone id which assassin bug it is?

More photos: [I would add more but I think this should be plenty]

I at least think it's quite a pretty specimen (to betray my mammalian aversion to bugs).

species ID

I feel reasonably confident this is a late-instar Acanthocephala declivis nymph (that is, almost-but-not-quite-adult).

Compare your pictures with those on bugguide of a similarly-aged individual, or the bugguide ID page. Also see the key here; which gives three characters for declivis

  Humeral angles of pronotum broadly expanded, extending laterally well beyond maximum lateral abdominal margin. Distal dilation of hind tibia broad until apex, then curving in at right angles to tibial shaft. Anterior pronotal lobe with 2 small shining blunt tubercles along midline

If you look at your pictures, you'll see that you're three for three here: the broad 'shoulders' (pronotum), the right-angle in the leg flange (dilated tibia) just above the the 'ankle', and the two rounded bumps on the pronotum (visible in photos 1 and 3).

original answer / working towards the ID

You're right on track, it definitely looks like a true bug (Hemiptera/Heteroptera). Possibly immature if it looks wingless. Maybe some kind of Assassin Bug (Reduviidae)? They don't all have burly forelimbs. You might also want to consider Coreidae, for instance the genus Leptoglossus (pdf on Leptoglossus in Georgia).

You could try this key to Florida bug families, it looks pretty user-friendly.


Why can't we half-close our eyes? Can we half-close our eyes such that they don't vibrate?

If not, then why we are unable to half-close our eyes properly?

Alternatively, why isn't it possible to keep the upper eyelid close to the lower eyelid without it vibrating?

The motion of the eyelid is driven by the levator palpebrae superioris, i.e. elevating muscle of upper eyelid, and it can be positioned to the intermediate, half-closed positions. At least I can do it.

Yes, this muscle tends to shake or oscillate simply because it's a very weak muscle. It's similar with the muscles controlling the motion of the little finger (or ring finger). Vibration and "noise" is present in all muscles but the stronger muscle you have, the more accurately the random motion is averaged out.

If you connected $N$ eyelid muscles so that they move in unison, the noisy vibrations would be reduced by the factor of $\frac{1}{\sqrt{N}}$. This is the well-known scaling of the statistical errors in physics etc.

I would think that this question was totally appropriate at the Physics Stack Exchange.


Base-stacking interactions versus hydrogen bonds Is it correct that the hyperchromic shift in DNA is a result of the disruption of the base-pairing hydrogen bonds, but the actual denaturation of dsDNA has more to do with the base-stacking interactions? Why does separating the strands have any effect on the stacking of the bases? Why wouldn't the bases in ssDNA still experience stacking interactions?

I really appreciate any help with this. Thanks!

For a direct reference on the contribution of these two forces see here.

If it helps, think of the double helix of dsDNA as a more rigid structure than ssDNA, which flops around and generally is capable of a lot of steric freedom that dsDNA doesn't have. This freedom means that the bases of the ssDNA backbone may not always be in the correct orientation for stacking, because the two strands of the helix aren't forcing the bases together into that orientation. "Usually the DNA double helix is considered to be a relatively rigid structure. Certainly it is much more rigid than its component single strands." (see the review for a much more detailed discussion of this issue)

It's true that base stacking still occurs in ssDNA, it's just not enforced in the same way. It also appears to be somewhat sequence-specific, occurring more in polypurines than polypyrimidines, possibly because purines are bulkier molecules with more steric hindrance.

For a related conversation see here.


Order of events in hibernation Arrange this in sequence :

  i. Heat loss exceeds heat production.

  ii.As body temperature falls, heat loss decreases.

  iii.Body temperature equals environmental temperature.

  iv.Metabolic activities fall to the basal level.

I am confused between i,iii,ii,iv and iv,i,ii,iii.

I think the order i,ii,iii should be correct, since the fall in temperature occurs after the heat loss exceeds production and will continue only till the temperature equals the ambient temperature. iv is the reason for i. Hence iv,i,ii,iii sounds pretty convincing to me.

With i,iii,ii,iv , the main problem is that there can not be any appreciable fall in temperature ii after the temperature equals the environmental temperature iii. And iv seems more probably to be the reason for i rather than the reverse


Are spinal nerves myelinated and unmyelinated at the same time? I was trying to answer this question when I remembered that the somatic axon is myelinated, while both sympathetic and parasympathetic preganglionic axons are also myelinated. Are they only myelinated or are they both myelinated and unmyelinated? Thanks
Edit:
This is a question from an old lecture quiz (previous year) and unfortunately I do not have the answers for the questions. The wording of the question was

Spinal Nerves are
a.) myelinated
b.) unmyelinated
c.) answers a and b
d) none of the above"

Spinal nerves are mixed nerves containing afferent and efferent neurons of various types. Anatomically, they protrude from the spinal column bilaterally at each vertebral level. They contain both myelinated fibers (e.g., A fibers) and unmyelinated fibers (e.g., C fibers).

The answer is (c): both myelinated and unmyelinated.

Please note that spinal nerves are NOT located in the spinal cord, despite the fact that neurons in each spinal nerve will either originate or terminate there. A spinal nerve is a peripheral structure. It starts at the point where the dorsal and ventral root converge (See April's Clinical Anatomy, Ch. 1). If you have the opportunity to observe back surgery or dissect a human cadaver, you can see and touch a spinal nerve. They are cable like structures containing bundles of many many many axons, but no neuron in its entirety. A nerve is not a neuron. This is a common misconception.

Just to add, the details here may seem like trivia, but they are not. Similar questions (and questions that require you to understand the distinction between a nerve and a neuron) are often asked on US medical licensing exams. This is because they are relevant to understanding and interpreting neurological symptoms and physical exam findings.


computing relative synonymous codon usage from a coding sequence alignment while accounting for phylogenetic inertia? I would like to compute the relative synonymous codon usage (RSCU) from coding sequence alignments. But since the coding sequences from an alignment are not independent realization, the statistics (RSCU) need to account for the phylogenetics autocorrelation present in the data. How can I do that?

It looks like you want to test a very specific hypothesis. Wether a sequence accumulates more non-synonymous changes than expected given its phylogenetic backgroun. The programme CODEML, included in the package PAML was designed specifically for this:

http://evomics.org/learning/phylogenetics/paml/


How compatible are mammal wombs? I had read about science working towards the creation of artificial wombs however I wonder how compatible are mammal wombs and connected systems to develop fetuses. What species are so compatible that they would be able to surrogate the embryos and fetuses of another species?

In short: Not completely, but more than you would expect.

The project to clone a mammoth considered using an adult female elephant as a surrogate mother, so in theory closely related species can do this.


Why should we preceed neostigmine by atropine in tubocurarine toxicity? Why should we precede neostigmine by atropine in tubocurarine toxicity ?

I know that neostigmine act as anticholinesterase thus increasing the number of Ach molecules rendering them able to displace the tubocurarine, but I don't get the idea of atropine I know it's muscarinic inhibitor but we are speaking about nicotinergic receptors?

Tubocurarine is a non-depolarising neuromuscular blocking aqgent, that is, it acts as a competetive antagonist of Acetyl Choline at the Nicotinic receptors.(Toxicity/Effect: $-N$)

Atropine is a competitive antagonist of the muscarinic acetylcholine receptor, classified as an anticholinergic. (Effect: $-M$)

Neostigmine blocks acetylcholinesterase, increasing the concentration of ACh at, and stimulating both muscarinic and nicotinic receptors. (Effect: $+M+N$)

Hence, to counter the only nicotinic deficiency of ACh, we give Neostigmine, which will also stimulate the muscarinic receptors, leading to muscarinic side effects. To counter the latter, atropine is given. A similar formulation is used in a disease like Myasthenia Gravis, with a functionally similar lesion.
$$(+M+N)+(-M)+(-N)=0$$


Sansevieria species specification needed What are the botanical differences between the species S. parva and S. senegambica? Please highlight the main ones.
I have 2 groups of plants. One with label "Sansevieria dooneri" (a synonym of S. parva) and one with label "Sansevieria senegambica" and sadly both groups look awfully the same at first sight.

You could use this key to the genus. The differences between both species should become obvious when tracing back the decision tree. It seems that they can be distinguished mainly by the leaf size/shape of adult plants.


What is the use of having a surrogate mother in animal cloning? In animal cloning, an ovum is collected by an animal and processed to form an embryo after fusion, which is going to be inserted to a surrogate mother. So my question is that why can't the embryo be inserted the animal that gives the ovum as they are both maternal?

It would make the result at least a little ambiguous. How would you establish with high confidence that the offspring was the results of your implanted cloned ovum and not a naturally fertilized one? DNA testing would have to be quite extensive to establish that offspring was a clone and not the result of an ordinary pregnancy. If you use a surrogate mother, the offspring will have DNA quite distinct from the surrogate.


Psychrotrophic Bacteria I want to know what gene or protein makes bacteria psychrotrophic, as opposed to regular bacteria that prefers warmer conditions. If you don’t know exactly, and you have suggestions as to where I can find the name of the gene, that would be great. I would also need the gene to be accessible so if anyone knows anything, please let me know. Thank you!

It is not necessarily about special (psychrophilic) genes, but rather about psychrophilic variants of their mesophilic and thermophilic homologs.

In general, lower temperature means lower rate of enzymatic reactions.

To cope with this problem, psychrophilic bacteria encode enzymes with highly mobile surface loops (higher mobility, higher catalytic rate).

Thermophilic bacteria have a different problem: enzymatic reactions are fast, but the enzymes are unstable; to cope with this problem, thermophilic bacteria encode enzymes with more rigid surface loops (more rigid, more stable).

Sočan et al. (2018) Catalytic Adaptation of Psychrophilic Elastase. Biochemistry 57: 2984-2993.
Åqvist (2017) Cold Adaptation of Triosephosphate Isomerase. Biochemistry 56: 4169-4176.


Is this a saltwater millipede? I spotted this millipede-like creature in Hervey Bay, Australia at low tide, just kind of hanging out at the bottom of a small saltwater tidepool.

It's several inches long, composed of a large number of segments, each of which appears to sport a pair of legs.

Hard to tell from the photos, but the creature is aquatic and in both instances was observed moving around under about an inch or so of water.  No specimens, alive or dead, were observed outside of the water.

They leave obvious trails behind them in the sand at the bottom of the tidepool as they move across it, and I assume they have some ability to burrow into the sand as I saw far more trails than I did creatures.

What are these things?

This is indeed a polychaete worm, and likely a member of the beachworm family Onuphidae.

From the Marine Education Society of Australasia  :

  Polychaetes are particularly common on and in muddy and sandy shores. Their most obvious feature are the pairs of parapodia appendages. One pair comes from each body segment. These parapodia are used for crawling and swimming. "Para" means "like", and "podia", "pod" or "ped" means "legs". These parapodia are often tipped with hardened spine-like setae or dorsal cirri.

You can find some good informaiton on beach worms here, and information on the distribution, abundance and
population dynamics of various species here.

I'm sure a quick message to Dr. Pat Hutchings, the Austrtalian Museum's polychate expert, would prove to be be your best chance to get a species identification.

For those interested in additional polychaete identification, you can download a digital ID key.


can somebody please Identify this queen ant? hi, i found this queen in France and i want to know if it is a species i can take back home to England. i cant identify her since the only queens I've ever kept are Lasius Niger so i would like some help please!!

There are 4 main families in France. Formicinae, Dolichoderinae, Myrmecinae ans Ponerinae. This is a an ant in the subfamily Formicinae because it is large and has only one segment between the thorax and the abdomen. You can deduce that because the thorax and the abdomen seem very close. This particular ants is a queen of the genus Formica (wood ants) from the general aspect. The presence of wings indicate this is a reproductive individual and because the eyes are small compared to the rest of the head it is a female. The color and the general shape and the size would allow any trained observer to identify the genus Formica, although no formal criteria can be seen on this picture. Formal criteria require inspection of the funicula, a part of the antenna, which cannot be seen on this picture. For references please visit http://antarea.org, http://cle.fourmis.free.fr and read Seifert - Ameisen Mittel und Nordeuropas. Lutra.


What ecological niche do disk shaped fish exploit? I looked up "Early Triassic" to get a sense of what that meant and I ended up on this image of marine life at the time. I noticed some disk shaped fish (#8 in the picture:  Bobasatrania (durophagous actinopterygian)) that looked, to me, like Permit or a Sunny.

I wondered, what ecological niche are disk shaped fish exploiting? Why is this particular body type repeating itself 250 million years later?

EDIT per answers:
I view them as same thing. I don't mean to suggest an animal can only exploit one niche, nor that a given niche can only be exploited by one animal. For example, birds with short, thick beaks like parrots eat seeds that are tough to crack. They give up the ability, perhaps, to get at some more delicate flower nectars. Brightly colored poisonous animals are easier to spot, but they are poisonous. So, over time, they are, as a specie, less likely to get eaten. What do disk shaped fish give up by being disk shaped, and what do they gain?

I believe what you're referring to are fish with the compressiform body shape (fish with a narrow flattened body). The advantage to this body shape is that it allows the fish to swim very quickly for short periods of time. This would, I assume, be an advantage both as predator and prey in that it can use a quick burst to escape from something else trying to eat it and also allow it to use a quick burst to catch food for itself.

--added--

I just re-read your question and caught the "ecological niche" part, which is different from evolutionary advantage. I'm not 100% sure regarding this (I'd say 80% sure though), but I don't think that an animal has to fill a specific ecological niche in order to survive - it just has to...survive. Surely animals that fill specific niches can gain an evolutionary advantage by filling a niche, but it is not (to my knowledge) a requirement.


Do the pH and other ions affect the hydrolysis of ATP ATP hydrolizes to ADP and phosphate in a strongly exergonic reaction and is used for energy transfer and short-term storage in cells.

ATP is stable inside a cell, so a significant activation energy must be necessary for the reaction.

However, the English Wikipedia article implies that stability of ATP is not a given, but depends strongly on the properties of the surrouding solution:

"ATP is highly soluble in water and is quite stable in solutions between pH 6.8 and 7.4, but is rapidly hydrolysed at extreme pH." and
"ATP is an unstable molecule in unbuffered water, in which it hydrolyses to ADP and phosphate."

How does the pH affect the hydrolysis of ATP?
Why is it even relevant if the solution is buffered or not? (Do the ions stabilize the molecule somehow?)
Are there other effects that influence stability in animal cells?

Stability of ATP is largely due to Mg2+. ATP in cell is actually Mg2ATP2-
The Mg ions stability the negative charges on the phosphates. pH is also important of course, but Mg is key, hence you see Mg2+ all the time in biochemical reactions where ATP is involved.


Do unique communities of bacteria form inside water storage in plants? I assume that plants, like animals, have an ability to fight off bacteria that invade their cells (support: here and here.

However, water often harbors quite a bit of bacteria in even unsuspecting locations (e.g., see here).

Moreover, plants store a lot of water in their vacuoles.

I was wondering, whether the water stored in plant cells tends to harbor bacteria...

If so, are the bacterial communities in such water-storage organelles unique to plant vacuoles or do bacteria get transferred with the water as it moves through the plant?

As stated in Plant Signal Behav. 2010 Dec; 5(12): 1568–1570:

  Phytopathogenic bacteria do not enter plant host cells, but proliferate in the intracellular space.

But as they can reach the apoplast, pathogenic bacteria can take advantage of environmental humidity levels and manipulate water content inside plant leaves to reproduce and spread infection as shown in
Nature volume539, pages524–529

So yes, bacteria can infect water inside plants but usually not inside the plant cells themselves. As they infect the intracellular space, they can spread in the water and infect the whole plant. It is also to mention that we are not speaking about the same bacteria as in standing water or something else. Viruses on the other hand can infect the plant cells themselves.


Is beauty universal? I don't know if this is off topic at all, but there are a lot of things that humans tend to consider beautiful which other animals in nature also seem attracted to. For example, bees pollinate the most vibrant flowers. Birds of Paradise appear to demonstrate a selective advantage to looking pretty. Peacocks flaunt their looks. Songbirds sing beautiful melodies. Butterflies are amazing. Some spider species have bright colors and perform cute dances. It seems like these examples demonstrate an evolutionary advantage not just for things that stick out from a crowd but also that look good to us humans.

So I guess my question is, is beauty universal? Are there aesthetic characteristics that are attractive to all these different kinds of animals, that would signal something good for others to see, and that different animals including humans would universally recognize as being nice?

Fitness

Fitness is a trait which, when high is pretty much always attractive to potential mates in all species. However, fitness is definitely not an "aestetic characteristic".

Traits that are often correlated with fitness

There are some "aestetic characteristics" that are correlated to fitness in many species, such as body weight. Such trait are therefore often correlated with what individuals find appealing.

Body weight is a standard examples. Heavier individuals often have better competitive abilities, better foraging abilities and therefore have a higher fitness. As a consequence body weight is often used a s a proxy for fitness.

Relative body characteristics

Novel traits in a population can be evidence of parasitism and therefore would tend to be considered as non-attractive. However, counter to this intuition, it has been shown typically in birds having high sexual selection, that individuals having novel traits are more attractive.

Why is there a lack of generalization?

To build the intuition I would just say that given the gigantic phenotypic diversity that exist among all species that perform some level of mate choice, it is pretty clear that you will not find a simple morphological trait that will be attractive to all species.

Mating preferences evolves. Individuals that are attracted toward individuals that will yield to a high progeny (and low sexual conflict and low transmission of parasites) have higher fitness their preferences increase in frequency in the population. As a consequence, individuals like whatever is (should rather say 'was') favoured in the population. Now, in some population individuals are selected to be small, or to be big or any other things. This is the process of natural selection applied to mating preferences.


Where does weight go when you lose it? When one loses weight, where does the lost poundage (I assume comprised mainly of fat) go?

Is it urinated out? Defecated out? If a combination of both, does the percentage of each differ depending on how much of what your are losing was pure fat?

You breath it out, for the most part. Fat is "burned" to convert the carbons to CO2, which is breathed out. There's not very much fat-derived carbon in each breath, but you breath a lot, all day long.

At rest, an average 70 kg person consuming a mixed diet (respiratory quotient 0.8) exhales about 200 ml of CO2 in 12 breaths per minute. Each of those breaths therefore excretes 33 mg of CO2, of which 8.9 mg is carbon. In a day spent asleep, at rest, and performing light activities that double the resting metabolic rate, each for 8 hours, this person exhales 0.74 kg of CO2 so that 203 g of carbon are lost from the body. ... Replacing one hour of rest with exercise that raises the metabolic rate to seven times that of resting by, for example, jogging, removes an additional 39 g of carbon from the body, raising the total by about 20% to 240 g. ...
Our calculations show that the lungs are the primary excretory organ for fat.

--When somebody loses weight, where does the fat go? Ruben Meerman and Andrew Brown, BMJ 2014; 349


RNA isolation from Drosophila head I need to isolate RNA from Drosophila head. I basically chop the head off and first homogenize it with a homogenizer (similar to this: http://www.omni-inc.com/omni-tissue-homogenizer-th-package-p-11.html) and further homogenize it with 22G needle in TRIzol reagent. I use TRIzol RNA isolation for larvae brain a lot and have no problem with the method itself. However, with adult I got really low RNA concentration which is weird.

I thought that maybe I have problem with homogenization itself, or I overlook something (such as extra centrifugation or different kind of homogenization etc). Does anybody have experience with it?
Thanks.

It doesn't seem like a homogenization problem. Nonetheless you can try this:

Suspend the heads in trizol
Homogenize by passing through 30/31G needles (insulin syringe) up to 10-15 times.
Heating a little might help but I think it is unnecessary for these tissues.

Insulin syringe is much better than the hand held homogenizer. Freeze-thaw 1-2 times if you want (helps in homogenization).

During extraction you can add 5M LiCl (100µl) + Ethanol (1ml) to 400µl aqueous phase (instead of isopropanol), keep at -20⁰C for 1-2h before centrifuging. Alternatively you can add a little RNAse free glycogen to Isopropanol during precipitation.

PS: the liquid Nitrogen trick that rg255 mentioned is for quickly getting heads and avoiding the pain of dissecting each head.


Where do I get an annotation file for yeast genome with ENSEMBL ids? Even the annotation files hosted on  the Ensembl site have systematic names (starting with Y..) instead of ENSEMBL ids (starting with EN..).

I bet there would be a place where I can get an annotation file (GFF3 preferably). Please let me know if you know such.

With a further search for the answer, I realised that unconventionally, ENSEMBL ids for yeast start with Y. That is strange. I guess this is because the yeast annotations are primarily maintained by SGD (yeast genome database) and ENSEMBL just hosts a copy of that.

Also these ids are called Stable Gene IDs.


What is this tree and fruits? Please help me identify this tree and its fruits that have sweet taste and very small soft seeds:

It grows in the Mediterranean region.

It's a sycamore fig (Ficus sycomorus)- a type of Mediterranean fig.

For details: see this wiki page


What are phenetic analyses used for? Phenetics (grouping of organisms based on similarity) used to be claimed to be an alternative to cladistics, but now it is widely accepted that phenetic analyses cannot be used to infer evolutionary relationships. However, phenetic methods like neighbor-joining trees are still being developed today.

Are phenetic analyses still valid today for purposes other than determining evolutionary relationships, or are they completely obsolete? Does anyone have an example of a recent paper that uses phenetic analyses in a valid way?

As usual, a rant from Joe Felsenstein's webpage seems relevant. Specifically, this:
"There is no consensus, even among systematists, as to what the word "cladistics" means."
Everyone seems to have agreed that phenetics--which is to say the blind faith in the results of clustering algorithms such as neighbor-joining etc.--is on its own not very useful, compared to a principled dedication to placing organisms taxonomically into monophyletic groups.
However, the hard-line cladistics point of view (e.g. Willi Hennig society) is that no method of inference other than maximum parsimony (in one of its various flavors) is acceptable, for obscure philosophical reasons that no one cares about. Frankly, for any realistic purpose, cladistically unacceptable methods such as Bayesian inference and likelihood methods perform the best. From cladistics wiki:

Although traditionally such cladograms were generated largely on the basis of morphological characters and originally calculated by hand, genetic sequencing data and computational phylogenetics are now commonly used in phylogenetic analyses, and the parsimony criterion has been abandoned by many phylogeneticists in favor of more "sophisticated" but less parsimonious evolutionary models of character state transformation. Cladists contend that these models are unjustified.

In other words, cladistics is more of a philosophical point of view than a group of methods. There are "soft" versions that everyone pretty much agrees on, namely the principle that monophyletic groups are preferable to paraphyletic groups. But methodologically, it's just a lot easier and more workable to use non-cladistic or even phenetic techniques rather than the (computationally frequently more onerous and not necessarily more accurate) parsimony techniques of cladistics.
For a (fairly) recent apologia specific to neighbor-joining, see here.
In short, given the highly heuristic nature of most science, most workers aren't really paying attention to these debates, and just use the tool that works for the problem they're working on. And in many cases those methods are phenetic, even if cladists claimed a victory of principle.


Does every wave length of UV kill bacteria? Will every wave length of UV work for killing bacteria? So will UV A, UV B and UV C all work? Or will only the shortest of the three, UV C, work? Also, will the average UV lamp help against bacterial growth (if it is shone on an object for 3-5 minutes for example)? What about a longer period: a bacterial colony in a petri dish under an average household UV lamp for a day? Would the growth be reduced noticeably? Or would the change be too small to notice when using the average UV lamp? Does the type of UV also matter for this (A/B/C)?

The CDC's disinfection guidelines lists UV radiation between 328 and 210nm as effective for disinfection, with a maximum of bactericidal activity occurring between 240-280nm. At this wavelength DNA damage (Thymine dimers) is induced with a high rate.

Due to practical reasons UV light is mostly used to disinfect water, if used in rooms there is some effectiveness against microorganisms in the air and some on surfaces, but on one hand the effectiveness is reduced  by square with the distance from the UV source and on the other hand you need completely empty surfaces where nothing casts shadows. The other problems are plastic materials which may get damaged by repeated UV exposure.

Have a look at this reference (only available via Google Books): "Principles and practices of disinfection, preservation and sterilization." and this subchapter.


Why don't people seem to die from salmonella in bites? As far as I know, reptiles have salmonella in their mouths as part of their digestive process. Every time I hear about someone being bitten by an python or alligator or monitor either at a zoo or in the news or from a private owner, it seems like whoever is bit recovers with ease.

How come something as virulent as salmonella that can evade an immune response doesn't cause whoever gets bitten to nearly immediately become septic? Is it because salmonella only attacks epithelial tissue and there isn't much of that deep in an arm or leg?

Salmonella infect via the fecal-oral route. They have proteins on their surface that match our gut cell surfaces, allowing them to attach and invade the gut. Those cell markers aren't present when you are bitten. it's the same reason that plant virus dont make us sick.

https://www.ncbi.nlm.nih.gov/pubmed/17593246

this is a bit heavy if you dont usually read primary papers, but looking for "Salmonella route of infection" or similar will yield the same kind of information


When did mouth pipetting stop becoming a way to handle liquids in a lab? Almost all modern lab protocols have an addendum prohibiting pipetting by mouth, instead mandating that a Gilson pipette, a rubber pipette ball, or a serological Pipet-Aid be used.

However, it was clear that some time in the previous century, prior to the invention of the aforementioned tools, many labs did in fact use mouth pipetting to transfer liquids, some of which were highly hazardous. An example can be seen here (from this IO9 article, which dates the photo to the year 1943):

When did pipetting by mouth stop being recommended in labs?

Mouth pipetting, while almost unheard of in modern laboratories in developed countries, is still very much a current protocol in many parts of the world.

For example, this paper analyses the proportion of clinical labs in Pakistan and found evidence of poor biosafety practices (emphasis mine):

  Results: A total of 1,647 (92.4%) males and 135 (7.6%) females
  participated in the study, with over half (59.7%) having more than
  five years of work experience. Results showed that 28.4% of the
  laboratory technicians from Punjab, 35.7% from Sindh, 32% from
  Balochistan and 38.4% from Khyber Pakhtoon Khawa (KPK) did not use any
  personal protective equipment. Almost 46% of the respondents (34.2%
  from Punjab, 61.9% from Sindh, 25.2% from Balochistan and 85% from
  KPK) said they reused syringes either occasionally or regularly.
  Furthermore, 30.7% of the respondents said they discard used syringes
  directly into municipal dustbins. The majority (66.7%) claimed there
  are no separate bins for sharps, so they throw these in municipal
  dustbins. Mouth pipetting was reported by 28.3% technicians.

Additionally, a Google Scholar search for papers published in the past 5 years involving mouth pipetting turned up 670 hits out of 284000 total hits, a proportion of 0.23%. This is further evidence that this dangerous technique has not been fully eradicated from labs.


Method for preparation of LB agar plates with Ag+? I need a method for preparing LB agar plates with 1 mM concentration of AgNO3.
I can not seem to find a method online, does anyone know of one that I could use?

Here are my main questions regarding the method:

a. Do I add the silver before or after I autoclave?

b. do I add the silver in a liquid form for powder?

Thanks.

You add the silver after autoclaving. Just make sure that you make your stock concentration of silver in sterile water to avoid unwanted contamination. Do it in liquid form; it is easier to dilute from a stock.


What is the name of this moth found in Virginia USA? Found in Virginia, USA on Nov 1 2015, 10:34 AM.

Oh, found it. It is called a Euonymus Leaf Notcher Moth. It is an invasive species from Asia. It was first found in Maryland and Virginia in 2001.

http://www.insectid.ento.vt.edu/exotic-pests/euonymus/


How to measure the biomass of hydroponic plants in netpot/rockwool DWC system? I'm doing an experiment with 4 kale plants, each in their own small deep water culture (DWC) system. Each plant was transplanted in rockwool with netpots and clay pebbles. But I need to periodically and accurately measure the biomass of each plant. The roots have grown through the rockwool and netpots and I don't want to rip out the roots.

Is there an easy way to do this?

If you did enough replications in your experiment, you could harvest one or more plants and measure fresh weight, and then gently oven dry for about 48 hours at like 160 degrees F and then take a dry weight as a measure of biomass. I don't know a non-destructive way to do it. A lesser alternative would be to measure plant height and number of leaves, though this would be less accurate. There are devices that measure leaf area, and I know a simple, low-tech way to measure leaf area.


Rate-determining steps in enzyme catalysed reactions According to my chemistry book, there are 3 simplified steps within an enzyme catalysed reaction:

S + E → ES
ES → EP
EP → E + P

Where S is substrate, E is enzyme, ES is enzyme substrate complex, EP is enzyme product complex and P is product.

It is my understanding that at first, when substrate concentration is low the rate determining step is step 1, as this is the slowest step in the mechanism.

When you increase substrate concentration to a certain level, where there are no free enzymes remaining to bond with them, adding more substrate will not make the reaction faster, so the order has become 0 with respect to substrate conc.

Is the rate determining step now 2 or 3? I thought it would be 3 as that is the step that frees up more enzymes which could go on to catalyse more reactions. My book says that it is step 2, as "it depends on how fast the ES can convert into EP". But surely this step won't free up more enzymes to catalyse reaction further?

Is the book correct? Can anyone help me understand this?

This is enzyme and substrate concentration specific, since the reaction rate depends on the reaction rate constant k that depends on the enzyme. However if there is a large amount of P present in the solution the EP -> E + P reaction slows down so this can be the rate determining step. On the other hand if you dynamically remove the P molecules from the system the ES->EP can be the rate determining step.


Can we artificially increase human growth using HGH? Robert Pershing Wadlow was a man who lived in the first half of the twentieth century. He had hyperplasia of his pituitary gland, which caused him over-produce human growth hormone (HGH), and as a result, he grew to nearly 9 feet (2.75m). He had difficulty managing his body size and died at age 22, with no sign that this growth was slowing down.

HGH can be used for medicinal purposes, and it seems that doctors prescribe it for conditions like chronic underdevelopment and HGH deficiencies.

Putting aside ethical or government regulation issues, is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH? If not, what was different about Wadlow's case?

You asked

  ... is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH?

For an adult, the answer is no. Human growth means skeletal lateral growth, which is indeed mediated by human growth hormone. But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.

From the cancer.gov site on Bone development and growth:

  When cartilage growth ceases, usually in the early twenties, the epiphyseal plate completely ossifies so that only a thin epiphyseal line remains and the bones can no longer grow in length

Further reading: NEJM Osteogenesis: The Development of Bones

This point is usually reached around the early twenties in humans. The case mentioned in your question is different because in this case, the human growth hormone was "given" before this process had finished and thus the bones grew longer. He was 22 when he died, so we will never know if he would have finished growing in his mid- to late twenties.

Giving adults (that don't suffer from an HGH deficit) more human growth hormone has been done and does not result in lateral growth, but it does result in increase in lean body mass in both young adults and the elderly


Is a butterfly one or two animals? I have read somewhere that a butterfly might be two animals that combined together. One animal was a worm-like creature and the other an insect.

And the insect basically hatched inside the worm. Somehow they combined into one creature.

Is there any truth in this? Wouldn't this mean a catterpillar and a butterfly would have different DNA?

But in that case why would a butterfly lay eggs that turned into caterpillars?

There was a paper by: Donald I. Williamson, published in the Proceedings of the National Academy of Science (PNAS) August 28, 2009 https://doi.org/10.1073/pnas.0908357106, and communicated by Lynn Margulis.

Lynn Margulis, as a member of the National Academy of Sciences, could publish papers in PNAS without adequate peer review. Members of the academy were afforded this honor, because they have achieved the highest levels of science, and supposedly, have few peers who can review their work.

Margulis was known for her work on the origin of mitochondria from the engulfment of prokaryotes, and also the Gaia hypothesis (that the Earth is itself, a living organism). That may have predisposed her to the ludicrous idea that butterflies were the result of some strange symbiosis from onycophorans (Velvet worms).

The whole thing was a huge embarrassment to PNAS, and Margulis. It would never have been published if it had been objectively peer reviewed, and was formally rebutted as wrong, and without any merit whatsoever. See: https://blogs.scientificamerican.com/observations/controversial-caterpillar-evolution-study-formally-rebutted/


How to manufacture different sized micelles in nano -scale? I am trying to answer q5:

  "How can you manufacture micelles in A) nanometerer -scale B) and in ten nanometer -scale?"

  My Thinking

    Observations and some thinking

    Oil in water forms a micelle here, not making it soluble.
    Whey protein in Water forms a micelle or is this due to other reason? Protein folding with hydrophopic-tailed-and-hydrophilic-headed-particels? Is this micelle or not?

    Required Vocabulary about one answer

    what is IVC?
    PLoS?
    "[E]xtrusion step" = some sort of burst?
    PCR=Polymerase chain reaction here.
    monodisperse = A collection of objects that "have the same size, shape, or mass." (source
    here).

A key factor that determines the radii of a micelle is the critical micelle concentration. The other is the the hydrophobicity of the micelles which can be measured using the contact angle. A lipid nanoparticle has a minimum size on the order of 50 nm due to the surface tension of the lipid bilayer. However, micelles can be much smaller.

As for the creation of uniform nanoparticles, I am going to claim that what I say next can be in no way a reasonable answer to a HW problem. Why? Because the information is hidden in some obscure PLoS paper (Stapleton and Swartz) with 7 citations using IVC. Typically, micelles created for emulsion-PCR are created by vigorous mixing and followed by an extrusion step. However, this creates a polydisperse droplets. Alternatively, if you were to use a microfluidic device, then more monodispersed droplets can be formed. The control of droplet size can be achieved by varying the flow rates of the aqueous phase and the oil phase as well as changing the surfactant.


Why do bulls have a hump? Camels have a hump as an adaptation to the heat. They store fat so that it minimizes the insulating effect the fat would have if distributed over the rest of their bodies.

Why do buffaloes/ oxen/ bulls have a hump then? The climates they are found in, I assume, are not as hot as that of the camels.

Bison humps are made of muscles, huge muscles. According to this and this pages bisons use their heads for snowplowing. This hump provides head support. It seems that also other animals have structures like that: giraffes, rhinoceroses, elasmotheriums,... this list can go on since this structure should be homologous of other animals'. From this page rhino humps made from muscles, nuchal ligament, fat, and dermis. And from the page, probably fat quantity depends on the nutritional state of animal.

I searched nuchal ligament, the remarkable structure of hump according to rhino page. This is a ligament spans from upperback vertebra to neck vertebra and to skull. Can be found on humans too. Also muscles of hump should be homologous to humans' notice that vertebras have spines not just for supporting ligaments they also for muscles. Human skeletons just don't have vertebra with long big muscle connection points and huge neck/back muscles connecting huge bones, this is why we don't have a hump or an obvious large hump. And I think even camels do have slighly bigger muscular humps but theirs are covered with big fat hump.

Bison skeleton and elongated spines supports huge muscles and ligaments.

Horse's nuchal ligament

Human nuchal ligament

Human nuchal ligament drawn with red lines and muscles (bison hump also consist of muscles).

Giraffes' this is an energy saving feature. Giraffes don't need to use muscles to hold their neck. They just use when flexing their necks down, when drinking water etc.

According to Wikipedia, for an alternative hypothesis Ouranosaurus have a hump. (Other hypothesis is display sail or termoregulation sail of course. Also spinosaurus have this kind of alternative hypotesis but this hypothesis not accepted much as sail. and spinosaurus' spine different from bisons. Bison spines concentrating at shoulder but spinosaurs' not at the shoulder. You can find spinosaurus info from this page.)


Why do earthworms have so little colour? Earthworms (or at least the ones that I have seen) tend to be pinkish, but with the front dorsal region being a camoflagued brown. Why is this the case, rather than the entire body or back being pigmented. I couldn't find any reference to the reasons behind earthworm colouration

Here is a picture from the wikipedia page on earthworms, showing the concentrated pigmentation

The reason appears to be the light cells of Hess, which are light-sensitive cells distributed over the back of earthworms, being more concentrated towards the head


probe amplification in MLPA I'm reading an article about MLPA (Multiplex ligation-dependent probe amplification) and I got stuck on this sentence:

  The advantage of splitting the probe into two parts is that only the ligated oligonucleotides, but not the unbound probe oligonucleotides, are amplified.

The principle I don't understand is why won't the unligated oligonucleotides be amplified? As is my current understanding of the PCR, the primers should normally anneal and produce fragments which would end at the end of an oligonucleotide (at the "ligation site" - so they would be shorter, but they should be there), am I wrong?

I work for MRC-Holland, the developer of MLPA, and what Kacper explains is indeed the case. Any RPO (right probe oligo) that is not ligated is also amplified in the MLPA reaction, as the reverse primer can bind to the primer binding site of the RPO. HOWEVER, since this unligated RPO oligo LACKS the binding site for the (fluoresently labelled) forward primer, the amplification ends here. LIGATED probes, in contrast, contain the binding site for BOTH primers, and hence are amplified exponentially. Furthermore, the fluorescent label is only incorporated in the amplicons that results from ligated probes.


Why are there species instead of a continuum of various animals? As I understand it, various animal traits have to evolve gradually, but what happens to the species that are "neither here nor there"?

To put it differently, if a species evolved from another, it did so because it's somehow better, right? So why are there examples of the original species not being extinct?

What factors determine weather some species "stick"?

Mathematician/computer programmer's answer here:

There is a continuum of different animals — in fact it's pretty fair to say that every animal occupies a different place on this continuum. They're just not uniformly distributed over the continuum; they're clustered around forms that are most likely to survive and reproduce, and the lowest-energy paths between them.

This is because evolution is basically a stochastic optimization algorithm, one that finds the "best" set of parameters for maximizing some function by randomly perturbing an initial set of input values. In fact, some of the best optimization algorithms today are based on ideas drawn directly from evolution and called "evolutionary algorithms".

In mathematics, given enough time, these algorithms will all converge on one optimum solution and nothing else. Why isn't it like that in nature? Because in mathematics, the "fitness function" that we're optimizing for stays the same for a given problem for as long as the algorithm runs. It represents the specific problem we're trying to solve. In nature, there's no outside force imposing a fitness function; an organism's survival depends on millions of factors in its environment which change over time, many of which depend on the survival and properties of the other organisms in its environment (competition, symbiosis, predator/prey relationships, etc.) This is a chaotic system so complex that it could easily go for billions of years without reaching a steady state, and even if it did, external changes (like the odd asteroid impact, to use an extreme example) would still come around to shake things up.

Another reason for the clustering is because a lot of the "intermediate states" in the genetic space have a fitness of zero — these are the states between species that can't interbreed, or that have sterile offspring. The categorization of "species" is based on this, and although it's not exact, it's still generally true that the more different two creatures are, the less likely they can have viable offspring. This makes evolution more likely to explore the spaces near already-successful organisms, and less likely to produce radical new things by hybridization.