Metabolic activity postmortem I read some papers about studies on metabolism in post-mortem tissues in human, but I do not exactly the reason about why our brain continues to have activity after death.

Your question is a little vague and as Christiaan mentioned, linking to the papers would be useful. If I understand, though, you want to know why cellular metabolic activity that takes places after someone dies?

If that's the case, the answer is essentially that whatever kills a complex organism in the sense of causing the heart to cease beating, doesn't immediately cause every cell in the body to stop functioning at the same moment.

Now for a slightly longer answer...Consider someone who suffers a heart attack and dies. Blood stops flowing through their veins and cessation of breathing means gas exchange stops. For cells with extremely sensitive oxygen and nutrient demands like cardiac cells, cell death begins to occur rapidly. Other cells farther down the blood and oxygen supply chain have a greater tolerance to disruptions in nutrient supply and would have at least some store of nutrients to work with after blood flow stops. Those cells will keep doing whatever they were doing for a little while; metabolizing nutrients, transporting metabolites, transcribing genes, etc.

After a while, though, even they will feel the lack of oxygen. At that point, most cells will switch over to anaerobic respiration. The eukaryotic fraction of cells in our body isn't particularly good at this, but can struggle on for a little bit until they simply run out of fuel and begin to die, largely through apoptosis.

Apoptosis of some cells will actually help prolong the lives of some of the cells neighboring the apoptotic ones, an effect that probably encouraged the evolution of apoptosis. After a while, though, too much apoptosis will have occurred and an uncontrolled sort death called necrosis will begin, leading to cascades of cell death and cessation of cellular metabolic activity. This process can take days to occur, depending on many variables surrounding the death of the organism.

So far, this has all been about eukaryotic cells; cardiocytes, adipocytes, myocytes, etc. These are the smallest fraction of cells in our body, by cell count. The rest of our bodies are composed of prokaryotic, or bacterial cells. This is our microbiome and this is where (for me) things get really interesting.

Although our microbiome exists in a symbiotic relationship with our eukaryotic cell fraction, many members of the microbiome are less dependent on the nutrients found in our blood system than those eukaryotic cells. The cells of our microbiome are also frequently much more capable of surviving in low-oxygen or even anaerobic environments. These parts of us will continue to thrive for some time after we "die".

Some of our microbial cells, if left to their own devices, could even find new environmental niches outside our bodies and continue to live long after "we" have died. The quotes around 'die' and 'we' become necessary at this point because from here, questions of identity and life branch into the philosophical.

This became a lengthy answer, but I find it a really interesting topic. Here's a nice article from the Guardian, that discusses post-mortem cellular metabolism and our microbiomes in particular: https://www.theguardian.com/science/neurophilosophy/2015/may/05/life-after-death


What is the advantage of the inverted image on the retina? Recently, I learned that the image of the world which we see actually reaches the retina inverted.
This is due to the fact that the retina lies behind the focus of our eyes.

I have two questions:

When the retina lies behind the focus and the lens in our eyes has a spherical shape, shouldn't left and right also be interchanged?
What is the advantage of this? Why does the retina lie behind the focus and not in front of it?
Or doesn’t it matter since our brain is not a real screen and it’s only a question of the correct interpretation of the electic signals?

There may be no advantage of the inverted image on the retina. But there is an advantage with the lens that refractes the image inverted.

Our eye lens is of convex in nature. Now lets see what is the advantage of convex lens being our eye lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php

The light from the object, when reaches the convex lens it gets refracted and gets "converged" and is a "real image" and also "diminished" but the problem is it makes the light inverted.

Now let us see what happens if our eye lens is a concave lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php

In this case, when the light from the object from a distance reaches the lens, the lens "diverges" the light, also it "enlarges" the image, but it produces an "erect" image but the major problem is that the image is "virtual".

We know how evolution works, it selects more advantageous option generally.

Case - 1: If the lens is convex, the only problem the eye has to handle is that the image is inverted.
Case - 2: But if the lens is concave, it should converge the diverged light, it should diminish it and it should also make it real.

If we take both cases into consideration, case - 1 seems to be easily handled, that's why we have inverted image falling in the retina. There maybe no other specific advantage associated with it.


Is the leading strand consistent in the same chromosome with multiple replication forks? If a chromosome has multiple origins or replication, do those origins necessarily pick the same DNA strand as leading and the same one as lagging, or can they be of opposite orientations, sending replication forks in opposite directions and therefore picking different leading vs lagging strands?

Replication proceeds in both directions from a single origin of replication, so the same strand acts as both the leading or lagging strand for the two different replication forks.


How can I interface cAMP signal or membrane potential from slime mold to an electrode? I am very much interested in measuring cAMP (cyclic adenosine mono phosphate) signal and membrane potential from amoeba. Since I want to try this as a hobby, what are the basic steps I must do to view these signals on a CRO (cathode ray oscilloscope). Cyclic-AMP being a biochemical, how can I view it as a corresponding electric signal?

For cAMP there is only one electrophysiological technique I've found.  You can use cyclic nucleotide-gated channels in the cell as a secondary indicator of cAMP activity.  When cAMP increases in the cell, these channel will fast gate which you should be able to pick up.

The issue is standard CNGC's are not overly sensitive to cAMP and are typically more sensitive to cGMP.  But there have been mutants created that have a high affinity for cAMP.  You can transplant these in and have an easier time with the detection.

This paper goes into a a lot more detail on it.


What is the change in ratio of histone to protamine in men with infertility called? I am neither a biology researcher nor a student. In a paper (written by a biology researcher) I am translating into English, there is the following statement which, according to the text, must have a name and I fail to find the English name:

  It is showed that in men with infertility histone to protamine ratio changes and the change is called ...

What is the change called? I guess it's something unnatural/abnormal.

It is termed "abnormal packing".

Source: "Sperm Chromatin: Biological and Clinical Applications in Male Infertility and Assisted Reproduction" by Armand Zini & Ashok Agarwal (2011), p 172.


Prader-Willi Syndrome and Angelman Syndrome? On the website http://www.whatisepigenetics.com/fundamentals/2/ it states that

  the imprint disorders Prader-Willi syndrome and Angelman syndrome, display an abnormal phenotype as a result of the absence of the paternal or maternal copy of a gene, respectively. In these imprint disorders, there is a genetic deletion in chromosome 15 in a majority of patients. The same gene on the corresponding chromosome cannot compensate for the deletion because it has been turned off by methylation, an epigenetic modification.  Genetic deletions inherited from the father result in Prader-Willi syndrome, and those inherited from the mother, Angelman syndrome.

To me it seems like this is suggesting the same problem in both Prader-Willi and Angelman sydrome- lack of expression of a particular gene. However in Prader-Willi syndrome it is the paternal chromosome that is missing and the maternal copy of this gene is silenced by methylation and the reverse applies for Angelman syndrome. Therefore it seems that in boh cases the problem is the lack of expression of this gene. Why, then, if both are caused by lack of expression of this gene, do these two illnesses have such different symptoms (constant hunger in Prader-Willi syndrome and mental disability and jerky movements in Angelman syndrome)?

Within that region, there are multiple genes.

  Although the same gene may control imprinting for both disorders, the
  gene(s) causing their phenotypes differ. AS results from
  underexpression of a single gene, UBE3A, which codes for E6-AP, a
  protein that functions to transfer small ubiquitin molecules to
  certain target proteins, to enable their degradation. The genes
  responsible for PWS are not determined, although several maternally
  imprinted genes in 15q11-q13 are known. The most likely candidate is
  SNRPN

From this paper: http://www.ncbi.nlm.nih.gov/pubmed/11180221


What is the use of crystallized Photosystems from cyanobacteria? I read a lot of articles about techniques for the crystallization of Photosystem I and II from cyanobacteria. My question is what is the reason for that and what can you do with Photosystem crystals?

The main purpose of crystallizing a molecule or molecular complex like a  Photosystem is usually to provide a crystal for X-ray crystallography.  A crystal has its molecular components arranged in a structured systematic repeating pattern, and this repeated pattern allows the X-rays to reveal the 3-dimensional shape of one of the components.  Knowing the shape is of biological interest as it suggests how the molecules perform their function.


How do crocodiles stay fit? My 8 year old son asked me a question I could not answer (and Google, at least in so far as we tried, was no help either).

We were watching a documentary about Salt Water Crocodiles in Northern Australia.

The crocodiles seem very energy efficient: they barely move if they don't absolutely need to (and when they do, it is mostly to eat). Particularly, they hardly ever run, but when they do they are very fast and powerful.

So the question he asked me was: how can crocodiles remain so fit if they don't do any exercise?

If humans just sat around and moved only to eat, ran only when they absolutely had to, our muscles would atrophy. Other mammals seem to be in a similar boat to us humans.

Why not crocs? What distinguishes animals that need to exercise to be strong from animals that don't?

This is the closest question I could find here, but I don't think it assists in answering this question: Do insects' muscles become stronger with exercise?

Let us start with difference between humans and crocodiles. There are lot of differences but the one which matters in current discussion is thermophysiology.

Unlike humans, crocodiles are cold blooded animals (more specifically ectotherms). These animals needs to get heat from environmental sources to maintain their body temperature. As contrast to humans who can get heat from internal metabolism. That is the precise reason crocodiles are seen always not moving and basking in sun light when it is cold (while go to shade or water if it is hot). Read this for more elaborate strategies they use. If you want scientific reference, you can check this, this or this.

On your exercise point, there are few reports which suggest exercise can enhances aerobic capacity in young crocodiles. In this study they actually put crocodiles on treadmill and checked affect on their respiration. This report suggest  crocodile uses 3 different kinds of muscle mechanisms for lung ventilation. These three act differently in different conditions (means one acts during rest while other during high metabolism). However I couldn't find any information regarding atrophy.

  how can crocodiles remain so fit if they don't do any exercise? What distinguishes animals that need to exercise to be strong from animals that don't?

Short answer: Their body metabolism.

Their body metabolism is different from human's. Although doing exercise  might help in their aerobic capacity as mentioned in reference above.


How to read this diagram? I have diagram of oxidative decarboxylation of pyruvate pathway. The pathway is between glycolisis and Krebs cycle.

How to read this diagram?

This excerpt from Harper's Illustrated Biochemistry, 30E, page 173.

Texts usually have a verbal explanation of these kind of diagrams, so look in the text where it references Figure 17.5 and read the section before and section after.

That being said, if you start at the top with pyruvate, it enters the cycle where the curved circles touch on pyruvate dehydrogenase, which catalyzes its decarboxylation. That product then enters into the next cycle where the disulphide bond is broken and it is added to one of the sulfurs. Co-enzyme A then reacts with that and you get Acetyl CoA as a byproduct and dihydrolipoamide. The cycle continues and you get one hydride (I think) and one proton transfer to FAD and the reformation of the disulfide bond. You then have a hydride transfer to NAD+ and a deprotonation to regenerate FAD.

So each place a curved arrow touches another is what goes into the reaction and then following the split of the arrows is the product that comes out of the reaction. Where there are transfers to different circles means that there are different enzymes catalyzing the reactions.


Does homeopathic or herbal treatment of cancer have any scientific recognition? Even though we have a very high tech society, cancer is still a serious issue. We humans still are not entirely capable of fighting cancer.

Radiation and chemotherapy are still considered the best methods for treating it and frequently, even these don't work. And, as for this disease, it is a phenomenon of uncontrolled cell growth that has lead to the death of many people. Within these main two treatments, there is plenty of controversy surrounding applying radiation and chemo in a proper sequence.

However, there are also some different methods known and available on the market to treat cancer. Among them, homeopathic and herbal treatments are the most common. So, my question is, do they really work and is there any scientific evidence of that?  If yes then what is it?

The methodology behind homeopathy is scientific nonsense.  If you dilute anything a billion times, it will have no chemical effect, not even if you shake it all the while.  So no, homeopathy does nothing for cancer, or any medical condition at all.

Of course plants can have active compounds in them, once scientists have identified those compounds, they can be tweaked to make them act better in the human body, and then manufactured under strict guidelines to ensure purity, and tested to determine the optimum dosage; then it's just medicine.  Taxol comes from yew trees, it doesn't mean that native herbalists were successfully treating cancer with it for hundreds of years.  Native herbalists were using willow bark, which contains salicylic acid, which has anti-inflammatory properties, but chemists improved on it, reducing some of its negative side effects, by modifying it to acetylsalicylic acid.

Millions of people get cancer.  Doctors get cancer.  Herbalists get cancer.  If curing cancer was as easy as mixing some leaves in a poultice, people would do that.


Which bird of Upper Michigan is it? While doing morning-walk in Keweenaw Penisula, Michigan; I found this juvenile bird wandering around looking for her mother !

Can someone spot which bird is it?

Based on the location and picture I believe this a Spotted Sandpiper (Actitis macularis) chick. Once they hatch, they are out of the nest, the one you are holding looks fairly small still, must have hatched recently.

You can find more information about them here.


Are the human genes' promoters all known? It seems to be a basic question, but I couldn't find a certain answer.

The human genome is known for more than a decade, and is available through several data providers as the NCBI etc. For the genes' promoters however there seems to be much less information. There are some characteristics known (like the TATA box, which appears in ~25% of human genes), some prediction methods (like CpG sites appearance), some rough estimations for the location (100-1000kbp long, in the adjacent 2kbp upstream from the TSS), but I couldn't find any data set with a closed list of human genes' promoters.

Is this really yet to exist?

Nope. The human genome is still quite unexplored, new genes are still being discovered and the annotation of non-protein-coding regions (that include promoters) is still far from being complete. For example, look at the Statistics comparison of the current and previous Human GENCODE Release, it clearly shows that the annotation of the human genome is still an ongoing process.


Why does T-cell Cancer Therapy require a large tumor mutanome? An article I read about Neuroblastoma states that the fact that Neuroblstoma has a small mutanome means that it is not viable to apply the classic T-cell immunotherapy. Why is this so?
The article can be found here: Neuroblastoma: Developmental Biology, Cancer Genomics, and Immunotherapy

Understanding the link between the size of the tumor mutanome and its immunogenicity requires a basic understanding of T-cell development and regulation.

When normal human cells degrade proteins via the proteasome, some fragments of these proteins, called peptides, are bound to specialized cell-surface proteins called MHC. T-cells express a specialized receptor, called the TCR, which recognizes peptides bound by MHC proteins on other cells. The specificity of the TCR, what peptide/MHC combinations a T-cell can recognize, is randomly generated by targeted mutations and VDJ recombination in the TCR genes during a T-cells development. Each clonal population of T-cells (T-cells derived from the same precursor) have a unique TCR that recognizing different peptide/MHC pairs. When a T-cell's TCRs recognize a peptide/MHC combo on another cell, the T-cell is activated.

Because the TCR is generated randomly, many TCRs in T-cell precursors can recognize peptides derived from normal human proteins. To prevent these precursors from becoming T-cells that can attack the body, they are regulated in several ways. Many self-peptide recognizing precursors are destroyed in development, others are converted into regulatory T-cells that instead produce anti-inflammatory cytokines that tune down immune responses. Those those that escape these regulatory processes are later inactivated by other means.

What does this have to do with cancer? Well, most of a tumor's proteins are normal human proteins, and the human body does its best to suppress immune responses against normal human proteins, making it hard to generate an attack against cancer cells with T-cells that recognize normal self-peptide/MHC. Worse, overcoming this protective response could lead to an auto-immune attack on normal, healthy cells. Therefore, we want to make or use T-cells that recognize mutant-peptide/MHC combos. Such cells would not attack or be effectively suppressed in normal tissues, but could attack tumors.

However, to get these ideal, tumor-targeted T-cells, we need the tumor to produce mutant proteins whose peptide fragments ARE DISTINCT from the peptide fragments of normal proteins. Some tumors have far more of these kinds of mutations than others, and not every mutation is immunogenic (not every mutation can be differentially recognized by T-cells). For example, point mutations (single amino acid changes) that activate proto-oncogenes like BRAF don't necessarily lead to the production of structurally different peptide fragments. A larger mutanome offers a greater chance of immunogenic mutations.


What is the difference between sinew and tendon? I wonder what the difference between sinew and tendon is. I searched for it but didn't get any clear answer:

https://www.quora.com/Whats-the-difference-between-sinew-and-tendon:

  They are often used interchangably but to be technical, a tendon
  connects a muscle to a bone. The term sinew also seems to include
  ligaments which connect bones to bones. It is however, not a medical
  term.

https://answers.yahoo.com/question/index?qid=20070410182936AA2Kcnk

  Sinew is another word for muscle which is the functional unit of
  movement.

  Tendons connect bone to muscle to make movement possible: The muscle
  contracts and pulls the bone that it's connected to Source(s)

http://the-difference-between.com/tendon/sinew :

  Sinew is a synonym of tendon. As nouns the difference between sinew
  and tendon is that sinew is (anatomy) a cord or tendon of the body
  while tendon is (anatomy) a tough band of inelastic fibrous tissue
  that connects a muscle with its bony attachment.

http://www.thefreedictionary.com/sinew

  sinew = tendon

https://en.wikipedia.org/wiki/Tendon

  A tendon (or sinew) is a [...]

Is sinew a synonym for tendon, and if not what is the difference?

They get used somewhat interchangeably, which blurs the lines on the definitions.

When I had my anatomy classes, sinews were regarded as an inclusive class, which included both ligaments and tendons.

For the breakdown:

Tendon: Fibrous tissue that connects muscle to bone.
Ligament: Fibrous tissue that connects bone to bone.
Sinew: Includes both of the above.


How can we distinguish blended flavors? As far as I know, humans can distinguish between 5 basic tastes based on various molecules in food and their interactions. There's a level to all 5 so there can be an endless variety of tastes, and we can recognize them with some precision. What surprises me is that we can often distinguish the original flavors in a mix - for example in a salad or even more so in a blended juice. Shouldn't we perceive an entirely new flavor having the average of each basic taste?
Not entirely sure this belongs on a biology forum, but I hope someone can explain :)

You're talking about the difference between "taste" and "flavor." In common speech we use these words synonymously, but they actually mean different things.

Taste refers to the five sensations your tongue can detect -- sweet, sour, salty, bitter and umami. There's growing evidence for a sixth taste, "fat."

Flavor refers to the combination of several factors:

1) taste, as just described,

2) the aromas of esters, flavinoids, ketones, and other compounds in your food, detected by the nose. This happens a) before you take a bite, and b) as you chew and swallow, releasing different compounds and higher concentrations into your nose through your retronasal passage,

3) physical sensations such as texture, heat and cold, visual appearance and even sound (for example, the crunch of celery or potato chips)

4) chemesthetic effects, like the astringency of tannins or the "artificial" heat of chili peppers. (The compound responsible for chili heat actually down-regulates physical heat receptors so they're more sensitive. Menthol up-regulates them to create a cooling sensation.)

5) Emotional and social factors, like the memory of your grandmother's homebaked bread, or many people's aversion to raw fish.

All of this put together is why blackberries and strawberries are both sweet and tart, yet blackberries taste like blackberries and strawberries taste like strawberries.

Hope that helps!

References:

-- The collected works of Karen Page & Andrew Dornenburg

-- "Tastebuds And Molecules," Francois Chartier

-- LOTS of personal empirical evidence (I'm a chef)


What causes the range of severity of neurological deficits in Down's syndrome? It's known that the severity of symptoms caused by a trisomy 21 varies from individual to individual. Part of the explanation for this range of severity is the finding that 94% of Down's syndrome sufferers have a full trisomy, ie., all of the cells in their body have an extra copy of chromosome 21, while others have an underlying translocation (mostly a chunck of chromosome 21 being attached to 14). The last group has mosaic Down syndrome, where just a portion of cells is affected due to errors later in development.

However, this cannot be the only cause of the variation, as it would basically mean that 94% of all Down's syndrome patients should have similar complaints. Indeed, symptom variability is greater, as far as I am aware. I am specifically interested in the range of mental deficits caused by Down's syndrome:

  The majority of children with Down syndrome function in the mild to moderate range of mental retardation. However, some children are not mentally retarded at all; they may function in the borderline to low average range; others may be severely mentally retarded.

What is the source of the variability in the neurological deficits? For the sake of answerability it may be best to narrow the scope down to the larger chunk of Down's syndrome sufferers with a full trisomy. Does any, or all of the variability in neurological deficits has to do with the stochastic process of X-inactivation?

The symptoms of Down syndrome occur due to overexpression of genes present on the duplicated chromosome.

If possessing an extra chromosome meant an equivalent change in gene expression, one would expect to observe 50% more protein production for having 3 rather than 2 copies of a chromosome. However, due to complexities in regulation at the level of transcription, translation, and protein degradation, the actual expression levels vary substantially. These complexities can arise from alleles present on chromosome 21 or elsewhere on the genome. I will present some examples from three categories of variation that are known to contribute to the spectrum of symptoms in Down syndrome.

1. Complexity of chromosome duplication

Down syndrome is sometimes caused not by a complete, but rather a partial trisomy 21 (Antonarakis et al., 2004). These variations can also partly explain the severity of symptoms because some individuals do not possess a full duplication. You mention this in your question, but as you note, this is a fairly rare occurrence relative to full trisomy, so let us consider other contributions...

2. Variation of expression levels in normal individuals and those with trisomy 21

It turns out that among the genes expressed on chromosome 21, mRNA levels vary between normal individuals by as much as 40-fold! (Deutch, et al. 2005; Stranger, et al. 2005) This expression variability can explain the susceptibility of different individuals to trisomy 21, depending on the expression levels of the alleles they possess.

Among the different genes present on chromosome 21, some expression levels are consistently elevated in Down syndrome across individuals, some have overlapping but significantly different distributions (suggesting some Down syndrome patients have expression levels in the normal range and others do not), and others are indistinguishable between patients and controls (Prandini et al., 2007).

Presumably, genes in the first category contribute most to the shared phenotype of Down syndrome, and genes in the second category contribute most to the variation. Perhaps alleles that produce mRNA transcripts at the low end of normal for those genes are less susceptible to the effects of chromosome duplication.

A case study: Amyloid precursor protein

One protein of interest in particular is the amyloid precursor protein, APP, which is also associated with Alzheimer's disease (which shares some phenotypic characteristics with Down syndrome). APP expression varies widely among tissue types and individuals. Therefore, although APP mRNA levels are significantly elevated in Down syndrome individuals, the distributions between controls and Down syndrome are very overlapping; for example, see Figure 2B from the Antonarakis 2016 review.

3. Interactions with genes on other chromosomes

The third contributor to the variation of symptoms is the interaction of duplicated chromosome 21 genes with alleles located on other chromosomes. Just for an example where some of the genetic basis is understood, Down syndrome individuals are susceptible to certain leukemias, which are also associated with specific alleles on other chromosomes (Antonarakis, 2016). It seems that trisomy 21 affects histone modification in the areas of those alleles (Lane et al., 2014) and promotes proliferation of B-cells. Therefore, Down syndrome interacts with those other oncogenes to produce a greater combined risk. Individual with Down syndrome but not possessing the other alleles are less susceptible to the increased risk of leukemia

Similar interactions are likely with other systems that are influenced by Down syndrome, though the full molecular basis of all of those interactions are not fully understood. The Down Syndrome Genomes Project aims to, among other things, discover these other alleles outside of chromosome 21 that contribute to Down syndrome symptoms, which may also help understanding of the contribution of those alleles to other disorders (Antonarakis, 2016).

References:

Antonarakis, S. E. (2016). Down syndrome and the complexity of genome dosage imbalance. Nature Reviews Genetics.

Antonarakis, S. E., Lyle, R., Dermitzakis, E. T., Reymond, A., & Deutsch, S. (2004). Chromosome 21 and down syndrome: from genomics to pathophysiology. Nature reviews genetics, 5(10), 725-738.

Deutsch, S., Lyle, R., Dermitzakis, E. T., Attar, H., Subrahmanyan, L., Gehrig, C., ... & Antonarakis, S. E. (2005). Gene expression variation and expression quantitative trait mapping of human chromosome 21 genes. Human molecular genetics, 14(23), 3741-3749.

Lane, A. A., Chapuy, B., Lin, C. Y., Tivey, T., Li, H., Townsend, E. C., ... & Yoda, A. (2014). Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation. Nature genetics, 46(6), 618-623.

Prandini, P., Deutsch, S., Lyle, R., Gagnebin, M., Vivier, C. D., Delorenzi, M., ... & Baldo, C. (2007). Natural gene-expression variation in Down syndrome modulates the outcome of gene-dosage imbalance. The American Journal of Human Genetics, 81(2), 252-263.

Stranger, B. E., Forrest, M. S., Clark, A. G., Minichiello, M. J., Deutsch, S., Lyle, R., ... & Deloukas, P. (2005). Genome-wide associations of gene expression variation in humans. PLoS Genet, 1(6), e78.

(note: the two references I have linked here: Antonarakis 2016 and Prandini et al 2007, are, respectively, a nearly direct answer to the posed question that establishes the current state of knowledge about symptom variability, and an original research paper that provides much more detailed genetic analysis of the variability of expression of many relevant genes than would be appropriate for an answer here; I highly recommend them both for further reading on the subject)


What is the minimum functional biological light sensor? As a follow up to this question regarding the evolution of the eye, it was suggested that primitive eyes only needed to evolve a light sensor and could perhaps use the existing biochemical cascade infrastructure.

What is the minimum of this biological light sensor? Please provide a detailed biochemical description of how many proteins are involved and their interactions which can be "hooked up" to the existing biochemical cascade infrastructure. (to the best of our knowledge)

The minimum biological light sensor is just an existing signaling molecule that, by chance, also has some change in its activity due to light.  There are several ways this could happen.

One extremely simple example would be based on a G-protein coupled receptor (GPCR).  GPCRs are a family of related signal transduction proteins (the largest family) that sit on the surface of a cell's membrane.   Each one is sensitive to a molecule or small group of related molecules.  When exposed to the molecule it is sensitive to, the GPCR sets of a series of chemical cascades that trigger some activity in the cell.  For example, it can serve as a signal for the cell to move towards the place where the chemical was detected, or move away.

Now, imagine that, just by chance, the molecule the GPCR is sensitive to has some sensitivity to light, in that when exposed to light the molecule either has a larger or smaller chance (even slightly) of binding to the GPCR.  This is not improbable, a ton of biological molecules have this characteristic, in fact many have substantial responses to light even though they are not involved in light-sensing pathways.  A good example is called "photoisomerization", where the same molecule can have more than one shape, and switches between two shapes when exposed to light.

This would be a biological light sensor.  Not necessarily a very sensitive one, but once you have such a basic light sensor, natural selection would take over and lead to stronger and stronger effects.

In fact, this is pretty much how our eyes work today.  It uses a GPCR whose target is a molecule that changes its shape when exposed to light, which makes it no longer able to bind to the receptor, shutting of the signaling cascade.  What is more, this molecule is not only used in sensing light, it is a precursor to a molecule needed for gene transcription and signaling.

In fact, you can splice light-sensitive GPCRs from bacteria (which are different than those in animals) into non-light-sensitive animal cells, and those molecules will automatically integrate with existing GPCR signaling cascades, rendering the cell light sensitive.


Calculating the frequency of a recessive allele in case of three segregating alleles Is it correct to say:

A.  f(A) = p; f(a) = q
B.  p = f(AA) + ½ f(Aa)=$\sqrt{f(AA)}$?

Also,

  For a gene locus segregating more than two alleles, the frequency of
  each allele is the frequency of its homozygote plus 1/2 the sum of the
  frequencies of all heterozygotes in which it can occur.

For example, I have this data on blood-types from a population: 42,4% type A, 8.3% type B, 1.4% type AB, 47.9% type O. Plus we know that p(A)=0.250, p(B)=0,050, p(O)=0,692.
When I try to calculate p(O) in different ways, I get p(O)= $\sqrt{0.479}$=0,692
If I calculate p(O) as:p(O)= 0.479+½*0.424+½*0,083=0,7325
 As the result, I am getting two different frequencies for p(O). What am I getting wrong here?

Welcome to Biology.SE

A few issues about your post

You should always limit your post to a single question.

Make sure to define what the function f() and p() mean.

Use points (.) instead of comas (,) for the numbers.

You should show how you made your calculations otherwise we can't tell what is right and wrong.

Your question

  is $p = f(AA) + \frac1{1}{2} f(Aa)=\sqrt{f(AA)}$ correct?

$$f(AA) = p^2$$
$$f(Aa) = 2pq = 2p(1-p)$$
$$f(Aa)/2 = pq = p(1-p) = p - p^2$$
, therefore

$$f(AA) + f(Aa)/2 = p^2 + (p - p^2) = p = \sqrt{p^2} = \sqrt{f(AA)}$$

So, yes you are correct


The number of nipples (breasts) a species has? Only mammals have mammaries and mammary glands.

What evolutionary factors determines the number of mammaries (nipples/teats/breasts) a species has?

Is it always an even number?

The number of mammary glands a species has is related to litter size. The relationship generally follows the "one-half rule," which states that the average litter size is equal to half the number of mammaries. The number of mammaries also tends to put an upper limit on litter size. It's not necessarily a hard limit, but survival tends to drop noticeably when number of offspring being nursed exceeds number of mammaries.

The number of mammaries is almost always even, but a notable exception is the Virginia possum, which has thirteen.

Gilbert, A.N. 1986. Mammary number and litter size in Rodentia: The "one-half rule". Proc. Natl. Acad. Sci. USA. Vol. 83, pp. 4828-4830.


anyone can help identify this aquatic microganisms? I extracted from fish excretion and at 400x
At the moment i have yet to try any medication because i don’t know what this is. Can someone who has seen this before share the light? thanks!

It's a Rotifer, commonly called wheel animal It uses the hooks to attach itself to the fish's gills.
https://www.google.com/search?tbm=isch&sa=1&ei=1t4qXJS_Jaiu0gLYppCYBw&q=rotifer+under+microscope&oq=rotifer+&gs_l=img.1.1.0l10.83680.92883..95716...0.0..0.181.993.1j7......0....1..gws-wiz-img.......0i67j0i10i67.8Yg5stvFiH4

https://l450v.alamy.com/450v/k42bdt/rotifer-lapadella-apsida-female-free-swimming-microscope-freshwater-k42bdt.jpg
I hope this helps


In the lysogenic cycle, does the provirus split from the cell's main genetic material for replication? In a diagram of the lysogenic cycle sent by my instructor in a video, it shows the provirus splitting from the cell's main DNA when the dormancy period ends and the viral DNA is "activated". Is this how it happens, or was he just trying to illustrate the activation?

I guess a better way of phrasing this would be, is the viral DNA replicated as part of the cell's normal DNA, or is it replicated separately?

Thanks!

evamvid

When the virus is integrated into the hosts genome (and becomes a provirus) it is replicated with the cell genome, since it is now part of it. When the provirus gets activated (this happens by changes in the host's environmental conditions or health), it will get transcribed.
This is followed by the translation of the viral proteins which then leads to a cell which exclusively produces viruses until its resources are exhausted and the cell gets destroyed.


Why does Rigor Mortis occur after death? After someone dies they become stiff, this is termed Rigor Mortis and happens because the cells run out of ATP (I think). But why do the cells need it to remain flexible?

You are right that ATP is needed in relation to Rigor Mortis: This for ion pumps to maintain concentration gradients in cells. Without a constant supply of ATP to the pumps, calcium starts to diffuse from the extracellular matrix (and other intracellular compartments with high concerntations of calcium) into the sarcomere where it binds to troponin, a regulatory protein in skeletal muscles. This holds myosin the actin filaments together creating the effect of rigor mortis.


Why deoxyribose for DNA and ribose for RNA? Why is DNA made out of deoxyribose and RNA made of ribose? Why can't they both use ribose or deoxyribose? I think that the deoxyribose gives an advantage in storing genes, the job of DNA and ribose is better dealt with outside the nucleus...but why?

Nice question which leads to the fundamentals of DNA and RNA.

DNA (Deoxyribonucleic acid) is the core of life in Earth, every known living organism is using DNA as their genetic backbone. DNA is so precious and vital to eukaryotes that its kept packaged in cell nucleus, its being copied but never removed because it never leaves the safety of nucleus. DNA directs all cell activity by delegating it to RNA. RNA (Ribonucleic acid ) have varied sort of biological roles in coding, decoding, regulation, and expression of genes. RNA carries messages out of the cell nucleus to cytoplasm.

  The structure of RNA nucleotides is very similar to that of DNA nucleotides, with the main difference being that the ribose sugar backbone in RNA has a hydroxyl (-OH) group that DNA does not. This gives DNA its name: DNA stands for deoxyribonucleic acid. Another minor difference is that DNA uses the base thymine (T) in place of uracil (U). Despite great structural similarities, DNA and RNA play very different roles from one another in modern cells.

  http://exploringorigins.org/rna.html

RNA has three main characteristics that differs it from DNA

RNA is very unstable and decomposes rapidly.
RNA contains Uracil in place of Thymine
RNA is almost always single stranded.

DNA and RNA use a ribose sugar as a main element of their chemical structures, ribose sugar used in DNA is deoxyribose, While RNA uses unmodified ribose sugar.

Ribose and Deoxyribose

  From the fig above we can see that the principal difference between
  the two molecules is the presence of OH in ribose (2' tail) and absence
  in deoxyribose. There is a difference in one Oxygen atom as the name
  stands de-oxy ribose. Both Ribose and deoxyribose have an Oxygen(O)
  atom  and a Hydrogen (H) atom (an OH group) at their 3' sites. The OH
  groups are very reactive in nature, so the 3' OH tail is required for
  phosphodiester bonds to form between nucleotides in both ribose
  and deoxyribose atoms.

Answer

DNA is such an important molecule so it must be protected from decomposition and further reactions. The absence of one Oxygen is the key for extending DNA's longevity. When the 2' Oxygen is absent in deoxyribose, the sugar molecule is less likely to get involved in chemical reactions( the aggressive nature of Oxygen in chemical reactions are famous). So by removing the Oxygen from deoxyribose molecule, DNA avoids being broken down. In an RNA's point of view the Oxygen is helpful, unlike DNA, RNA is a short-term tool used by the cell to send messages and manufacture proteins as a part of gene expression. Simply speaking mRNA (Messenger RNA) has the duties of turning genes ON and OFF, when a gene needed to be put ON mRNA is made and to keep it OFF the mRNA is removed. So the OH group in 2' is used to decompose the RNA quickly thereby making those affected genes in OFF state.

Finally, the ribose sugar is placed in RNA for easily decomposing it and DNA uses deoxyribose sugar for longevity.

  References

  Flesh and Bones of Metabolism -  Marek H. Dominiczak

  Genetics For Dummies -  Tara Rodden Robinson


What do halophytes do with the salt? The answer to "How do some plants grow in salt water, while others die?" offers some hints as to how salt-tolerant plants store salt by shifting it out of cells, and also can deal with higher salt concentrations in cells, but what happens after that?  Do the plants somehow excrete the salt? Store ever-increasing amounts in more and bigger vacuoles? Convert it into something more useful by chemical reactions? Reach equilibrium concentrations with the water in which they grow and rely on osmosis?

It seems to this layman that plants growing in salt-water in the tropics will transpire quite a lot of water, and if that's replaced with salt water, they'll take up quite a lot of salt.

There are a couple of strategies that salt-tolerant plants can use to survive in high-salt conditions.

Plants can increase the concentration of compatible solutes in their cell to the point where the intracellular concentration of solute approaches the concentration of the water in the environment. By doing this, the plants are able to minimize water loss through osmosis, while ensuring that the cells do not reach harmful levels of salinity.

However, compatible solutes are often not enough to completely combat the effects of salt stress. Salt stress creates higher concentrations of oxygen free radicals, which can cause harm to DNA and other cell components. Mangrove trees have been found to have heightened expression of repair proteins and anti-oxidants when exposed to salt stress.

Additionally, mangroves have been found to be able to excrete salt from their root cells and their leaves. They have ion-transporters which actively pump sodium ions out of their cells into the extracellular space. They have salt-filtering mechanisms that allow them to uptake the water from salt-water without up-taking the salt in the water.

So in conclusion, salt-tolerant plants sequester some salt within their cells, but also use ion-pumps and compatible solutes to limit the concentrations of salt within their cells. They can selectively uptake water from salt water, and use repair mechanisms to limit the damage of high salt concentrations in their cells.

Kao, C.H. 2015. Mechanisms of salt tolerance in rice plants: compatible solutes and aquaporins. Crop, Environment & Bioinformatics 12:73-82.

Wang, L., Pan, D., Lv, X., Cheng, C.L., Li, J. Liang, W., Xing, J, and W. Chen. 2016. A multilevel investigation to discover why Kandelia candel thrives in high salinity. Plant, Cell & Environment 39:2486-2497.

Srikanth, S., Kaihekulani, Lum, Y., and Z. Cheng. 2016. Mangrove root: adaptations and ecological importance. Trees 30:451-465


How are electrons entering the electron transport chain in cellular respiration energised (excited)? In photosynthesis, electrons are excited by light energy from the sun (photoactivated).

How do they become excited in human cellular respiration?

I believe it has something to do with NADH and FADH2.

It may be useful to start with a quotation from the Introduction to Ch. 9 of Berg et al. Biochemistry (6e) that addresses the question, more or less as asked. I can’t find a link to the pages in the 5e online so I will transcribe it from my text:

  “A principal difference between oxidative phosphorylation and
  photophosphorylation is the source of the high energy electrons. In
  oxidative phosphorylation these electrons come from the oxidation of
  carbon fuels to carbon dioxide. In photosynthesis these electrons are
  excited to a higher energy level by the energy from photons.”

It is important to think about one of the ways in which the excited electrons are used in photosynthesis. To quote from earlier in the Introduction:

  “In essence, light is used to create reducing potential.”

What this means chemically is that in photosynthesis the electrons have sufficient energy to reduce NAD+ to NADPH. In the biosynthetic (dark) reactions of photosynthesis the NADPH can be used to reduce carbon dioxide to sugars from which glucose can be produced.

So glucose is a reduced compound and can be thought of as ‘embodying’ the excited electrons, as its oxidation to carbon dioxide generates NADH (from NAD+). Hence:

There is no need for any additional excitation of electrons — that was done originally in photosynthesis.


What controls the southern range of willows? Many willows (Salix spp.) grow in northern states but do not grow in southern states, for example Salix viminalis.

What mechanisms control the southern range of temperate hardwoods such as willow? Is it disease? Temperature sensitivity of respiration? Water use efficiency?

The distribution of temperate hardwood forests, as well as deserts, tundras, savannahs, and other ecosystems, is determined primarily by average climate conditions, specifically average annual temperature and precipitation. You can see how biomes are related to climate in this figure, taken from Whittaker (1975):

Temperate forests tend to be between 2.5-17°C, and between 800-2500 mm precipation. These are not exact boundaries but reflect long-term climate conditions. As climate changes, so will the distribution of the biomes.

Temperature is important in many ways.  For example, most temperate trees go dormant during the winter. This requires metabolic preparation by the tree. If the weather turns cold too fast, then the trees may be be properly prepared. Alternatively, if the weather warms to quickly the trees may not be able to come out of dormancy properly. This technical report (Coder 2011) provides more detail.

The precise mechanism that restricts the distribution of any one species would require experimental determination. As it turns out, Populus trichocarpa (black cottonwood), plus other Populus and Salix (all in the family Salicaceae) are quickly becoming model organisms for study. This should shed more light on specific distribution limitations, such as changes in soil nutrients, light intensity, or other environmental parameters. There are now regular symposia held on these model organisms. You can read an introduction to one symposium here (Tognetti et al. 2011).

As a side note: One must be careful about the mapped distributions of popular trees like willows. Many species, including Salix viminalis, have been introduced far outside their native range, including through out the eastern United States, as shown by the map you linked to. The native distribution of the species is the Palearctic (Eurasia), shown here.

Literature Cited

Coder, K.D. 2011. Trees & cold temperatures. Environmental Tolerance Series WSFNR11-12, Warnell School of Forestry and Natural Resources, University of Georgia, USA.

Tognetti, R. et al. 2011. Fifth international poplar symposium: Poplars and willows: From research to multipurpose trees for a bio-based society.

Whittaker, R.H. 1975. Communities and Ecosystems. MacMillan Publishing, New York, USA.


Leaf formation on unknown tree: cocoon or something else? A small tree in my yard has leaves which appears to double over themselves. The first two pictures show this phenomena, and the third is the same tree to maybe aid identification.

I can't absolutely guarantee when this first appeared, but I believe it was this growing season, and I know it's been there at least a month (unless it's reoccurring, I am not tracking the individual leaves).

My first thought is cocoons or some other insect behavior. Can anyone tell me what it is?

(What kind of tree it is will also be valuable, in case we can't find the answer to the leaf question here)

EDIT: Location is outside Boston, MA (USA).

Based on the location and assuming this isn't a domesticated hazelnut there are two likely hazelnut species.  The lack of the distinctive "beak" seen on the Beaked hazelnut means this is most likely an American hazelnut (Corylus americana):

The hairs along the young branch are also consistent with this (see for example the Plant Guide from the USDA).

Note, however, there are hybrids between American and European hazelnuts so it is beyond my ability to be completely sure by visual inspection alone.


Deletion of codons at the start of a sequence in preparation for heterogeneous expression. Why? I am reading a patent where they isolate a gene from cDNA constructed from RNA extracted from plant matter.

The subsequent step (in preparation for heterogeneous expression in E Coli.) puzzles me:

The codon optimization I can understand but this part confuses me "...remove the first 23 codons from the DNA sequence and replace [the start?] by the ATGGCT sequence."

Why would one remove a set of codons at the start of a sequence? How did they decide how many to remove Is there an obvious reason I am missing?  Also what is special about the ATGGCT sequence.

Any ideas why they would do this?

The start of the new sequence (1650 bp) looks like this:

atggctaccg ataatgacag ctctgaaaac cgtcgtatgg gtaattacaa gccgtccatc       60

tggaactacg acttcctgca gtccctggct acccgccaca atatcatgga agagcgccac      120

whereas the original sequence (1710 bp) was this:

atggattctt ccaccgccac cgccatgaga gctccattca ttgatcatac tgatcatgtg       60

aatctcagaa ctgataacga ttcctcagag aatcgaagga tggggaatta taaacccagt      120

Another point I am confused about is that 1710 - 23 x 3 + 6 is 1647. But the new seq. is 1650 bp. What gives?

The easiest answer would be to ask the authors of the patent.
Several other possibilities (see comments) were excluded, such as:

restriction sites which interfere with cloning
signal peptide
proteolytic cleavage

Although it's just a theory, removing part of the N-terminus might improve protein stability and half-life time because the first 30-40 amino acids lack an ordered structure (as judged by submitting the structure to Phyre). Those structures are known to aggregate and influence protein stability.

References:

The use of systematic N- and C-terminal deletions to promote production and structural studies of recombinant proteins.

Sequence composition of disordered regions fine-tunes protein half-life

Production of prone-to-aggregate proteins


What is the C765-Gal4 driver? What is a gene driver and what does C765 stand for? Is Gal4 a transcription factor?

Source: "Dynamics of Dpp Signaling and Proliferation Control"

C765 is a transgenic Drosophila strain that has a specific Gal4 expression pattern ("embryonic salivary glands and larval wing and leg discs").

Gal4 is a transcription factor from yeast which binds an upstream activating sequence (UAS) and also happens to function in other species (like flies). In the Gal4/UAS system, a strain expressing Gal4, under the control of a tissue specific promoter or a minimal promoter in an enhancer trap, is crossed with a strain expressing a gene of interest flanked at the 5' end by the UAS. The F1 generation will thus express the gene of interest tissue specifically (ie only in the tissue(s) expressing Gal4).

[source]

Further reading:

Phelps CB, Brand, AH. 1998. Ectopic Gene Expression in Drosophila Using Gal4 System. Methods 14(4):367-379.


How do I find the sequence of the phage BxB1 gene? Specifically, I'm trying to find the sequence of BxB1 and its att sites.  I have success finding the att site sequences, but I'm having a bit more of an issue with finding the sequence of the actual recombinase.  I've looked through Genebank, but I can't find a definitive sequence of the BxB1 recombinase.

How should I go about looking for this sequence?

EDIT: One more thing I'm concerned about is the validity of the sequences that I do find.  For example, I have seen that Addgene has this pCAG-NLS-HA-Bxb1 sequence.  However, I'm not sure how to verify that this sequence is correct.

http://phagesdb.org/phages/Bxb1/ here you can click "Locally BLAST this genome" it will give you the sequence in FASTA format and then you can click BLAST if you want additional information about the sequence, alignment, etc


What is the best current understanding of how yeast transformation works? I would like to get myself up to speed with what is currently known to science about yeast transformation. Specifically, transformation of plasmids and linear DNA fragments. I am particularly interested in practical aspects, such as:

What is salmon sperm for? What if I don't use it? What if I use more?
What is the relationship between number of cells, amount of transforming DNA, and transformation efficiency?
How does choice of electroporation cuvette gap size affect efficiency?
What can I do to get more colonies after transforming my yeast?
What steps can I skip to make the transformation quicker if I am doing an easy transformation?
How do different genetic backgrounds and media affect efficiency? Are there any common ones that reduce efficiency substantially? Are there any uncommon ones that increase it substantially?
What is the effect of post-transformation "recovery" time (eg. culture 12 h without selection and then plate on selective medium)?
Is making spheroplasts worth it?
Does the same transformation protocol work for different species (S. cerevisiae, S. pombe, C. albicans, etc.)?
Is there a coherent theoretical framework for understanding what actually happens when yeast are transformed, as opposed to "you mix some chemicals with DNA and throw cells in, abra kadabra, transformants come out"? The sort of theory I'm asking about would be useful in predicting conditions for better efficiency.

I am not expecting you to comprehensively answer these questions in your answer. This would make for a very long answer, and each of these could be a question here in its own right.

Instead, I want the answer to name reference materials which can be studied to learn more about the points above. For example, recent reviews or textbooks by established experts in the fields would be quite useful.

I have never worked much with yeast, but I can still give some answers:

Salmon sperm is used as a the so called "carrier DNA". It is thought to bind to the yeast cell wall and thus prevents that the DNA which shall be transformed does so. This raises the transformation efficiency. See here for more details: "Transformation of yeast by lithium acetate/single-stranded carrier DNA/polyethylene glycol method.".

Effect of the recovery time: In this time you typically give the cells the chance to recover from the relative rude treatment and to express the resistance gene (when used) before moving them to a selective medium. This raises the efficiency of the transformation.

Spheroblasts: As far as I remember they are terribly fragile and painful to handle. However, when you succeed making them, you have cells which take up high quantitaties of DNA which makes them pretty efficient.

I think these reviews are definitely worth looking at (they also contain a lot more references):

Genetic Transformation of Yeast
Transformation of Saccharomyces cerevisiae and other fungi - Methods
and possible underlying mechanism
Foreign gene expression in yeast: a review

If you have a chance to get hands on a copy of "Methods in Yeast Genetics: A Cold Spring Harbor Laboratory Course Manual", I think this will be very helpful.


observed luminescence in a piece of plaice A plaice fish bought for human feed has been cleaned and cooked.
Some parts of the raw body have been left out of the fridge at about 22°C for about 15 hours.
During the following night a luminescence phenomenon has been observed on the meat of the fish.

The second shot has been taken in a dark environment with a professional camera using a high sensitivity and long-time exposure.

What could it be?

It's probably bacteria.

Here's a pdf describing the phenomenon, along with an in-depth history of the reported occurrence, which should tell you everything you might want to know.

  These seafood products exhibited luminescence due to the presence of certain bacteria that are capable of emitting light.  Luminescence by bacteria is due to a chemical reaction catalyzed by luciferase, a protein similar to that found in fireflies... Most of these species require salt except for the two nonmarine luminescent bacteria.

There is some link to potential pathogenicity, so I'd recommend not eating it.  That document also requests that you contact the researcher, so why not?  Here is a potentially-relevant paper but 1. is very old, 2. is in Russian, and 3. I have no access to it.  And this supposedly tells you how to isolate them.


Deterministic model of lambda-phage lysis/lysogeny [MATLAB] Project 1 Base:

Can someone please help me understand what I need from Project 1 Base code to do questions 1 and 2 from the first image? I'm new to MATLAB so a thorough explanation would be great.

For homework questions, the policy is to see some work from the poster.  Since you don't know programming, I've outlined what the code is doing, beyond the simple operations (+, -, /, *, ^), to get you started.  I think you should be able to implement the models with this information, and I'd be happy to confirm your own answers.

So the best way to figure out what any line of code means, in any language, is to type it and see what happens. To help you get started with programming in MATLAB:

Any text following a % (on the same line) is a comment: it does nothing in the program, and is only there for you to write notes to yourself.

The first two sections, Time-Related Constants and Simulation Constants, are just setting variables. It's like saying x = 3, so that later on you can do other operations with x.

The semicolon at the end of a line (in MATLAB) suppresses the output of the line. See what happens if you type x = 3; versus x = 3 at the command prompt.

In iteration constants, length is just a function that tells you the length of the vector.  X_rna_0 was previously initialized to go from 0 to 1.4 in steps of 0.2: the syntax is vector_name = start:step:end.

The simulation variables section is creating xyz-matrices, with all values initialized to zero.  The length in x is xr_max, and so on.  The idea is that, later on, at each step in Euler's method and each value of xr_max and xp_max, you'll save the value of X_rna.

The initial conditions are being set using meshgrid, which is best explained here.  The : means all of the rows/columns, corresponding to position: say you had a 3 x 3 matrix called apple.  apple[:,1]  gives you all the first column (1) of all three rows.  apple[1,:] gives you the first row (1) of all three columns. The .' means that the matrix is being transposed: again, the best way to see what's going on is to create a matrix of your own, perform the operation, and see if what you get is what you thought it would be.

For loops, you can read about here, for a start.  I do not think understanding this loop requires more information than that page.

Dot before ^2 means that each element of the matrix is being squared; you are not multiplying the matrix by itself.

That should decipher most of the code for you.  If you have further questions, feel free to comment here.

EDIT: Question 2 asks you to make a plot.  A plot of y vs. x would be made by typing plot(x,y)

Also, help on a particular MATLAB function can be accessed by typing help name_of_function.


what is the name of this small plant with yellow flower? Can someone please help me find the name of this flower. The close I got to is maybe some kind of diasy?.

Location: Hyderabad, India

This looks like Sphagneticola trilobata also known as Singapore daisy, creeping-oxeye, trailing daisy, and wedelia.  It is now found throughout the Neotropics but is native to Mexico, Central America, and the Carribean.  It is a weed that is classified in the top 100 worst invasive species in the world.

Source: Sphagneticola trilobata (ePlants)


Alternative plant taxonomies to Linneaus In addition to Linneaus-inspired taxonomies of the botanical world, I suppose there are some other proposals for different kinds of taxonomic accounts, perhaps for specific sub-domains of botany or perhaps historical. I'd be keen to learn about those.

Additionally, if any of you know there are some other alternative non-taxonomic approaches to botanic classification that are widely-used in sub-domains or in the early days of science, I'd be keen. I guess there are still some "common sense" classification to be made between use (ornamental/non-ornamental; medicinal/edible/poisonous), but perhaps there's more.

The most common alternative to taxonomic classifications are functional classifications. Emphasizing ecological similarities rather than similarities in relatedness, they can be regarded as complementary approach to, but not as a replacement of taxonomy. Why do we need this? Because species often perform very similar tasks, exhibit very similar characteristics and, most importantly, are very, very numerous (there are ~ 300,000 vascular plants). Reducing this redundant complexity is crucial for decision-making in conservation politics or the projection of vegetation change under future climatic conditions (Woodward & Cramer, 1996).

The idea behind this is to use functional traits, such as seed size, height, photosynthetic pathway, root density, etc., as a surrogate of a species' ecological 'role' -- its response to environmental factors and its impact on ecosystems. Seed mass for example (functional trait), is a proxy for the dispersal ability of a plant (function, performance). You should have a look at Lavorel et al. (2007), there is a nice table (too big to include here) that links specific traits to the actual ecological functions they describe. But look at this figure from the same paper:

By applying multivariate statistics like cluster analyses or ordination methods, species can then be classified into functional types. To make up one example, a functional type that might emerge from species with the following traits

height: > 20 m
seed size: > 0.5 cm
woody: yes
Specific leaf area: low

would certainly represent climax forest trees. This classification does not distinguish between individual species, because, from an ecosystem perspective, they all are functionally roughly equivalent.

For further research google 'Functional trait', 'Plant functional type' or have a look at refs 3 and 4.

Citations:

Woodward, F. I. and Cramer, W. (1996): Plant functional types and
climatic change: introduction. Journal of vegetation science, 7(3):
306–308.
Lavorel, S., Díaz, S., Cornelissen, J. H. C., Garnier, E., Harrison, S. P., McIntyre, S., Pausas, J. G., Pérez-Harguindeguy, N., Roumet, C., and Urcelay, C. (2007): Plant
Functional Types: Are We Getting Any Closer to the Holy Grail? In: Canadell,
J. G., Pataki, D. E., and Pitelka, L. F. (editors): Terrestrial Ecosystems in a Changing
World, Global Change—The IGBP Series, pages 149–164. Springer Berlin Heidelberg.
Halloy, S. (1990): A morphological classification of plants, with
special reference to the New Zealand alpine flora. Journal of
vegetation science, 1(3): 291–304.
Leishman, M. R. and Westoby, M. (1992): Classifying plants into groups on the basis
of associations of individual traits–evidence from Australian semi-arid woodlands.
Journal of Ecology, 80: 417–424.


connect three coding sequences with IRES To express two proteins at once in mammalian cells, expression vectors carrying an IRES (internal ribosomal entry site) are available. Does anyone know any attempt to express three proteins using two IRESs or more. The third gene may be expressed very low, but it may be acceptable depending on experiments if it works.

You might be interested in the Foot and Mouth Disease 2A Peptide, a self-cleaving peptide sequence that can be inserted in between two proteins. The proteins are translated as one sequence, but cleaved at the 2A peptide to form 2 proteins. If I'm reading the source right, they used 4 genes in a row with 2A peptides between them. The 2A peptide has the advantage of being much smaller than most IRES elements, while being more reliable than IRES or internal promoters.


What range of dose should be used? This is a dose-response experiment testing a new cancer drug.  the darker line represents cancer cells.  what range of dose should be used? I think it's 2-4 because this affects cancer cells only.  is this correct?

In the most basic sense you want to kill the most cancerous cells whilst minimizing the regular somatic cell death. Almost all cancer medications affect regular cells, too - though the better ones do so at a minimum whilst being effective. In reality, it's also nearly impossible to kill all of the cancerous cells. The goal is to bring them below detectable levels, which can allow the body to finish the job. Leaving significant amounts of cancerous cells alive won't do the patient any good - they'll just continue to proliferate and the patient will be back for more operations or treatments soon.

So, with the goal of minimizing benign cell cost and completely eradicating the cancerous line, on your crude chart that falls at about "4".


What kind of hawk is in this picture? I found this hawk(?) sitting on a fence near a small duck pond with a fountain near my workplace in Fort Smith, Arkansas, USA. There are some wooded hills (deciduous) nearby. It let me get within 3 meters or so before flying up to a tree across the pond. Based on measurements made of the fence it was sitting on, I'm guessing a height of 50 cm (20 inches) head to tail, I assume it'd have a wingspan of 60-70 cm perhaps (24-28 inches).

My best guess it either the Red-shouldered Hawk or Red-tailed Hawk. Unfortunately, I couldn't get a good picture of its back/tail. Any idea what species this is? I came across the bird during winter.

It looks very much like an immature red shouldered hawk.

  Immature Red-shouldered Hawks can be tricky to identify. Immature Red-tails show a belly band and are less heavily marked on the upper chest than young Red-shouldered Hawks.

Red shouldered hawks are smaller and like deciduous forests, like perching on wires, branches, etc. Red tailed hawks are usually birds of open spaces. They hunt from lower down than red tails, and they're often found near water (especially rivers and swamps), as they like frogs and snakes.

  Look for Red-shouldered Hawks in deciduous woodlands, often near rivers and swamps. They build stick nests in a main crotch of a large tree. During migration, Red-shouldered Hawks often move high overhead along ridges or along the coast.

Limited to a phone for a while and can't do much (I'm a dinosaur) but info and pictures here.


what would be the scientific name of this variety of dove recently i came across a small dove who had its feathers tied by a rubber band so that it $would'nt$ fly. it looks some what like this

i was stunned by seeing it as i have never seen a dove in brown colour. and after staring it for some time i noticed that it's feathers or hairs near the neck region were made into a cluster that makes it look like $spike$ $hair$ $style$

so in short what would be the scientific name of this dove ??

It's a rock pigeons (Columba livia).

The Color coding of Pigeon

There are three genes responsible for pigmentation in pigeons.

  – Tyrp1 gene produces a protein that helps make the pigment eumelanin.
  Pigeons with blue-black feathers have normal Tyrp1. Ash-red and brown
  birds pigeons contain different mutations in the Tyrp1 gene, which
  leads to less or different pigmentation.

  – Mutations that affect the Sox10 gene override colors determined by
  various versions of the Tyrp1 gene. Regardless of whether the Tyrp1
  version makes pigeons blue-black, ash-red or brown, mutations that
  regulate the Sox10 gene result in red pigeons.

  – Mutation of the Slc45a2 gene decreases the intensity of colors
  determined by Tyrp1, Sox10 and their mutants. Depending on the version
  of the Tyrp1 gene – blue-black, ash-red, and brown − pigeons harboring
  the mutant Slc45a2 gene still display the same colors, but in
  watered-down or diluted versions, less intense than those with normal
  Slc45a2. For example, a pigeon with both the ash-red version of Tyrp1
  and the mutant Slc45a2 gene has ash-yellow feathers. Pigeons with
  Sox10 and Slc45a2 mutations are yellow, which is the dilute form of
  red.

Source: http://unews.utah.edu/news_releases/birds-of-a-different-color/

Source: University of Utah


A website for identifying birds I am not sure if this is the right place to ask this question, but I guess that ornithology enthusiasts (or ornithologists) will have the best knowledge about it.

I am wondering if there is a website which would identify birds by their looks. For example, I would specify that the bird is similar to a sparrow in size (just a little bigger), it has a gray back and yellow-ish-orange-ish belly and it would tell me the exact species.

Does such a website exist?

There are actually a few, the problem with these websites is that they usually cover only a part of all birds on this planet. I use:

Bird identifier: Usefull website for a lot of European birds.
Backyard Bird Identifier: Useful for some European birds but
mostly for North American and Canadian birds.
All about Birds: Useful, but needs more knowledge for the identification

What I also do is using Google with a description of the bird, which sometimes works surprisingly well.


Insect Identification - Black Cicada I came across a black cicada in northwest Missouri last week (May 2015). I am only familiar with brown cicadas. What makes this black one different? Is it a different species, or do the brown cicadas change color at some point in adulthood?

A little digging on wikipedia seems to have answered my question. This picture of a 17 year cicada, Magicicada septendecim is pretty close to what I saw.

Furthermore, this seems to match the time and place, as the Kansas Brood of 17 year cicadas is scheduled to emerge this year and should appear in the Missouri-Kansas area. It also explains why I'm not familiar with these cicadas, 17 years ago I wasn't paying attention to them.


Do spouses begin to share genes over time? I apologize if this hypothesis sounds strange by I was wondering if any research had been done on a phenomenon which I've seen and have corroborated with many other - the idea that over time spouses tend to start looking similar to each other.

My hypothesis is that this is really a one-way street with the wife tending to look more like the husband. The reason being that after coitus her body is flooded with his genetic material which may lead to some mixing of DNA outside of the egg. Furthermore once the woman is pregnant she enter into a symbiotic relationship with an organism whose DNA is approximately 50% foreign. Her body must then adapt to the presence of that new genetic material.

I realize this may sound strange and Lamarkian but I was curious if the phenomenon itself had been investigated.

Microchimerism (Mc) is an interesting concept, and

  refers to the harboring of a small number of cells (or DNA) that originated in a different individual. Naturally acquired Mc derives primarily from maternal cells in her progeny, or cells of fetal origin in women.

In women, it has nothing to do with transfer during/after sex but rather is due to the presence of the developing fetus.  There is definite long-term persistence of microchimerism, although not much is yet known about its effects.  Here is a nice and free review from 2010 dealing with the subject.  Most if not all of the effects have to do with immune function, in particular autoimmunity.  It is definitely not a mechanism by which couples begin to look similar.  That is social, in particular a result of living in the same environment with similar activities and tastes.  Male contribution to cellular content in the embryo is almost nil, as sperm die and the transcript count in the successful sperm is puny compared to the egg.  Most RNA content in the embryo is maternal until it switches to embryo.


What was the first gene(s) found to code for ncRNA I could not find a source that states what the first gene found to code for ncRNA was. Someone told me, however, it was a gene that coded for either rRNA or tRNA. To this point in time I have had no other confirmation that this is true.

The first eukaryotic genes cloned were the 18S and 28S rRNA genes from the frog X. laevis as described here: http://www.genome.gov/25520303

And yes, they are definitely ncRNA genes.


Why isn't hearing the same as tasting? How do we feel and differentiate external stimuli? When I was at school, I learned that:

Skin, tongue, ears, and other sensory organs have sensors/convertors that turn external environment stimuli into "electric" signals.
Neurons send information as electric propagation of K+ / Na+ along their axon. Hence, the real nature of the stimuli is definitely lost in translation.
Each region of the brain is a cortex specialized for vision, sound, smell, and other sensations yet they all are made of the same neurons.

So:

Then how do we feel? How are "electric" signals turned into taste or smell?
Why does the brain not feel the same way about these different stimuli, rather than only differentiating amplitude and frequency of the signal?
Why do we even feel pleasure or pain at all? A machine would just transfer the information.

That part was never explained to me. Is it quantum (entanglement?) physics-related? Or even metaphysical? Does anyone really know?

Philosophically speaking, I am not even sure I taste things or feel music the same way other people do.

The problem you are seeking an answer to is referred to as the hard problem of consciousness, the term originally coined by David Chalmers, or more generally the mind-body problem.

Just how "hard" this problem is seems a bit unclear; some people argue it isn't truly "hard" at all, but they make these claims in support of their own particular views of the nature of consciousness. Since not everyone agrees with them, it seems like to at least some extent the "hard problem" description is appropriate.

There certainly are quantum explanations, and you will find proponents like Stuart Hameroff, but most neuroscientists consider his theories to be crank science since he hasn't provided any evidence of his theories, only hand-waving explanations of how they could be plausible.

There are also metaphysical explanations, going back to the dualism of Rene Descartes. The problem with these metaphysical theories is that they aren't scientifically disprovable, and the more we learn about the brain the more of its functions can be explained physically. Dualism is ultimately a religious or philosophical stance rather than a scientific one.

There are several neuroscientific theories of consciousness, including integrated information theory(IIT) and global workspace theory(GWT). For IIT, consciousness occurs through the integration of information in a causal structure like the structure of a brain. GWT proposes that consciousness occurs through the transmission of information through particular central brain structures. In both, the qualia that are experienced occur through the neural substrates of either the processing or the information carried. Hearing and tasting are different because they involve different groups of neurons and synapses; you don't typically taste a sound because the parts of the brain that process taste are not getting direct auditory information.

However, that doesn't mean that senses are completely disconnected: it is possible to form relationships between senses by association, like how both written and spoken language evoke the same meanings, or how certain colors seem to be associated with "hot" versus "cold" temperature.

As far as what it means to experience things how others do, I'd recommend Nagel's What Is It Like To Be a Bat? which argues that subjective aspects of consciousness cannot be completely understood, but that there are objective features that can be understood. So, although you cannot know that others taste or feel music in subjectively the same way as you, you can objectively understand that other people can taste sweet and sour, can hear music in a similar frequency range, etc.


What happens when the parietal cells of gut epithelium becomes partially non-functional? The options are

a) The pancreatic enzymes will not work properly
b) The pH of the stomach will fall abruptly
c) Steapsin will be more effective
d) Proteins will not be adequately hydrolysed by pepsin into proteoses and peptones.

The answer is D because pro enzyme pepsinogen gets converted to active pepsin in presence of HCl.

But, Why can't the answer be B ? Because if HCl is not secreted by perital cells then obviously pH of the stomach is going to fall down ?

Parietal cells are responsible for acid secretion (HCl) in the stomach.

pH is inversely correlated to H+ concentration; the higher the H+ concentration, the lower the pH.

If the stomach's parietal cells become partially non-functional, there will be less acid secreted into the stomach (a lower H+), and the pH will rise.

Answer (b)

  (b) The pH of the stomach will fall abruptly

is the opposite of what would be expected to occur.

The correct answer is d), for the reason you listed.

  Proteins will not be adequately hydrolysed by pepsin into proteoses and peptones.

Regulation of Acid Secretion


What concentration of sugar is optimal for baker's yeast fermentation? I'd like to do an experiment on what concentration of sugar would be best for fastest yeast fermentation. I'm thinking to put some active dry yeast into different concentrations of sugar water and measure the fermentation activity after a certain amount of time (like 15 minutes or so). I know at a certain concentration the yeast will effectively die as the sugar solution becomes hypertonic, but I don't really know what range would be most effective right now. Any papers I've found are on yeast for alcohol.

When glucose and fructose are fermented separately, the uptake profiles indicate that both sugars are utilized at similar rates. However, when fermentations are conducted in media containing an equal concentration of glucose and fructose, glucose is utilized at approximately twice the rate of fructose. The preferential uptake of glucose also occurred when sucrose, which was first rapidly hydrolyzed into glucose and fructose by the action of the enzyme invertase, was employed as a substrate. Similar results were observed in the fermentation of brewer's wort and wort containing 30% sucrose and 30% glucose as adjuncts. In addition, the high levels of glucose in the wort exerted severe catabolite repression on maltose utilization in the Saccharo~ myces uvarum (carlsbergensis) brewing strain. Kinetic analysis of glucose and fructose uptake in Saccharomyces cerevisiae revealed a Km of 1.6 mM for glucose and 20 mM for fructose. Thus, the yeast strain has a higher affinity for glucose than fructose. Growth on glucose or fructose had no repressible effect on the uptake of either sugar. In addition, glucose inhibited fructose uptake by 60% and likewise fructose inhibited glucose uptake by 40%. These results indicate that glucose and fructose share the same membrane transport components

References

D'Amore, Tony, Inge Russell, and Graham G. Stewart. "Sugar utilization by yeast during fermentation." Journal of industrial microbiology 4.4 (1989): 315-323.

Thirwell, A.J. and R.L. Busby. 1982. Liquid sugar as a brewing adjunct. Inst. Brew. Proc. Conv. (Aust. and N.Z. Sect.) 17:77 84.
, http://www.123HelpMe.com/view.asp?id=121963


Effects of selection on effective population size Background

The effective population size ($N_e$) is a central concept of evolutionary biology and is influenced by several parameters. For example: sex ratio bias affects $N_e$ $\left(N_e = \frac{4N_mN_f}{N_m+N_f}\right)$ and varying population size over time influences $N_e$ $\left(N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}\right)$. There is a post on how overlapping generations influences population size.

Question

Selection also influences the effective population size. Intuitively, I'd expect that the higher is the fitness variance, the lower is the effective population size as fewer individuals contribute to the next generation. Am I right? How (what is the mathematical formulation) does fitness variance influences the effective population size?

From Conner and Hartl's A primer of ecological genetics:

  "Any variance in reproductive success among individuals greater than
  random expectations, a commonplace concurrence in natural populations,
  reduces effective population size."

So yes, selection does reduce the effective population size and for the reason you suggest - it removes some individuals from the mating pool/ reduces their contribution to the next generation. Mathematically it can be derived as

$N_e \approx \frac{ 8N_a}{V_m + V_f + 4 }$

where $V_m$ and $V_f$ are sex-specific variances of offspring production (males are often more variable in reproductive success than females).

They give an example of selection affecting $N_e$, in a population of deer 33 males had four times the variance ($V_m$ = 41.9) in reproductive success of 35 females where variance was $V_f$ = 9.1. Thus effective population size was

$N_e \approx \frac{ 8 * (33 + 35)}{41.9 + 9.1 + 4 } = 9.9$

The notation $N_a$ is the actual number of individuals in the population. This can be seen in the calculation of effective population size when the number of males and females are not equal

$N_e = \frac{4 N_m N_f}{N_m + N_f} = \frac{4 N_m N_f}{N_a}$

An example is a population of 80 males and 80 females compared to a population of 70 males and 90 females. Both populations have equal sizes but effective population size is reduced by unequal sex ratios

$N_e = \frac{4 * 80 * 80}{160} = 160 \neq \frac{4 * 70 * 90}{160} = 157.5$


Can you identify this insect (orange back, 6 legs)? Found a couple of them in central europe on a zucchini plant (in august).

They are about a centimeter in size.

Tried looking for insect with orange back and 6 legs but no result.

[EDIT from comment]: The insect in this post looks pretty similar. There is a difference though - the one in my picture has orange legs not black ones. (maybe different stage of larvae or different species of ladybug or just random?)

It is a harlequin ladybird larvae.

This is one of the most variable species in the world, with an unusually broad range of color forms. It is native to eastern Asia, but has been artificially introduced to North America and Europe to control aphids.

I figure that Wiki is saying "it has some of the highest color variability of any wild plant or animal".

wiki: harlequin ladybird


Which sex has higher variance of reproductive rate in modern societies - male or females? Who has a more varied reproduction rate in modern western societies - men or women? The average rate is the same of course, but I wonder which sex have higher variance - higher variance means that reproduction is more concentrated in some subgroup of given sex so this subgroup transfer their genes at higher rates then average rate in whole population. The next question would be 'is that subgroup somehow homogeneous' ?

Sperm are cheaper than eggs

According to Bateman's Principle the males of a species are (typically) more able to produce a greater variance in the number of offspring. This is because generally the males can produce many gametes and achieve many matings whereas females are limited by the number of eggs, resources, and time lost to pregnancy. Therefore, just by simple logic, it would appear likely that males have greater variance in mating success (strong/attractive males would be able to mate with many females while weak/unattractive males would have little to no offspring). See Wikipedia for an introduction to Bateman's Principle. Also see this paper about sexual selection and mating success variance.

An Example

An extreme example of higher variance in male mating success is that seen in lekking species. These species form groups of males called leks where females enter and choose mates. Often one/few males will sire the majority of offspring in the next generation. Fallow deer are one lekking species where males have higher mating success variation than expected by chance.

In Humans

Here is a blog post discussing a paper which showed that males have greater reproductive success variance than females in humans. In the paper see table 1 (Vm:Vf column) which indicates the majority, particularly those close to ancestral type lifestyles, have much greater variance in male reproductive success. Only one measured (Finland) is the reverse pattern.


What are the potential dangers (if any) facing the twin girls recently born in China with their CCR5 gene modified? According to this Nature news article, a Chinese researcher claims to have made the world's first genome-edited baby using the popular CRISPR–Cas9 genome-editing tool. A gene called CCR5 was modified before the embryo was implanted into the mother. The CCR5 gene is known to produce a protein that is utilized by the HIV to enter human immune cells, and the genome editing performed is expected to make the babies HIV-resistant despite their father being HIV positive.

As a Chinese, I am deeply concerned with the ethical consequences and scientific impacts of this highly controversial experiment. However, to form an opinion for myself, I believe that I first need to know the potential dangers, either expected or speculated, that the twin babies might face in their life. Unfortunately I am not familiar enough with molecular biology to be able to know and judge these myself, and the reports in the media seem very vague on this issue.

So please let me ask: What are the potential dangers (if any) facing the twin girls, and how sure are we now about these dangers, their consequences, and possible countermeasures?

Important notes:

  I am not going into the ethical aspects of editing/removing CCR5 in human embryos, neither will I discuss potential effects of introducing that mutation into the human population. Both of these are very important issues, but out of the scope for this answer.
  As of now I'm not aware of any reliable sources of what was actually done in this case, so I will also keep my answer general / hypothetical without going into any specifics of these particular girls.

That out of the way lets get into the potential problems that could be caused by removing the CCR5 gene from  human embryo using the CRISPR-cas9 system. These can mainly be grouped into two classes: off-target or side effects of the procedure itself and any effects of a non-existing/functional CCR5 by itself.
One additional point I want to mention is that removal of CCR5 does not make one completely immune to HIV, because some strains of the virus (can) use the CXCR4 as a co-receptor instead.

1. CRISPR-Cas9 off-target effects

The CRISPR-Cas9 system has become very popular with scientists in the last few years, because it allows genome editing in very many organism with previously unmatched efficiency and speed. However, people only recently  - when the potential medical use of the system was being considered - started to look into the specificity of the system. What they found was, that while CRISPR-Cas9 is supposed to be very sequence specific it often also induces mutations in genes that were not supposed to be targeted.
There is a quite a lot of ongoing research to reduce these off-target effects, one good example being to use two variant copies of the system that each only cut on strand of the DNA at neighbouring sites (instead of cutting both strands at one site as is normally done).
If such mutations occur while genome editing an embryo the possible effects are very hard to predict - it could be anything from completely harmless to cancer inducing. If one wants any reliable estimate for this, it would be necessary to check for any off-target mutations by sequencing the whole genome of the edited embryo. That however requires (even with very modern techniques) removing at least a single cell from the growing embryo before the IVF procedure can take place and might therefore reduce chances of the IVF being successful.

Main source: Extensive review to CRISPR off-target effects

2. Side-effects of CCR5 removal

Normally it would be very hard (read: basically impossible) to predict what potential side effects the removal of a specific gene would have, even if there are e.g. mice where this has already been done but only studied for specific medical aspects. In this particular case however, we are in luck because there is a naturally occurring mutation called CCR5-Δ32 that also renders the protein completely dysfunctional. We can therefore pretty safely assume that the CCR5 removal by CRISPR-Cas9 will have similar effects to this mutation.

Since CCR5 is a gene expressed by immune cells, it  - unsurprisingly - has influences on various immune functions, but mostly seems to be affect infectious diseases. As this review puts it:

  In summary, there are ample data to suggest that CCR5 is involved in both positive and negative regulation of immune functions that relate to the regulation of leukocyte trafficking during infectious and postinfectious diseases.

One particular risk that seems to correlate with non-functional CCR5 is both initial infection and disease progression by flaviviruses. It has been reported that the CCR5-Δ32 mutation increases the risk of being affected by both the Tickborne encephalitis (TBE) virus and West Nile Virus, both of which can affect the nervous system if the diseases progresses far.


Is p53 a cyclin dependent kinase? I've been reading some research papers about p53 and associated tumour suppressor proteins, such as p21. I see them referred to and associated with cyclin-dependent kinases. Is p53,p63 et cetera part of the CDK family?

No, p53 and other tumor suppressor proteins do not belong to Cyclin dependent kinase(CDK)family. p53 blocks the cell cycle by promoting the synthesis of Cyclin dependent kinase inhibitors (CKI proteins). These CKI proteins bind with the Cyclin and CDK complex and inhibit the cell cycle at G1 checkpoint.

(Image Source:  https://www.khanacademy.org/science/biology/cellular-molecular-biology/stem-cells-and-cancer/a/cell-cycle-regulators)

p53 also plays role in activating DNA repair enzymes and if DNA is not repaired, p53 will promote apoptosis, so that defective DNA is not passed on.

These all proteins are structurally homologous to p53, so together they are known as p53 family.

(Via: https://www.frontiersin.org/articles/10.3389/fonc.2014.00285/full)


Primary cilia: what cell types have non-motile cilia that migrate? My understanding is that there are two broad categories of cilia: motile and non-motile (also called primary.

Examples of the former include sperm flagella and the cilia of epithelial cells that line the airways.

Examples of the latter are mostly single cilia that protrude from the cell and act as an antenna, usually packed with certain receptors (HH pathway, Notch pathway etc.)

In the inner ear, a primary cilium called the kinocilium extends out of the center of the apical side of hair cells and migrates to the lateral side over the course of a few days. This cilium is non-motile, it is simply anchored to a basal body which is pulled to one side of the cell.

Does anyone know of another such example in any other tissue? A single non-motile primary cilium whose basal body migrates along the apical plane of the cell after docking with the cell cortex.

Thanks.

It's hypothesized that planar cell polarity is many cases functionally associated with asymmetry of (primary) cilia (Axelrod (2008)). So, the phenomenon of primary cilium migration could be not that infrequent. One example is the development of ependymal cells in brain ventricules: They are multiciliated and the cilia are motile, but ciliogenesis starts from a single cilium, which is not motile and which migrates from the apex to the rostral end of the cell:

Mirzadeh et al (2010)
Bayly & Axelrod (2011)

Seemingly less clear (for me, at least) cases are non-motile single cilia on the lens fiber cells and may be, embryal node cilia (which are motile in the mature state):

Wallingford (2010)
Sugiyama et al (2010)


Can PCR duplicates have complementary sequences? It is common when analyzing paired-end whole-genome shotgun sequencing data to check for and eliminate PCR duplicates. The reasoning is that the probability of sampling a fragment of the genome of the same exact length from the same exact position in the genome multiple times is extremely low. Therefore, if you see multiple read pairs with the same exact sequence in both pairs, these don't represent independent events but are multiple copies of the same event.

My question is whether PCR duplicates can be reverse complements of each other. All the PCR duplicates I've observed myself have been exactly the same sequence on exactly the same strand. Is there a technical reason why this is the case, or is it possible that PCR duplicates could not be on the same strand as each other?

The standard directional Illumina library prep protocols that are used at the facility in my building follow the schematic below:

So, I guess this provides a potential technical explanation for your stranded duplicates, with the broad simple answer being it depends on the protocol used to make the libraries.


Do flowers transpire? I have googled this out but no where found a satisfactory answer. The definition of transpiration states that it is the evaporative loss of water from the aerial surfaces of the plant but I am really unsure as to whether flowers transpire or not.

Short answer: yes.

Floral parts, as petals and sepals, have stomata, and transpire just like a normal leaf or a primary stem (that is, a stem covered by epidermis, not periderm). And, besides stomatal transpiration, flowers have cuticular transpiration, like most of structures covered by epidermis.

This is a SE micrography of a petal's stoma:

(source: http://www.sciencephoto.com/media/32403/view)

There is a very famous experiment that we make with the kids in primary school: take a white flower and put it in a vase with coloured water. The petals will become coloured. This experiment shows that there is an ascendent flux of water, and this flux depends on transpiration. You can see it here: https://youtu.be/y9hprlmck44


T7 phage promoter action in mammals Does anyone know if the T7 phage promoter is efficient in mammalian systems?

Amazingly, yes.

See High level gene expression in mammalian cells by a nuclear T7-phage RNA polymerase. The authors recognize that the T7 RNA polymerase tends to work only in the cytoplasm thus is unable to transcribe genes in the nucleus. To remedy this limitation, the T7 polymerase was fused to a nuclear location signal peptide to localize the polymerase correctly.

Promega sells a T7 expression system for RNAi production.