From refseq ids to Go term Ids I have a list of Refseq accession numbers such as :

YP_009448812
YP_009448725
YP_009448701
NP_659591
around 10 000 acc_numbers...

and I'm looking for a tools in R or Python in order to get the corresponding Go term ids.

I tried the packages (org.Mm.eg.db) and (GO.db) but it does not work.

> Term(names(get(get("YP_009165174", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009165174" not found
> Term(names(get(get("YP_009448701", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009448701" not found
> Term(names(get(get("NP_659591", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "NP_659591" not found
> Term(names(get(get("YP_009448812", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009448812" not found

Does anyone have an idea? Thank you for your time. I cannot find a egREFSEQ2EG for viruses.

So, I've looked a bit into this and the way you want to do your analysis won't work as you planned it. The main reason for this is that the GO database does not contain any virus species (as fas as I could see). The existence of the species you want to analyse in the database is important, because you need to have a background or reference gene set in order to perform enrichment analysis. Even if you're just interested in the IDs and want to perform the analysis by yourself, this means that you're unlikely to find anything for your genes/proteins in the GO databases.

Your best alternative is to use other annotation databases and either rely on their annotation or map their annotation to GO term ids (here is a list of all databases that allow this).

Your best bet for this is probably the UniProt database, since that should have entries for most of your proteins (though not all will have annotated GO terms). UniProt also offers an ID mapping tool that should be able to convert your RefSeq IDs to uniprot IDs, and also comes with an API for python. Do note that some of your IDs (the YP_ ones) are provisional RefSeq entries and the webpage tool only finds them in the 'UniParc' database (not UniProt KB).

Once you have the the UniProt IDs you should be able to map the available GO terms from there (see the last entries of the first link above).


C-myc/anti-myc Ab Interaction with Fusion Proteins I am going to prepare a c-myc fusion protein with the following configuration:

(28-residue signal sequence)-(c-myc)-(GGSGGGSG Linker)-(Protein of Interest (POI))

POI is a transmembrane protein and the 28-residue signal sequence is needed for membrane incorporation in ER.

My concern is the disruption of the c-myc/anti-myc Ab interaction due to the fact that c-myc being fused on both ends. Does anyone have any experience or reference with a similar construct?

After some further research, I found papers reporting successful co-immunoprecipitation experiments with POI-myc-His fusion proteins.

Moreover, I figured the signal sequence will be cleaved by signal peptidases which will leave the c-myc tag exposed on N-terminus with only an extra residue. I don't think that one extra residue will create a problem.

Here's the tool I used to figure out where the signal sequence will be cleaved:
http://www.cbs.dtu.dk/services/SignalP/

Here are the references for POI-myc-His experiments:

DOI: 10.1016/j.cub.2006.08.085
DOI: 10.1073/pnas.97.2.668


What is the map unit between the genes? While doing some biology I came across this question:
The following tables present results of plant crosses involving two linked genes: S is a seed-color gene, and L is a plant-height gene. Each gene has two alleles with one allele exhibiting complete dominance over the other allele. Dominant phenotypes are yellow seeds, and tall plants; recessive phenotypes are green, and short, respectively. Assume that crossing-over between two genes occurs once.

Calculate the map unit between gene L and gene S. (One map unit = distance of 1%
recombination)
This question confuses me because what I understand from the table is that from crossing over we get short flowers with green seeds(0.01) and tall ones with yellow seeds(that 0.01 from 0.51). So as a result from the fertilization we get a 0.02 frequency, that as I understand also equals the recombination rate. And so the map unit would need to be 0.02*100= 2%. But the response I have to get is 20%, which I do no understand how to get to.

Here's a hint: you're right about 0.01 being the recombinant (crossed-over) double homozygous recessive offspring. I think you're forgetting that each offspring contains 2 gamete haplotypes, and so predicting the percent of offspring with a given genotype involves multiplying the frequencies of the individual gametes that produce that offspring. To calculate the gamete frequencies (and thus the recombination frequency) you need to reverse that multiplication process.
Full answer:
I find it easiest to deal with uniform genotypes first. Of the 4 offspring phenotype categories, only the double homozygous recessive category (short/green) has uniform genotype - llss. If l and s were unlinked, 1/16 of the total offspring would be short/green=llss.
However, many fewer than 1/16 are short/green=llss, so linkage is confirmed and (as you note), ls must represent one of the crossed-over haplotypes. The other crossed-over haplotype is then LS. Thus, the parental (non-crossed-over) haplotypes must be lS and Ls.
Let's call r the recombination distance (in map units) between l and s. Each recombination between l and s produces 2 recombinant gametes: 1 ls and 1 LS.  Thus the fraction of ls gametes - f(ls) - will be (r/2)/100 and the fraction of LS gametes - f(LS) - will also be (r/2)/100.  Since each F1 offspring consists of 2 gametes, the fraction of offspring with an ls/ls genotype will be f(ls) x f(ls) = (r/2)/100 x (r/2)/100 = r^2/40000 = 0.01 (from F1 data).
Solving for r, r^2 = 0.01 x 40000 = 400, so sqrt(r^2) = r = sqrt(400) = 20.
r = 20 map units


Why does the membrane of a neuron not stay at its depolarized state? When an action potential is transmitted along the axon, the membrane reaches its depolarized state by opening Na+ channels. Both K+ (potassium) and Na+ (sodium) are now on both sides with close to equal concentration-ratios. It is the next step that confuses me: the K+ rushing out of the cell, thus repolarizing the membrane.

Wouldn't the two substances balance themselves out according to the Electric-/Substance-Concentration-Gradient once the Na+/K+ channels are open? I don't understand where that energy comes from, the energy that not only mediates polarization, but also the subsequent re-polarization.

Three facts:

The K+ ions are heavily concentrated on the inside while the Na+ ions are heavily concentrated on the outside

The Na+/K+ ion pump is unidirectional. It can only pump K+ ions inside the cell while expelling the Na+ ions.

Finally only the Na+/K+ ion pumps can restore the ionic equilibrium.

The full scene:

Once the threshold is reached the Na+ voltage gated channels open up. So Na+ ions rush in, causing depolarisation.

Then the Na+ channels close while the K+ channels open. This causes rushing of K+ ions outside, thus slowly reducing the potential difference starting the process of repolarisation

Now the Na+/K+ ion pumps are geared up as the extracellular concentration of K+ and intracellular concentration of Na+ ions are high (which is the ideal environment for the pump to work.

PS:
Without the high extracellular concentration of the K+ ions the pump can't function any faster than the basal rate even though the intracellular concentration of Na+ ions exceed the normal value by many times. High concentration of K+ ions in the extracellular environment is essential for restoration of the ionic equilibrium.

Edit:
I meant unidirectional in the sense that when actively pumping sodium is always pushed out while potassium is always pushed in.
Thanks to AliceD for pointing out that when the gradient is reversed, the pump synthesizes ATP due to forced movement of ions in the opposite direction.


variation in expression accounted for a SNP -- what's a usual percent? I am reading a GWAS paper that found a SNP associated to predisposition to colon cancer and was assessed for gene expression of the nearby gene. They found that the genotype accounted for 55% of the variation in the nearby gene expression. 55% sounds like a lot to me, what is the usual percent accounted for a significant SNP in a study like this?

 Dunlop MG, Dobbins SE, Farrington SM, Jones AM, Palles C, Whiffin N, Tenesa A, Spain S, Broderick P, Ooi L-Y, et al.. 2012. Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal cancer risk. Nature genetics 44: 770–776.

eQTLs (expression quantitative trait loci) are variants that affect the expression of one or more genes.

There have been several 'genome-wide' studies of SNPs that directly affect expression. The actual effect sizes are hard to pin down in most of them, but in the supplementary data for this paper is a list of the SNPs with the largest effects and coefficients of determination.

There are several common SNPs (cis-acting) that account for >50% of the variation in that genes expression in this (European) population cohort. That being said, that vast majority of variants account for much less variation in the expression, but this is to be expected.

I therefore can fully suppose that a disease-linked SNP could affect the expression of a gene to that degree, particularly if it is an oncogene or tumour suppressor.

Reference:

 Wood AR, Hernandez DG, Nalls MA, Yaghootkar H, Gibbs JR, Harries LW, Chong S, Moore M, Weedon MN, Guralnik JM, et al.. 2011. Allelic heterogeneity and more detailed analyses of known loci explain additional phenotypic variation and reveal complex patterns of association. Human molecular genetics 20: 4082–92.


What type of jellyfish is this? Friends of mine recently came back from a visit in kenya and on the kenyan beach they said they found several jellyfish with "sails" on their head. We tried finding out what they were and found one image online that was exactly the type of jellyfish they found:

What kind of jellyfish is it?

The guide told them that they're dangerous and those are just the corpses without stings or something, but nobody knew it's name.

If the jellyfish your friends saw actually look like this and if they were small (Wikipedia says they're usually less than 7 cm in length), they're likely Vellela vellela or sometimes called By-the-wind Sailors for the way the raised part catches the wind and is blown along the ocean's surface.

Wikipedia writes

  ...all possess nematocysts, in some species the nematocysts and toxins
  therein are more powerful than other species. V. velella's nematocysts
  are relatively benign to humans, although each person may respond
  differently to contact with the nematocyst toxin. It is wise to avoid
  touching one's face or eyes after handling V. velella, and itching may
  develop on parts of the skin that have been exposed to V. velella
  nematocysts.

Some photos.

Source

Source


Viral mutation rates and replication TL;DR
What's the relationship between the following?

Mutation rates (expressed as "mutations per year" for a virus like e.g. COVID-19 (SARS-CoV-2). E.g. this article mentions "The rate looks to be about 24 mutations per year"
Actual virion replication error rates in a single host cell, measured as e.g. error rates per released virion from the infected cell, i.e. (# of mutated released virions) per infected cell.

Assumptions
I would assume that mutations happen at a single virion-cell level because there are differences in e.g. nucleotides in RNA  between:

the virion infecting a cell (e.g. ACE2 for SARS-CoV-2)
the released virions from that same single cell

If so, wouldn't one argue that:

replication errors (at the nucleotide and thus released virion level) can easily happen, potentially billions of times during the infection of a single host organism
there is no "single successful" mutation or RNA variant within a host, rather, we have a distribution of RNAs, many of which could be simultaneously transmitted to another host organism?

Further context
I quote from e.g. this paper:

On a per-site level, DNA viruses typically have mutation rates on the order of 10E-8 to 10E-6 substitutions per nucleotide site per cell infection (s/n/c). RNA viruses, however, have higher mutation rates that range between 10E−6 and 10E−4 s/n/c

Again, wouldn't that mean that a single host could 1) easily generate many mutations of the same virus and 2) pass most of those uniquely generated mutations to another host? If so, how come we can simply say "24 mutations (over time) per year"?

Since no one else has done so, just gonna expand on what occurred here in the comments (mostly from @Alex Reynolds):

tl;dr: natural selection exists.

Longer version:

Mutations/replication errors/whatever will happen in the creation of new virus particles within a host cell. There is some distribution of number of mutational events that will occur as a function of the number of new RNA molecules created per cell and the replication error rate. Some subset of these RNA molecules will be packaged into new particles, yielding a new generation of viruses that get a chance to infect. Yes, this is potentially a large number of new mutations per infection event.
Some large proportion of these new particles will contain non-functional RNAs, due to inactivating mutations of one kind or another. Most of the new mutations will be worse at being a virus than the originally infecting virus (their immediate parent). So therefore, they will be outcompeted by non-mutated forms.
Among all those viruses which continue successfully infecting throughout the course of a year, on average we observe 24 substitution mutations in the genome over the course of that year. Every transmission chain included in the group of viruses at the end of the year must have remained viable for infection of hosts. In other words, it has survived natural selection.

In population genetics, this phenomenon is known as "mutation-selection balance"- e.g. new mutations arise in the population at a rate that is limited by the action of natural selection (at equilibrium).

Genotype-phenotype maps

What of course I am leaving unstated is exactly why "...new mutations will be worse at being a virus than the originally infecting virus..."

This is very hard to predict in many cases. In some cases it is very obvious why a mutant is bad at being a virus, if e.g. an essential gene is deleted from the RNA genome. But for many single mutations we don't really understand what their effect will be on virus function, we just observe that they drop out of the population due to negative selection.

If you are interested in this question, I recommend looking into genotype-phenotype maps. I know Jesse Bloom has done some work on influenza in this field, here is one example of such a paper. It is generally extremely laborious to do this kind of work, so relatively little is known about the functional effect of any specific mutation in any specific genome.

Hope it is helpful to have all that written out.


Name of scientist who discovered lifesaving drug and chose not to patent it? I recall reading about a 20th century scientist who made a life-saving drug that could have patented it and made millions. He chose not to and saved the lives of millions around the globe.

I thought it was Frederick Banting - but it doesn't sound quite right.

None of the others in this list seem quite right.

My question is: What is the name of scientist who discovered lifesaving drug and chose not to patent it?

Dr Jonas Salk or Dr Albert Sabin who did not patent their respective polio vaccines. There are some more such researchers so I am not sure who exactly you are looking for but this would be a start.


Why do the ancestors of birds still exist? If I am not mistaken, scientists believe that birds are evolved from reptiles. Why do the ancestors of birds (that is, reptiles) still exist?

Introduction to phylogeny
Short Intro to Speciation
Let's talk about speciation. Speciation is the process by which a single lineage split into two. This happens in a number of ways (allopatric vs sympatric vs parapatric, BDM model and others). I will consider a simple case of allopatric speciation below as it is the simplest one to understand (although not necessarily the process causing most speciation events).
Following the story of a lineage through its speciation events
Think of a population at time $t=0$. Let's call this species A (for Ancestor). Imagine that an ecological change brings a barrier right in the middle of the range of this population of A. Such a barrier could be originally caused by a fire, or a river that has changed direction or a mountain range "popping up". The two now isolated populations are free to diverge randomly through time. This is what we call a speciation event. Note that under this model, there is no necessary need for selection to explain speciation. Let's call the two diverging population B and C which exist at time $t=1$.
Now, imagine C goes under another speciation event and split into the populations D and E. In the same time, population B may have changed quite a bit so that we might want to call them F. Here is a diagram of the situation
  F           D ----- E     t=2
  |               |
  B ------------- C         t=1
          |
          A                 t=0

A is an ancestor of B,C,D,E and F and does not exist today. B is an ancestor of F but does not exist today. C is an ancestor to both D and E and does not exist today. Let some more time pass by and you may eventually end up with the following tree
  G ----- H       K   I ----- J t=3
      |           |       |
      F           D ----- E     t=2
      |               |
      B ------------- C         t=1
              |
              A                 t=0

At time $t=3$, only species G, H, I, K and J exist today, the other are ancestors of current species. Let's expand this tree even further.
  L ----- M   N       O       P ----- Q      t=4
      |       |       |           |
      G ----- H       K   I ----- J          t=3
          |           |       |
          F           D ----- E              t=2
          |               |
          B ------------- C                  t=1
                  |
                  A                          t=0

You will note that lineage I went extinct at some point between $t=3$ and $t=4$.
Naming subsets of the tree
Reptilia
I am now suggesting to give a generic name for all the lineages present in the tree we drew (which we call a phylogenetic tree by the way). Let's call them Reptilia. So all the species A,B,C,D,E,F,J,I,J,K,L,M,N,O,P and Q are Reptilia.
Birds and Mammals
Now let's consider a subset of this tree. Let's consider the subset made of the species J, P and Q only. Let's call them birds. Let's also call mammals the subset composed by the species G,L and M.
Lizards (and others)
Finally let's call lizards all reptilia that are not birds, nor mammals (in reality it would be more correct to call this group lizard_crocodile_turtles_snake_amphibians_tuatura). Of course, the right tree is much bigger! By the way, you can explore the tree of life yourself on OneZoom.org.
What is a taxon
By the way, a group of species is called a taxon (plur. taxa).
Monophyletic taxa
It might be straight forward to you that there is something fundamentally different between the groups that we called mammals, birds and reptilia to the one that we called lizards. Indeed mammals, birds and reptilia are called monophyletic as they are composed of a given ancestor and all its descendants. lizard on the other way is not monophyletic. A monophyletic taxon is also called a clade. Below is a graph representing what a monophyletic taxon is. It also uses the terms polyphyletic and paraphyletic to describe different types of non-monophyletic taxa

Concept of species
You might want to learn more about the issues behind the concept of species in the post How could humans have interbred with Neanderthals if we're a different species?
Concept of taxonomic ranks
What we decide to call a class, an order or a family is also somewhat arbitrary too. For example, we generally consider the monophyletic taxon Mammalia is a class. However, there is no non-arbitrary reason for calling Mammalia a class rather than Eutheria (eutheria = placental mammal).

Online resources
I suppose the above answered a big part of your question. You will be able to read all of what I just wrote (and much more) on any good introductory course to evolutionary biology. Consider having a quick look at Understanding Evolution by UC Berkeley for example as @MattDMo suggested in the comments.
Issues in your post
There are issues in your post that cannot be addressed in a single post (another reason for you to follow a quick intro course to evolution). Below I consider your post piece by piece mainly to point to some issues

Scientists believe

Terrible statement. By belief, we often refer to a non-justified belief, that is a belief about the world that is not justified (in science, the method of justification is called "the scientific method"). The statement, therefore, suggests that non-justified beliefs have a place in science while they don't. By being a little lose on the semantic, one could say that scientists "know" or they don't know but they don't believe without good reasons to believe.

that birds are evolved from reptiles

This is misleading (and it mislead you) because by "reptile" you think of a lineage that currently exists. Also, the expression "are evolved from" sounds very wrong. The expression "has evolved from" would be more correct.

evolution occur so that the organism can survive in the environment by developing new characters

This is wrong both in terms of the semantic (issue of causality when saying so that) and in term of the definition of evolution. You seem to confound evolution with natural selection.

According to natural selection

Natural selection is a process, not an explanation. It is like saying "according to gravity". The semantic is wrong, you should say "according to the theory of gravity" or "according to the theory of evolution" (or eventually "according to the theory of natural selection").

According to natural selection, those with favourable variations will survive and those with unfavourable die

You seem to apply that statement to population-level fitness (which would be mainly wrong) rather than to fitness variance within a population.

Why do the ancestors of birds (that is, reptiles) still exist?

The ancestors of birds don't exist anymore. I hope that was made clear from the above explanations.

Why didn't they get eliminated by natural selection?

This sentence suggests that you do not really understand what natural selection is but this is a story for another time. You can learn about natural selection on Understanding Evolution by UC Berkeley.


Is cell wall and cytoplasm an organelle? So cell wall is an organelle?
Whereas, it is not a membrane-closed organelle?

Cytoplasm is an organelle?
Whereas, it is not a membrane-closed organelle?

Wikipedia gives quite clear and sourced answers in this case:

an organelle is a specialized subunit within a cell that has a specific function. Individual organelles are usually separately enclosed within their own lipid bilayers.
Under the more restricted definition of membrane-bound structures,
some parts of the cell do not qualify as organelles. Nevertheless, the
use of organelle to refer to non-membrane bound structures such as
ribosomes is common.[11] This has led some texts to delineate between
membrane-bound and non-membrane bound organelles.[12] The non-membrane
bound organelles, also called large biomolecular complexes, are large
assemblies of macromolecules that carry out particular and specialized
functions, but they lack membrane boundaries.

To answer our question, the cell wall can be considered an organelle as it is a subunit with a defined (set of related) function(s).
The cytoplasm in itself is difficult to consider as an organelle, but the cytoskeleton can be considered one.


Do humans have a "dominant" neurotransmitter system/sensitivity within their brain? I've recently heard a podcast, in which Dr. Helen Fisher suggests that there are "4 broad personality types", and each one is associated with a particular neurotransmitter:

The corresponding Platonic thinking style, Keirsey temperament type (according to some readers, not Fisher herself), and color can be seen in parenthesis.

Explorer (creative; Artisan temperament, yellow) = dopamine
Builder (sensible; Guardian temperament, blue) = serotonin
Director (reasoning; Rational temperament; red) = testosterone
Negotiator (intuitive; Idealist temperament; green) = estrogen/oxytocin

I'm interested if there's indeed scientific evidence to support that for different people their affinity for a certain neurotransmitter is increased to such degree that it manifests in a noticeable difference in personality?

Dr. Helen Fisher's conclusions are plain bunkum. What does it even mean when she says associated with a particular neurotransmitter? The sheer work required to even get at this question is vast and difficult so it is unsurprising that she is venturing as much as a guess.There is scientific evidence to support different neurotransmitters systems can go awry in diseases but Fisher is overinterpreting the literature. Take a look at the neurotrasmiter table and you can see what each does and how malfunctions can result in certain diseases.
http://en.wikipedia.org/wiki/Neurotransmitter

Also testosterone and estrogen are thought of primarily as hormones not neurotrasmiters.So Fisher is saying women(who have more estrogen) are better negotiatiors whereas men(more testosterone) are directors. Even these banal conclusions are contentious and debatable.


ID of a pair of similar-looking birds in NT, Australia I spotted these two birds in Yellow Water, Kakadu NP. They were not in each other's vicinity, so it's not a pair in the sense that they were mates (not that I can tell at least :-).

Their appearance is quite similar, so I'm expecting they are the same species of bird. They look like egrets to me, which are common water fowl in the wetlands of Kakadu. However, they may in fact be different species altogether. One has these speckles on the wings, the other one doesn't, by the looks of it.

Can anyone help me ID these birds?

Where: Yellow Water Region in Kakadu NP, Northern Territory, Australia;
Size: Not too big, my guess is about 20 to 40 cm from beak to tip of the tail (about a foot or so);
When: Southern hemisphere's spring, early September; the end of the dry season;
Time of day: afternoon.

I think these are most likely nankeen night heron (Nycticorax caledonicus). The only that does not fit is your size estimation. See the images (from here):

I think the first image shows a bird which still has parts of its juvenile feathers, which look pretty different (from here):

A lot of information about these birds can be found here and here.


Are there multiple meanings to "clone" as in "clone a gene"? I originally thought that cloning a gene meant to put it into bacteria and have them express it. But sometimes I see it used and it seems like it's just a synonym for "identify the sequence and/or location of". So what does "clone a gene" really mean"

"Cloning a gene" also just means making tons of copies of it, like in PCR, so you can sequence it


What is the largest animal that has no hard parts? Some examples of "hard" animal parts are bones, cartilage, and exoskeletons. What animal has the most mass while being completely "soft". I don't think it's the colossal squid, since it has a hard beak and cartilage in their mantle. My guess is the heaviest jellyfish.

Please forgive me for plagiarizing the open source wikipedia, here are some species of large soft bodied animals. I honestly don't think I could re-write this more clearly for any logical reason:

Citation:

The lion's mane jellyfish (Cyanea capillata) is the largest cnidaria species, of the class Scyphozoa. The largest known specimen of this giant, found washed up on the shore of Massachusetts Bay in 1870, had a bell diameter of 2.5 m (8.2 ft), a weight of 150 kg (330 lb). The tentacles of this specimens were as long as 37 m (121 ft) and were projected to have a tentacular spread of about 75 m (246 ft) making it one of the longest extant animals

The largest roundworm, Placentonema gigantissima,[174] is a parasite found in the placentas of sperm whales which can reach up to 9 m (30 ft) in length

The largest nemertean is the bootlace worm, Lineus longissimus. A specimen found washed ashore on a beach in St. Andrews, Scotland in 1864 was recorded at a length of 55 m (180 ft).[183]

There are a couple of animals that are of interest but they are not technically soft bodied:

The colossal squid (Mesonychoteuthis hamiltoni) is projected to be the largest invertebrate. Current estimates put its maximum size at 12 to 14 m (39 to 46 ft) long and 750 kg (1,650 lb),[185] based on analysis of smaller specimens. In 2007, authorities in New Zealand announced the capture of the largest known colossal squid specimen. It was initially thought to be 10 m (33 ft) and 450 kg (990 lb). It was later measured at 4.2 m (14 ft) long and 495 kg (1,091 lb) in weight

The largest known species of sea sponge is the giant barrel sponge, Xestospongia muta. These massively built sponges can reach 2.4 m (8 ft) in height, 80 kg and can be of about the same number of feet across at the thickest part of the "body". Some of these creatures have been estimated to be over 2,400 years of age.

https://en.wikipedia.org/wiki/Largest_organisms#Invertebrates


What DNA has the most info for getting a person's likeness? I understand that DNA can come from hair but also from other places.

Let's suppose a person gets their DNA mapped by a company (there are some companies claiming to offer analysis of DNA.. e.g. maybe $200 and maybe some may send the DNA on a DVD)

I understand from this link that human DNA should fit on a DVD

https://stackoverflow.com/questions/8954571/how-much-memory-would-be-required-to-store-human-dna

Would it be possible to get a person's likeness..  if not now, then in future, based on the DNA I might be able to get sent to me digitally.

And presumably the DNA of a 28 year old would be the most ideal for getting (in a computer program) the likeness/image of that person at 28 - the age the DNA was taken?

I hear of the cost of sequencing the human genome to be millions or billions.. Is that more about scientists figuring out what the DNA does, rather than capturing it all?

For example, if I got my DNA captured by a company for $200, then in 50 years time or the future when technology develops, could I use it to produce a likeness of myself?    Or would what a company would send me, not really be all my DNA or be vastly insufficient to create a likeness?

I'm interested in if the kind of test that copmanies off for $200 provides all the information to create an exact replica.

Is a complete replica of a person possible in theory? (e.g. if in future they have a machine to build somebody from DNA) (with the information gathered and that could be sent to the customer by a DNA test for $200, or is it impossible even in theory because the DNA collected and sent is insufficient?)

I'm more interested in the possibility of (in theory) getting a really good likeness, than the personality of a person.

If a company only collects Saliva, is that just a fail.. would they need hair too and DNA from all sorts of human parts, in order to get a good likeness? or better likeness?  Or would it not matter whether it's the hair or the saliva?

Except for Red Blood Cells, every somatic cell contains two copies of the autosomal chromosomes and a pair of sex chromosomes, either XX or XY (Assuming an average human being) One set is maternal and one is paternal
Some lymphocytes actually recombine their chromosomes, so their DNA will be functionally different to all of the other somatic cells in the body.
Gametes undergo Meiosis and will be haploid, only containing one copy of each autosomal chromosome and one of the sex chromosomes
Cells accumulate mutations over time. The closest you could probably come to an exact clone of a person is if you harvested one of the cells from the eight-cell stage of development. The other seven are able to go on and produce a viable and healthy person. The harvested cells DNA would be the closest to the DNA that combined in the fertilization of the egg. The next closest would likely be stem cells from cord blood. Then probably neurons, as they tend to divide the least.
As the link you posted said, ATCG can be represented in a two bit code, so for about 6 billion bases, you would need about 1.5GB of storage (You need to capture both sets of chromosomes in order to produce a person).

There are places where you could compress the data. Telomeres could be removed and just added back after the fact, as there is likely a standard length for each chromosome of the six nucleotide repeats.
Though you could have a minimum of a two bit code, you would really need a larger data set. You would need metadata, so things like polarity of DNA and chromosome number.
You might also want data about the alleles of each and every gene, that way any errors could be fixed. If you are making the DNA from a data set, there is no sense keeping any genetic defects or diseases in the sequence when you remake it.

Craig Venter, one of the protagonists of the Human Genome Project has a company that is able to produce synthetic DNA for a whole organism. They have reportedly produced a synthetic bacterium, so in theory, they could print DNA from a database and recreate an entire genome, though at what cost and how long I am not sure.
The Original sequencing of the Human Genome did cost Billions of Dollars, however today's sequencing machines can produce an entire genomic sequence more in the range of thousands of dollars. I am not sure if they have broken the $1,000 threshold yet.
Most of the commercial companies do not produce full genomes. They likely do not even sequence a full exome (The areas of all genes that make up the coding sequences of mature mRNAs). They likely do some form of polymorphism analysis to determine if for any given gene you have certain allele other than the Wild Type allele. In this kind of analysis, you do not really need a full sequencing to determine what gene a person has, you only need to identify areas of key differences to determine what is what. That being said, the data collected by a commercial genetics company would likely not be sufficient to recreate an entire genome.
Another important factor is Epigenetics. Just because you have the entire base sequence of the person, doesn't necessarily mean that synthetically creating all 46 of that person's chromosomes would give you the necessary material to transfer into an enucleated oocyte to then produce a new person. You would likely also want to capture the epigenetic encoding as well as the full genome. The epigenetic code that you would likely want would be from one of the cells from the 8-cell stage of development I mentioned earlier. While we have been able to clone adult mammals by nuclear transfer, those animals have had issues with cancer and premature aging. This may have something to do with telomeres, but it also may have something to do with the epigenetic code in early development.
There are other considerations in development as well. There is exchange of nutrients between mother and fetus during development. There is also a sharing of immunity and probably hormonal signals from the mother that can effect development.
Also women are mosaics. A woman would also have the added challenge that every single one of her cells has one of her two X chromosomes inactivated, so depending on which one is inactivated, at random, will determine which of the two X alleles she will be expressing in that cell. It is very possible that her clone would be different from her in appearance.

That is a pretty extensive list. I probably have missed some things. One thing I have definitely left out are all of the structural proteins of chromatin and how to package the DNA into a nucleus. We do not yet understand all of the mechanisms to compact DNA down into a nucleus, so we would have to answer all of those questions before we could figure out how to print and package the DNA to make a clone of a person from a database of their genome.

As we have not currently cloned a human, then it is difficult to say if it is possible. Things that we can do, even in other mammals do not always translate to humans and human cells. There would also be significant ethical hurdles to overcome and based on the current sentiments, it is unlikely, even if we have the technology, that society would allow human clones to be produced.


(A)sexual reproduction of plants Are all plants capable of sexual reproduction? Some can do asexual reproduction as well but I haven't found any plants that aren't capable of sexual reproduction. Is it correct to say all plants are capable of sexual reproduction?

No, it's not. There are common plants that can only reproduce asexually.

It's likely you can buy produce from several plants which are unable to do so at your local supermarket. The most famous example is, of course, the banana which is a sterile mutant and all bananas of a particular variety are clones, but some seedless varieties of grapes and oranges would also count (although most seedless fruit you find in the supermarket are actually produced with hormonal treatments rather than being asexual varieties).

These plants are examples of artificial selection but there are also examples of plants that have lost the ability to sexually reproduce in the wild. The evening primrose is a good example, with some 30% of species in the genus Oenothera having evolved to be asexual (Hollister et al, 2015), but this is not the only example. It is likely that, just as in animal species, asexuality has short (on an evolutionary timescale) term advantages but results in lower fitness in the longer term.


How does waking up from an alarm clock work? During sleep, one's brain is shut down. All it can do is to see some dreams from the semi-conscious mind.

Then how does it hear when the alarm clock rings?

The brain does not "shut down" during sleep. While not everything about sleeping is understood, we do know that certain areas in the brain remain active during sleep. There is a good overview on sleep on the website of the National Institute of Neurological Disorders and Stroke.

  Until the 1950s, most people thought of sleep as a passive, dormant part of our daily lives. We now know that our brains are very active during sleep. Moreover, sleep affects our daily functioning and our physical and mental health in many ways that we are just beginning to understand

As for hearing, that part of the brain doesn't shut down during sleep - and for good reasons. Sudden, loud noises for example may be a sign of immediate danger. Any animal that just stops hearing a third of the day would be at a huge disadvantage.

The brain even processes the sounds we receive during sleep and doesn't wake on every loud noise. You might find the following article interesting: How do we hear while we sleep?

  Using electrodes implanted directly on the human cortex, a Johns Hopkins University undergraduate has located the part of the brain that appears to process sounds while people sleep. This site, in the frontal lobe, may be part of a vigilance system that, for instance, rouses a mother when her baby cries but lets the woman sleep when a truck rumbles by.

Alarm clocks are usually designed to just get louder and louder until we do wake up. Even despite that, some people actually do manage to sleep "through" the sounds, for example of they were very tired and haven't yet had enough sleep. This is speculation, but maybe in that instance the brain prioritizes sleep.

Other articles on the subject are for example Odd Sound Processing in the Sleeping Brain and Auditory information processing during human sleep as revealed by event-related brain potentials, but the main point is that we don't stop processing what happens around us just because we are asleep.


What specimen of caterpillar is this? Early this morning, I found this beautiful caterpillar specimen crawling over a leaf:

This specimen was found today morning (spring season) in Brazil at Porto Alegre City 30°01′59″S 51°13′48″W. With approximately 1 Inch long.

What kind of specimen is this?

This appears to be a "Monkey slug" caterpillar (Phobetron spp) of the family Limacodidae (or slug moths).

According to these sites (here and here), caterpillars of this type are commonly referred to in Portuguese as "Lagarta-Aranha" (or "lesma-macaco") [literally, "spider caterpillar" and "monkey slug" in English].

The most common Phobetron species I can find in Brazil is Phobetron hipparchia.

The caterpillar of this species appears to be quite variable (ranging from browns to reds in color) as is made apparent by here, here, and here

 Phobetron hipparchia  (Source: http://caterpillars.unr.edu/)


Why are animal births not taken as seriously as human births? When humans give birth, more than often medical assistance is needed. Others gather around and frantically look for any way to help. But when an animal gives birth, it is usually seen as a moment where you give the female its space and let the birth occur naturally and without any assistance. The animal is of course in serious pain just as a female human but this is more than often not taken into account. Why is it that animal births are not taken as seriously?

Our heads are bigger.

There's some debate on the issue, but in essence, human brains, and therefore heads, are very large relative to our body size.  This is handy for all the intelligent things we like to do, but can be rather painful during birth.  Because we walk upright, the size of a newborn's head is actually a non-trivial fact during the birthing process.  There are two major implications.

The first is that human birth hurts.  You can watch the birth of other animals and they seem to brush it off, but for humans, forcing that huge head through a relatively small birth canal is difficult.  Evolution has (supposedly) limited the size of the hips because, while that would allow an easier birthing process, it would negatively impact our ability to walk.  As such, it has to hurt.

Secondly, in order to make the process easier, humans rotate during birth.  The end result is that, unlike even other closely related primates, humans come out backward in a way that is very difficult for a birthing female to attend to.  This almost requires having another person or two on hand to help out.  This would, of course, be a huge reinforcement for social connections.

A few books I know of touch on this.  Up From Dragons deals with the brain size/hip size issue and The Invisible Sex talks about rotation during the birthing process and the social implications.


Is the Michael Jackson skin pigmentation disease realistic? Quoting wikipedia:

  Jackson's skin had been a medium-brown color for the entire duration
  of his youth, but starting in the mid-1980s, it gradually grew paler.
  The change gained widespread media coverage, including rumors that he
  might be bleaching his skin. According to J. Randy Taraborrelli's
  biography, in 1986, Jackson was diagnosed with vitiligo and lupus; the
  vitiligo partially lightened his skin, and the lupus was in remission;
  both illnesses made him sensitive to sunlight. The treatments he used
  for his condition further lightened his skin tone, and, with the
  application of pancake makeup to even out blotches, he could appear
  very pale. Jackson was also diagnosed with vitiligo in his
  autopsy.

1) Is this plausible?

2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

1) Is this plausible?

It is absolutely plausible. His particular condition was called Vitiligo
 (as stated in your quote) and isn't that uncommon, albeit not usually as severe.

Skin pigmentation expression changes over time, sometimes dramatically.

  2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

Vitiligo is a very well-documented disease, and like every disease, there's a broad range of affectation. Treatments options are very limited, and so makeup or other methods are often used to disguise the affected skin.

Here's some more pictures of people with Vitiligo at varying stages:


Why only water in liquid form is essential to live? My question is:-
Only liquid water supports almost every living organism's metabolism, neither the vapour nor the condensed form of water does so. What is the chemical & the biological reason behind this fact?

A layman's view of the problem :

Let's assume that water in liquid form was not necessary and organisms could survive on solid or gaseous water. What would some of the difficulties be to sustain such a life form?

Solid Form of water

How would the organism move without breaking or tearing itself apart? How would essential substances be transported from one part to another of the organism body?

Gaseous form

What would be the size of the organism? Gas has a much bigger volume than water.
In order to transport nutrient molecules within the a gaseous body, a huge air pressure needs to be generated. Also, how will gravity be overcome while transporting these molecules? A lot of energy will be required to maintain such pressures.

I guess nature (which always takes an optimal path) asked such questions and found that water in it's liquid form was the most suited to support life on Earth.

It need not be water alone. Other liquids may be able to support life as well. Only, we haven't discovered them yet. But whatever the substance, it's liquid form would seem to be an optimal solution for life.


Is there an advantage to linear chromosomes? The DNA copying enzymes have a hard time working to the end of a chromosome. For circular chromosomes this is not a problem, since there is not a sharp 'end'. However, for a linear chromosome, without extra mechanisms in place, a bit of DNA is lost off the end of the chromosome after each replication. Because of this, eukaryotes have a telomere to cap off their chromosomes.
In most cells of a mutli-cellular organism, this telomere is slowly worn away after each reproduction leading to apoptosis. Cells that need to reproduce indefinitely such as germ and stem cells have to invest in extra mechanisms to replenish the telomere. For multi-cellular eukaryotes I can see how this might be usefull (for instance as a cancer counter mechanism). However, multi-cellular organisms evolved from single-cell eukaryotes.
I cannot see a reason for wanting apoptosis in a single-cell organism. However, single cell eukaryotes (say yeast) still have linear chromosomes with telomere caps. What advantage did linear chromosomes provide single-cell eukaryotes to offset the extra investment in reparing the telomere?

Related questions

What is the advantage of circular DNA in bacteria?

I think it is the wrong question. You assume that eukaryotes developed from a single-cell organism with circular DNA. Then, clearly, there must have been an advantage of (newly) developing a linear genome. But eukaryotes could have developed from an organism with linear DNA, too. There are still a few bacterial species with linear chromosomes, so this is not unlikely. We don't know, however.

On the other hand, if linearisation developed independently, you can learn from bacteria why it might have occurred:

J. N. Volff, J. Altenbuchner: A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. In: FEMS microbiology letters. 186, 2, May 2000, 143–150, PMID 10802162. (Review).

Abstract:

  Bacterial circular chromosomes have sporadically become linearised
  during prokaryote evolution. Unrelated bacteria, including the
  spirochete Borrelia burgdorferi and the actinomycete Streptomyces,
  have linear chromosomes. Linear chromosomes may have been formed
  through integration of linear plasmids. Linear chromosomes use linear
  plasmid strategies to resolve the 'end-of-replication problem', but
  they have generally retained from their circular ancestors a central
  origin of replication. Streptomyces linear chromosomes are very
  unstable and at high frequency undergo amplifications and large
  deletions, often removing the telomeres. At least in Streptomyces,
  chromosome linearity is reversible: circular chromosomes arise
  spontaneously as products of genetic instability or can be generated
  artificially by targeted recombination. Streptomyces circularised
  chromosomes are very unstable as well, indicating that genetic
  instability is not confined to the linearised chromosomes. Bacterial
  linear chromosomes may contain telomere-linked regions of enhanced
  genomic plasticity, which undergo more frequent genetic exchanges and
  rearrangements and allow differential evolution of genes, depending on
  their chromosomal location.


Spatial resolutions in optical microscopy I have read that different optical imaging techniques such as  such as wide-field microscopy, confocal microscopy or STED microscopy can theoretically achieve a different spatial resolution.

However, I was only able to find information about the STED microscopy's spatial resolution (5.8 nm) on Wikipedia.

Does anybody know of any references or recommended reading (preferably free) where I can learn more about different optical microscopy methods and how the cope with the diffraction limit?

The theoretical resolution for an optical microscope depends on the wavelength used, but is close to 0.22 um (220 nm). Confocal microscopy does not greatly improve axial resolution; it dramatically improves the in-plane resolution (x and y directions, by excluding extraneous light). Theres not a lot to do to "cope" with that using those techniques. If you need more resolution, you can use the super-resolution techniques you mention, or the good old TEM.

There is some more information on the Nikon website: http://www.microscopyu.com/articles/formulas/formulasresolution.html

and on Olympus website: http://www.olympusconfocal.com/theory/resolutionintro.html


Is "A" inhibiting "B" and vice-versa, a positive feedback loop? If product A inhibits the expression of product B, and product B inhibits the expression of product A, is this a positive feedback loop?

My thinking was to consider the scenario that A starts off high, and so B is naturally low. Then, a large amount of B is added to the system. This inhibits the production of A, so the level of A falls, and that in turn enables the production of more B, which further decreases the production of A and in turn further increases the production of B, in a never-ending cycle. This runaway amplification is characteristic of positive feedback loops, whereas negative feedback loops cause a return to equilibrium.

Yet the Wikipedia page says that, for it to be a positive feedback loop, it must be set up so an increase in A causes an increase in B.

So what is it?

The situation that you presented in which an entity A inhibits the production of another entity B which in turn inhibits A, is a positive feedback.

In a network path or a loop the overall sign of the loop/path is the product of the signs of individual edges (interactions). In this case it is negative times negative which gives a positive sign to the loop.

In simple words, a positive feedback should lead to an entity promoting its own production, directly or indirectly; it can auto-activate itself, activate an activator or inhibit an inhibitor. In this case A inhibits its inhibitor. Sometimes you can have large loops like this:

This is still a positive feedback.

Moreover, your case would exhibit (with the right parameters) the dynamic properties of positive feedbacks (such as bistability and hysteresis).

Sometimes people also refer to this type of positive feedback as double-negative feedback (which I personally do not like because it is misleading).

  Positive and negative feedback loops may consist of a single component
  that activates and represses directly its own activity, respectively
  (Fig. 1B,C); or they may include several components and involve
  indirect interactions (Fig. 1D–G). The overall sign of a complex
  feedback loop (i.e. positive or negative) depends on the constituting
  elementary interactions (Fig. 1D–G).(1) For example, two mutually
  repressing components form a positive feedback loop (PFL, also termed
  “double-negative feedback loop”).

  Mitrophanov & Groisman, 2008

However, not all positive feedbacks lead to runaway amplification. That is a property of an unstable system. The degradation of the molecules (or death) ensures a finite (and stable) steady state. Sometimes (with certain parameter combinations, as previously mentioned) positive feedbacks can have two stable steady states. Depending on the initial condition, the system can settle to either of the states. In your example the two states can be — High-A Low-B and Low-A High-B.

Further reading:
Mitrophanov, Alexander Y., and Eduardo A. Groisman. "Positive feedback in cellular control systems." Bioessays 30.6 (2008): 542-555.


How can I make a protein interaction/protein-complex network? Let's say I have a list of proteins ID. I would like to know whether I can find any complex based on that list. Any example, explanation is appreciated.

An example input is what you see below. What can I do with the following list of protein IDs? These IDs are from human.

P41182,P56524, P41182,Q9UQL6, P41182,Q8WUI4,Q92793,Q09472,Q9Y6Q9,Q92831

This is not a trivial task depending on how well studied your network is or what information you want to gather. It sounds like an interaction dataset is what you want rather than scouring the PDB for static structures (that would be such a hit and miss process I'm not sure it's worth bothering).

Upload you list of gene codes to string-db.

You'll see the network here, and structures are made clear of known complexes in an expandable thumbnail.
It's a limited web-server tool, and whilst very powerful, isn't very flexible. Cytoscape might be needed for a more novel study because it is scriptable.

You can probably stop here and investigate your network.
From string-db download the .txt file (TXT - simple tab delimited flatfile). I think it's an old-school save icon on the web-server, although if you're uploading multiple identifiers, it is simply the "save" button at the top left.
Download Cytoscape here.
Then use File>Import>Table>From file.
This will build an interaction network and you'll see which genes/proteins interact with one another.

Catch: whilst this provides spacial information, you can't get a picture of temporal information: i.e you know what is interacting, but not when nor for how long.


How long ago did the mutation arise that gives rise to sickle-cell disease? Is it known how long ago the mutation arose in Africa that gives rise to sickle-cell disease and protects from Malaria in heterozygote carriers?

In a fairly recent review P W Hedrick surveys a number of gene variants associated with resistance to malaria.

He explains that:

  The impact of malaria is thought to have increased between 10,000 and 5,000 years ago when there were the beginnings of agriculture and consequently more human settlements. During this period, the numbers of both the human population and the mosquito vector increased, resulting in higher spread of malaria.
  Recent molecular studies suggest that malaria in humans from Plasmodium falciparum may have originated from gorillas. Using these data, an initial timeline for the origin of P. falciparum as a human pathogen suggests that it may be more recent than previously thought.

As you can see from his Table 1 (reproduced below), the S variant of β-globin is suggested to have arisen 1440 years ago.

The study of the origin of sickle cell anaemia is complicated by the fact that the allele responsible is found associated with five different β-globin haplotypes (four from Africa, one from Saudi Arabia/India). This has sometimes been interpreted as indicating that the allele arose on several independent occasions. However, the picture is complicated by patterns of human migration, and recent papers suggest that the observed distribution of the S variant is not inconsistent with a single origin, e.g. this paper.


What is the distance between the insertion of the distal end of the bicep tendon and the head of the radius? I was unable to find a source that could provide a measurement for the distance between the insertion of the distal end of the bicep tendon and the head of the radius.

Does anyone know a source that might be able to provide this data for the average adult human?

From {1}:

  Abstract
  PURPOSE:
  There is little information in the literature describing the anatomy of the biceps tendon insertion. The purpose of this study was to map the footprint of the biceps tendon insertion on the bicipital tuberosity and to report on the relevant anatomy to assist surgeons with correct tendon orientation during surgical repair.
  METHODS:
  Fifteen fresh-frozen adult upper extremities were used in this study. The relationships between the long head of the biceps tendon, the short head of the biceps tendon, the muscle bellies, and the distal tendon orientation were examined. The length, width, and area of the biceps tendon insertion were measured.
  RESULTS:
  In all specimens examined, the biceps musculotendinous unit rotated 90 degrees externally from origin to insertion. The long head of the distal tendon was inserted onto the proximal aspect of the bicipital tuberosity, while the short head of the distal tendon was inserted onto the distal aspect of the tuberosity. The lacertus fibrosus, in all specimens, originated from the distal short head of the biceps tendon. On average, the biceps tendon insertion started 23 mm distal to the articular margin of the radial head. The average length of the biceps tendon insertion on the tuberosity was 21 mm, and the average width was 7 mm. The average total area of the biceps tendon insertion (footprint) was 108 mm(2). The average area of the long head of the biceps tendon insertion was 48 mm(2), and the average area of the short head of the biceps tendon insertion was 60 mm(2).
  CONCLUSIONS:
  Landmarks have been identified that will allow anatomic orientation of the distal biceps tendon during operative repair. The distal short head of the biceps tendon has a consistent relationship with the lacertus fibrosus and a distinct insertion on the bicipital tuberosity. The dimensions of the distal biceps tendon footprint have been determined to assist with bone tunnel or suture anchor placement during surgical repair.

(bicipital tuberosity = radial tuberosity)

Some figures from the same study:

FYI:

How correlated are the lengths of tendons in different part of a human body?
How can I measure my tendon length?

References:

{1} Athwal, George S., Scott P. Steinmann, and Damian M. Rispoli. "The distal biceps tendon: footprint and relevant clinical anatomy." The Journal of hand surgery 32, no. 8 (2007): 1225-1229. https://www.ncbi.nlm.nih.gov/pubmed/17923307 ; https://scholar.google.com/scholar?cluster=16116840451671820399&hl=en&as_sdt=0,22 ; http://www.sciencedirect.com/science/article/pii/S0363502307005163 ; http://dx.doi.org/10.1016/j.jhsa.2007.05.027 ; http://sci-hub.cc/10.1016/j.jhsa.2007.05.027


Ventricular Filling : Systole or Diastole? As the Blood goes down from the Atrium to the Ventricles:

The Tricuspid Valve ( Right Atrioventricular Valve)
Bicuspid Valve (Mitral Valve )

The atrial pressure is INCREASES WHEN ATRIA ( THE ATRIA CONTRACTS AT THIS STAGE/ATRIA SYSTOLE) Thus:

fills the ventricles with blood ( blood goes down from the atria to the ventricles)
The Tricuspid/ Bicuspid valves OPENS since there is a higher pressure of Atria than the Ventricle

Questions:

Is the Ventricular Filling, (When Blood from Atria fills the Ventricles) itself a DIASTOLE or SYSTOLE
So during the Ventricular Diastole
Ventricular Filling is Diastole?? ,
Is it when VENTRICLES are filled with blood :

  it increases THE PRESSURE IN IT SO THAT IT MAKES A
  (** VENTRICULAR DIASTOLE /VENTRICULAR CONTRACTION **)

I also saw in here that:
" The P wave represents the atrial electrical depolarization. This phase is ventricular diastole. During filling, pressure within the right atrium increases, pushing blood across the AV valves into the right ventricle."

I'd also like to clarify:

    Shouldn't it be  WHEN IT FILLS THE VENTRICLE is filled,
     THE PRESSURE GOES LOW in atria gradually within the???
    I get it that the atrium has a HIGHER PRESSURE BEFORE FILLING and it makes the (TRICUSPID AND BICUSPID) valve OPEN

Kindly clarify through diagrams and steps, I'm somehow confused. Thank you!
You can kindly watch this short clip of video and this may help me clarify things:

http://highered.mheducation.com/sites/0072495855/student_view0/chapter22/animation__the_cardiac_cycle__quiz_1_.html

Ventricular diastole is a period in cardiac cycle during which the ventricles are filling with blood. During this period, the atria are contracting and the ventricles are relaxed.

The diastole consist of this: atrioventricular valves open, atria contract (atrial systole), blood flows from the atria to the ventricles, the atrioventricular valves close.

When the term systole or diastole is used without saying is it atrial or ventricular, it means it is ventricular. For example, systolic blood pressure is the blood pressure during ventricular systole and diastolic during ventricular diastole.


How many plants are needed to survive in an airtight chamber? How large a garden do you need if you are to survive on them producing enough oxygen in a closed chamber?

And which are the most effective plants?

According to this news article, in a NASA experiment one man survived for 15 days in a sealed chamber containing 30,000 small wheat plants. If you read the article you will find that this did not produce a completely balanced system - some excess oxygen had to be removed, and some extra CO2 had to be pumped in.


Purpose of dilution streaking or streak purification In dilution streaking a drop of liquid culture is collected with an inoculating loop and then streaked across the agar plate surface. At the end of the streaking the number of organisms clinging to the loop until only single cells are deposited at a given location and you get colony-forming units.

I am wondering now what exactly the purpose of this streak purification is. If you want to grow your bacteria why would you not just put a few drops of the liquid culture on the agar plate? Why is it particularly useful to use this technique? Or, why would you choose this method over the "spread plate" technique, where a liquid culture undergoes a set of dilutions first and each dilution is then placed directly on the surface of separate agar plates.

The purpose of this technique is to dilute the bacterial cells so much that you get single cells, as can be seen on the image of the plate. You can then pick the colonies grown from these single cells, characterize them, test them for the mutations/plasmids, or whatever change you introduced, and can be sure that you have only the descendants of a single cell in your culture.

This way you ensure that you don't grow a mixture of different cells with different characteristics, of which one will eventually overgrow the other one. The streaking is a fast and reliable technique, which works especially well when you want to test a larger number of bacterial cultures. It also allows to check a stock culture very fast for contaminations with other bacteria by simply inspecting the single colonies by eye (different bacteria often look different).

Diluting the cultures would work as well, but needs to be done in more than one step and is more work when you want to do it for more than one culture. Also for dilutions you often plate more than one plate to be sure to have a plate with single colonies (when the cell number is unknown).


Human perception of time depending on age From what I can tell and what thus far all people with whom I discussed this subject confirmed is that time appears to "accelerate" as we age.

Digging a little, most explanations I found basically reduced this to two reasons:

As we age physically, a time frame of constant length becomes ever smaller in contrast to the time we spent living
As we age socially, we are burdened with an increasing amount of responsibility and thus an increasing influx of information which impairs our perception of the present

To be honest, neither sounds entirely convincing to me because:

In my perception "local time" (short time frames that I don't even bother to measure on the scale of my lifetime) is also accelerating. Just as an example: When I wait for the bus, time goes by reasonably fast as opposed to my childhood tortures of having to wait an eternity for those five minutes to pass.
Even after making a great effort to cut myself off from society and consciously trying to focus on the moment, the perceived speed of time didn't really change. (Although I did have a great time :))

Which leads me to a simple question (and a few corollaries):

Am I just in denial of two perfectly plausible and sufficient explanations, or are there actual biological effects (e.g. changes in brain chemistry) in place, that cause (or at least significantly influence) this?
Is there a mechanism, that "stretches out" time for the young brain so that weight of an immense boredom forces it to benefit from its learning ability, while it "shrinks" time as the brain "matures" and must now act based on what it has learned, which often involves a lot of patience?
If there is such a mechanism, are there any available means to counter it? (not sure I'd really want to, but I'd like to know whether I could)

This is not really a biological answer, but a psychological one:

One important fact to consider is that the perception of time is essentially a recollection of past experience, rather than perception of the present.

Researchers who study autobiographical memory have suggested that part of this effect may be explained by the number of recallable memories during a particular time period. During one's adolescence, one typically has a large number of salient memories, due to the distinctness of events. People often make new friends, move frequently, attend different schools, and have several jobs. As each of these memories is unique, recollection of these (many) memories gives the impression that the time span was large.

In contrast, older adults have fewer unique experiences. They tend to work a single job, and live in a single place, and have set routines which they may follow for years. For this reason, memories are less distinct, and are often blurred together or consolidated. Upon recollection, it seems like time went by quickly because we can't remember what actually happened.

In other words, it can be considered a special case of the availability heuristic: people judge a time span to be longer in which there are more salient/unique events.

Incidentally, (and to at least mention biology), episodic memory has been shown to be neurally distinct from semantic memory in the brain. In particular, a double dissociation has been shown for amnesics who suffer from semantic or episodic memory, but not both.

My apologies for the lack of citations, but a good bit about autobiographical memories can be found in:

  Eysenck, M.W., & Keane, M.T. (2010). Cognitive Psychology: A
  Student's Handbook.

You may also be interested in some responses or references to a related question on the Cognitive Science StackExchange:

Perception of time as a function of age


Is the rate of photosynthesis higher than the rate of respiration? In photosynthesis carbon dioxide is used up and oxygen is produced and at the same time plants respire too. So oxygen is used up and carbon dioxide is produced.
Then the net exchange of gases should be zero. If this is so, then why do we say that plants maintain the level of oxygen and carbon dioxide in the atmosphere?

So, is the rate of photosynthesis higher than the rate of respiration in plants in a year(overall)? What is the net exchange of gases annually?

The net exchange of gasses in any area will be different depending on the number of plants and what plants they are.  This is because it depends on the number and size of leaves, and because chlorophyll is essential for photosynthesis, it also depends on the amount of chlorophyll in the leaves. Therefore that part of the question is very broad.

Overall, photosynthesis (oxygen production) is higher than the rate of respiration in plants during a year.

Aerobic respiration continues all the time in plant cells (in light and in darkness), using up oxygen and making carbon dioxide. Photosynthesis, in contrast, occurs only in light and uses up carbon dioxide and makes oxygen. The more light there is, the more oxygen is produced.

There is a light intensity at which respiration and photosynthesis cancel each other out. This is called the compensation point. Below this level carbohydrates are used up and the plant cannot grow.

This and more can be read in this document from the Royal Society of Chemistry


Is Norway spruce (Picea abies (L.) Karst.) isohydric or anisohydric species? Question from a thesis defense list ask me this. But I can't find the exact answer on the internet or in books. In my thesis, I described isohydric plants, for example maize, lupin, pea, poplar. This plants response to a decrease in soil water in same way. How Norway spruce response to decrease in soil water? As a isohydric plant or anisohydric?

Thank you for your time and help.

This review paper states that spruce is isohydric, citing Physiologie und Ökologie der Gehölze by Lyr, Fiedler, & Tranquillini:

  Spruce appears to reﬂect an isohydric strategy (Lyr et al. 1992), reducing stomatal conductance at early stages of soil drought.

It's important to note that this is not a binary distinction, isohydric and anisohydric are two extremes in a spectrum of how plants respond to drought.


What is a DNA-binding domain? I am confused about the term DNA-binding domain. Does it mean that there are some parts of the DNA that tend to coil up? Does it happen because some proteins tend to stick around that area? Also it is my understanding that with some proteins DNA (say for bacteria like E. coli) tends to coil up. Do we know what is the approximately the size of these coils? What is a ‘motif’ in this context.

Welcome to Biology.SE!

The term "domain" in biochemistry and molecular biology is usually used to refer to a part of a protein that has a conserved structure and function, is similar between related proteins, and can generally exist or function on its own if it was separated from the rest of the protein. A DNA-binding domain is a protein structure that has a high affinity for DNA, and so binds to it when the two molecules are in the same vicinity. An example is a type of protein called a transcription factor, which binds to DNA in the nucleus of the cell (in Eukaryotes, bacteria and Archaea don't have nuclei - the DNA just floats free) and causes changes in the transcription of genes. The following image from WikiMedia shows how transcription factors work in general.

"DNA coiling" is a very generic term that describes many different things. The basic structure of DNA itself is a coil, with two sugar chains (the deoxyribose in DeoxyriboNucleic Acid or DNA) coiling around each other, and attached by nucleic acid bases. In the eukaryotic cell, individual strands of DNA are associated with structural proteins to create chromatin, which is what makes up chromosomes in the nucleus of each cell. In the first stage, naked DNA is wrapped or coiled around structural proteins called histones into a structure called a nucleosome. These then stack into a "solenoid" or fiber structure, which makes up so-called "relaxed" chromatin - regions of the genome where active transcription is taking place. If a part of a chromosome has been marked as inactive, or during certain steps in the cell cycle when one cell splits into two (mitosis), the fibers further coil into condensed chromatin, forming the typical structure many people associate with chromosomes. This image, from Wikipedia, visualizes each step in the process.

The word "motif" can sometimes mean the same thing as domain - for example, someone might refer to a "DNA-binding motif" in a protein. However, a motif is typically smaller than a domain, can occur in DNA, RNA, and proteins, and has to do with the specific sequence. A "structural motif" in a protein is something like a helix-loop-helix or a beta-hairpin turn that can appear in multiple different kinds of protein domains, and doesn't necessarily have the same exact function in those different domains, but typically has a fairly conserved sequence that is very similar. As an example, the zinc finger motif is found in protein domains that bind DNA, RNA, and other proteins.

All of this terminology can be very confusing at first, but if you stick with it it'll get easier over time. Biochemistry and molecular biology are fascinating fields, so keep up your studies!


How are new chromosomes replicated into the next generation via sexual reproduction? If an individual has a new chromosome, which is very unlikely to happen, he will not have any luck in finding a sexual partner with this same trait. How will the offspring inherit this trait. And given that extra/fewer chromosomes are often undesirable traits (e.g. Turner Syndrome) how can it propagate?

I assume that humans and rats have different number of chromosomes, so a common ancestor must give a lineage where some individuals had a different number of chromosomes than their parents.

You are right that a person with an abnormal number of chromosomes will be unlikely to find an "equal" partner to mate with. This does not prevent a chromosome aberration from spreading though, and it is not necessary that the mutation is initially beneficial for it to spread. While it is true that many chromosomal aberrations may be detrimental and cause various syndromes, a chromosome split or multiplication may also be netural except for the matter of reproduction. A change in chromsome number will not be inherited deterministically, but can give rise to various new permutations in the offspring due to the mechanics of chromosome segregation during meiosis.

You can find a good explanation at Scienceblogs.com: http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/ :

  The net result [of a chromosome split] is that although this
  individual is fine and healthy, a significant number of his or her
  gametes may carry serious chromosomal errors, which means they may
  have reduced fertility. They aren’t sterile, though; some of their
  gametes will have the full complement of genes, and can similarly
  produce new healthy individuals who will probably have fertility
  problems. (...)
  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant. Which leads to another misconception in
  the question: something doesn’t have to provide a benefit to spread
  through a population! Chance alone can do it. We don’t have to argue
  for a benefit of chromosome fission at all in order for it to happen.


What kind of spider is this and is it poisonous? A brown furry diamond shape on its back and brown joints all on black body. Caught entering my house in Trinidad (small island off South America) -- killed the first one, this is the second.

It's a Mygalomorph spider, of the sort which are usually called Tarantulas.  This is told by the two long, upcurved spinnerets and the large, dish-shaped carapace, with the eyes clustered in a clump - looking rather like the disk of the USS Enterprise from Star Trek, if the command bump was placed near the front edge.  I'm not sure which species it would be, but the good news is that like almost all spiders, it's pretty much harmless to humans.  These guys do have large fangs, though, so if you got bitten by one, you'd feel it.  As far as I'm aware, the venom of South American species is no big deal, so the feeling of being poked by a big needle is likely to be the worst effect.  Presumably they were entering your house to hunt for the small animals which share your home with you - large insects, small mammals and lizards, maybe.  I'd post an image, but I'm not sure which tarantula this would be (not really being a tarantula guy), and you could probably do as good a job of searching the internet as I could.  However, here is a resource I was able to turn up with a short search:

ttfnc.org/livingworld/index.php/lwj/article/download/479/462

As I said, I'm not really a tarantula guy, and so am not confident as to a specific ID of this spider.  However, having been pressed for an image, there are in this article some images of a spider which may or may not be yours.  The images are, however, tarantulas from Trinidad.  You will need to page through to the end of the article to see them:

http://sciencepress.mnhn.fr/sites/default/files/articles/pdf/z2017n2a5.pdf


How important is getting enough glucose for maximal brain performance / cognition? I know from many studies that have been done, that resting versus active use of the brain has relatively similar overall energy expenditure levels.

On the other hand, however, we know that the brain along with our eyes require glucose in order to function properly. Ketone bodies, lactate, etcetera may act as glucose sparing agents, but certain parts can definitively only use glucose as an energy source.

Anecdotally, I’ve noticed that when performing low intensity mental tasks like jogging or hiking for example, if I haven’t eaten for a while and am in a fasted state, I might get hungry for a bit, but if I just keep on going, after a while I feel fine and can pretty much go on forever after that. With high intensity mental tasks like programming though, the feeling of hunger doesn’t really seem to go away, and if I try to push through it, it just results in consistent brain fog and an inability to perform at any meaningful level.

My theory is that in cases where high mental performance is not required, alternative sources of metabolism provide the needed energy to function, and where intensive cognition is required, the rate of glucose production is unable to keep up with demand from the parts of the brain that depend on it which effectively creates a bottleneck in the cognition process causing the aforementioned brain fog and low performance.

Is this what is actually happening though? I’d like to think that it makes sense, but I’d prefer to have a biologically accurate understanding first and foremost.

In short: skipping a meal lowers blood glucose levels, which can reduce cognitive performance, for example, memory.

Let's say that between meals you are in fasting state for 8 hours during which you do some desk work and some moderate exercise for 1.5 hours. With such level of physical activity, your last meal and your glycogen stores should provide enough glucose for all your body needs, including the brain. So, during this time, you do not need any ketones or lactate as additional source of energy. According to Medical Hypotheses, 2014:

  Estimated amount of glycogen in the human organism is about 200–500 g,
  and in certain specific conditions could reach up to 1.0 kg, which
  seems to be optimal for human organism. This amount is definitely
  sufficient for keeping optimal concentration of glucose in the blood
  during usual fasting periods not exceeding 24 h (between meals, during
  sleep, in case of exercise, etc.)

Skipping a meal can lower your blood glucose levels. According to WebMD:

  Normal blood sugar levels are less than 100 mg/dL after not eating
  (fasting) for at least eight hours. And they're less than 140 mg/dL
  two hours after eating.

  During the day, levels tend to be at their lowest just before meals.
  For most people without diabetes, blood sugar levels before meals
  hover around 70 to 80 mg/dL. For some people, 60 is normal; for
  others, 90 is the norm.

Blood glucose fluctuations related to meals:

Image source: Wikipedia, Creative Commons License

In some studies (AJCN, 1998), skipping breakfast was associated with lower blood glucose levels and worse memory test but not intelligence test results:

  This article compares the findings of three studies that explored the
  role of increased blood glucose in improving memory function for
  subjects who ate breakfast. An initial improvement in memory function
  for these subjects was found to correlate with blood glucose
  concentrations. In subsequent studies, morning fasting was found to
  adversely affect the ability to recall a word list and a story read
  aloud, as well as recall items while counting backwards. Failure to
  eat breakfast did not affect performance on an intelligence test.


Retrovirus Production I have been having difficulties with low transduction efficiencies of my retrovirus production. I expand my plasmid of interest (on MiG-GFP plasmid) in DH5α E Coli for ~24 hours, purify with Qiagen midi prep kits, then put on ~90% confluent 293FT cells with either retronectin or polybrene for 24 hours. I then change media and harvest supernatant at 48 and 72 hours of incubation with the 293FT cells. I then expose 3T3 cells to varying volumes of the virus containing 293FT media and am able to transduce about 10% of the 3T3 cells, which is really low. That being said, here and there I am able to get very high transduction efficiencies on the 3T3 cells, but for unknown reasons. I have tried concentrating the virus but transduction efficiencies don't increase all that much. And I have tried growing up the plasmid in Stbl3 cells, which if anything gives me worse virus.

Anything here jump out as being responsible for low transduction efficiencies. Or is there another way somebody does this that works really well?

In my experience, transduction efficiencies skyrocketed when I applied a spin-infection procedure. A 30 min low speed centrifuge with the virus changed a lot. Here is the TRC protocol for this: http://www.broadinstitute.org/rnai/public/dir/download?dirpath=protocols/production&filename=TRC%20viral%20infection%20200909.pdf


How do the chromosomes arrange themselves after fertilization in humans? In human reproduction the male produces sperm containing 23 chromosomes and the female has the oovum containing 23 chromosomes , so after fertilization the zygote contains 46 chromosomes. What I want to know is , how do the chromosomes identify each other and pair up,  fir example say ,how does chromosome '1' of the male pair up with chromosome '1' of the female to make set '1' of the zygote?

After fertilization the diploid cells divide by mitosis.  Chromosomes don’t need to pair with their partner during the eukaryotic cell cycle.  After S-phase each chromosome has been duplicated (so there are 46 + 46 = 92).  The two daughter chromosomes resulting from semi-conservative DNA replication are held together at one point: their centromeres. In M-phase two microtubules from opposite poles of the mitotic spindle will attach to the kinetochore that assembles at those centromeres.

Nowhere in this process is the maternal chr1 required to interact with the paternal chr1.

The pairing that you are refering to takes place much later after the new primordial germ cells haved developed into the germline, leading to meiosis.  The molecular details of homolog pairing during meiosis are best understood in the model organism C. elegans where each chromosome has specific cis-acting sequences that are recognized by different trans-acting factors that lead to recognition and then pairing, followed by synapsis, and eventually crossing over.


Parallel DNA double-helices with Watson–Crick base-pairing: Why do they not occur? I know that parallel DNA helices exist and are governed by Hoogsten base pairing, but why can’t they be possible with Watson-Crick pairing? In the diagram below, if we were to flip one of the strands while keeping the other the same, it appears as though hydrogen bonding is still possible.

The only specific suggestions that I could find was because of the DNA replication process and the negative polarity of hydoxyl group on the phosphates. Moreover, after flipping one strand, the DNA nucleotides form enantiomers. Are these possible reasons, or are there others?

“The only specific suggestions that I could find was because of the DNA replication process and…”

No. The explanation can have nothing to do with DNA replication. If the structure does not exist, you can’t replicate it, if it does, Nature will evolve a mechanism. (The related SE question, mentioned by @Gilleain, asked whether it could still replicate if it were parallel, i.e. using the enzymes that have evolved for parallel DNA.)

  I know that parallel DNA helices exist…

Let us clarify this first. Perhaps the most extensive parallel duplex DNA, the structure of which has been determined, is that described by Parvathy et al.. The two parallel strands of this are shown below:

The following points should be noted:

This parallel DNA (and the shorter examples that preceded it) is not a pure stretch of complementary base pairs.
It is stabilized by what the authors refer to as “CC+ clamps” at either end. One is left to conclude that without these the duplex would not form.
All the complementary base-pairs are of the type AT (actually reverse Watson–Crick base pairs). Presumably GC base-pairs would have destablized the structure.

(You can inspect this structure in three-dimensions here. Choose ‘Licorice’ style and colour ‘by chain’ and notice the non-planarity of the three base ‘pairs’ at each end.)

So although the question refers specifically to parallel DNA helices with Watson–Crick base pairs, it should be recognized that extended parallel DNA helices composed of any kind of complementary AT and GC base pairs are not found, and the question applies equally well to them.

  “In the diagram if we were to flip one of the strands while keeping the other same, hydrogen bonding is still possible”

The diagram in the question is two-dimensional; DNA is three-dimensional. It is only by considering the three-dimensional structure of DNA can you approach this question.

So how would one do that? One must consider the free energy of alternative structures in the relevant millieu to determine which will occur (i.e. be more thermodynamically stable).

This will tell you whether single DNA strands with parallel sequences will form a double-stranded (ds) structure or not.
This will tell you whether ds-parallel DNA is more or less energetically stable than a ds-antiparallel DNA. Hence, even if both can form (which I doubt, without some special circumstances*) the lower thermodynamic free energy of the anti-parallel dsDNA would give organisms adopting it an evolutionary advantage.

And the answer to the question?

It seems unlikely that one single factor is responsible or it would have been pointed out in elementary text books such as Berg et al..

To answer would require a complete theoretical analysis of the structure or structures. First one would have to build a model of a proposed parallel structure that could accommodate Watson–Crick base pairs. This in itself is a problem because there are likely to be many alternative structures. Perhaps there are computer programs that can find the structure with the lowest energy. This would be calculated in the classic manner, calculating the positive contribution of hydrogen bonding (which depends on distance and angle), ionic interaction etc.*  against the negative contribution of charge and steric repulsions.

*Etc? The two-dimensional diagram fails to consider the contribution of base stacking (how could it?), which contributes to a considerable extent to the stability of nucleic acid helices, as the original cover design of Stryer’s Biochemistry is a constant reminder:


Mathematical models of lineage selection I'm interested in the concept of lineage selection (Aboitiz, 1991) as an explanation for why traits would be selected for that enhance the rate at which evolution can occur, rather than directly enhancing an individual's fitness. (Such traits could include gene duplication; body plans that can easily be adapted to new niches; learning (which enhances evolution due to the Baldwin effect) and so on. Questions about the evolution of such traits are collectively termed "evolution of evolvability.") The term "lineage selection" does not refer to group selection or kin selection, but simply to selection between distinct genetic lineages in a mixed population.

What I would like to know is whether a mathematical theory has been developed along the lines of the Price equation that can capture the concept of lineage selection and make predictions about it. Lineage selection does not appear to be modelled by the Price equation itself, at least not in a straightforward and obvious way, because on the face of it the Price equation only directly accounts for the relation between a trait and the number of offspring in the next generation, rather than the number of surviving descendants several generations later, which is what is required for lineage selection.

The reason I'm looking for a mathematical model is that there are a number of intuitions that many people seem to share about lineage selection and I'd like to understand what assumptions are needed in order for them to be true. In particular, it seems clear that large populations are needed for lineage selection to be effective, and I'd like to understand precisely the relationship between population size and the effectiveness of lineage selection. (My intuition is that with a population size of around a million, lineage selection can select for traits that have a beneficial effect around 20 generations later, since $1,000,000\approx 2^{20}$, but this intuition lacks a formal basis.)

A literature search did not turn up anything along the lines of what I'm looking for, but this is not my main field and I may simply not know the most appropriate search terms to use.

The writings by Samir Okasha (philosopher of biology/science) could be a good starting point. In his book Evolution and the Levels of Selection, he explicitly uses the Price equation to discuss selection at multiple levels (e.g. chapter 2.3: Price's equation in a hierarchical setting), and also derives a multi-level version of the Price equation:

$$\bar{w}\Delta\bar{z} = Cov(W,Z) + E(Cov_k(w,z))$$

where the first part on the right hand side represents collective-level selection and the second part particle-level selection. This is mostly aimed at aspects of group-level selection though. There is also a chapter on "Species Selection, Clade Selection, and Macroecolution" (ch. 7), but this is not directly tied to the Price equation. A note though; I own the book and have read parts of it casually, but I haven't worked with the Price equation myself, and I haven't checked exactly how the extended version of the Price equation is developed and used in the book.

A couple of references that might be useful are Frank (1998) (and other papers by him) and papers by Vrba. The work presented in this recent conference abstract by Rankin, Fox et al (2014), "Using the Extended Price Equation to Analyze Species Selection in Mammalian Body Size Evolution Across the Paleocene/eocene Thermal Maximum", seems to describe exactly the type of theoretical developments that you are looking for (I didn't attend the conference, and haven't heard the talk though).


Do all cells have the same DNA? According to genome.gov, All the cells in a person's body have the same DNA.

I understand that the main reason parents and children have different genomes is because of random mixing of 2 genomes, but that there are also very small differences caused by random mutations.

If all of a person's cells have identical genomes, then does that mean that random mutations only occur in gametes?

I also understand that if sunlight hits my arm, it can cause random mutations.

So do all cells in a person's body really have the same DNA?

All cells in a person’s body have roughly the same DNA. As you point out correctly, mutations can happen in any cell at any time. They are frequently caused by

UV radiation
Chemicals (think of the correlation between the development of lung cancer and smoking)
Replication of DNA during cell division
Integration of foreign (e. g. viral) genomic material
On purpose by the body’s own enzymes

That last point brings us to cells of the immune system, some of which (classically T- and B- Lymphocytes, but there is emerging evidence for others) generate variance within their genomic DNA on purpose.

Red blood cells lack a nucleus altogether.

Gametes only have half the body’s genome, as you already pointed out.

Finally, although having the same base sequence, epigenetic modification of DNA molecules by, for example, Methylation makes DNA chemically different even between cells of the same type.


Identity by descent among unrelated individuals I was reading a couple of papers which talk about IBD (Identity by descent) among unrelated individuals (for eg. http://www.pnas.org/content/109/4/1193.long). However they do not seem to clearly define what they mean there. I was wondering how IBD is defined in such a context. I'd appreciate any help (especially suggested references to look this up).

The definition of IBD is always the same - an allele or segment of alleles which is shared between two individuals because of descent from a common ancstor.
In the context of this paper, the authors are referring to segments of the genome between individuals which are IBD. In this case, they are looking at recently isolated populations who are likely to share longer stretches of IBD with one another. This is the case because each individual within a relatively isolated population is likely to be, on avergae, more related to another individual than in an outbred population. In general, it it much easier to detect longer segments of IBD than shorter segments, and this is why they choose to study isolated populations. Also, you can be much more sure that longer IBD segments will share a common ancestor with one another.
More specifically, they define a 'large' IBD segment is one which is longer than L centimorgans of length. Additionally, they define 'IBD-sharing' level between two individuals, as the probability that a randomly chosen genomic position on homologous chromosomes from each of the individuals lies in a large IBD segment shared by the two individuals. Thus IBD sharing takes values between 0 and 1.
There are several different methods, such as PLINK, fastIBD and GERMLINE which can identify IBD segments and their corresponding lengths from genotype data.
If you are interested in a relatively accessible guide to understand the principles of both single locus and segmented IBD, then I would recommended checking out Graham Coops's population genetics notes, section 2.2.