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Is there an RGB equivalent for smells?
Millions of colors in the visible spectrum can be generated by mixing red, green and blue - the RGB color system. Is there a basic set of smells that, when mixed, can yield all, or nearly all detectable smells ?

It would be so cool if this could be used in video games. Like if the player walks into this room, make the smell equal to $x$. But I think we have to wait a long time until this becomes possible haha.

Not an answer, but instead of and RGB style system (with 200 receptors) some of the more experimental systems mix common sents to get a new smell. There are a few "sents" that make up a large selection of artificial smells in our food an fragrances.

Actually, RGB can't reproduce the entire visible spectrum. If you're curious, read up on the color triangle. The mind-blowing thing for me is that how the primary colors were chosen is somewhat arbitrary, but they do correspond to where each type of cone (we have three types) is most responsive.

The question was whether there is a combination of basic smells that, when combined, would allow us to experience the equivalent of a 'smell rainbow'.  i don't think anyone has answered this yet

It's probably also worth mentioning that there's no consistent theory for what smell actually is - i.e. alternatives like vibration theory which describe things shape theory can't (but vice-versa is also true). Once it's known how it actually works then it can be broken down into its basic components and categorized into the resulting "human perception spectrum" like RGB does for light.

in a way, the answer to your question is 'we have no idea' - it is tempting to imagine, but our sense of smell is much more personalized than our visual system and, across individuals there is really minimal similarity in activity in the piriform cortex (for instance) where odors are interpreted after initial decoding, compared to the visual cortex.

@Kevin you make me nostalgic. Back in 2001 (I was 10 then) computer magazines were crazy over scent reproduction for movies, web perfume catalogs, web tours (click a door, wait 10 seconds to download, repeat). I remember them noting that audiovisual storytelling will elicit desired reactions (mountains evoke awe) but smells wont (rotten wood may evoke nostalgia instead of the intended disgust). Here is a link from those times: https://www.wired.com/1999/11/digiscent/

There are about 100 (Purves, 2001) to 400 (Zozulya et al., 2001) functional olfactory receptors in man. While the total tally of olfactory receptor genes exceeds 1000, more than half of them are inactive pseudogenes. The combined activity of the expressed functional receptors accounts for the number of distinct odors that can be discriminated by the human olfactory system, which is estimated to be about 10,000 (Purves, 2001).
Different receptors are sensitive to subsets of chemicals that define a “tuning curve.” Depending on the particular olfactory receptor molecules they contain, some olfactory receptor neurons exhibit marked selectivity to particular chemical stimuli, whereas others are activated by a number of different odorant molecules. In addition, olfactory receptor neurons can exhibit different thresholds for a particular odorant. How these olfactory responses encode a specific odorant is a complex issue that is unlikely to be explained at the level of the primary neurons (Purves, 2001).
So in a way, the answer to your question is yes, as there are approximately 100 to 400 olfactory receptors. Just like the photoreceptors in the visual system, each sensory neuron in the olfactory epithelium in the nose expresses only a single receptor gene (Kimball). In the visual system for color vision there are just three (red, green and blue cones - RGB) types of sensory neurons, so it's a bit more complicated in olfaction.
References
- Purves et al, Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Zozulya et al., Genome Biol (2001); 2(6): research0018.1–0018.12
Sources
- Kimball's Biology Pages

It's fascinating. Are there people who can approximately evaluate the 200-parameter RGB smell counterpart? Do dogs have more than 200 or is their smell superiority caused by something else?

@LubošMotl - Dogs have higher sensitivity, i.e., more receptors in terms of sheer numbers. Their olfactory spectrum is not so different than ours afaik

Thanks! Maybe they're less pretentious, too. I think that if a man weren't feeling painful, he could smell quite some details about many things and other people, too. ;-)

Also, dogs get a lot more practice, starting from a very young age. Though it turns out humans aren't too bad at it if they really try. Read Surely you're joking Mr Feynman for details.

@LubošMotl AliceD's second paragraph alludes to the fact that the olfactory responses don't have a great correspondence to the chemical structure... There are certainly variations in odor sensitivity and discrimination between people, but it isn't at all clear that the 200 "smell motifs" have any particular meaning individually. This seems like a difference from RGB where there is a perception of the individual colors, but maybe not: for example, it seems silly from a perceptual standpoint to say that white is "more red" than black, though this is clear in RGB or physical terms.

i think the idea of a base set of odorants, like red green and blue, is flawed, although this is a nice summary of how olfaction works

@dblyons - Overmind's answer below seems supportive too

The information in Purves is significantly out of data with the fields current literature. The olfactory code has still not been worked out, though it is likely combinatorial. There is also extinguishing effects. After a certain point, ORs are taken off the surface of the OSN, and the ability to detect that volatile chemical diminishes.

@AMR - long time no see! yes of course there's adaptation; just as in the visual system. The senses are complicated.

Can those inactive pseudogenes be used to send information over smells?!? No I don't believe in government conspiracies, why do you ask?

If there are $100$ kinds of receptors there should at least $2^{100}$ distinguishable scents. How can there only be $10000$?

There are many, many more parameters than 200! As an example, look at the nomenclature system for olfactory receptors (ORnXm).

"OR" is the root name (Olfactory Receptor superfamily)
n = an integer representing a family (e.g., 1-56) whose members have greater than 40% sequence identity,
X = a single letter (A, B, C, ...) denoting a subfamily (>60% sequence identity),
m = an integer representing an individual family member (isoform)

Members belonging to the same subfamily of olfactory receptors (>60% sequence identity) are likely to recognize structurally similar odorant molecules.
So, if we have 56 families, and each family has 26 possible subfamilies that can each detect a specific range of molecules, then you have a 1456-characters "alphabet" to describe all possible smells. Now humans will have more or less of each type, some types will not be there but be present in dogs, etc... Now if you take any actual smell (complex molecules with multiple odorants), it will be represented by any number of specific receptors going on at the same time. So if we set a limit of 100 receptors activated simultaneously per whiff (imaginary, no idea what the real number is), there are 1456^100 possible combinations of receptor activations for any 100-odorants smell.
References:
Glusman G, Bahar A, Sharon D, Pilpel Y, White J, Lancet D (November 2000). "The olfactory receptor gene superfamily: data mining, classification, and nomenclature". Mammalian Genome. 11 (11): 1016–23. doi:10.1007/s003350010196. PMID 11063259.
Malnic B, Godfrey PA, Buck LB (February 2004). "The human olfactory receptor gene family". Proceedings of the National Academy of Sciences of the United States of America. 101 (8): 2584–9. Bibcode:2004PNAS..101.2584M. doi:10.1073/pnas.0307882100. PMC 356993Freely accessible. PMID 14983052.
Glusman G, Yanai I, Rubin I, Lancet D (May 2001). "The complete human olfactory subgenome". Genome Research. 11 (5): 685–702. doi:10.1101/gr.171001. PMID 11337468.

This seriously needs a reference or two.

I added three...

Having the possibility to name such a big number of genes in a family doesn't actually mean, that there are so many genes. Your first reference tells us that there are 330 human olfactory receptors (rather than 1456), so please read these references.

If you re-read the answer, it is clear that the 1456 is a maximum. I was not limiting the answer to humans either. If there are 26 possible subfamilies, the number is 1456. Even if humans only have 330 receptors, what is important is how many different families and subfamilies are they distributed into. Just as an exercise, let's say those 330 receptors are part of 330 subfamilies (1 of each). Let's say a typical smell has ~20 odorant molecules. That is 330 ^ 20 possible combinations of receptor activation.

Most of the olfactory genes are pseudogenes.

Nonetheless, I have updated my numbers in my answer. Thanks. +1

This seems to be addressing how many smells there can be, rather than how many axes. Compare: with RGB, there are three axes, but we often encode colors using a level from 0 (black) to 255 (very bright) on each axis, giving 256^3 colors. By comparison, you are saying one way to think of smell is as a 330-axis thing with only levels 0 (not present) and 1 (present), which would give 2^330 possible smells, but then constrained so that at most 20 axes are 1 at a time, which reduces the space to 330 choose 20 (not quite as big as your 330^20). But that doesn't mean there are 330 choose 20 axes!

@DanielWagner - indeed, man can discern millions of colors

Where is your evidence that there are 26 possible subfamilies - from the 26 letters in the alphabet? I'm terribly sorry, but biology doesn't work that way.

@AliceD The ability of man to discern millions of colors is a bit dependent on circumstance... The studies that report people can determine millions of colors are really talking about contrast sensitivity. The number goes way way down if you would instead present colors sequentially. Even the paint colors in a hardware store can't be reliably distinguished when they aren't held together.

Yes, it certainly is. But I cannot guarantee that all have been properly determined.
For that, we would have to find the basic unique values (like the Red, Green and Blue in the case of colors).
Currently, we have 10 unique human detectable smells:
The wood-like smell, the floral/fragrant one, non-citrus, chemical, sharp(garlic-like), sweet, menthol, peanut-like, lemon and decay/dead-like (those are labeled by researchers as W1 to W10). A reference of the 10.
The your RGB-like-values for smell should be something like that.


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Are there parts of DNA that do not have genes?
A question in my genetics class is "Are the number of genes proportional to the genome size?"
The answer is "no," and is it because the genome is the entirety of all the DNA in an organism, but that there are some segments of DNA that don't have genes on them?  Can someone explain this?  Thank you!

there are many parts of DNA that are not genes - these are things like enhancer sequences or other regulatory coding regions that are not expressed... where have you looked for this answer?

Most the genome is not coding for proteins. Here is a pie chart of what the human genome is made of

As you can see, only 1.5% of the human genome codes for proteins. The term gene is often a bit vaguely defined but if we assume that a gene is all the exons, all the introns and all the regulatory sequences, then 25.5% of the human genome are genes. So, yes many "parts of the genome" do not contain genes.
Now, it is worth highlighting that there is a very high correlation between the genome size and the number of protein-coding genes among lineages. Consider the below graph based on data from NCBI genome reports and styled after Koonin (2011).

There is a high correlation but there are also important outliers. See for example the eukaryotes (green dots) at the bottom right of the graph (probably mainly polyploid plants) that have very big genomes but relatively few protein-coding genes.
So, even though there is a strong correlation, it was quite obvious to me that the answer your teacher was expecting was no, because most of the genome is not coding and despite an existing correlation between genome size and number of genes among lineages there exists species with a very high density of genes and others with a very low density of genes in their genome.

Please add citations/sources for your images.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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How is color information transmitted from the eye to the brain via the optic nerve?
I would presume that is has something to do with synapses and specific chemicals starting specific charges through the optical nerve's sub-components, and that this is somehow interpreted by the brain to configure an actual image; but in all honesty I have no idea.
The eye is obviously quite complex, and as I am not massively associated with all the terminology yet, I would be grateful for an answer in layman's terms.

Color vision in layman's terms:
The eyes contain a photosensitive layer much like a digital camera called the retina. In the center of this layer is a 3 mm-wide spot called the fovea that contains high densities of photosensitive cells, called the cones. Cones are photon hungry and operate only in bright light (photopic vision). They are called cones because of their conical shape. Rods are abundant in the periphery and mediate gray-scale night vision (scotopic vision).
The cones in the fovea are present in three types: red, green and blue cones - hence they convey color images much like digital pictures, namely as a bunch of pixels with a mixture of red, green and blue.
The cones in the retina are the first nerve cells (called neurons) in a long chain of neurons. The cones are hence called primary neurons. They connect to secondary neurons, namely the retinal ganglion cells (RGCs). These cells have long protrusions called axons. These axons bundle together to form the optic nerve. Each cone in the fovea connects to one RGC. The optic nerve extends from the retina to the brain. Information is sent through the optic nerve in the form of electrical pulses, just like a photosensitive chip operates in a camera. The information from the optic nerve eventually reaches the primary visual cortex in the brain, also referred to as V1 or striate cortex (Fig. 1).
In the visual cortex, there is a retinotopic map, meaning that a topographic representation exists in the brain that matches the retinal image. In other words, images are projected faithfully on the brain's surface as neuronal activity. The brain's job is to process these images further and generate conscious perceptions out of them; we see with the brain, not the eyes (a famous quote from Bach-y-Rita).

Fig. 1. The visual system. source: IEEE
References
- Kolb et al., Webvision. The Organization of the Retina and Visual System. Utah University
- Purves et al., Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001

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Creating BLAST database with nucleotide "place holder"
I have a set of nucleotide sequences that contain some special characters with multiple meanings:

H -> C, A or T
K -> G or T
M -> C or A
R -> G or A
S -> C or G
W -> A or T
Y -> c or T

I would like to create a BLAST database with that sequences.
The "place holders" seem to be a known vocabulary (at least for the query sequence).
It is also possible to create a database (using makeblastdb), with sequences containing the "place holder" characters. However, the characters are always recognized as mismatch.
Is there a way to tell BLAST recognizing the characters above as match if the query sequence fits?
If not, I could imagine to "expand" all combinations for each sequences by replacing the "place holder" with it's concrete nucleotide, but that may grow up the database... Or is there another solution to face that problem?

There is no such option. You would have to edit BLAST source code.

I had thought so, thanks for confirming! Modifying the sources would be an option of course, but to much effort for me. Just for interest, is there a public repository for the BLAST sources? I didn't find one (only the downloadable zip package).


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Do two hormones have the same effect on a cell if the second messenger is the same?
There are so many hormones/cytokines/neurotransmitters and receptors, all of which act through about 4-5 second-messenger systems. So if one particular cell has receptors for say, two different hormones which act via the same second messenger, is there any way that the cell can distinguish the two stimuli? I’m guessing there must be some distinguish between the two, otherwise, wouldn’t the effect of both the hormones be the same?
For example, in a hepatocyte, beta-adrenergic receptors and glucagon receptors both act via Gs-coupled receptors, downstream of which, cAMP is increased. Since the cAMP is the same, the changes it would make are also the same. So does it to the hepatocyte, make no difference if the first messenger was epinephrine or glucagon?
I’m assuming the receptors would make a difference, but aren’t the coupled G-proteins (Gs) also the same? Is there a difference of amplitude?
Note: I understand that it is not necessary for the hormones to produce an exclusively different effect. I also understand that systemic effects can be different because of differential distribution of receptors. My question pertains to the effects on a single cell.

Technically, yes. But signalling molecules/receptors often elicit multiple responses.

Thanks @wysiwig could you pls give an example?

Here is some further discussion on the question https://www.reddit.com/r/Biochemistry/comments/5pig7x/do_two_hormones_have_the_same_effect_on_a_cell_if/

Sorry. I just forgot. I'm a bit occupied right now. Will get back. Ping me if I forget again.

@WYSIWYG the reditt thread I started is good.. but could you give a referenced answer? Thanks :)

Perhaps an interesting read with an example is the following: https://www.ncbi.nlm.nih.gov/pubmed/24365330
Two ligands (LH and hCG) binding the exact same receptor, yet differing in their actions. Part of the difference is mediated via the second messenger they share (cAMP).

I have edited the post. Please note the term is "second messenger", not "secondary messenger". These have different linguistic implications. Suffice it to say that a second messenger is not secondary, it is integral to the response which consists of 1-2-3 (or more).

Secondary signaling molecules like cAMP, Calcium, and Ras-Raf are common in many pathways and I think its a way of integrating different signals.We cannot say that at a moment only one pathway operates in a cell or a single pathway will be enough for a process to happen.I think common second messengers is a resource and time-saving method adapted by our system to coordinate different response efficiently.https://www.nature.com/scitable/topicpage/cell-signaling-14047077
Then how a cell can identify which pathway and process should go on? I think that each time this second messenger will make a small change in choosing down stream effectors.Like Calcium binds to calmodulin which in turn choose next binding partner.Maybe the number of second messengers like concentration and affinity decide which downstream effector will be appropriate for the required stimuli.You can see in this link about how different secondary messengers make different results https://www.ncbi.nlm.nih.gov/books/NBK9870/
About GPCR, more than 800 GPCR are there and you can see from this link http://jcs.biologists.org/content/116/24/4867
So, Do two hormones have the same effect on a cell if the second messenger is the same?
I think yes, see this table (https://www.ncbi.nlm.nih.gov/books/NBK21705/)

Here, from the table, you can see adrenaline and glucagon are having the same effect in the liver cell and both have cAMP as a second messenger.But in cardiac muscle and intestine, adrenaline is having a different function. So I think it depends on the cell also.

So is your answer to the poster’s question Yes or No? And why exactly?

I think yes, for details you can see my edited answer.Thank you


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Can epigenetic structures carry a trait?
Can epigenetic structures cause a trait to manifest in a person if the trait is not already in the DNA? In all my readings I have yet to find a definitive statement that it is impossible.

I'm not an expert on this and it's really complicated, so I'd rather not give an answer. But take a look at research on transgenerational epigenetic inheritance TEI. By chance I read the abstract of a paper today that might be of interest for you as well. Rawlik et al. conclude that differences in DNA methylation patterns in humans are mainly driven by genetic differences in cis - so the differences is actually 'DNA-driven'.

Yes, epigenetic changes does affect the phenotype. This is here the whole interest behind epigenetic. Environmental variation (incl. parental care) affect epigenetics which in turn affect the phenotype (incl. behaviour) of an individual. It is pretty much clear from the wikipedia definition of epigenetics

Epigenetics studies stably heritable traits (or "phenotypes") that cannot be explained by changes in DNA sequence.

The term "phenotype" (or "phenotypic") is actually present 3 times is the first small paragraph of the wikipedia article.
For example, you can read here on wikipedia an example of a study showing that maternal care affect epigenetic variations which in turn affects stress level later in life as measured by HPA.

Please forgive my ignorance, but is the quote you cite equal to "Epigenetics studies stably heritable traits that cannot be explained by DNA"?

Replace "DNA" by "DNA sequence" or "amino-acid sequence" and you're good. The term epigenetics is typically poorly defined but most often we are thinking of methylation occuring directly on the DNA (hence the importance of saying "DNA sequence" and not just "DNA") or on histone tails. The definition as presented might also make some people in the field of niche construction unhappy but this is a story for another time. You should have a look at this post for more information


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How do you call "pocoya" bird in English?
I am translating a Spanish book and I have here a bird named in Spanish "pocoya", about which I know the following:
1) it flies at night
2) it makes sounds that allow to confuse it with an injured animal
3) it lives in Nicaragua or at least lived several centuries ago.
My own research brought me here: https://en.wikipedia.org/wiki/Pauraque and here: https://en.wikipedia.org/wiki/Ocellated_poorwill.
I don't know which one of them it could be, nor how it could be in English (the first article doesn't have an English version) when spoken (my indigenous people can't use Latin names, for sure...)
Thank you in advance for your  quick response!

I have done some reading based on your descriptors of the bird and your examples, the bird in question is a nightjar and I think they are referring to the Common Paruaque. All nightjars fit your first 2 points, the 3rd point is the only clue we can use to determine what species of nightjar you are describing. There are 11 species of nightjar is Nicaragua.
It seems the Common Pauraque (Nyctidromus albicollis) is commonly known as the "Pocoyo" in spanish, but the spelling may not been certain. Here's a quote from page 9 of an article on the birds of Nicaragua from 1957:
"The species is known in Nicaragua as “Pocoyo” (exact spelling uncertain)".
Reference.
The other bird you describe, the Ocellated Poorwill (Nyctiphrynus ocellatus) is referred to as the "Pocoyo ocelado".
The only other nightjar that might be called Pocoya is the Common Nighthawk (Chordeiles minor), but it is referred to as "Anapero".
I believe when referring to "Pocoya" it is most likely the Common Pauraque as the Ocellated Poorwill would have another descriptive word in it's name in spanish.

Les Beletskys' ecotravellers wildlife guide to Costa Rica says the Spanish name of the Pauraque is 'Tapacaminos Común', probably because it often rests at the road. They also say it is extremely common in Costa Rica and the most abundant caprimulgid of Central America.

Thank you! Yes, my doubt primarily raised from the fact that initially in the description of Nyctidromus albicollis I found that it barely flies. After that, when I discovered pocoya, I assumed pocoyo and pocoya should be two different, distinct names, and happily decided pocoyo will be Nyctiphrynus ocellatus while pocoya is Nyctidromus albicollis. https://vianica.com/sp/animales/aves/chotacabras-y-estaqueros/127


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Are brassica oleracea cultivars the same species?
I used to think Brassica oleracea cultivars (e.g., kale, cabbage) were different species originating from the same species Brassica oleracea.
But it seems I were wrong, right?
If so can we breed two different cultivars with each other, e.g., cabbage + cauliflower?

Cultivars are, per definition, the same species of plants. Animal breeds are the same species too, think of the bewildering phenotypical variety of dogs for example; they are still the same species, i.e., Canis lupus.
To your question - Yes, cabbage, broccoli, cauliflower, and Brussels sprouts are the same species.
Hybrids of these plants are called cultivars; broccoli and cauliflower yields broccoflower for example. However, I wasn't able to find evidence of a hybrid between cabbage and cauliflower - a cabbaflower?

These are the same species. There are people working on new cultivars. This species can also cross with some of the other brassicas - search for 'The Triangle of U' for further information on interspecific hybrids in this group.


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Is a set of chromosomes made up of many copies of DNA, or is one complete string of DNA broken up into one set of chromosomes?
I know technically the question isn't really accurate but hopefully it gives the essence of what I'm trying to ask.
By the way I was taught in school, I was under the impression that a chromosome was made out of multiple complete copies of DNA. But, what I'm reading online makes it sound like a single complete string of DNA is broken up into sections and those sections are wound into chromosomes (so that one complete set of chromosomes would make up one complete string of DNA).
I'm assuming neither are 100% correct, but could someone explain it in a way that I can understand?

please cite what you are reading online

I agree with @tyto-alba, but over generations the separation can break down. Crossing-over occurs, even between the Y and X chromosome, duplications of chromosomes occur, crossing over between unusual chromosome pairs occurs, horizontal gene transfer/between species gene transfer occurs, etc. The genome is never fused as one entity, save for in prokaryotes, but chromosomes aren't perfectly isolated.

A chromosome is one long molecule of double-stranded DNA.  As a diploid organism, you (almost certainly) have two copies of each autosomal chromosome; one from your father, one from your mother.  You (almost certainly) inherited one copy of the X chromosome from your mother, and you either have a second one from your father, or you inherited a smaller Y chromosome instead.

Is a set of chromosomes made up of many copies of DNA?

Yes, 23 different chromosomes (discrete ds DNA molecules) form a set of the pair in human beings.

Or is one complete string of DNA broken up into one set of chromosomes?

No. No such string of DNA with all the chromosomal materials fused together exist in any stage of a cell's life.
When a cell in not dividing  it has 46 discrete ds DNA molecules.
Here's a karyotype of human male:

From: wellcomeimages.org

For this answer it might be useful to understand the different "stages" of genetic information.
The very root of genetic information is DNA. A section of DNA makes up a single gene. Genes are physically represented by loci (points) on a chromosome. What's more, chromosomes can fall into two categories: allosomes and autosomes. The former are what determines your gender, they contain all of the genetic data required to form the various proteins to eventually build your reproductive organs. The latter is everything else: your hair colour, eye colour, specific enzymes, etc are all made here.
This is useful to this question because it means that each chromosome contains sperate genes to control set functions. Thus, each chromosome is part of the same set of DNA - in the sense of the same genome (the complete genetic code in a given organism).
It would then be logical to arrive to the result that, in terms of your question, chromosomes are part of the same DNA "chain". One structure cut into chunks, if you will.
Hope that helps.
EDIT: My reference is: Genetics By, B. Guttman, A. Griffiths, D. Suzuki and T. Cullis.
EDIT: Please bear in mind that each chromosome is itself it's own module.

Very interesting! I always assumed that DNA was one long strand. I didn't know that it doesn't exist as one entity, but rather is broken up into chromosomes. And I assume the entire DNA (I guess the correct term would be "genome"?) comprises all the chromosomes and the mitochondria (I think)?

Good, I am glad! Yes genome would be the correct term. No. Whist chromosomes make up your genetic information, mitochondria are actually ancient bacteria that formed a biotymbiotic (both parties gain value from the following action) with a human cell, as ATP (energy) is formed by the mitochondria and the cell provides other necessities for the bacteria (mitochondria). So the mitochondria remains in the human. The bacteria has its own genome and is thus separate from our DNA.

-1: I'm sorry but this is just too inaccurate. To focus on the most glaring mistake, chromosomes are most certainly not part of the same DNA chain! Each of them is a distinct molecule.

That is correct, in the sense that they are completely separate from one another as distinct entities, but they are still ultimately part of the same genome, of which I think is a suitable answer the question he is asking. They are certainly not copies of the same DNA if that is the answer you are supporting.

I completely agree with @terdon. Chromosomes are not part of the same "DNA chain". You are implying that eukaryotic multi-chromosomal DNA somehow has a "natural state" where you can connect all the chromosomes together, if you wish. A genome is not a "chain" - it is composed of individual, separate elements (chromosomes), which exist independently - you cannot just splice them together and expect them to work in the same way. Telomeres are one reason, the issue of multiple centromeres and what happens during mitosis (independent assortment) is another.

MattSMo, yes I understand that. But I used the word 'chain' (with quotation marks to show that it wasn't really the correct term) to convey the idea that his second suggestion in the question itself was the correct one of the two. I apologize if my wording seemed inaccurate, for this is my first answer so I this feedback on board. I think I was just trying to convey my meaning in a way much more related to the context of the question - I didn't want to go information overboard.

Your second assumption is right. Dna is broken into various parts and then arranged into sets of chromosomes


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How does CpG island methylation lead to gene silencing?
I see often the blanket statement that CpG island methylation can lead to gene silencing.  However, I have been unable to find a straightforward explanation of the mechanism by this.
Is it a purely physical block of binding for transcription factors?  Does the methylation create a tertiary structure that is compacting the DNA?  Does it recruit histone modification factors that compact the chromatin?
Please feel free to cite literature so I can go read the papers.

CG methylation has long been associated with gene silencing due to the generally negative correlation between gene promoter methylation and transcription levels.
When CG methylation occurs in the promoter or enhancer region of animals (where these 'CpG islands' tend to be), methylation seems to impede (to some extent) transcription factor (TF) binding.  That is the baseline mechanism for gene repression.  The altered chemical properties of the DNA make it less favorable binding site for its cognate TF.
In some cases, methylation clearly prevents TF binding.  For instance, some TFs bind DNA to block methylation, which facilitates access of another TF or set of TFs to the bound DNA (for instance, this paper by the Schubeler lab about NRF1).  In the case of other TFs, their binding is less reliant on methylation state, possibly due to the strength and breadth of the binding site (for instance this work from the John Stam. lab about CTCF).
Methylation also can affect nucleosome positioning and stability in some contexts; the nucleosome effects are poorly understood currently  because nucleosomes and methylation likely feedback on one another.  See this work from the Zilberman lab for an example.
The role of a higher-order repressive structure forming is arguably not obvious yet; for instance, histone H1 bining does not appear to be heavily influenced by methylation state (although this is somewhat contentious because there is often a positive but weak correlation at repressed elements in the genome between H1 and methylation--for instance just pubmed 'h1 chip' with reviews and read a recent one).  More certain is the relative change in location of methylated promoters within the nucleus to a place of transcriptional 'silence' (inactivity).  These repositioning phenomena are under intense investigation; you can learn more about this by googling for 'nuclear topology and gene repression' or something like that.
hope this helps


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Why are most fishes vertical?
Why do most fishes have a "vertical" body shape instead of a "flat" one ?
Here "vertical" means that the body(from a front view) is roughly orthogonal to the horizontal plane, and a "flat" body shape means something like a frog's or a bird's with spreading wings.
PS: This question was raised when I was thinking how I can swim faster.

Is you question really why is the fish's mass usually distributed into a truck-like shape (rather than into a tank-like shape) or whether they move their fins perpendicular to the direction of gravity?

It is about body shape or mass distribution.

I suspect it has a lot to do with the efficient arrangement  of muscles for propulsion.  The typical fish undulates from side to side, so considering leverage &c, a body that's deeper than it's wide probably works better. Wider fish like rays & anglerfish either use a different propulsion mechanism, or are sedentary.  Whales & dolphins move their flukes vertically, and AFAIK are always more round than tall.

While the most popular image of a fish for many is as you say, a more "vertical" than horizontal body shape, however there are many different adaptations to body shape depending upon the lifestyle of the fish. An ultimate example would be the flat fishes, such as flounder and halibut, which lay on one side essentially flat on the ocean floor or other similar surface. These fish however have adapted to have both eyes on one lateral side. There do exist other fish, such as some angler fish, especially in the family Lophiidae, which are more wide than tall, and they sit on the ocean floor and use a lure like appendage to attract prey so that they can ambush it, using their fins more to walk along the bottom surface. The feeding/hunting style is also highly related to the body shape of a fish, some shapes are more suited for moderate constant speeds, while others are suited for short quick bursts. Generally though, flat fish are not well suited for swimming at the middle of the water column, giving them a smaller habitat in which to live, while the more commonly found fish body shapes are used by much more species throughout the water column.
More information from MEER:
More information regarding Fish locomotion on Wikipedia.

Rays are flat too. Cetaceans also are broad and they are decent swimmers.

The flat fishes seem to be to be sort of an extreme example of a "vertical" body orientation, at least in that their developmental dorsal-ventral axis is the long way, it's just that they live on their sides. Rays of course are quite the opposite.

I think we can all agree that cetaceans are not fish, but their body shapes and locomotion patterns are worth looking at. Unlike most fish, cetaceans use their horizontal caudal fins in an up and down movement, whereas most use their vertical caudal fins for a lateral to lateral movement. I agree that flatfish are an extreme example, however monkfish are a different example, although they are quite sedentary and their fins have developed more to propel them along bottom surfaces like feet than they are adapted for swimming.

The link talks about the balance of stability and speed. I assume the most hydrodynamic shape (eels) is the best for speed so how does the tall shape help the stability? I'd guess "gravitational" stability (the ability to balance gravity) is what we talking about here.

Some fish are built for short rapid movements while some are able sustain fast movements for long periods of time, like tuna. Gravity is not a factor in the sea, but buoyancy is. However buoyancy is controlled with a swim bladder in most fish. Here stability refers to a fish's ability to make angular turns and resist opposing currents etc.

Swimming below the water surface, when you can tune your body density to obtain neutral buoyancy (as fish do), the axis of the swimming motion with respect to vertical is indifferent.
And indeed, there is a very wide variety of orientations of body plan for fish, from the vertical axis dominated body plans and motions (e.g. bream) to the more horizontal body with vertical swimming axis (e.g. monkfish) of mixed motion (e.g. many rays) and down to flatfish. The evolutionary constraints are thus rather on other advantages awarded by specific body plans (e.g. camouflage, angle of vision,...)


text:
Is the human eye supposed to see the lense effect?
Just as the GoPro cameras, we need lenses to be able to focus. Nevertheless, we can see the "fisheye effect" on the shots taken by GoPros. I am talking about this:

Is it possible to notice the "fish eye effect"? Or does the brain somehow eliminate this distortion?
[EDIT:]
My insufficient knowledge of optics tells me that, as we have lenses in our eyes, we should see the worlds through a thicker layer of mass in the middle of our field of vision, and through a thinner layer of mass on the margins of our field of vision. We know that our vision is reversed when it enters the eye. Is it inflated in the middle as well?
Is there any "distortion" in the proportions of different parts of the image (that is filtered-out at brain), or the does the image formed in retina have the proportions of different parts same as the actual scene?

Human eyes do not have the same optical properties as fish-eye lenses. As should be plain from your everyday experiences using your sense of vision, we do not see a fish-eye effect.

@MattDMo ...because the brain "filters" this effect out?

Why would the effect be there in the first place?

@AliceD Because we watch the world through lenses and there is a thinner layer of glass in the middle than on the margins.

Probably the OP is asking if there any 'distortion' in the proportions of different parts of the image (that is filtered-out at brain), or the image formed in retina have the proportions of different parts same as the actual scene.

@WYSIWYG Could you please move this question to Cognitive science?

@MattDMo We also don't see our "blind spot," nor do we see the world upside down.  It's also hard to notice depth of field.  But we know all these things must exist because our eyes are physical optical systems.  The OP's question is a good one to ask, and I'd also like to know how the distortion (which is guaranteed to exist) gets filtered out.


text:
Do Osteichthyes fishes have any cartilage?
Higher vertebrates, such as mammals, birds, reptiles and amphibians have both bone and cartilage.
But do Osteichthyes fish (Bony fish) have any cartilage? Or do they only have bones?
I've searched the web but I could not find anything helpful.

Yes, Osteichthyes do have cartilage. For example, Ancient origin of lubricated joints in bony vertebrates shows images of cartilaginous tissue in the joints of several bony fish.  More generally, cartilage is required for normal bone development, and Osteichthyes are no exception (e.g. Distinct patterns of notochord mineralization in zebrafish coincide with the localization of Osteocalcin isoform 1 during early vertebral centra formation).


text:
What's this spring-like structure in the plant parenchyma cell?
I observed a transverse section of an amaranth stem in biology lesson today. When I boost the magnification to 600X, I found this spring-like structure in one of the parenchyma cells near a vascular bundle. I could only find one of these in the section. Can anyone tell what structure is it?

It looks like a part of a xylem cell (particularly vessel). Take a look at pics in wiki article. Another good example is here on pic. 36. Possibly you have dragged a part of it during cutting. So it is presumably not a part of parenchyma cell.

I came here to ask the same question. Thanks for the answer and links!


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What is the speed of blood in when flows through the fingertip?
What is the average speed of blood as it flows through the index finger on the right hand?

The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters. You are asking a seemingly specific question but with almost no details, like if I asked "what is the average speed of a person?" Well, do you mean their average max running speed? Their day-averaged velocity including walking, sleeping, driving? Average of all people or just adults? As-is, your question is far too broad.

@BryanKrause I'm asking for use in a heart rate detection application which detects the heart rate based on the user's fingertip pressed against the camera. I'm not knowledgeable about veins and such.

@BryanKrause because of that, which of those blood vessels would directly impact what I'm doing?

Why do you think velocity is important for that?

@BryanKrause my algorithm is slightly different than other ones out there, because it attempts to find the user's blood speed as well. That's why I'm asking.

I see - interesting approach, but I just don't see any meaningful interpretation of the blood speed in that context, because it will vary greatly, even within individual vessels. You can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.

@BryanKrause I'm not actually using this speed value to estimate the volume; rather, I've already built an algorithm that can do that, and I'm merely looking for an average blood speed value I can use to compare to see if my algorithm is accurate.

How do you plan to convert speed (distance/time) to volume/time?

This reference gives about 10-20cm/s in the major arteries and 5 cm/s in the major veins of the index finger in 5 male subjects, though there was a lot of variation.
The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters.
Because it will vary greatly, even within individual vessels, you can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.


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If a mother had a child with her own son, could a paternity test yield positive result for the son's father?
Let's imagine a family composed of Mr A and Mrs B, who have a son named John.
Now, if for whatever twisted reason, John had a child with Mrs B, could a paternity test yield positive result for Mr A ?
Since John's genes all come from Mr A and Mrs B, the child's genes would all come originally from Mr A and Mrs B as well. Thus it seems to me like the test could suggest Mr A is the father of the child.
Or would there definetly be some "red flags" that suggest something wrong happened ?
Like, for example, if the child is a girl, that would mean both of her X chromosomes originally came from Mrs A (since John's X chromosome comes from his mother, as for all males), possibly even the same chromosome twice.
Let's consider that only Mr. A is tested, and not John. Would the child be considered genetically close enough to Mr. A that a test could attest that he is probably the child's father, granting there is no other test showing someone else as a much more likely candidate ?

Let's approach some different methods of distinguishing parents:
1: The Y chromosome. These are passed down from father to son. Therefore, if the baby is male, its Y chromosome will be the same as John's and his father's - it will be indistinguishable who it's from.
2: The X chromosome. A male baby always has one of the mother's X chromosomes. A female baby always has its father's X and one of the mother's X. A male baby of John and Mrs B would always end up with one of Mrs B's X chromosomes, meaning that this can't distinguish the father. A female baby would have two X chromosomes from Mrs B (because John's own X came from her), proving that it is the product of incest.
3: Mitochondrial DNA. mtDNA is passed on from mothers to their children, never from the father. Therefore regardless of whether John or Mr A is the father, the baby would have Mrs B's mtDNA - not useful.
4: DNA fingerprint. This is primarily based on stretches of the human genome that contain repeats of short DNA sequences (so-called STR/short tandem repeats, or VNTR/variable number tandem repeats). In both cases, the sequence is the same in individuals, but the number of repeats is extremely variable and each human therefore has a (possibly) unique combination across the different repeat locations in the genome. Because children inherit 50% of their DNA sequences from the father and 50% from the mother, John himself will have his mother's characteristic lengths in 50% of repeat locations and his father's in the remaining 50% of locations (roughly). A child of John and Mrs B would have MrA's repeat lengths in 25% of locations and Mrs B's in 75%. The fractions "100% Mr A" vs. "50% Mr A" vs. "25% Mr A" can be distinguished by this method.

Sorry to answer a really old question but I've been researching this exact topic and this post often appears near the top of search engine results, and I think it could use some more info; the top answer does a great job outlining the technical factors at play, but it neglects to consider a couple of practical factors that will affect the outcome of paternity testing in the real world. I am going to assume we are using commercial paternity testing services widely available to the general public, and not a service that is specifically more precise.

Because only Mr. A is being tested and not John, there is a significant possibility that commercial paternity testing services will return a "false positive" for Mr. A being the father. These testing services have articles specifically mentioning scenarios just like this one, sans mention of incest. According to these articles, it is not unthinkably uncommon for two potential fathers to be closely related, i.e. brothers or father and son. Quote: "When the two potential fathers share a father and son relationship, it must be mentioned to the testing facility beforehand, as failing to mention this might result in a high false-positive result." The ubiquity of this kind of disclaimer across articles from multiple different paternity testing services suggests that false positives in scenarios like this one are not only possible, but especially likely if the testing service is not made aware of any of the broader context.

What are the chances that Mrs. B participates in the test? This reduces the likelihood of a false-positive scenario. Quote: "[...] your best chance of receiving an accurate result lies in both parties agreeing to take the test. But in this case, the likelihood of success further increases if the mother agrees to undergo a test as well, which will help isolate the genetics of the offspring to an easier degree." So even if John does not participate at all, if Mrs. B participates, it will reduce the chances of a false-positive scenario. For most commercial paternity testing services, the participation of the mother is an optional feature offered at additional cost for greater certainty. Greater certainty would only be required if there was reason to doubt the results of a standard paternity test, so in a scenario that makes the fewest assumptions, Mrs. B does not participate, leaving increased probability of a false-positive.

This is probably the biggest factor overall — will the paternity testers be specifically told anything that might indicate the situation is non-standard? Or will it just be a blind test of "Is Mr. A likely the father of Mrs. B's latest child?" Even if the testing service is not advised of specific details like the possibility of incest, if any questions of the test's potential validity are raised, they are highly likely to ask for additional samples, if for no other reason than to upsell you — these are commercial services after all.

In summary, for a real world commercial paternity testing scenario, it appears to be a numbers game that's difficult to predict; if the test really is just a DNA sample of Mr. A and the child with no additional context, then yes, there is a strong possibility that a testing service will determine it's "close enough" and send back a "positive" result. They quite literally admit this. The likelihood of that outcome depends on the policies of the testing service and the personal standards of the personnel doing the testing (and, lets be honest, whether their lunch break is about to start!) whether a "close" result like this one would be considered "close enough" to send back positive, or whether it warranted a closer look and/or request for additional samples.
Sources:

Home DNA Direct
DNA Center
Easy-DNA

No, Mr. A would not be flagged the father.
This is becasue when a parental test is done they look to what genes have the mother, the father and the baby. First they look at what genes has the mother and the baby. The one missing should be from the father.
In this case it could be possible that for example:
Mr. A: 1 gene Red hair, gene Blond hair.
Mrs. B: gene Brown hair, gene Black hair.
John: gene Brown hair (from his mother), gene Blond hair (from his father).
If the baby has: gene Black hair (from mother) and gene Brown hair (from John. Then that would prove the hair color is not from mr. A. He doesn't have those genes.  So he isn't the father.

This answer is technically inaccurate. DNA testing doesn't work like this.

@anongoodnurse, you say it doesn't work like this, downvotes my post, and then you forget to post how it is done yet... Why don't post how it is done then? It is very easy to say 'You are wrong', but then come with arguments to support your argument. :-)

The way it is done has already been explained in the other answer. No need to repeat. The gist is the child-mother offspring will have approximately 75% maternal DNA and 25% (original) paternal DNA.

@Tenzin, there are an infinite number of wrong answers. It is not our responsibility to prove them all wrong, it is your responsibility to justify your answer and provide citations.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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How do point mutations arise from mistakes in DNA replication?

Hi! I'm trying to make sense of this illustration (from the textbook Biological Science by Scott Freeman).
The general question is: How do point mutations arise from mistakes in DNA replication?
If you don't mind, however, I'd like to explain how I interpret the illustration so you can see the confusion. As the original molecule of DNA is replicated (in gray), a mistake occurs in the synthesis of the bottom strand in the new molecule (the noncomplimentary bases G and T have been paired together). Now, it seems like a second replication is required for the mutation to arise: the defective molecule is replicated resulting in two new molecules, one free of mistakes (because it takes as its template the top strand) and one "wrong" where the mutation is present.
But my doubt is, wouldn't the middle molecule already constitute a mutation? If a mRNA were to transcribe that sequence, the codon is already different from the original molecule. Must a DNA molecule be replicated two times for a mutation to arise (where the first time a mistake is made and a second where such mistake is, let's say, "consolidated")?
Thank you very much in advance.

Welcome to Biology.SE and congratulations for asking a question that explains so well the origin of your misunderstanding (+1).

Source of your misunderstanding
Your misunderstanding is very comprehensible as the figure is misleading.
The figure only shows a single event of replication. What you see as a second replication resulting into two double stranded molecules is NOT an event of replication. It actually represents the two possible outcomes from a 'mismatch repair mechanism'. The term DNA replication written on the figure should be replaced by Possible outcomes of DNA repair. The molecule that contains the G-T mismatch is therefore just a temporary state that will very quickly be changed to either the T-A state (bottom right of your figure) or to the G-C state (upper right of your figure). More information below.
DNA repair

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome.

The type of DNA repair that is of interest on the figure is called "DNA mismatch repair"
DNA mismatch repair

DNA mismatch repair is a system for recognizing and repairing erroneous insertion, deletion, and mis-incorporation of bases that can arise during DNA replication and recombination, as well as repairing some forms of DNA damage.

There are specific enzymes to repair a mismatch such as the G-T mismatch represented on your figure. These enzymes can either repair G-T into G-C or into A-T. If the repair is A-T (lower outcome in the figure) then a mutation would have occurred. If the repair is G-C (upper outcome in the figure) then we are back to the original sequence and no mutation would have occurred.
Note that the probability of the two possible outcomes is different from 0.5 as these enzymes have ways to try to figure out which was the original strand and which was the newly replicated strand. You can learn much more about the mechanism of DNA mismatch repair on the wikipedia > DNA mismatch repair.

Thank you very much for this excellent explanation. I have corrected the figure in my textbook and I've certainly solved my confusion thanks to your answer.


text:
Why are root hairs mostly unicellular?
Most root hairs are unicellular but why is it so? What advantages does a plant derive from a unicellular root hair that it couldn't have if it was multicellular?

I have edited your question because 'Root hair cells are unicellular' is wrong it should be root hairs only.

@SanjuktaGhosh are you sure? I need some one to confirm this . There's naught like "hairs"

@Abcd Seemingly User SanjuktaGhosh meant "A Cell" means unicellular because Uni=1. You can't get a "multicellular cell". That is impossible due to Grammar. For example we could found "Multicellular stem-hairs" but not "stem-hair cells are multicellular"

@AlwaysConfused nothing = naught

Root hairs are not like our hairs. They are called hair just because they are hair-like projections. They are usually difficult to see without microscope, and found only at the delicate, growing region just above the tip. You could see them well in Chilli (Capsicum sp) Sprouting seeds quite well.

@Abcd A cell cannot be unicellular. That's all.

@AlwaysConfused in English language there's no word such as" hairs "right?

@Abcd "Hairs" is a valid word in English. However, "hair" can refer to either a singular hair or to a whole section, so that the correct usage when you are talking about "hair color" or getting a "hair cut"  or referring to "pubic hair" is to not use "hairs": it's more of a synonym for "fur" in these contexts. However, "hairs" still is correct and used in certain contexts such as a descriptive context: "oh look at all those little hairs on that caterpillar!" or if you are referencing numbers "his head was bald except for 4 hairs" and a few other contexts.

I though that unicellular is attribute for organisms, not organs

@altroware How else you could characterize the particular cell-number of projecting structures? As well this (hair-like projections) is not the only field where the term unicellular or multicellular is quite commonly used. In many other similar cases,  Such as structure of a gland, sporangia etc, or developmental mode (eusporangia vs leptosporangia) etc.

A couple reasons come to mind.* The purpose of root hairs is absorbtion. If you consider multiple cells along the length of the hair,  additional cell walls and plasma membranes would somewhat impede the movement of nutrients.
More importantly, the absorbtion is a function of the surface area of the hair. Smaller diameter (one cell thick) hairs provide greater surface area to volume ratio. While it's true that a larger diameter, due to multiple cells, might offer greater overall surface area, it would come at the expense of requiring more volume compared to a greater number of smaller hairs.
For example, suppose you have a certain volume of cutoplasm to spend on making root hairs. For the sake of the example, suppose the hairs are of a fixed length. If you make the hairs half the diameter you will be able to provide twice the overall surface area using the same volume of material.
* By this I mean I don't know the ultimate (evolutionary) reason and I doubt anyone does. This is probabably not an active area of research and you're not likely to find definitive answers with research. So, my answer, if you will, is conjecture.
That said, it is educated conjecture. In 24 years of teaching AP Biology, the relationship of volume versus surface area has arisen multiple times. One of the exercises I gave my students, in preparation for the exam, was to find at least ten examples. Some of the best students found many more.

Can you please add some citations to your answer?

@BryanKrause I think this answer is primarily based upon logic. Still, if there pre-exists any published documents; that would be purely hypothetical. It doesn't seems plants would die if someone developed by GM some > 1 cellular root-hairs. It happens maybe just because this trait evolved accidentally

@AlwaysConfused I don't disagree with the logic posted, there should still be citation just because that's how this site works. I've gotten a lot of criticism myself when I've posted uncited answers :)

@BryanKrause This is simple math, as diameters increase, volumes get larger faster than surface area. As far as afirming these reasons are an ultimate cause, I doubt that can be done; that's why I phrased it in the manner I did. Maybe you'd like to put this question in the catagory of requiring an "opinion based" answer. But, as an educatior, I think it's a good one for offering opportunities to model generalized scientific reasoning. Surface area versus volume ratio is a recuring theme in Biology, explaining  a myriad of observations.

I'm not arguing with the math or the logic. I am saying you should find an authoritative source that agrees with what you wrote. Sometimes, especially in biology, the most obvious math or logic turns out to be wrong because of some other misunderstood concept. I don't think that's going on here, but just to have a reference to a biology/botany textbook that says this fact, rather than person on the internet @bpedit says this fact is just part of the good standards on this site.

I've made some edit, corrected spellings and improved format. I think you meant bullet by ' * ' . You can roll back if you prefer the previous format.

@SanjuktaGhosh Thanks, but the reformatting loses the meaning of the asterisk which was meant to address Bryan's comments.


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What does fluorogenic mean for fluorescent probes?
Many fluorescent probes are described as being fluorogeninc as an advantage for fluorescence microscopy but what does fluorogenic mean? Dictionary definitions state that it means generating fluorescence, but i've read somewhere that it involves switching the fluorescence on or off for super resolution microscopy. I just want to understand the exact meaning in this context. Thanks in advance for the help.

@BryanKrause Sorry bout that, check edits for clarification. thanks

@BryanKrause here's one example, albeit a poor one, "fluorogenicity provides a high signal-to-noise ratio"

@BryanKrause Thank you so much Bryan for the help. It's now clear to me what it means thanks to your explanation.

I summarized my comments into an answer and added some references for anyone else that stumbles across this.

The usage of "fluorogenic" is typically applied to probes that are not currently fluorescent but can be, typically by some enzyme action or other reaction. For example, see here, here, or here. Essentially they are precursors to the fluorescent molecules of interest.
As one example, you could get a higher signal to noise ratio if you only "activated" the fluorogenic compound in one area, perhaps inside cells vs in the extracellular space, for example, so you aren't dealing with stray light from that "unwanted" signal.
References:
Shieh, P., Hangauer, M. J., & Bertozzi, C. R. (2012). Fluorogenic azidofluoresceins for biological imaging. Journal of the American Chemical Society, 134(42), 17428-17431.
Lukinavičius, G., Reymond, L., D'Este, E., Masharina, A., Göttfert, F., Ta, H., ... & Blaukopf, C. (2014). Fluorogenic probes for live-cell imaging of the cytoskeleton. Nature methods, 11(7), 731-733.
Friscourt, F., Fahrni, C. J., & Boons, G. J. (2012). A fluorogenic probe for the catalyst-free detection of azide-tagged molecules. Journal of the American Chemical Society, 134(45), 18809-18815.


text:
Reason for hiccups?
I recently fed my axolotyl an earthworm, which is good for them. I was rather kind and made sure that the said earthworm was quickly despatched beforehand. Now, watching the axolotyl whilst swallowing the worm, he exhibited a series of rhythmic "hiccups". It got me thinking. Maybe hiccups are an ancient evolutionary means of ensuring that live prey are killed by the movements of the diaphragm muscle to protect the ingestor, whether the prey is eaten on purpose, or by error. Even herbivores may have hiccups because they may swallow, say a snake or something by accident. A horrible thought, I know, but it may make evolutionary sense ! Although I understand that only mammals have diaphragms, perhaps this is an evolutionary muscular trait which stems from a common anscestor which has been refined in animals. I would be very interested to hear anyone else's thoughts. Many thanks, Donna Skelly.

This phenomenon seems to be typical to mammals only.

Non-mammals don't have a diaphragm.

This paper, linked from the Wikipedia page that Sanjuka linked, suggests an older evolutionary role for hiccups, but I think this is all quite controversial and not well worked out. I'd also caution that hiccups are using machinery that exists for other purposes, so there might not be a great evolutionary reason or origin besides "it wasn't harmful enough to be selected against."


text:
Have bacteria evolved antibiotic resistance in a laboratory setting?
Is it possible to breed a strain of bacteria in a laboratory setting so that it gains resistance to an antibiotic, replicating the kinds of resistance seen in wild, and has that been done?

Yes, many times.
For just one example, see this paper; you could also see this review for numerous examples.
These are examples of spontaneous mutations that lead to antibiotic resistance, so this is sort of an extreme version of evolution of antibiotic resistance. You could also say that antibiotic resistance "evolves" in terms of selection any time an experiment is done that uses a resistance gene to mark a subset of cells, which occurs on a daily basis in labs all over; fortunately these experiments use antibiotics that aren't used to treat patients.


text:
Is Plasmid pGLO a stable or unstable plasmid varient ?
Is plasmid pGLO a stable or unstable plasmid varient?

What research have you done before asking it here?

What do you mean by an unstable plasmid?

The GFP protein is an unstable variant

The pGLO plasmid uses a stable version of GFP. This is stated in the pGLO education series protocol, and wiki.
I could however, engineer to be unstable if wanted.
https://en.wikipedia.org/wiki/PGLO


text:
Australian Tree Identification - maybe pine?
Can you help identify this species?

(Link to imgur album with all images)
It was growing next to the Yarra River (maybe 10 meters from the bank) in Melbourne. At first I thought it was a type of pine however this page says Australian pines at not actually true pines. It does look much like some of the images of Australian Pine Casuarina equisetifolia
However the Wikipedia page for Casuarina equisetifolia says there are 2 subspecies, equisetifolia and incana. Equisetifolia is only found in Southeast Asia & northern Australia so that rules that one out. Incana is found on the east coast of Australia (eastern Queensland, New South Wales) - could it also be found as far down south as Melbourne?
I've also compared it against all the pines on this site as it specifically shows Australian species.
From there I thought it looks a bit like a Port Jackson Cypress Pine Callitris rhomboidea but the needles look longer and narrower.
I think it also looks a little like a Narrow Leaved Wattle Acacia linearifolia if you ignore the yellow flowers.
I'm carving a spoon out of some of it's wood so would like to know for sure what species it actually is. Any help greatly appreciated.
UPDATE:
I went back to the tree to get some more photos but the whole tree had fallen in the river!

I did get a branch off it however to get a close up of the nodes / internodes but I could not find any seeds or cones.

FINAL UPDATE:
I've tried to get a close up of the apical portion (the top bit right?). My twig sample has started to dry up a bit so this is the best I could get.

ONE MORE UPDATE
Due to my last pictures being rather fuzzy I got out the DSLR and the tripod. These photos are very high res and around 8mb each so may take a while to load...

You've correctly observed, it looks like Casuarina sp (an angiosperm) and some member of cupressaceae (Callitris , Juniperus etc) of conifer group of gymnosperm. Like those plants, in OP's specimen, green, narrow things are seemingly stem-branches (and not leaves at all) because they're clearly differentiated into nodes and internodes.

Could you find any reproductive structures like cones/ seeds etc? Also it would do help if you add a close-up of the nodal region of green axes (likely there is some small leaf or scale-like thing) and the internodes. Is the internode-axis a bit angular or prism-like? (as seems from the picture). How many angles, if so.

I'll go back to the tree to get more close up pictures

After more research I now think it is Casuarina obesa - Swamp Sheoak but will still get some more close up pictures (when it is not raining)

Those are great photos!

@AlwaysConfused - I've added a close up of the nodes / internodes - but a shame the whole tree has fallen in the river!

Ahh I'm so sorry I forgot to mention close-up the apical portion (which this photograph do not incluse) of these stem axes. Casuarina sp. male inflorescence occur at tip portions; such as in Casuarina equisetifolia and your mentioned species C. obesa. Was there something that looks like earbuds?  Unfortunate the tree is falling in water.

But still this photo would help. Did you have a  twig sample of it?

This Melbourne tree map website may help you.

My tree was just a bit off that map. Yes, I do have a twig sample. I'll photograph some more tonight.

From the ridges and furrows on its stem it seems quite like Casuarina sp. But otherwise, from its branching and greenness of older (seemingly woody) twig portions, it looks far different. I've never seen it but I'll continue trying. I can't even conclude about its systematic position. However, from last updates it seems there are some yellow coloured flowers or anthers or cones but it is very hazy.

Native cherry, Cherry ballart or Cypress cherryn belongs to the sandalwood family of plants.
http://en.wikipedia.org/wiki/Exocarpos_cupressiformis

I think your right. All the pictures on this page of Exocarpos cupressiformis match all my photos

I did some research following the latest answer on species of Exocarpos. I believe it is Exocarpus cupressiformis as well.
You can refer to this Australian website for a key to determine the actual species of Exocarpos : http://plantnet.rbgsyd.nsw.gov.au/cgi-bin/NSWfl.pl?page=nswfl&lvl=gn&name=Exocarpos#4
Also, as I researched, I found other Exocarpos species to mismatch with your images, except for two; Exocarpos cupressiformis and Exocarpos strictus. One mismatch of E. strictus was with the way flowers were arranged in your last few pictures.
Find below the pictures of flowers of E. cupressiformis (First) and E. strictus:

You can see that E. strcitus has the flowers blooming on stem edges and not at all on tips. In contrast, your images show flowers clustering at tips just like E.cupressiformis.

You are most welcome.


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Left and Right Handedness
Today I found out that the gene for being Left-handed is dominant while Right-handed is recessive. I personally am left handed and so is my father. My mothers father is also left handed and I was wondering whether or not I am homozygous or heterozygous for the left handed gene. Is there any way to determine this without getting genetic testing or by actually having kids? Thanks.
Source: My science teacher

Welcome to SE Biology. Could you edit your question to include a source showing that there is dominance for left/right handedness? It will allow people to more accurately address your question.

Handedness is not determined by a single gene.

I'm afraid your science teacher is wrong. Handedness is a complex trait. It is not determined by a single gene, and can't be described as being dominant or recessive. Handedness does apparently have a genetic component, but many other factors are involved as well. See the Wikipedia article on handedness:

Handedness displays a complex inheritance pattern. For example, if
  both parents of a child are left-handed, there is a 26% chance of that
  child being left-handed. A large study of twins from 25,732
  families by Medland et al. (2006) has indicated that the heritability
  of handedness is roughly 24%.
To date, two theoretical single gene models have been proposed to
  explain the patterns of inheritance of handedness, the first by Marian
  Annett of the University of Leicester and the second by Professor
  Chris McManus of UCL.
However, the growing weight of evidence from linkage and genome-wide
  association studies suggests that genetic variance in handedness
  cannot be explained by a single genetic
  locus. From these studies McManus et
  al. now conclude that handedness is polygenic and estimate that at
  least 40 loci contribute to determining this trait.

What may be confusing is that the preferred hand is often called the dominant hand, but that usage of the work 'dominant' is unconnected to the concept of dominance in genetics.

True. However, assuming a single pair trait, as described, the answer to the question asked would be: Nope, can't tell what pattern someone has on a gene pair with a strict dominant/resessive expression unless the recessive is displayed. You would need to check genetics directly or breed enough to get statistical probability on your side. The latter is less certain and would require considerably more patience. Kids can be quite a headache.


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Why have people much more different cells than rice plants, while they have roughly the same number of genes?
Rice plants have about two times as much of genes in their DNA than humans have. Then how is it possible that people have much more different cells than a rice plant has?

Did you have any reference about number of genes in rice plant is almost same as human being? and are these genes present as copy of few genes? or it tells about number of specific genes? OP looks something different from C-value paradox (that deals with DNA amount, not gene number). Interesting.

See https://medium.com/.../human-genome-shrinks-to-only-19-000-ge...
The rice plant cell contains 30 000 genes.

Actually, rice has about twice as many genes than humans (you can check yourself on bionumbers). But who cares? It is not because two species have the same number of genes that they would look alike. Human and rice have quite different genes. Numbers in themselves do not matter.
Consider the situation where Paul has twice the number of clothes in his wardrobe than Jack, it does not necessarily mean that Paul and Jack dress up differently. Conversely, when playing poker, Paul always has the same number of cards in his hands than Jack, yet their hands may well be very different.
Generally speaking 'higher plants' tend to have way more genes than 'higher animals'. There are several hypotheses for that. Plants are more often polyploid and therefore have more neofunctionalization. Also, plants don't move. It is not impossible that they would need more genes to cope with a more varying environmental conditions.

@Remib- I know the number doesn't count, but why do half the number of genes can produce so much more different cells in the human body?  Can it be that the proteins in humans, coded for by the genes, are complexer than those in a rice plant? Or can it be that the amount of non-coding DNA is much bigger in humans than in rice plants? Or do more combinations of genes (and genes can be used in many different cells) produce more combinations of proteins which more different cells?

@descheleschilder I would say the determining factor in "number of cell types" has mostly to do with regulation of genes. If you have two regulatory genes, just "on" and "off" could give you up to 4 cell types, but having three levels of each could give you 9. There are certainly way more than 2 regulatory genes, and they can regulate each other, to the point that there is a potential for essentially an infinite number of cell types in a human or a rice plant. The question is whether it is advantageous to develop a new cell type, not the number of available genes, for rice or humans.

@BryanKrause-In that case, why can't rice plants and humans make the different cells they need (which is much bigger in humans) with much fewer, but equal amounts of genes? If the number of regulatory cells is n, then they can give rise to $\ 2^n $ cell types. So if there are 10 of those genes the number of different cells they can give rise to has already grown to 1028 (the same genes can take part in the formation of different cells). And those regulatory genes can give rise to many new advantageous cell types, depending on the varying circumstances, by turning on or of different genes.

The biggest difference though between rice plants (or other plants) and humans is that human cells contain much, much more non-coding DNA, which in my opinion is the cause of the big difference in different kinds of cells.

@BryanKrause-Are regulatory genes bound to specific genes which code for a protein, or can they regulate all genes?

If Paul has twice as many clothes as Jack, Paul can show a bigger variety of clothes. Or put them on all together, which Jack can do too. Insofar the fact that plants are non-moving, don't you think that moving creatures encounter more diversity in their surroundings? Why doe polyploidy implies more neofunctionalization?

It is not because two species have the same number of genes that they would look alike. But how can fewer genes make a living organism more complex?


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How does P-protein (phloem) help in sealing of wounds?
While I was reading a book I found that "P-proteins in the sieve elements of phloem help in sealing  of wounds along with callose".
So how does p-protein do that, moreover how can it reach to other parts of plant body in order to seal the wounds?


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Does an organism have only certain antibodies for life?
Before birth, in the bone marrow millions of different B-cells are formed. These cells are differentiated and express different antibodies.
Are these the only B-cell types you will ever have? Or can the body generate new types of B cells, with new antibodies to deal with newly encountered threats?

Are these the only B-cell types you will ever have? Or can the body generate new types of B cells, with new antibodies to deal with newly encountered threats?

New B cells are constantly formed throughout one's life; the B cells that are present in the newborn are constantly supplemented by newly formed B cells.

... there is no statistical difference in the rate of production of new immature B cells in the marrow of young and old animals. In total, our results confirm previous work showing that mature B cells in old mice have a slower turnover, but more importantly suggest that the defect in mature B cell turnover is not due to a decline in B lymphopoiesis, but rather an inability of the newly made cells to replenish the peripheral compartments.

--Aging and developmental transitions in the B cell lineage.
But the second part of your question seems to have a misconception.  The newly-formed B cells have no relationship to newly-encountered threats.  No matter what new pathogens you encounter, your newly-formed B cells don't reflect them; they are formed randomly, and it is only by chance that any particular B cell might be able to react with a new threat.  Fortunately, there are so many B cells that the chance of at least a few reacting is very high, even though only a tiny fraction of the whole B cell population can do so.
Although new threats (mainly) require new B cells, repeated threats don't -- once a B cell is stimulated the first time, it undergoes a pathway that functionally makes it longer lived and more effective, so that on repeat exposure these optimized B cells are called in and there's much less need for the new naive B cells.

After the body is alerted to the presence of antigens, it calls in the artillery, which in this case are the white blood cells (phagocytes). The phagocytes digest as many of the antigens as they can, and then report back to the lymphocytes (B cells). The digested antigen material inside the phagocyte is then given to the lymphocyte, so it can produce an antibody to neutralize the antigen. This is similar to using snake venom to make anti-venom.
If the antigen attacks again in the future, the lymphocytes 'remember' the antigen and release the antibody, which they already know how to make, saving time and getting rid of the antigen before the human is even aware of its presence or it's excretion from the body. This is the basic concept behind vaccines and immunity. So to answer your question, yes, we can and do form new antibodies regularly. If we didn't, every new virus strain would be fatal.
Edit: As requested this is a source I found that is way more detailed and science-y - https://www.ncbi.nlm.nih.gov/books/NBK26884/

This answer is misleading.  You are describing what happens with mature B cells following antigen exposure, which is a completely separate thing from whether newly-formed B cells continue to arise throughout an individual's life.

@iayork Damn you're actually right. Probably should have read the question better but this is all I remember so I thought I've give my two cents.

@user45808 that's fine, but unfortunately your two cents are irrelevant and somewhat misleading. Not all white blood cells are phagocytes, not by a long shot. Similarly, not all lymphocytes are B cells. Digested antigens are not "given to" the lymphocyte like a delivery person handing off a package - they are presented on the antigen-presenting cell's surface for cognate receptors to bind to, recognize, and stimulate the resting B (or T) cell. Also, not all cell-mediated immunity to repeat exposures to antigen happen without the host's knowledge - some infections still take time to fight off.


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Why does a high osmotic pressure pull water in, yet a high hydrostatic pressure pushes water out?
When I normally think of high pressure, I think of it as pushing something away from the zone of high pressure.
Yet for a high osmotic pressure, water is pulled IN to this high osmotic pressure region.

Why is this the case?

Are you telling about reverse osmosis? Could not understand which context you are asking. Yes osmotic pressure is a negative pressure (i.e. its value is negative) but hydrostatic pressure (in plants, the wall-pressure is a form of hydrostatic pressure) is a positive pressure.

Thanks for the response @AlwaysConfused.  Sorry if it was unclear. I am just confused as to why a "high osmotic pressure" like in the picture above, doesn't push water away from the high pressure region.  Because if we are talking about e.g. air pressure, the air would be pushed away from the high pressure region.

The diagram you mentioned; involves a very confusing theory, commonly given at school kids' textbook, but there is exception to this theory, and one of my chemistry teacher once told me not to follow this. Well I'll take some time to write more elaborate answer.

Great question, the answer has to do with the definition of osmotic pressure and the difference between this pressure and "hydrostatic pressure" which is the water pressure you are thinking of.
Here is the definition of "osmotic pressure" given by Google:

the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis, often used to express the concentration of the solution.

Osmotic pressure in this definition is best illustrated by the commonly used tool to show osmotic pressure, often seen in a textbook as something like this:

In this picture, osmotic pressure is roughly how hard do you have to push down on the water on the right to make the levels the same on the left and right, despite the difference in concentrations. Osmotic pressure is not a pressure of water, as your question seems to imply, it is a pressure of the solutes in the water.
If it helps, I think it would be appropriate to think of this as sort of a "suction" on the water. Net flow of water stops when:
osmotic pressure - hydrostatic pressure = 0
...on the right side of the diagram.

Hi, @Bryan. Another user was asking about this and was confused about the pressure being applied to the pure solution. I think the quote about pressure being applied to the pure solution is a widely spread error (or maybe the pressure is doing something weird). As you say, you're pushing down on the right (non-pure) side of the tube and textbooks agree with this. So it might be a good idea to fix the quote in your answer. Thanks

What is "Osmotic Pressure"?

Consider the following system -1 :

Fig.1:  Left container: Pure water (Solvent). Right container: Solution of glucose (solute) in water (solvent); separated with a semi-permeable membrane.
In this system; as we know, water (solute) will flow from left container (Lower concentration of solute) to the right (higher concentration of solute); and such phenomenon is called Osmosis. If we use more-concentrated sugar solution to the right-container; the "tendency" to take water from the left container. We need to "define" this tendency.
Why the flow is taking place? Whatever going on molecular scale; on gross-scale we can imagine a 'pressure' that is driving the solvent only. (As we know, to pump a fluid we need to generate a difference in pressure). But it is not actually a real pressure. It is just used to measure/ describe the "Tendency to suck solvent". Now we have to "define" this pressure.

Consider the following system - 2

Fig-2: A piston has been added on the second container of system-1, with which a variable (as we wish) amount of pressure could be applied on the content of right container.
We can see the following 3 conditions:
A. Below a certain applied pressure, osmosis continues, but the rate is lesser than no-piston (system-1)
B. At certain applied pressure osmosis stops.
C. Above certain applied pressure; the solvent follow a reverse path. i.e. get squeezed out back-to left container. This is called Reverse osmosis.
Condition- B; i.e. the applied pressure at which the flow stops, is considered as the magnitude of osmotic pressure.
--------------------------------------------------------

Why osmotic pressure pulls the water in?

Better to ask,

Why a solution try to suck solvent through a semi-permeable membrane? Or why a solution do have an osmotic pressure?

According to this article ( * ) by Frank G. Borg ;

The standard treatment of osmosis in thermodynamics employs the concept of the
  chemical potential and does not give any clues how the process "really" works.

The answer is controversial; and there are 3 hypotheses.

The theory you mentioned: the  concentration of water explanation-

Fig: 3, Diagram taken from (**) experiment- article by Robert J. Kosinski and C. Kaighn Morlok
This theory tells; if we increase concentration of solute in a solution, the concentration of solvent would decrease.
But they also told that this theory doesn't work. See appendix section of the paper.

The Handbook of Chemistry and Physics has a large section on
  solutions of common solutes, and it discloses that a 0.2 M solution of NaCl has a markedly higher water concentration (995 g/L) than a 0.2 M solution of sucrose (958 g/L) (Wolf et al., 1982, pp. D261 and D270). Yet our experiments will disclose that a potato cores loses water to a 0.2 M solution of NaCl but it gains water from a 0.2 M solution of sucrose.

The “bound water” explanation for osmosis

Fig 4: The “bound water” explanation for osmosis. Diagram taken from following (**) research article by Robert J. Kosinski and C. Kaighn Morlok.
According to this hypothesis; due to the attraction (or hydrophilicity) the solute molecules bind the water; thus decrease water's concentration.
The paper told this theory is proven wrong because:

If the bound water explanation
  were true, we would expect that a greater mass of hydrophilic solute would bind more water. Whether a certain mass of solute is present in a few large molecules or in many small ones shouldn’t matter.

And in wikipedia's language (latest edition),

" The "bound water" model is refuted by the fact that osmosis is independent of the size of the solute molecules—a colligative property".

But this argument is not clear to me, I confess, because if solute particles break into fragments; the exposed area should be increased, so, more surface area would become available to get bind with solvent; and vice versa if more than 1 solute particles bound with each other the surface area should get decreased. So I did not understand why they thought the attraction model conflicts with number-of-particle theory.

the number of particles” explanation (According to the article by Kosinski and Kaighn, it is as same as Van't Hoff 's theory). According to this theory; only the number of particles per certain amount of solution; (and not its chemical nature) determines the osmotic pressure. i.e. osmotic pressure acts as Colligative property of a solution.

Though its derivation is thermodynamic (using concept of energy loss-gain); (And I confess, I've not understood whole mathematical derivation), I could not found any portion of it directly claiming a physical mechanism.
However according to wikipedia;

It is hard to describe osmosis without a mechanical or thermodynamic explanation, but basically, there is an interaction between the solute and water that counteracts the pressure that otherwise free solute molecules would exert. One fact to take note of is that heat from the surroundings is able to be converted into mechanical energy (water rising).

Reference:

Plant Physiology by Taiz and Zeiger, Ed3, Sinauer.
* What is Osmosis? Explanation and Understanding of a Physical Phenomenon / Frank Borg ,  Jyväskylä University, Chydenius Institute
** Challenging Misconceptions about Osmosis / Robert J. Kosinski and C. Kaighn Morlok
My high-school chemistry textbook, দ্বাদশে রসায়ন (Chemistry for class 12), 3rd edn 2008/ Mitra, Paul, Choudhury.
Wikipedia

Osmotic pressure is simply... Negative pressure exerted by solutes in the solvent.. That will draw the solvent into the solution.
External pressure,(+VE)exerted on the solution side to prevent the flow of solvent into solution across semipermeable membrane measures... Total magnitude of OSMOTIC PRESSURE (-VE) created by solutes.

Hi and welcome to Biology_SE. Answers are much more appealing if they cite references to books/papers and if they are formatted in a more organized layout.