Why are there splice variants within the same organism? What might contribute to the need for the feature? I only know splice variants are produced by different combinations of introns and exons. I wish to know why there is a need of such function. Perhaps using the same amount of DNA sequence to produce multiple proteins saves genetic material. Also, I want to know what contribute to the need for splice variants feature (e.g. evolutionary pressure, the need to increase the complexity)

I find that in human, protein CD81 is predicted by Ensembl to have a lot of splice variants (http://grch37.ensembl.org/Homo_sapiens/Gene/Splice?db=core;g=ENSG00000110651;r=11:2398547-2418649;t=ENST00000475945). However, only 1 of them is characterized. Thus, splice variants seem redundant. Any examples of splice variants actually carry different function?

The reason is very simply to provide enough variation in a limited sized genome to produce the repertoire of proteins produced by the cells of multicellular organisms. It is also a matter of efficiency and reduced energy consumption.

Consider that on average there are about 100,000 unique protein types being produced in a human cell [1], but the human genome is estimated to contain only 19,042 protein coding genes [2], then the cell needs some way to vary that limited instruction set.

Also remember that differentiated cell types express certain genes but not others, and produce different proteins that other cells do. So that implies that there are more than 100,000 different types of human proteins, and far fewer than 19,042 genes being expressed in any one cell at the same time.

So without splice variants, our genomes would either need to be far larger than the approximately 3 billion base pairs it is already or our repertoire of proteins would be significantly less. We would also have a lot of redundancy, as many common exons would have to be repeated over an over again. That would require a lot more energy for DNA synthesis, and nucleic acid synthesis, etc. The process would become inefficient rather quickly and would likely make complex multicellular animal life untenable.

There is a bit of an error in your question. Splice variants are identified by the mRNAs that are produced, and exons are defined by the sequence that is in the mature mRNA. Introns are, by definition spliced out of the pre-mRNA, meaning that splice variants are not "produced by different combinations of introns and exons." Splice variants will only consist of different combinations of exons. The only time an intron would be found in a mature mRNA is if a splice site is mutated and it is no longer recognized by the spliceosome, so it leaves the intron in incorrectly. This will generally result in a non functional protein.

EDIT

  The collection of components required to carry out the intricate processes involved in generating and maintaining a living, breathing and, sometimes, thinking organism is staggeringly complex. Where do all of the parts come from? Early estimates stated that about 100,000 genes would be required to make up a mammal; however, the actual number is less than one-quarter of that, barely four times the number of genes in budding yeast. It is now clear that the 'missing' information is in large part provided by alternative splicing, the process by which multiple different functional messenger RNAs, and therefore proteins, can be synthesized from a single gene.

-Expansion of the eukaryotic proteome by alternative splicing: Nilsen and Graveley

  Alternative splicing of pre‐messenger ribonucleic acid (pre‐mRNA) allows the generation of different mRNAs from the same gene. Evolution of alternative splicing affecting translated regions of mRNAs permits the synthesis of different proteins from a single gene, significantly increasing the diversity of the protein repertoire.

-Patthy, László(Apr 2008) Alternative Splicing: Evolution. In: eLS. John Wiley & Sons Ltd, Chichester.

Also while I am not one to accept a Nobel Prize at face value, they are usually awarded when the field accepts the explanation of the hypothesis. The 1993 Nobel Prize in Physiology and Medicine was awarded to Richard J. Roberts and Phillip A. Sharp "for their discovery of 'split genes'."


How to do a blast search for similar sequences? Tried doing a Blast search for a PPO gene in an advocado genome: https://www.ncbi.nlm.nih.gov/blast/Blast.cgi?PAGE_TYPE=BlastSearch&PROG_DEFAULTS=on&BLAST_SPEC=OGP__3435__73885&DATABASE=GPIPE/3435/current

However there are no matches, which may be because it is a different species with a slightly different sequence? The genome I am searching is known to contain PPO.

As stated in the comments here, there is no complete genome sequence for avocado as of yet, though people appear to be working on it.

However, there are a large number of ESTs and doing a BLAST of their translations with the tomato PPO sequence (tblastn) gives some hits.

Here is a link to that BLAST.

  However there are no matches, which may be because it is a different species with a slightly different sequence?

This is precisely the problem that BLAST was designed to solve.


Why has our nose evolved with the nostrils facing down? For most animals, the whole bottom of their face sticks out and they have a snout with a mouth and nose at the end.  But humans have a flat face and just a nose that sticks out.  We used to have the whole face sticking out, but our jaws got smaller and smaller.  Because our noses still needed space to do their job, they had to stay sticking out.  People who come from very cold areas have bigger noses than people from where it is hot, so they can warm the air up more.

Why has our nose evolved with the nostrils facing down? Is it because we were water animals, and that would help with water coming in?

I have not been able to find any studies that look specifically at the genetic mechanism for nose development. I certainly do not know but I'll offer up two hypotheses.

My first hypothesis is that the elongated nose is a remnant of the elongated lower face of our ancestral species, as you note in your answer. Take a look at this brief YouTube video (1:17 long, the part relevant to this answer begins at 33 seconds) of a time-lapse composite showing the develop of the human face. Our face develops as two separate halves that meet together in the middle. That's what creates the philtrum under our nose.

Watch the especially carefully from the 54 second mark to 1 minute mark. Note that our nostrils are pointing directly forward and the overall region looks somewhat like a pig snout. The mouth is vertical aligned with the front of the nose. The overall face is much more rectangular and the eyes are on the sides of the face.

Then, the face begins to become rounder and flatten. The eyes move to the front of the face and the recesses our our eye sockets recede. The lower face below the nose recedes, becoming flatter. The only part that does not recede is the nose area. The flattening of the lower face may actually cause the nostrils to turn downward.  Our nose does not develop outward from a flat face but instead is left behind as the rest of the face flattens.  This would be my initial thought as the primary reason for the shape of the nose and direction of the nostrils.

My second hypothesis (and honestly independent of the comment by @Remib) is related to our sense of smell and taste. Although our ability to detect flavors is a complex process, the primary sense involved is smell (Shepherd 2006). Therefore, downward-pointing nostrils are located directly above the mouth so we get a good smell of the food just before it enters the mouth, perhaps enhancing our flavor-sensing ability.

  Shephered, G.M. 2006. Smell images and the flavour system in the human brain. Nature 444: 316-321.

Note that these two hypotheses are not mutually exclusive. The downward pointing nostrils may be a remnant of our facial development but provides an (adaptive?) advantage for flavour perception.


Variation in MHC in humans What evolutionary process lead to so much variation in MHC? What is the advantage of having such variation?

Here are two free articles that go into the subject very nicely, I think:

Major Histocompatibility Complex (MHC)
How pathogens drive genetic diversity: MHC, mechanisms and misunderstandings

The MHC loci are the single most important determinant of our immune system's response to foreign invaders and are absolutely necessary for discrimination between self and non-self.  Because of the massive diversity amongst those pathogens, no one single MHC allele will allow the best response.  For example, the delta-32 deletion that bears resistance to HIV also increases susceptibility to West Nile; if you're more likely to suffer from the latter, that is a fitness reduction that could be selected against.  Thus, more alleles will survive in the population as all can be advantageous.  This is called balancing selection.

Additionally, the microbial invaders mutate and evolve much, much faster than our genome does, so you want to have the greatest breadth of MHC present in the population and in an individual in order to maximize resistance to whatever may arise.  At a population level, it is also advantageous because it means that the entire populace won't succumb to a certain infection.  If everyone has similar alleles one virus could wipe everyone out; we observe something similar happen with our crops, for example, when grown in massive monocultures.  There is also a fair amount of evidence, mainly in humans and mice I believe, supporting a role for MHC in mate selection.  Individuals seem to find potential mates with different MHC alleles more attractive, presumably to maximize the fitness of their offspring.

MHC is an absolutely fascinating subject (I'm researching it at the moment!).


What happens once a brain is full? I just read the answer to this question, and it got me thinking...

If the human brain (or any other brain) has a finite amount of storage, what would happen once the brain has taken in its maximum amount of information?

This is, or course, assuming that the individual can live long enough to acquire that much information.

I would take a guess that just like how we forget things all the time, the new memories would "override" some older ones.

Has there been any research or hypotheses on a brain's behavior once the its storage has maxed out?

It's very likely that memory is "lossy" and holographic, such that you can keep adding more information indefinitely, but retain it with less and less accuracy.

Memory isn't a digital storage system with X gigabytes of capacity, and the inputs to memory aren't neat little packets. What we remember are a web of associations and patterns. Vastly oversimplified, we group similar memories together into a baseline, and remember the deviations from that.

If you walk the same route to work every day, you take in a huge amount of information the first few days: stretches of residential buildings, cars parked on the street, portions of curb painted red, trash in the gutters. In successive days different cars will come and go, front yards will get overgrown and trimmed, etc, but these details get mixed in with what you saw the first few days into a blurrier and blurrier sort of average. Trillions of impressions from hundreds of days take up very little more capacity than the first day did, and still tell you what you need to know about the route.

Imagine that there's a particular green car of common make and model, that was parked in front of a certain house about 3/4 of the time for the first hundred days you walked the route. Your memory reduces this to something like "green car usually along here somewhere". If the green car stops parking there, you'll probably notice "green car not there today" because that's a contrast to the common case that you've memorized. But if a week goes by with no sightings of the green car, it's very hard to remember which day you last saw it, because you don't remember individual sightings. (I actually had this happen to me with my own car; I discovered it stolen on a Wednesday and could not for the life of me recall whether I'd seen it on Monday or Tuesday even though I'd walked past the spot it should have been parked both days.)

As you remember more things, you remember them in less and less detail; you can't remember if you've been to New Orleans once or twice; you can't remember which memories were from your first trip to Las Vegas or your second, etc. So the brain never becomes full, it just becomes fuzzy.


Is the serum concentration of calcitriol different at different times in the day? Given that calcitriol has a relatively short half-life in adults it would be possible that the serum concentration is at different times of the day different if it gets produced in different quantities at different times of the day.
Is this the case or is the level relatively constant over the day and doesn't follow a daily rhythm?

Calcitriol, or 1,25-dihydroxyvitamin D, is produced in the kidney by 25-hydroxyvitamin D-1α-hydroxylase from it's precursor, 25-hydroxyvitamin D.

Calcitriol has a plasma half life of about 6 hours. It is tightly regulated. This regulation involves a negative feedback loop on its own synthesis and via an inhibitory effect on PTH synthesis, and control by downstream effects (plasma phosphorus, calcium, FGF-23 and others).

25-OH-D, the precursor, has a plasma half life of about 2-3 weeks, and except in chronic deficiency or other pathologic states, is in plenty of supply for the appropriate production of calcitriol. Because of this, it is unlikely that, for example, daily changes in sun exposure or nutritional intake would propagate down to production of the active metabolite.

The image and a good review of Vitamin D can be found in this NEJM article

References ranges at my lab and in Lange's guide to diagnostic tests do not include any interpretation suggestions for plasma or serum 1, 25-dihydroxy vitamin D (calcitriol) at different times of day. Notably, though, this test is not often done clinically. It's primarily for the case where a patient has high calcium, low PTH, and no malignancy has been found.

Despite this (reference ranges do not distinguish between times of day), there may be a circadian rhythm within that range. Regulators and downstream effects of calcitriol do show a circadian rhythm, as is demonstrated in this classic 1972 study:


Definition of Phenotype I'm not a biologist but, I'm trying to enter molecular biology from a perspective. I have noticed that concept of genotype is quite well defined while phenotype is not. If I understand well, gene expression builds up enzymes that ultimately control all chemistry inside the cell, and which are sensible to the environment. Then, how correct/incorrect would it be to state that "phenotype is the enzyme composition within the cell"? Is it at least a good approximate idea?

Genotype:

Simply genotype is the inherited genetic information an individual has, and is conceptually quite easy to grasp. For example, if height is determined by gene $A$ and there are two alleles (variants of the gene, $A_1$ and $A_2$), then the three possible genotypes at that locus are $A_1A_1$, $A_1A_2$, and $A_2A_2$.

Phenotype:

The definition of a phenotype is a little more difficult to grasp, in part because it's so broad. As a quantitative geneticist I would say its any characteristic of an individual that can be measured. There's an enormous variance in the phenotypes that are used, they can be characteristics that are physiological, morphological, behavioural, life-history, even fitness itself. Personally I've used phenotypes from gene expression, which is one of the "lowest" (most close to genotype on the bridge between genotype and phenotype) phenotypic levels, through to lifespan, rates of ageing, and lifetime offspring production. Phenotypes are determined by genotype and/or environment (all non-genetic effects). For example, height may be affected by several genes, but it is also affected by nutrition during development and growth (among other things). As an evolutionary biologist, I feel the need to point out that selection operates on the phenotype, it is because genotype often has some effect on the phenotype that we see evolution by inheritance of genetic information.

Correctness of your statement:

  "Phenotype is the enzyme composition within the cell"

Would be sort of incorrect. It certainly wouldn't be appropriately defining phenotype as a general thing. It would be saying that phenotype means enzyme composition within cells, and the appropriate sentence depends on what you are trying to say. The following would say that, in the discussed case, the enzyme composition of the cell is what you consider to be the phenotype:

  "In this study the enzyme composition within the cell is the phenotype."

Whereas, the following defined the concept of phenotype:

  "Phenotypes are characteristics which could be, in principle, measured, such as the enzyme composition within a cell."

The problem of your statement is it makes it sound like phenotype, as a general thing, is enzyme composition within cells. It's kind of a problem of while enzyme composition of a cell can be a phenotype, not all phenotypes are enzyme compositions of cells. Similarly to all humans are mammals but not all mammals are humans.


Which hydrophobicity scales are best for detecting transmembrane regions, and why? There are many hydrophobicity scales for protein analysis.

Broadly, I gather the differences between them are from the experimental method to acquire the data and the normalisation (or lack thereof) of the data.

To detect/predict transmembrane segments one method is to use a window of 19-20 of these residue scales to detect a region of hydrophobicity above a threshold. The Eisenberg et al. scale is used by uniprot for example.

Uniprot don't seem to explain their choice of using the Eisenberg et al. scale.

Why might one use a certain scale over another when predicting transmembrane segments?

This has been studied by some of my labmates in Why is the biological hydrophobicity scale more accurate than earlier experimental hydrophobicity scales? I am not involved in their research, but here is the gist of the paper:

Different scales are, as you say, developed based on different criteria. In particular, Eisenberg scale is one of the consensus scales, that is hopefully at least as good as all of its components. It was believed that there were no big performance differences between scales. This could be why Uniprot doesn't specify their choice of scale: at the time, it didn't matter too much. A study in 2009 showed that the new UHS scale was actually better than others.

The results of the benchmark are that the differences are indeed not so big: roughly $\pm2\%$ in difference in prediction accuracy. The overall winner? Hessa, scoring $1.29\ \sigma$ over the average of the scales, but closely followed by UHS, PM1D and PM3D. Eisenberg performance, by the way, is average.

Final note: they found that a near optimal window size for all the scales was 21 with double the weight in the central third.


Does anybody know what this shark is eating? Looking for a species identification on the orange fish that the shark is eating. The shark is a goblin shark filmed as part of the BBC's 'Legends of the Deep: Deep Sea Sharks'.

The fish in this image is Helicolenus dactylopterus. Shown below;

This fish, is more formally known as a Blackbelly Rose-Fish. This fish, is one of the Goblin Sharks' many prey in the deep sea.

In the photo you posted it looks as if the Goblin shark effortlessly and oddly so caught the fish - it did. This is due to how it consumes most of its prey:

  When they approach it their jaw goes out similar to how a human can stick out its tongue. Then with a sucking motion they draw they prey into their mouth where very powerful teeth are waiting to consume it.

Goblin sharks are quite terrifying...


In the NCBI Taxonomy tree what does "no rank" mean? NCBI publish their taxonomy browser at https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi

While many taxa have a well defined rank (Order, Family, Genus etc..), some of them have "no rank".

For example, Amniota:

  Taxonomy ID: 32524
  Genbank common name: amniotes
  Inherited blast name: vertebrates
  Rank: no rank
  Genetic code: Translation table 1 (Standard)
  Mitochondrial genetic code: Translation table 2 (Vertebrate Mitochondrial)

What does "no rank" mean?

Well, welcome to Phylogenetic Systematics.

The Linnaean Taxonomy is a rank-based classification system. When Linnaeus first proposed it in 1735, in his famous Systema Naturae, he created 5 ranks: Regnum, Classis, Ordo, Genus and Species (in Latin).

Today (more on that below) Linnean Taxonomy uses 8 main ranks:

Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species

If you add the prefixes super-, sub- and infra- to that, you get more ranks.

However, in the 60's, a new systematics was proposed by Hennig, called Phylogenetic Systematics. I'll not explain in details what Phylogenetic Systematics is in this answer, there are plenty of good sources for you to read about. My point here is only one: showing you that there is no rank in Phylogenetic Systematics.

Have a look at this cladogram:

The group made by A + B is a monophyletic group. The group made by A + B + C + D is also a monophyletic group. The same way, the group made by A + B + C + D + E + F + G + H is a monophyletic group (by the way, there are 7 monophyletic groups in that cladogram). And all those groups have names.

Now comes the important part: in Phylogenetic Systematics, the number of monophyletic groups between the more exclusive set (you) and the more inclusive set (your very first ancestor, more than 3 billion years ago) is enormous! It is, of course, way bigger than 8 (or than 32, if you add all those prefixes). Even if you add uncommon ranks, as Tribe  or Section, you don't get even close to the number of monophyletic groups between you and your oldest ancestor.

As I read some time ago in a phylogenetic systematics paper: "We need names. Lots of names!".

That's why modern taxonomy has a problem with the traditional notion of ranks, some biologists defending that we should drop the ranks altogether (except, of course, the Species). And that's why I was uncomfortable in writing today some paragraphs above: there is an increasingly number of biologists that use phylogenetic nomenclature, which is incompatible with Linnaean taxonomy.

So, to give you an example: Mammalia is a Class. However, Mammalia lies inside a higher group, that we call Synapsida. Synapsida is neither a Class nor an Order nor a Phylum... it does not have a rank. Synapsida, by its turn, lies inside Amniota (animals with amnion), which also doesn't have a rank...

The examples abound: Sauropsida, Eudycots, Opisthokonta, Reptiliomorpha, Viridiplantae etc are all groups without a rank.

Thus, when a biologist says "that organism is an Amniota", she/he is just saying that the given organism belongs to the monophyletic group called Amniota. If you ask him/her "what is Amniota? A Class, an Order, a Superfamily, a Subphylum?", the answer will be: "none of them". Monophyletic groups don't need to have a rank in Phylogenetic Systematics.

Finally, quoting the Taxonomy Help from NCBI:

  The ‘preferred scientific name’ for a taxon may be either formal (e.g. Homo sapiens) or informal (e.g. Homo sp. Altai, or uncultured fungus). Taxa above the species level may also be either formal (e.g. the order Mammalia) or informal (e.g. the unranked node eudicotyledons). (Emphasis mine)

Source: https://www.ncbi.nlm.nih.gov/books/NBK53758/#taxonomyqs.Overview


Isogametes and oogametes I have found the following definitions of different types of gametes:

isogametes: gametes looking and behaving the same;
heterogametes: gametes different in size or in behaviour;
oogametes: gametes different in size and behaviour.

I have some doubts about the exact meaning of behaviour in such definitions. I know that there exist species where gametes of the same mating type can originate a zygote, for ex. in some fungi.
Do differing heterogametes and oogametes always belong to different mating types?
Thank you very much for any clarification!

Allow me to start off with a nice picture showing the differences - note female gametes are on the left while male gametes are on the right in my examples:

Isogametes

For a gamete to be considered an isogamete the other gamete that it meets up with to produce is exactly the same in both size, structure and movement. [2] It is literally trying to find itself. The "male" and "female" are literally no different and it is impossible to tell which is which.

When you look at the picture the two gametes are exactly the same in every way except that they are facing each other in this picture.

The next two are forms of anisogamy:

(source: ulsfmovie.org)

Heterogametes

These gametes differ in at least one of the following:

size
structure
sex

Although it can also be a combination of these three things. [3] As you can see here the female can be structurally the same as the male. (Bottom and top examples of the second picture). From my understanding (although someone can come and prove me wrong) Oogametes are a specific from of heterogamous.

Oogametes

Oogametes differ in size, sex AND function. Females are stationary while males move. [4] Females are also much larger than males. (For instance in humans the cell that divides to make sperm divides equally while the cell that divides in the female divides to make one egg and three polar bodies.)


Why do I get cytosine to guanine/adenine transitions in bisulphite treated sequences? I got my sequencing results (bisulphite treated and non treated sequences of same species Allium cepa) and now I have to do analysis in Cymate online tool. I prepared all sequences as it is written in original Cymate paper (master sequence and clones - aligned in ClustalW, blunt ended).
My problem is that I got gaps in results (image is attached, it is from Cymate Result) on positions 27, 50, 58 etc.

When I looked back at my original alignment FASTA file and compared those positions, I noticed that those gaps are from C to A, or C to G transitions (and obviously Cymate outputs only C to C, and C to T cases).
Does anyone know why do I get those C to A, or C to G, are those some mismatches, should I manually remove it from alignment, or did I made some other mistake?
Any advice from you would be very useful for me!
My FASTA file alignment, which I uploaded to Cymate, is here (if anyone wants to check). First sequence is master sequence (non-treated, orifinal sequence) and the rest are clones (bisulphite treated sequences).

Consensus_cepa__(289_bp)
GAAAGCCAACCACCACATCCGCCATCCCTCACAGTATGCCAACGAGCAGCTGAATGACTCCGAACAACGCAAAGCATGACGCCCAAACCGACGAACACCCAACCGAAAGGCCACAAGCGCAACGTGCATTCCAAAACCCCATGAACCACCGAATCCTGCAATGCACACCACGCTCGACGCCATTCGCTACAGACCACATCGACACGAGCGCCAAGCCATCCATCACCCGAAGCCATCCACCCACTCACAAACATACCACGAAGCACAGCAAATATGAAGACAAACCCTC
MV_A_SP6_izrezani_s_primerima__(295_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAGATAAATAA-TTAAAATAACGCAAAACATAACGCCCAAACAGACGTACTCTCAACCTAATAACCTCGAACGCAACTTACATTCAAAAACTCGATAATTCACGAAATTCTGCAATTCACACCAAA--TATTGCATTTCGCTACGTTCTTCATCGACACGAAAACCAAAATATCCATTGCCAAAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC
MV_B_SP6_izrezani_s_primerima__(295_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAGATAAATAA-TTAAAATGACGCAAAACATAACGCCCAAACAGACGTACTCTCAACCTAATGACCTTGAACGCAACTTACATTCAAAAACTCGATGATTCACGGAATTCTGCAATTCACACCAAA--TATCACATTTCGCTACGTTCTTCATCAACACGAAAACCAAAATATCCATTACCAGAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC
MV_C_SP6_izrezani_s_primerima__(291_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAAATAAATAA-TTAAAATAACGCAAAACATGACACCCAAACAGACATACTCTCAACCTAATAACCTCGAACGCAACTTACATTCAAAAACTCGATAATTCACGGAATTCTGCAATTCACACCAAA--TATCGCATTTCGCTACGTTCTTCATCGACACGAGAACCAAAATATCCATTGCCAGAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC

I quickly aligned your sequences, and as far as I can tell, the answer is that your "consensus" sequence is a poor match for the 3 other sequences:
CLUSTAL format alignment by MAFFT L-INS-i (v7.310)

Consensus_cepa_ gaaagccaaccaccacatccgccatccctcacagtatgccaacgagcagctgaatgactc
MV_A_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtagataaataa-tt
MV_C_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtaaataaataa-tt
MV_B_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtagataaataa-tt
                .***..***.* ************** **********... ** **.*. *.***.* *.

Consensus_cepa_ cgaacaacgcaaagcatgacgcccaaaccgacgaacacccaaccgaaaggccacaagcgc
MV_A_SP6_izreza aaaataacgcaaaacataacgcccaaacagacgtactctcaacctaataacctcgaacgc
MV_C_SP6_izreza aaaataacgcaaaacatgacacccaaacagacatactctcaacctaataacctcgaacgc
MV_B_SP6_izreza aaaatgacgcaaaacataacgcccaaacagacgtactctcaacctaatgaccttgaacgc
                 .**..*******.***.**.******* ***. ** *.***** ** ..** ..*.***

Consensus_cepa_ aacgtgcattccaaaaccccatgaaccaccgaatcctgcaatgcacaccacgctcgacgc
MV_A_SP6_izreza aacttacattcaaaaactcgataattcacgaaattctgcaattcacaccaaatattgcat
MV_C_SP6_izreza aacttacattcaaaaactcgataattcacggaattctgcaattcacaccaaatatcgcat
MV_B_SP6_izreza aacttacattcaaaaactcgatgattcacggaattctgcaattcacaccaaatatcacat
                *** *.***** *****.* **.* .*** .***.******* ******* .. . .*..

Consensus_cepa_ cattcgctacagaccacatcgacacgagcgccaagccatccatcacccgaagccatccac
MV_A_SP6_izreza --ttcgctacgttcttcatcgacacgaaaaccaaaatatccattgccaaaaatcattcag
MV_C_SP6_izreza --ttcgctacgttcttcatcgacacgagaaccaaaatatccattgccagaaatcattcag
MV_B_SP6_izreza --ttcgctacgttcttcatcaacacgaaaaccaaaatatccattaccagaaatcattcag
                  ********.  *. ****.******. .****. .******..** .**..***.**

Consensus_cepa_ ccactcacaaacataccacgaagcacagcaaatatgaagacaaaccctc
MV_A_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
MV_C_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
MV_B_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
                 *.***** .* *** ***.**.**** **** **.* .******..**

I would suggest trying to come up with a different, more appropriate consensus/reference sequence. This one does not appear to be appropriate.
Granted, I have no idea how you came up with this consensus sequence (it certainly is not a consensus of the other sequences you show), and possibly there is something else going on that I am not understanding.
This does not seem to have anything to do with the bisulfite conversion, as the data also include changes that cannot be attributable to bisulfite, gaps, etc.
Knowing more about the whole workflow would help.
UPDATE
Also, while I'm not familiar with the workflow, could such gaps not be related to methylation on the opposite strand? E.g. CGTA-->TACG.
Is there a particular methylation context that you are looking at? CpGs only?
In some cases there is support for weird variants (e.g. consensus is not an outgroup).
If it's sanger data, it's always a good idea to directly inspect traces.


What is the nesting period of the European Turtle Dove in middle to southern Italy? While the breeding period to the north, in Switzerland, seems to be early May until early July, and I have not found any information for the Naples area.

Also, are they likely to nest a second time?

I think it would be difficult to answer except people living around or visiting frequently the Naples region as the bird distribution covers the whole central Europe during summer time.

Then my answer will focus more on the italian part.

One interesting reading would be this document from the European Commission.
Disclaimer: this document refers to biological aspects of the turtle dove, but the main topic is the pressure of the hunt on that bird.

In page 10 they mention that:

  Stable populations are found in central Europe: Italy, Austria, The Czech Republic and Slovenia (BirdLife International 2004a).

Page 14 table shows the period of migration and breeding countries (EU 25 only).

And in page 17, they shows that probably between 200'000 to 400'000 breedings pairs are present in the whole Italy (Estimation by Birdlife International)

Here are some refrences:

Breeding and distribution at IUCN
Distribution at avibase

As you can see the distribution os quite large and the figures of estimated breeding pairs very large.

You can also check the observations (not only breeding) with that avibase link.

For the probability to nest the same place, I would say it's possible as in general the birds can go to the same place as the previous year but I cannot say more if the European Turtle Dove have a different behaviour or not. If they have a quiet place where there are no disturbance (Hunting, human activities) or predators, they would probably come back to the same place.


Is the EC50 of an activating protein for an enzyme a good indicator for the binding affinity Kd? We work with a membrane protein system where measuring the affinity between the enzyme and the upstream activating protein has been difficult, and when measured in detergent solution, it is almost 100 fold lesser (ie ~100nM) whereas the EC50 in an enzymatic assay using vesicles in ~1-2nM. Would it be reasonable to say that the "real" affinity is ~1nM than 100s of nM based on the biochemical assay?

Alternately, is there a documented system where a huge discrepancy exists between measurements from direct binding and biochemical assays?

You can certainly get massive differences between EC50 and affinity. This is especially true for cell-based assays and membrane protein systems.

The reason why is because the appropriate time scales to achieve binding equilibrium (hrs for nM affinity, days for picomolar, feptomolar affinity according to back of the envelope calculations) may be and likely will be different from the appropriate time scales of activation, endocytosis, degradation, etc. Furthermore, you can have avidity effects that would not be apparent in a dilute membrane assay compared to a cell's surface. It could very much be that the dominant terms in mass transport change depending on the geometry and antigen density and while I'm not entirely sure bout vesicles vs. emulsions it is true for cancer models. Theoretical analysis of antibody targeting of tumor spheroids: importance of dosage for penetration, and affinity for retention.

Case study number I: hGH:hGHR interactions have been extensively studied and high affinity hGH have been produced. However, none of the variants showed improved EC50. It turns out that the binding was primarily influenced by the off-rates which were so slow, that affecting those values did little to the kinetics of the system. Growth Hormone Binding Affinity for Its Receptor Surpasses the Requirements for Cellular Activity

Case study number II: CEA-antibodies have been affinity matured to have pM activity compared to the wild-type nM affinity. However, the antibody had minimal effect on tumor uptake. As CEA gets endocytosed on the order of 30 minutes, all of the antibody was simply getting endocytosed rather than acting as an inhibitor. Directed evolution of an anti-carcinoembryonic antigen scFv with a 4-day monovalent dissociation half-time at 37°C.

(edit)
I realized that this answer is more applicable to IC50s vs. the EC50 experiments described above. However, many of the points remains. The Km between a substrate and its enzyme is a thermodynamic property where as the EC50 also has dynamic factors that may influence its measurement.

I would also add that simply adjusting the pH 2 units may result in a 2 orders of magnitude change in activity.

(edit2)
A further point to make about enzymatic assays is that from an observation of Michaelis-Menten kinetics, the KM of the reaction isn't the KD of the enzyme but alternatively the effective binding constant.

Recall that:

If there is a non-trivial kcat comparable to the dissociation rate kr, the enzyme will have an effective half maximal concentration that is significantly higher than the Kd. There are multiple ways how your assay can result in the discrepancies that you're seeing. The first would your strategy in measuring your EC50. If one is an enzymatic readout and the other is a binding readout, you would naturally have very different results.  Alternatively, the enzyme in the detergent system may be catalytically more active than the vesicle system resulting in a higher effective KM. Again, the pH thing.

Finally, there is always that awkward moment when you realized that you might accidentally have measured a titration curve rather than a binding curve.


Crusty eyes in the morning Often, after waking up from a night's sleep hard, flaky, pale yellow crystals are deposited around the eyelids (which easily wash off with water).

What are these? Why are they yellow? What are they made of? Is their amount proportional to the length of sleep?

This is quite common. It is most likely dried rheum (also know by slang terms such as "sleep", "eye boogers", "eye crusties", etc.).

Rheum is the result of dried mucus, tears (and the salt and minerals therein), as well as dead blood and skin cells.

Essentially it is all the stuff that’s normally in your eye that eventually dries up making the contents more condensed giving it a light yellow color. When all that stuff is in your tears it is spread out enough that your tears are still mostly clear.


What's the mixture of carbon and haemoglobin called I know of oxyhaemogloblin , the mixture of oxygen and haemoglobin  , but carbon and haemoglobin combination is what's confusing

I'm going to agree with the comment left by @anongoodnurse and assume you are looking for the terms that define CO2 + hemoglobin and CO + hemoglobin.

CO2 + hemoglobin = Carbaminohemoglobin

CO + hemoglobin = Carboxyhemoglobin


Help me identify the following insect This is my first post in this forum. I found the following insect at my kitchen in my apartment in Kolkata, India. Could you please help me identify the insect.
Thank you.
Best regards,
Saugata

Might be a red palm weevil

Rhynchophorus ferrugineus

https://en.m.wikipedia.org/wiki/Rhynchophorus


Are there multicellular isogamous species? Are there multicellular isogamous species?

Seeking through the examples of wikipedia I would tend to think that there are no multicellular isogamous species.

Our knowledge about the sexual transmission of mitochondria and
  plastids (hereafter organelles) in isogamous eukaryotes comes mostly
  from studies of the yeast Saccharomyces cerevisiae and the green alga
  Chlamydomonas reinhardtii which are both unicellular species. To
  investigate organelle inheritance in a multicellular organism with
  morphological isogamy, we studied the filamentous brown alga
  Ectocarpus siliculosus, in which each gamete contributes one plastid
  and at least one mitochondrion to the zygote. ...

2004 - Inheritance of organelles in artificial hybrids of the isogamous multicellular chromist alga Ectocarpus siliculosus (Phaeophyceae)

So it is possible, but it seems like very rare.


Degenerate Alignment Analysis Can someone please tell me what is Degenerate alignment analysis? Could not find a good article on the internet that could help me understand what it means?
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

First, degeneracy in a basic sense refers to redundancy of the codons in the genetic code.  For example, the amino acid proline is coded for by one of four codons: CCA, CCC, CCG and CCU. The third codon position (the third letter in each group of three) is called four-fold degenerate because it can change without affecting the coding for proline. Phenylalanine is two-fold degenerate because it is coded for by UUC and UUU.

However, this does not account for the alignment part of your question. Without more specific information (such as a reference you saw), I can't be certain of your intent but this paper by Morin et al. (2008) may be helpful. They had a series of small RNA sequences (each about 24 nucleotides long). They wanted to identify DNA sequences in the genome of Lodgepole pine  (Pinus contorta) and rice (Oryiza sativa). To accomplish this goal, they used degeneracy alignment. Here's the relevant section from their methods:

  altered to allow searches against genomic sequence. Alignments were kept if they were no shorter than L − 3, where L is the query sequence length. No more than a total of three mismatches or insertions/deletions were allowed within the aligned region.

Their approach was to find genomic sequences that correspond to the small RNAs. They allowed for some degeneracy, either in the genome or the RNA. The sequences could differ in length by no than three nucleotides or mismatches (an A in the query sequence but a C in the target sequence instead of a T; I'm assuming the query is RNA and the target is the genomic DNA). Their degeneracy alignment allowed for a small amount of freedom in identifying potential matches of conserved RNA clusters (high similarity) in the genomes of distantly related plant species.

  Morin, R.D. et al. 2008. Comparative analysis of the small RNA transcriptomes of Pinus contorta and Oryza sativa. Genome Research 18: 571-584.


What is optical density in Lowry's protein estimation method? I have a few questions:

What is an OD value?
Why do we use blank solution in Lowry's protein estimation method?
If The OD of a protein is 0.01, what does it mean?

Thanks in advance.

The OD measurement is the output of what the photometer measures. It is actually the amount of light which is scattered or absorbed by your sample - scientifically called extinction.
A blank is used to be able to substract the influence of reagents, light that is scattered on the surfaces of the cuvette (which is probably also not completely clean) and so on. Every of this influences reduces the amount of light which should reach the detector on the other side of the probe and give you false extinction readings. If you are using a colored detection sample (which colors deeper or looses color during the reaction) this is more obvious. The solution already has an extinction on its own which is not of interest. So you make a blank (which basically substracts all these influences from you sample reading) to correct for this. How this is done depends on the photometer. Some make a correction reading at the beginning, while others use a second cuvette (a blank cuvette) which is permanently measured.
It means that the protein gives you this extinction. Without a calibration curve (made from serial dilutions with known protein concentrations) it is impossible to make any further comment on this number.


FRET only works for interactions between 1nm to 20nm. FRET only works for interactions between 1nm to 20nm.

How can you be sure that the interaction that you want to study isn't less than 1 nm/greater than 20nm apart?

To get an elaborate answer on this one, I guess you should ask at physics. Very basically, FRET works by that an excited chromophore transfers energy to a nearby chromophore, through dipole-dipole coupling, which in turn emits energy (light) which can be detected. This is a quantum mechanic effect, i.e. these are very small energies. The emission energy between from the donor to the acceptor chromophore is inversely proportional to the distance between to the power of six according to the equation:

Where r is the distance and R0 the Förster distance between the donor/acceptor-pair (distance which the energy transfer efficiency is 50 %).This means that the energy to be detected very rapidly decreases. The Förster distance is in the range 2-10 nm for different chromophore pairs, which leads to the upper limit of FRET use.

The lower limit I don't know if it's due to steric effects or some quantum mechanical effect I do not know about. But since proteins are in the size range of the lower limit they must be in really close vicinity in order for their interaction to be detected using FRET.


Is there any non-pathogenic gram negative bacteria? In the category of Gram-negative bacteria, is there any non-pathogenic species? Is such a list of non-pathogenic gram-negative bacteria's available? Can you give maximum 5 examples of such bacteria which has been proved to be non-pathogenic and is gram-negative?

As Canadianer already mentioned in the comments, the majority of bacteria (this includes gram-negative bacteria) are non-pathogenic.

I think a prime example is the human gut flora. You can find loads of bacterial species living in your gut without doing you any harm, if anything they are doing you a favour by breaking down food.

Here some examples of gram-negative genera:

Bacteroides
Escherichia

Most species within those genera are non-pathogenic, however, there are exceptions.


Change in conditions of an ecosystem lead to change in organisms Let's think about the slash and burn method and its effects on the ecosystem.
Cutting down trees that rise all the way up to the canopy would expose the plants at ground level to more light, so would change an abiotic factor so changes the conditions required for survival. These plants are not adapted to the high light intensity so would find it hard to survive and compete, through inter-species competition, with newly arrived plant species that are much more adapted to the extra light intensity.

Obviously this would cause a dramatic reduction in the numbers of the previous plant species and would result in migration of the animals due to lack of food, assuming they can't feed on the newly arrived plants, and a change in the food chain.

In what ways do this affect the local and regional ecosystem, and what problems could it produce (both from an ecosystem and human perspective)? These types of land-use changes are often seen as problematic in conservation biology (as "...a bad thing"). Wouldn't the new plant species bring in new animals that do feed on them and a new equilibrium be reached just with different species? Is it to do with the reduced biodiversity or danger of extinction of indigenous organisms?

As you have probably realized I don't exactly understand this topic perfectly and would appreciate any amendments or extra information to the paragraphs above.
Thanks in advance.

I will try to provide a general answer, starting point and overview to this question, even though it is rather wide ranging and vague.

The biological process

If we start with your description of the process; you are correct that such a dramatic change in the environment as slash-and-burn agriculture will drastically change the living environments on the canopy floor (well, in the entire ecosystem).

To name a few, there will be changes in:

Light conditions, which will alter the competitive balance between plant species, where ones adapted to a closed canopy will disappear.
Moisture
Temperature (maximum, minimum and variance in temperature)
Nutrients The point of slash-and-burn agriculture is to provide a boost of nutrients for farming. However, the boost is short-lived and transient. Afterwards, you are usually left with a very nutrient poor soil, which is common in tropical forests. Tropical forests (where slash-and-burn is often used) are high in biomass, but most if it is bound in the standing biomass. When this is removed by clear-cutting, the natural cycling of nutrients is disrupted, and excess nutrients are leached out of the soil (Ricklefs, 2001).
Loss of host species This will lead to loss of primary consumers (specialists & generalists) feeding on them, and cascading effects into the ecosystem that depends on these.

All these changes and several others will dramatically modify the niche spaces and the competition between species in the forest patch, and most previous species will probably not be able to persist locally. New species will move in to fill the open niches, and over a (long) period of succession a new quasi-stable community will emerge. Due to the extremely high biodiversity in tropical forests it will almost certainly contain fewer species than the original community.

The question of whether the community will eventually return to its previous state (even if that will take an extremely long time), is a relatively open question, and also depends on the conditions at the specific site and if the spatial scale of the disturbance. The biggest issue for conservation biology is that these land-use changes generally happen at a large scale, so fragmentation of species habitats can lead to regional and even global extinction. Since many tropical species have small ranges and are not adapted to fragmented landscapes, many run the risk of going extinct. Therefore, even if the overall appearance of the original forest will return, it will contain a very different set of species. Land-use changes, even in the form of temporary slash-and-burn agriculture, also generally leads to continued/secondary exploitation of the area and seldom to restoration/regrowth (Meffe & Carroll, 1997).

I also want to point out that you are indirectly referring ("...new equilibrium be reached...") to the idea of a Balance of nature in ecosystems, which is largely seen as obsolete and incorrect. However, as shorthand or when referring to a dynamical equilibrium between multiple populations (with ongoing evolutionary change) it can be meaningful.

The philosophical issue

The question of whether an ecosystem change or extinction of species is "...a bad thing" is inherently philosophical and depends on human judgement. The philosophical foundations for conservation biology can be divided into instrumental values and intrinsic/inherent values. Instrumental values can then be subcategorized as services (pollination, water regulation), goods/resources, information (e.g. genetical info to be used in medical research), and esthetic/spiritual values. Intrinsic values refers to a specific value placed on species, ecosystems or evolutionary history due to its uniqueness and it is seen as independent of human needs and wants (although some argue that values independent of humans are impossible). Intrinsic values are also connected to the acknowledgement that organisms have interests and wants themselves (their own 'good'). Different people naturally weight these issues in different ways, and for some the short-term economical gains will weigh heavier. The long-term economic costs are potentially large, but less certain. From a strict biodiversity perspective (i.e. a species counting perspective), the change will certainly be negative, since the change in land-use will decrease diversity and probably lead to more 'trivial' species moving in. From the perspective of the original ecosystem (if it has a say) the change is per definition negative, since it will disappear.

The direct intrumental value of individual species are usually uncertain (irrespectivly of the direct rationales used), so the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. An example of ecosystem services from tropical environements can be seen in Ricketts (2004). However, sometimes functional diversity is emphasized which focus on preserving functional groups of species instead of 'general' biodiversity (i.e. specific species).


If a dead animal is electrified, will it decay? I was walking past some power lines today, and a flying fox (like a small furry bat, for those who don't know Australian fauna) had grabbed onto two adjacent power lines, completing a circuit, and as such died due to electrocution.

That got me thinking about whether or not the animal would decay in this situation. As far as I understand it, decay is caused by bacteria and other micro-organisms. Could they survive in this high-voltage environment? If not, will this poor flying fox be perfectly preserved until the next blackout occurs?

Environemental factors would degrade it (wind-water etc.).

But from what I know, electricity will follow a certain shortest path inside the body to close the circuit. The rest shouldnt be electrified and bacteria will be alive.

Bacteria are indeed not resistant to high levels of electricity and would die of it. The current would need to traverse the Entirety of the animal to kill every single bacteria which is highly improbable. Leave one alone, it will reproduce fast.

From what I researched, a constant electrical current of the power of an electric line would cook the animal in a short time. The flying fox you saw probably didnt have live current traversing him anymore and died from a quick jolt (this is a guess only).

Even in the extreme case that 100% of the bacteria would die, the dead animal would be recolonized by bacteria really fast. Even in the wires, wind or animals would carry bacteria.

Power lines are probably protected from arcing this way through anything that could touch them. Imagine if they werent, trees touching them would burn, shoes you throw and hang on them would be calcinated etc.

Off-topic: Are you sure he wasn't only sleeping on his improvised power-line hammock ? :P

Sources:

Conduction of Electrical Current to and Through the Human Body: A Review

Effects of high electric fields on microorganisms I. Killing of bacteria and yeasts


Are my plasmids single-stranded? Hi, in this agarose gel photo (70 volts, 3.5uL Gel Red in 30ml of TBE, 1% Agarose, 1 hour run), I've checked the digestion of a large plasmid (15Kbp, one cut site). The theory says that the digested plasmid (linearized) should migrate slower than the supercoiled form of the uncut one (bigger band of the Undigested Plasmid). In my case the digested plasmid is faster than the undigested one.
I've found that my digested plasmid could be single-stranded (http://bitesizebio.com/13524/how-to-identify-supercoils-nicks-and-circles-in-plasmid-preps/). Do you think that could be the case?

You assume that the undigested plasmid is supercoiled, but more probably it is in the relaxed circular form due to single strand nicks. This form migrates slower than linear DNA.


Human evolutionary innovation for rapidly restoring glycogen, and link to cardiovascular disease? I'm a physicist, not a biologist, but I'm interested in human evolution and its link to the physiology of endurance sports. Circa August 2019, I read an article in the newspaper whose contents I'll summarize below from memory. I mentioned this to a colleague who teaches anatomy and physiology, and he said that it sounded not very credible. I told him I'd find the article and send him a link, but I wasn't able to find it again. I'm wondering if anyone can help me find the original scientific paper, or a popularization.

According to this account, humans have a mutation, not present in other primates, so that when we eat, our glycogen stores are replenished quite a bit faster -- maybe by a factor of 2 or something. Of course digestion is complicated, and the speed of digestion depends on the macronutrient and even on the subtype of that macronutrient (e.g., we probably process maltodextrin faster than whole-wheat bread), but for typical foods I think the idea was that a human would rebuild their liver and muscle glycogen reserves in a few hours, as oppose to twice that for other primates.

The article also said that this evolutionary innovation had a cost associated with it -- that it led to an increased susceptibility to certain types of cardiovascular disease, which our close relatives don't get as easily.

Summary

We (Homo genus) used a lot more glycogen as we sweated while we foraged.
Our efficient metabolism allowed us to replete our glycogen stores with seemingly little trade-off.
Those same metabolic genes are associated with obesity risk
Obesity is a risk factor for heart disease

Sweat uses glycogen

...and lots of sweating was beneficial for our species survival

I think what you are indirectly asking about, as unlikely as it seems, is sweat production.

It is known that humans have a large number of eccrine sweat glands compared to other animals, for which glycogen is the primary energy substrate.
The ability to thermally vent via full-body eccrine sweat glands in this way, in conjunction with bipedalism, allowed foraging in the midday heat when predation is low.
This is limited to the genus Homo (Leiberman, 2015), although it is not clear exactly which mutations are responsible as far as I can tell.
Glycogen stores are more supported by their capillaries, and by extension have faster repletion, in primates in hotter drier climates and indeed in humans (Best & Kamilar, 2018).
Now at this point, you are thinking "Aha! More capillaries mean more pressure on the cardiovascular system and more disease".
I cannot find any evidence directly linking those two.

A note on glycogen production differences in our close relatives

The 1,4-alpha-glucan-branching enzyme indeed seems similar across close species.
So either we have relatively larger livers to cope with this, or some complex genetic mechanism produces more of the protein.
A quick BLAST alignment shows the identity of the 1,4-alpha-glucan-branching enzyme of chimpanzee species at >99% and E~0. The top results are shown below:

Entry   Organism    Organism ID Info            Status

Q04446  Homo sapiens (Human)    9606    E-value: 0.0;   Score: 3,814;   Ident.: 100.0%      reviewed
A0A2R9CB94  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
H2QMY2  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
G3SDH8  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,798;   Ident.: 99.4%       unreviewed
A0A096NQ25  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,729;   Ident.: 97.6%       unreviewed
A0A2K6ANP2  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,723;   Ident.: 97.3%       unreviewed
A0A0D9R0S5  Chlorocebus sabaeus (Green monkey) (Cercopithecus sabaeus)  60711   E-value: 0.0;   Score: 3,718;   Ident.: 97.4%       unreviewed
A0A2K5W1V0  Macaca fascicularis (Crab-eating macaque) (Cynomolgus monkey)   9541    E-value: 0.0;   Score: 3,716;   Ident.: 97.2%       unreviewed
A0A2I3GDY3  Nomascus leucogenys (Northern white-cheeked gibbon) (Hylobates leucogenys)  61853   E-value: 0.0;   Score: 3,714;   Ident.: 97.2%       unreviewed
A0A2K5I4Z7  Colobus angolensis palliatus (Peters' Angolan colobus)  336983  E-value: 0.0;   Score: 3,713;   Ident.: 96.7%       unreviewed
A0A1D5R8L3  Macaca mulatta (Rhesus macaque) 9544    E-value: 0.0;   Score: 3,712;   Ident.: 97.2%       unreviewed
A0A2K6KT87  Rhinopithecus bieti (Black snub-nosed monkey) (Pygathrix bieti) 61621   E-value: 0.0;   Score: 3,705;   Ident.: 96.9%       unreviewed
A0A2K6PB45  Rhinopithecus roxellana (Golden snub-nosed monkey) (Pygathrix roxellana)    61622   E-value: 0.0;   Score: 3,699;   Ident.: 96.7%       unreviewed
A0A2R9CB98  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I3T5K0  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I2ZFX5  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,675;   Ident.: 98.8%       unreviewed
A0A2K5QWD9  Cebus capucinus imitator    1737458 E-value: 0.0;   Score: 3,665;   Ident.: 96.0%       unreviewed
A0A2K6SM68  Saimiri boliviensis boliviensis (Bolivian squirrel monkey)  39432   E-value: 0.0;   Score: 3,661;   Ident.: 95.9%       unreviewed
F7FDF1  Callithrix jacchus (White-tufted-ear marmoset)  9483    E-value: 0.0;   Score: 3,627;   Ident.: 96.0%       unreviewed
A0A2K6ANP4  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,610;   Ident.: 95.3%       unreviewed
A0A2I3MXY4  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,607;   Ident.: 96.9%       unreviewed

Although this is only one protein of a multi-protein metabolic pathway, I think there must be something much more complex about how our glycogen is repleted to deal with the higher demand than simple differences in proteins.

Increase metabolism and disease

Humans have benefitted from a "thrifty genotype" when it comes to metabolism (Neel, 1999).
This, and the well-cited 1962 paper it is based on linking our faster metabolism to diabetes (Neel, 1962), may indeed be the paper you are looking for, but in my personal opinion, it is not very quantitative by today's standards and comes from the days before we had access to genomic data.

Although glycogen is only part of the story, it is generally accepted in the community that humans have an optimised metabolism. In terms of disease related to our metabolic evolution, GWAS showed that the genes that allow our increased metabolic activity is linked with obesity risk factors (Castillo et al., 2017).

To link that to your original question, obesity is linked with heart disease according to, well, everyone that has ever looked at it. Here is an NHS link to show it is a principal part of modern healthcare.

It may not be the exact answer you were expecting, so it will be fascinating if other papers corroborate this more directly.

Big brains need a faster metabolism

The scipop article you may have read could be from Science Daily, however this does not mention glycogen. This covers the Pontzer et al., 2016 paper which shows that we have a faster metabolism and this is linked with our brain size compared to our close primate relatives (another angle to the Leiberman 2015 paper discussed below).
The scipop article goes on to talk about research linking this to an increased risk of heart disease, not mentioned in the original Nature article.


How to determine whether the energy of a stem-loop fold is significant or not? If I have a predicted RNA stem-loop of energy -0.30 kcal/mol, and another of -4.9 kcal/mol, how do I tell whether such a structure is a significantly stable structure or not? Our two competing hypotheses are that there is some structure with sufficient energetic stability to fold inside a cell, versus the one that there is not.

You can convert the $\Delta G$ values into equilibrium constants $K$ using the formula

$$ \Delta G = R T \ln K $$

This might help you understand what those energies roughly mean.

But the more important and also more difficult part is judging how good your predicted free energies actually are. I assume you used a secondary structure prediction program like Mfold to calculate this. They typically have a several parameters you can adjust like ion concentrations and temperature, you should make sure that you have some appropriate values here.

Without knowing anything more about your system or data I'd ignore the -0.3 kcal/mole result, the -4.9 kcal/mole structure could be formed, but I wouldn't regard this as certain.

Now, in the in vivo situation the whole thing gets far more complicated. The presence of RNA binding proteins, helicases and the generally rather complex environment in the cell makes it much harder to predict which secondary structures will actually form.

If you wanted to know for sure you could e.g. do SHAPE experiments on your RNA. This is a technique that also works in vivo.


Flower identification (England, late May) I took this photo near Stratford upon Avon by the side of a road. Can anyone identify this flower?

MY guess would be Centranthus ruber coccineus, also known as red valerian. See this picture (from here):


Why does the hydrolysis of ATP increasing entropy increase the Phosphoryl-‐transfer Potential? I am currently taking a biology class. I do not understand this concept. I understand that the electrostatic repulsion of the negative charges, resonance stabilization and hydration stabilization all contribute. However, I do not understand why an increase in entropy would help. Wouldn't it be more favorable to have less entropy in a system?

The phosphoryl transfer potential is one way to think about the free energy available to do useful work when ATP is hydrolysed.
As you can see from the free energy equation below, a positive change in entropy will help to decrease (i.e. make more negative) the free energy change.
This is why an endothermic reaction can still occur spontaneously if the entropy change is big enough to create an entropy term that outweighs the enthalpy term in the Gibbs free energy equation.

ΔG=ΔH - TΔS
where:
T= temperature
G = Gibbs free energy
H = enthalpy
S = entropy


Why are human children more likely to get lice (nits) than adults? By my own experience, lice seems to be prevalent in the hair of human children, but not in adults.

My question is Why are human children more likely to get lice than adults?

Assumptions:

Can be referred to lice/louse/nits

Children generally don't care about their hair as much as adults do. So unless parents insist, they don't care for their hair as much (reference). Kids generally get lice because they are in close contact with each other during play-dates, slumber parties, and sports activities. They are also prone to exchange hair brushes and other personal items more often than adults (reference).

An interesting difference I came across between articles is that one article says that its

  theoretically possible to get infested if your hair makes contact with
  items such as hats, combs, or brushes (reference).

Another article insists that

  You’re extremely unlikely to get head lice by sharing hats, combs or
  pillows – a louse’s lifespan is very short once it’s removed from your
  head (reference).

Between the two, I believe that it is extremely likely that lice would spread if you use a infected hairbrush immediately after it was used by someone harboring the parasite since the time span is short.


Blebbistatin effect on vesicles Blebbistatin is a drug that specifically inhibits the assembly of myosin in the cytoskeleton. What effect would you expect blebbistatin to have on intracellular vesicles?

The formation of vesicles would cease.
The movement of vesicles within the cell would cease.
The vesicle membranes would fail and release their contents into the cytoplasm.
The vesicles would be unable to fuse with the plasma membrane.

I don't readily see how Blebbistatin would effect intracellular vesicles; I believe this ignorance comes from not knowing what myosin is and how it interacts in the cytoskeleton.

Blebbistatin inhibits myosin II by blocking it's attachment with actin. Myosin II and other actin based motors have shown to be involved in vesicle budding from trans golgi network. Given this information, I think correct answer will be

  The formation of vesicles would cease.

Following cartoon from (Stow et al 1998) shows proposed mechanism,

However looking at this paper, option (2) The movement of vesicles within the cell would cease, also sounds reasonable.


Does night sleep provide more energy-regain than sleep during the day? After reading this, I know that sleeping is an universal function, and that basically everything with a brain has the need to sleep.

However, I am still confused to what extent it is necessary to sleep at night to regain energy, or if some rest during the day provides a sufficient energy-regain?

I think the reason is primarily, that it is more quiet (the chance is very low that other people are disturbing your sleep) in the night as well as it is also dark. Keeping in mind, that the brain "gets tired" due to some proteins (melatonin) and in contrast, being more awake during the day, it seems to be just logical that the sleep in the night is healthier, thus providing more energy.


What happens when we re-start a PCR reaction? Recently when my PCR reaction was running there was power fluctuation and the entire lab was blacked out for a few minutes and unfortunately PCR that I was running got switched off. So, would it be okay to restart the PCR? What would happen if the same PCR program was run again?

The polymerase used in PCR is extremely stable at room temperature. I would expect you to be able to continue your PCR reaction from the cycle it was stopped at without too much trouble. However, it is important to not over cycle your product. This will produce non-specific products. If a clean result is imperative, take a 1-5ul sample from your original reaction to use as a template in a new reaction.


To understand Second messenger signalling in I/c and E/c I found this picture in my study materials.
I think it is too schematic and ignores the big pictures.

I think the thing connected to the hormone is receptor.
The second messanger is then connected to the receptor which stimulates the effector cell in the cytosol.
The cell then response both to cytosol and to extracellular space.
How do you understand this picture?

Do you know any similar pictures which present the same thing but clearer and more exactly?

I think the schematic you have there and the one that @Masi posted are pretty good.  A better way of getting a grasp of intercellular signaling would be to study a specific hormone and understand how each of the elements in the block diagrams here could vary.

For instance take a look at this diagram from a journal article where they are tinkering with yeast mating factor, one of the first discovered extracellular signaling pathways.

alpha factor and 'ligand' (I assume its not known at this point) bind to their receptors Ste2 and hGPCR respectively.  They then activate G protein complexes and both activate the same kinase cascade Ste4/18 -> Cdc42 -> Ste20 -> MEKK/MEK/MAPK/Ste5 which then may activate Far1 (or not) and Ste12.  Far1 and Ste12 are migrated into the nucleus to activate genes for cell reproduction.

By actually filling out the boxes in your diagram you can see dozens of different paradigms for how cell signaling may work, and why the diagram you have needs to be so simple.  Hope this helps.


Rescue cell lines function I'm reading in a paper in which the authors have made three cell lines to study the function of a gene of interest (Mbd3):

The one is knocked out for the gene of interest [Mbd3 -/-], the other is floxed for the one allele [Mbd3 fl/-], and the third is rescued knock out cell line [Mbd3 -/- (rescued)], that means that in the cell line of knocked out cells they have stably transfected a plasmid expressing the gene of interest. I am then wondering, why they use this rescue cell line, instead of using the wild type cells with the wildtype alleles of Mdb3?

Rescue experiments are the gold-standard for confirming that an effect is due to the gene of interest.

Removing a gene may have off-target effects but if you can return function to 'normal' by supplementing the gene back into the cell-line/animal then this is strong evidence that the gene and its product are the cause of effects that are seen in the experiment.

Wild-type cells would normally be included to show what 'normal' response  is.


What were the camels' humps good for back in the polar areas? I've heard that camels lived in the North America formerly and just in the last few thousands years they've migrated to the hot deserts. Thus they allegedly utilized the adaptations against the cold weather in the tropics.

One of this adaptations have been their humps. Clearly, it is useful not to have a thick fat layer all over your body in the hot weather. (I see it like a neural spine sail (which helps with thermoregulation to the desert fauna).) But how about the polar areas? All the other polar animals don't see to be restricted by the fact they save all the fat under their skin in any way.

So what were the original reason for the evolution of the camels' humps?

In my opinion there might be two reasons why the camel hump (rather than bump) might be one of the adequate adaptations of camels to living in the cold (additional to their flat feet giving hold on both snow and sand and tooth structure, Rybczynski et al., 2012). Both match the humps being fat storages in modern camels.

The first is also provided by Rybczynski et al. (2012):

  Their iconic hump(s), containing fat, also may have been adaptive. As seen in high-latitude ungulates today (Parker et al., 2009), fat deposits could have been
  critically important for allowing populations to survive and reproduce in harsh climates characterized by 6-month long, cold, winters.

Note that this refers to the nutritional value of the fat deposits and does not necessarily relate to maintaining body temperature.

The difference to modern camels would be that the fat storage in modern-day camels serves indirect water deposition (water can be easily gained from the fat stored in the humps and storing the water condensed in fat molecules is way more efficient than storing water directly). This relates to the second reason which, however, is more speculative from my part.

Cold - especially in plants - also implies drought as frozen water is not available. This does not need to apply to mammals as they can thaw ice, e.g. by licking. However, this might be critical as the body might lose some temperature during that process. Accordingly, fat storage might already then have been a means to storing water while keeping body temperature.

Alternatively, and maybe even more likely, the camel hump might have undergone a switch in function from storing a food source in archaic camels to storing water in modern camels as both can be achieved with fat deposits due to the chemical properties of fat.


Detecting Introns and Exons I know that when RNA is transcribed from the original strand of DNA it contains introns and exons, and that the introns are spliced out of the strand to provide genetic diversity. However, what I don't understand is, how does whatever is doing this splicing know whether the section it is reading is an intron or an exon? Are there start and stop codes like there are for polypeptides, or is it determined by epigenetic factors like methyl markers? Or is it neither?

Quick answer: we don't really know.
As WYSIWYG said, splice sites do have a sequence signature. The image below (taken from [1]) shows the consensus for human acceptor and donor sites:

In the images above, the size of a nucleotide represents its frequency at that location. As you can see, there is a clear signal around the splice sites and this signal is used by various programs that do splice site prediction. What is not quite clear yet is how the cell recognizes these signals. Sometimes a "perfect" (identical to the consensus) splice site is ignored by the cell in preference to one that we would consider "worse". This is further complicated by the presence of various downstream and upstream signals such as splicing enhancers, silencers and structural elements (loops, hairpins etc) in the mRNA molecule.
So, to answer your question yes there are start/end markers for introns/exons but they are far more complex than the simple START and STOP codons of transcription. We know know a lot about it but we still don't fully understand the details of splicing.

References
Brent MR, Guigó R., Recent advances in gene structure prediction, Curr Opin Struct Biol. 2004 Jun;14(3):264-72.


Do "transcription factor binding site" and "operator" mean the same thing? Can the terms "transcription factor binding site" and "operator" be used interchangeably in all contexts when referring to a DNA sequence, e.g. regardless of a cell type, whether or not the binding sequence is synthetic or natural etc.? If not, what are the differences?

As you no doubt know, the term operator was coined by Jacob and Monod as part of the formalism they developed to explain the properties of certain mutants in the lac operon in E. coli. In physical terms it is indeed the site of binding of a transcription factor, the lac repressor.

My understanding is that technically it is best to restrict the use of this terminology to bacterial systems in which the idea of an operon is useful. I don't think it would be wise to extend it to cover any site in eukaryotic DNA where a transcription factor is shown to bind.


Need help distinguishing between a primary and secondary source I am trying to figure out if the following article is a primary or secondary source.

I'm leaning towards secondary but here are my cases for both.

  Primary: Published in a peer-reviewed journal.

  Secondary: It seems to be mostly a summary of other works so it might
  not be original research.

Can anyone confirm this for me? Thank you!

Too long for a comment: Although this is a review article which summarizes the findings of other researchers, considers this as a primary article. The author gives you all the resources he used in the reference section of this article and summarises their finding. Additionally, review articles in renowned journals (and Genome Research is definitely such a journal) are peer-reviewed. Primary vs. secondary sources would be more the comparision of research articles and news articles. In my observation, news articles hardly ever name the sources or the original articles about which they report. Plus they sometimes have problems of getting the message wrong.


Deviation from Hardy Weinberg equilibrium (HWE) I have a set of 10 genes, each gene contains around 15 SNPs. I have tested the deviation from Hardy Weinberg equilibrium (HWE) for all SNPs. All of the SNPs didn't deviate from HWE, except 5 SNPs in ABCG8, they had p<0.05. I have found different factors that can affect the HWE. My question: Why for the rest of the SNPs met the HWE, why only 5 SNPs in ABCG8 deviate largely from HWE?

A significance test (i.e., p-value) allows us to reject the null hypothesis, but not to confirm it. In other words, when $p<0.05$ one can say that the conditions for HWE are not met, however $p>0.05$ does not mean that HWE holds - the conditions might still not be met, but we cannot prove it. Thus, by making statements such as All of the SNPs didn't deviate from HWE and the rest of the SNPs met the HWE one may be committing Type II statistical error.
As @MaximilianPress correctly pointed out, in this case one should not be making any statements about the SNPs with $p<0.05$ either, due to the high possibility of False discovery. Indeed, a p-value gives us the probability that the data would be at least as extreme as was observed, even though the null hypothesis is true. Given $N=150$ SNPs one expects about $$N\times\alpha = 150 \times 0.05= 7.5$$ statistically significant outcomes to occur by chance, even if the HWE holds. That is, one could be also committing the Type I error of rejecting the null hypothesis, when it is true. To exclude this error one needs to use a more stringent test, e.g., Bonferroni correction, i.e., testing against the significance level $N$ times smaller than the current $\alpha=0.05$:
$$
\alpha\longrightarrow\frac{\alpha}{N}=\frac{0.05}{150}\approx 0.0003
$$


Mathematical model for malaria The simplest malaria model is as follows:
$$\frac{dI}{dt} = \frac{\alpha \beta I}{\alpha I + r} (1-I) - \mu I$$

where $r$ is the natural death rate of mosquitoes, $\mu$ is the death rate of humans, $\beta$ is the transmission rate from infected mosquitoes to susceptible humans, and $\alpha$ is the transmission rate from humans to mosquitoes. However, for $I \ge 1$, $dI/dt$ is negative. Wouldn't that imply that the infected class is always shrinking from the start? How does this make sense?

I am afraid you may have to read your textbook more closely. The question on page 29 states that this equation models the proportion of infected humans. If $I$  $≥1$ that would mean that there are more people are infected than there are people in total - e.g. 3/2 of people are infected - this clearly doesn't make sense.

Thus $1≥I$ when using this model.


Do endosymbiotic organelles have Latin classification? Do endosymbiotic organelles such as chloroplasts or mitochondria have Latin classification?

As any other organelle, endosymbiotic organelles do not have a systematic name. However, their descendant prokaryotic organisms do have a genus name.


What does it mean to use DMSO as a dissolvant in biology experiemnts? In many biology publications, I saw that dimethyl sulfoxide (DMSO) is used to dissolve drugs. However, the cell-based assays are still performed in water-based medium such as RPMI or PBS.

My question is: If a compound is not soluble in water, what is the purpose of using DMSO? Although the drug can be dissolved in pure DMSO, won't it precipitate after putting the DMSO-dissolved compound into culture medium?

Usually such compounds are dissolved in DMSO to make a concentrated stock solution (e.g. 1000x), which is then diluted into the culture medium. Often, the compound is soluble in water at this lower dilution, but not at the higher concentration required to make a stock. Sometimes the compound has low solubility in water and much of it precipitates. This still lets us test the effect of the fraction that remains soluble.


Why does the HPV vaccine not work on already infected people? With my limited knowledge, I understand that the vaccine works by inserting fake HPV-like material in the body, thus inducing the immune system to build up defenses against it, so when the body is exposed to real HPV on the wild the immune system will be able to handle it.

That makes sense, however, why can't the body still build up the defenses when there was already an exposure? Specially when the HPV virus is "dormant" and undetectable.

EDIT: After the discussion with @Bob in the comments section below, the hypothesis is:

  In an infected person whose immune system was able to clear the acute
  infection, the virus (single infected cells) is constantly trying to
  enter lytic cycle again, only to be defeated by the immune system
  (because one infected cell leaving dormant state alone might not be
  effective); and then when the immune system is compromised for some
  reason, the virus is successful into entering lytic cycle and then
  there is a new clinical infection.

  If this is all truth, then the answer to the question is that the vaccine
  does "work" in the sense that the body still reacts correctly (by responding to the antigen)
  to it, but it is, in practice, useless because: 1) when the virus is
  dormant there isn't anything for the immune system to do; 2) when the
  virus strikes, the immune system was already exposed to it anyway, so
  it is generally able to fight and there is no need for the vaccine; 3)
  the infection will get clinical again only when the immune system is,
  for some reason, defective.

  The whole point of the vaccine is to never let the virus infect many (or any?) cell in order to avoid this situation where it is always trying to come back - and will do, when the immune system can't fight it off for some reason.

Please, if some specialist can analyze and comment on that it will be awesome.

More questions around it:

Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"?
How does the cell replication process impacts the 1) hypothesis? (Maybe it is not possible for the immune system to achieve a natural cure because the virus keeps constantly replicating.)
How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?
If the virus acts locally, is it possible for the vaccine to help other still-not-infected sites? In other words: is the natural immune response from the first infection in, say, the anus, worth anything for a subsequent infection in, for example, the oropharynx?

This is an excellent question, and it is actually being studied -- but for a different reason than your question suggests. HPV is a bit unique because there is some data showing that infected individuals can become "reinfected" with the same virus type, causing reactivation of the dormant/latent virus that they are already infected with. So the question in this case is whether administering an HPV vaccine to an already infected individual can help prevent (or minimize) reactivation of the latent virus.

Here's a journal article explaining some of this research. Please note that it is not standard medical practice to give HPV vaccine to already infected individuals. This work is still in the research phase, and is aimed at minimizing viral reinfection and reactivation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006803/

Simply put, a vaccine only works to prevent infection with a specific virus. It is rarely effective in treating a virus once a person has become infected. The reason for this has to do with how the immune system responds to its first encounter and subsequent encounters with a particular virus:

When the body encounters a specific virus for the first time, the immune system mounts a "primary" immune response specific to that virus. A primary immune response triggers the body to produce virus-specific immune cells that can generate antibodies against that virus. The body continues to make these immune cells in small quantities even after the virus is eliminated.

If the same virus is encountered again later, these cells will proliferate and immediately start producing antibodies against the virus. Thus, the body can mount a much faster and stronger "secondary" immune response. This prevents the viral load from reaching levels that produce physical symptoms, so the person does not become sick (or at most they may have milder symptoms), and the immune system is to able eliminate the virus more quickly.

The purpose of a vaccine is to trigger a primary immune response. With a vaccine, the body is exposed to a weakened form of the virus, and a primary immune response is triggered without the individual becoming sick. When the individual encounters the real virus, the body immediately mounts a secondary immune response, which fights off the virus much more efficiently and quickly, and the person typically has no physical symptoms.

Here's a more in-depth explanation on the difference between a "primary" and "secondary" immune response. Most cell biology textbooks (and all immunology textbooks) will have an explanation of this as well. This is an important concept in understanding how vaccines work:
http://www.microbiologynotes.com/differences-between-primary-and-secondary-immune-response/

If a non-vaccinated person is infected with a virus, administering a vaccine generally has no effect. At that point the body is already mounting a primary immune response, so a vaccine would serve no purpose. Because a primary immune response is slower than a secondary response, when a non-vaccinated person gets infected the viral load is able to increase more rapidly than it would in a vaccinated individual, resulting in the physical symptoms typical for that particular virus.

What makes "chronic" viruses such as HPV and Herpes virus (including chicken pox) harder to eliminate completely is that these viruses enter a dormant/latent (lysogenic) phase. At that point they become "invisible" to the immune system. Even if the person is not visibly sick, they are still infected with the virus. If/when the active (lytic) phase is triggered, the viral load increases rapidly -- more rapidly than if it were a new viral infection. The body still mounts a secondary immune response, but typically this will not completely eradicate the virus. As long as any amount of the virus is in the lysogenic phase, it remains "invisible" to the immune system.

With some viruses (e.g., chicken pox virus, which causes shingles) if a vaccine is administered during the latent phase, this can help somewhat with making symptoms milder if/when the lytic stage is ever triggered. But this doesn't work for all viruses.

If a targeted antiviral medication is available (e.g., Tamiflu for influenza; Harvoni for Hepatitis C) this can slow down the proliferation of the virus, allowing the immune system to "catch up" and eliminate the virus. Antiviral medications aren't vaccines. They are designed to directly target the virus and interfere with a biochemical activity that the virus needs in order to proliferate.

Currently there is no antiviral medication available for HPV, although a few drugs are being researched. One drug in particular (ranpirnase) looks promising, but it is still in early clinical trials.


Single long axon vs serial neurons Based on the comments in this post and also this chat. For discussions and speculations please comment in the chat.

The basic question is what is the advantage of having a single long axon such as that of sciatic nerve (~1m) compared to a series of neurons?

The primary advantage is surely the conduction speed which will get affected because of chemical synapses. However, gap junction synapses can reduce that delay. The larger volume of the soma of the post synaptic neuron may also reduce the conduction speed, but signal strengthening can also happen. Cell architecture can be adjusted to minimize the loss of speed.

The obvious disadvantage of having a single large cell is that there would be tremendous burden on the nucleus for the cellular maintenance. There would be delays in transfer of non-electrical signals such as biomolecules from axon termini to soma and vice versa. Long axons also means continuous transport along them which in turn demands large number of molecular motors and therefore ATP. Moreover, a small injury can disable the entire conduction channel. It can be imagined that this trait (long axons) can also be selected against; injury leading to inability to move and thereby causing perishment.

EDIT (Based on comments to Anne's answer)

Time is of course a valid advantage for having a single axon as an information conduction channel. However, the energy or the maintenance cost is the factor that I am actually interested in. Maintenance cost would increase with cell volume (in fact surface area) and having serial neurons would demand more energy (cumulative) than a single axon (including costs of maintaining a nucleus). However a long cell would need much higher number of molecular motors to maintain the traffic flow rate. All responses that require transcriptional control would be slow (such as response to injury). Moreover a single soma also imposes a limit on the number of mitochondria. There should be a limit on how long an axon can be. I am especially interested in case of big animals (with long hindlimbs) that also have a good reflex (perhaps camels, even horses).

Has someone tried to analyse the tradeoffs of having a long axon vs series of neurons connected by gap junctions? If not is this problem worth modeling or quite trivial?

Saw this in Quora:

  My first thought mostly agreed with the question details, except I'm
  pretty sure that the dorsal root ganglion (DRG) has a longer axon than
  the motor information carried in the sciatic nerve (which is the
  longest nerve in the body, but not axon).

Does this mean that sciatic nerve has serial neurons?

First, I must clarify that a nerve is not the same as a neuron. A nerve is a collection of axons (with each axon a part of an individual neuron) in the peripheral nervous system. Thus, when you mention “single long axon such as the sciatic nerve”, this is technically an incorrect phrase as the sciatic nerve is a collection of many long axons. If one of these axons is nonfunctional, this would not severely affect the function of the entire sciatic nerve. However, you are right that if the entire sciatic nerve is severed, then there would be serious consequences downstream.

Second, the primary advantage of conduction velocity is less dependent on length and more dependent on presence and degree of myelination (directly proportional to fiber diameter) and presence of nodes of Ranvier.

With regards to the content of your question, the advantage of length is exactly what one might think--- greater distance. The sciatic nerve is the longest nerve in the body in order for our nervous system to innervate as far as the tip of our toes. Having hundreds of side-by-side series of neurons compared to hundreds of side-by-side axons seems like a far less efficient system in a couple of ways in exactly the two ways you mention: energy and time.

Energy: Having serial neurons would require an increase the number of neurons needed to transmit a message. Having more neurons requires more Na+, K+ and Na/K pumps and individual channels, requiring more energy.

Time: Having serial neurons would also require an increase in the number of synapses between neurons— either electrical or chemical. If the synapses are chemical, then time is increased many-many fold. If the synapses are electrical, then time is slightly increased by 10-fold per synapse compared to chemical synapses, but this would still take more time compared to having a single axon with myelination and nodes of Ranvier which by about 100-fold faster than a single electrical synapse.

In summary, having longer nerves made up of axons rather than serial neurons is beneficial by improving energy and time efficiency, which allows our bodies to effectively innervate structures farther away.

Ref:

Regarding delay of conduction: Chemical v. Electrical/Gap  Ch 10 of Principles of Neuroscience- "Synaptic Integration in the Central Nervous System" (Siegelbaum,
Kandel, Yuste) 5th ed. McGraw-Hill Medical, c2013.
Regarding conduction velocity of myelinated versus nonmyelinated
cells

Regarding the ATPase absolute number increase in serial vs one long axon, I assume this will depend on the number of neurons in series. However, I read this paper, which says that increased length between each node of Ranvier has been physiologically associated with increased conduction velocity. This suggests fewer needed nodes, despite concentrated ATPases at these locations, and thus fewer ATPases. I haven't been able to find studies which compare ATPase concentration in the soma compared to nodes of Ranvier within axons.

Regarding energy use in soma vs axon, mitochondria are not only made in the soma but are concentrated in pre- and post-synaptic membranes (and growth cones). The more of these structures there are (as in serial neurons), the more presumed mitochondria. See mitochondria and neuronal activity.

Finally, my literature search could not find studies which showed longest possible energetically feasible length for myelinated or unmyelinated neurons.


Which grows slower: the thumb nail or the pinky nail? I notice that thumb nails and pinky nails grow slower than the 3 other fingers in the middle. But which one is slower, the thumb nail or the pinky nail?

I did some research and found out that it is actually the pinky that grows the slowest. See the decadal reports of Bean on fingernail growth or:

Gupta, Gita Rani, et al. "Human nail growth pattern and medicolegal aspect." (2005).


Why have humans evolved conciousness? Why did humans/animals evolve to become self-aware of their own thoughts.  That is, why don't humans act and compute like a machine, or walking zombie.  In my mind, such creatures would still be as smart and equally capable of surviving, the only difference being they don't experience the phenomenon of self-awareness. (To understand my question think: unconsciously sleep walking)

There have been many proposals over the years as to why human consciousness has emerged and how, or even what it is.

Most of us will not be surprised to know that there is no consensus about an answer here.  Its hard to draw a trend from a single example.

Here is a little survey of the one's I've heard.

We are intelligent because we have opposable thumbs and can use tools, which evolved our brains.  This is an old one - maybe as old as Darwin's time.  I think its mostly ignored now because so many animals - including pandas and other non primates have opposable thumbs or use tools or both.  (monkeys and chimps use tools, and recently crows have also been observed to use tools.)
brain size.  We do have a large brain to body size ratio.  There are other animals with similar ratios and they don't have internets.
We are 'self-aware'.  That is to say we recognize ourselves as an individual.  It was proven that other primates can recognize themselves in mirrors (putting a red dot on their forehead. when they see their reflection, they touch their own forehead).  So that's not exclusive either.  its not a bad idea, but so far it doesn't seem to make the
'We ate something' I once read a discussion of how humans might have ingested psychotropic plants or fungi.  As you can see, this was 2010.  Its not the worst idea, but its hard to prove.  Lots of experiments on cats since the '60s have not produced cat's who care to tell us if they are intelligent.  Maybe they are just too smart in the first place.

These theories, from when I was a student are so discounted now, you can't find too much record of anymore since they were pre-internet and also they seem so unlikely now.

More modern theories have locked onto social configurations of human societies which drive intelligent adaptations.  This is stemming from observations that human evolution (the rate at which genetic variants are retained in the gene pool) are accelerating since humans have become social.

These new theories while standing on some amazing evidence are still feeling around in the dark - stuff about how social interactions have created a preference for intelligence-like traits. There is probably something to that - once intelligence gets a toehold it is a clear advantage.  But how did it show up only once and why us? I think that's the hard part that science has, for the moment, given a rest.


Numbers in the names of tumor markers In tumor markers such as CA 125, CA 19-9 and many other, CA stands for Carcinoma antigen, but what about the number?

There are dozens of cell marker genes. The number refers to antigen protein from one of those specific genes. The number itself can be a result of any of a variety of things, from the order in which the protein was discovered to the corresponding antibody being the 125th antibody produced against the cell line or organism. These are often used as biomarkers of various cancers. CA-125, for example, is sometimes found at high levels on the surface of blood cells in women with ovarian cancer.


Meaning of the word Oleracea What does "oleracea", as appears in numerous plant species (scientific) names, mean? Examples: Euterpa oleracea, Brassica oleracea, Portulaca oleracea, Acmella oleracea, Spilanthes oleracea.

It means "vegetable".
I think it's because people use those plants for food