text:
Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection?
Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection? If so, is there a common notion of beauty between humans and animals?

Probably your query will be unresolved, but in researching deep water fish courting you will find info like:
they engage in parasitic mating, they digest their own face and whatever part of the female they’re latched on to via teeth so that they can become fused at a tissue level ... https://www.youtube.com/watch?v=XhsyZnVx2rQ perhaps best rephrase like: why do deep water fish have completely different and ugly facial proportions compared to most other vertebrates? Is it because they can't see each other.

I suspect the deep ocean fish look ugly to you because they are unfamiliar.  The iconic fish species with which humans have coexisted forever are all surface fish, with common adaptations for surface living in the light.  When one thinks of a fish the salmon or cod is what we think of.
The deep fish have different selection pressures.  They do not need to be streamlined or svelte.  A deep fish might think a surface fish is ugly because it cannot make its own light - how plain and dull.  How can the surface worlders find a good mate if everyone is dark?

The peacocks are also unfamiliar to me, yet their looks seems festive nevertheless. http://mirplaneta.ru/images/2/412.jpg

good info, they often swim slowly and have low energy so they are less streamlined. The goblin shark swims quite fast though and it is also one of the most strange of all sharks.  https://www.youtube.com/watch?v=fYpn2u2Wag4 .... https://www.google.com/search?q=goblin+shark&source=lnms&tbm=isch&sa=X&ved=0ahUKEwib47mA0-bgAhWQERQKHZ1bAGIQ_AUIDigB&biw=1431&bih=734#imgrc=AdlcEl7MK3cpcM:

@Anixx: Perhaps peacocks look beautiful to you, but how about vultures?  Yet both must be attractive to the opposite sex of their species, no?

@jamesqf perhaps in vultures looks plays less role in sexual attraction than obtaining resources?


text:
How is breathing involuntary if the muscles that control it are skeletal?
How is breathing involuntary if the muscles that control it are skeletal?  Breathing is involuntary. However, the muscles that control it are skeletal: intercostal muscles and the diaphragm. Are there other muscles involved? Is it that these skeletal muscles are being controlled and/or acting involuntarily?
Humans can both continue to breathe while asleep, and they can also intentionally take a deep breath.
How is breathing be an involuntary act, that can also be controlled?

There are other such muscles on "autopilot". Blinking is both voluntary and involuntary.

Breathing is controlled by both the Autonomic nervous system and the voluntary nervous system. You see this in instances where our breath rate increases in flight or fight situations glide to the secretion of Adrenaline and also when we intentionally increase the breathing rate when undergoing high levels of activity. This is due to the fact that the involuntary aspect of breathing is controlled by the medulla oblongata and the voluntary aspect s controlled by the cerebral cortex. The fact that it is controlled by skeletal muscles has nothing to do with how it is innervated. For example, Cardiac muscles are innervated by both the hearts own conducting system and by the Autonomic nervous system.
If you're wondering why the skeletal muscles dont get fatigued, it's because there is a small but significant rest period between each Breathing cycle (inhalation and exhalation). Therefore the skeletal muscles have a rest period. However if a high rate of breathing does occur for a sustained period, they will fatigue and that's why you get cramps after a marathon or a sprint.

Nice answer! Welcome. :)

I would argue that the problem here is more semantic than biological. We artificially classify processes into "voluntary" and "involuntary", but the reality is much more complicated. For example, is walking voluntary or involuntary? Well, if I decide to go walking, it may initially be voluntarily, but when I am walking, I am doing very little in the way of thinking about walking. Breathing is much the same way. There is BOTH a degree of conscious control from the cortex, and a basal regulatory system in the brain stem that keeps things going below conscious perception. Another way to look at this is that the conscious control from the cortex modulates the medulla based breathing system.

This could be a better answer without the (unrelated imo) philosophizing. "Involuntary breathing" is not semantic. We do it whether we want to or not; the brain will not allow us to forgo that activity. That makes it involuntary, and under the control of the ANS. There are also nerves in the CNS -> diaphragm that allow voluntary control, which can override the ANS to a point, but in the end, it's involuntary. Not semantics at all.

source: Stack Exchange

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

sort: votes


text:
What is the name of this moth and why does it have an extra wing?

Moth of length 15mm. Seen in Kerala, India on March 2019. Third Unusual wing part visible. Without mobile flash the colour of moth visible is completely black.

This isn't a moth, it's a planthopper (Order Hemiptera, suborder Auchenorrhyncha, infraorder Fulgoromorpha, Superfamily Fulgoroidea [in which there are over twenty families worldwide; which is represented here I cannot guess]).  The "extra wing" is the right hind wing displaced (more than likely due to injury).

@ArthurJFrost Can you please make this comment into a full answer? Then you can get the credit for it. Additionally, answering in the comments in not liked here.

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


text:
Are there health benefits to donating blood?
Donating blood is typically thought of as a commensal act, benefiting the recipient at no cost beyond time and inconvenience to the donor. Some even view it as a parasitic act, wherein the recipient benefits at some health cost to the donor. But it seems reasonable to posit the opposite.
Iron has been suggested as the reason why women have notably lower incidence of cardiac events than men, until menopause that is. Why? Because some blood loss every 28 days helps to reduce iron levels in the blood. Similar logic holds with metabolic syndrome and type 2 diabetes.
Additionally, treatment-resistant high blood pressure responds — unsurprisingly — quite well to blood loss, as a bit less blood means, all other things being equal, proportionately lower pressure.
But this is speculation. Is there any legitimate evidence of the health benefits of blood donation?

I believe a number of claims in this post come across as sensationalist or false. I recommend you cite sources that support these numerous claims. For example, who is referring to blood donation as a form of parasitism?? Where did you read/hear about prevalence of cardiac events? (what exactly is a "cardiac event")? What evidence do you have for the health benefits of blood donations -- who is making those claims and based on what scientific evidence? Please update your question explicitly indicating some previous research effort regarding these points.

Simple Google searches can bring up useful and informative sources rather easily (e.g., This report from Heart.org), so please do a bit more homework to improve your question. Thanks!

@theforestecologist I was unaware that the claims in the question were controversial enough to warrant evidence-based research. The Heart.org source you supplied strongly supports at least one of the claims, feel free to edit the question :) Finally, I used the words "commensal" and "parasitic" strictly in the ecological sense, with the second implying some form of harm to the donor resulting from some aspect of the donation process. This is as opposed to parasitism in the biological sense, which isn't the meaning at all. Unfortunately, English doesn't seem to differentiate between the two.


text:
What impedes the understanding of genotype/phenotype relationship without statistics?
Most genetic research tries to establish a relationship between a certain genotype and certain phenotype.
To me this is like trying to understand a system as a black box, where you try to establish a relationship between a certain input and an output. It seems unnecessary to me because it seems possible - even tough extremely complex - to establish a more mechanical relationship between the box’s system and its environment and make a mechanical model that would always be correct about the box’s outputs based on a combination of inputs.
What is the missing link that impedes science from creating a model of genetics that is 100% certain of the resulting phenotype based on a genotype? Is it just lack computing power due to the complexity of understanding genotype/phenotype as mechanical system instead of probabilistic one?

Perhaps you could clarify what you understand phenotype to mean, and what the determinants of a phenotype are.

The actual answer to this is in your question: "possible - even though extremely complex". Complexity both limits the current level of any science (as in, the more complex the system the more time it takes for scientists to figure it out. Consider the time it took between discovering DNA and sequencing the human genome for example), and even the level of understanding humans could ever realistically achieve (because chaos theory issues). But I think a good answer to this question would give examples of the current state of the science in terms of the mechanical genotype-phenotype relationship.

Many genes are not associated with phenotypes. Your question is not expressed in a contemporary manner. I have answered on the assumption that, in plain English, you want to predict what a gene does.

I’m not sure that this question is suitable for this list, which is intended for questions from students of biology, not questions from students of the physical sciences who would like biology to fit into the sort of framework they understand. However…
First, genetics has been variously defined throughout history — Wikipedia currently has “Genetics is a branch of biology concerned with the study of genes, genetic variation, and heredity in organisms”, but I do not think current research is concerned with “establish(ing) a relationship between a certain genotype and certain phenotype”. Phenotypes are not where it’s at.
I stand to be corrected, but I think the question behind the post can be put simply as:

Why can’t we predict the function of a gene and its product from the
  DNA sequence?

And the answer is simply:

Because the DNA sequence does not provide enough information for us to
  do that. For the benefit of the physical scientist I’d say it’s like trying to determine the value of several unknowns with an insufficient number of simultaneous equations.

Let me use some analogies to explain further.

It’s like trying to assemble IKEA furniture without instructions.
Or, worse, it’s like trying to determine the function of a single component of IKEA furniture without even knowing whether it’a part of a Rågifarsok or a Nässeltrjik.
Or someone thinking that the instructions for a Nässeltrjik will tell you how to build a Rågifarsok.
Or, if you don’t do IKEA, it’s like a person transported in time from the middle ages trying to guess what the blueprint for an internal combustion engine means.
Or for the same person to guess what a screwdriver does.

That’s why biology is an experimental science.


text:
Measuring transgenic gene expression with a microplate reader
I have been working on genetically engineering an E. coli strain to autotrophically oxidize arsenite into arsenate for bioremediation of arsenic contamination in groundwater. For my research, I have been finding ways to quantitatively measure how much arsenite the bacteria oxidizes over time.
After researching ways to quantitatively measure arsenite being oxidized, I have concluded to use the method of Johnson and Pilson (https://www.sciencedirect.com/science/article/pii/S0003267072800059?via%3Dihub).
The arsenate that is formed from arsenite oxidation forms a molybdenum-blue complex with phosphate in the water. As the concentration of arsenate increases, the absorbance value of the water should increase proportionally.
Here was my plan: First, after growing my transgenic bacteria on an amp-plate, I would pipette out various concentrations of cells and arsenite in wells of a 96-well spot plate. I currently plan to use the Fisher Scientific Multiskan FC microplate photometer. I planned on incubating the cells while shaking at 37 C. The main problem I have come across is that my experiment would not be controlled. Over time, the growth of cells will change the absorbance value, not just the molybdenum-blue complex. I need to isolate the variable of just arsenite oxidation.
I have thought of a few possible solutions, but I feel as if I may be missing something crucial. When learning about microplate readers, I know that researchers can use them to measure gene expression. How do these researchers eliminate the variable of cell growth effects on absorbance values?
For one, I have thought of finding a way to filter the cells to one side of the well where they will not affect the absorbance values. Would it be possible for me to cut out a dialysis bag to where it is dipping into the well? In that case, the cells could be suspended in the well, oxidizing arsenite (if my hypothesis is correct).
Anyway, I really want to find a simple method for quantitatively measuring arsenite concentrations over time using a microplate reader without having cell growth affecting absorbance values.

Spectophotometry
Does the photometer allow using different wavelengths of light? Perhaps using a spectrophotometer might give you a control and your desired value, i.e. blue light may be absorbed by your sample, but red might not? The absorbance spectrum of the molybdenum-blue complex is very specific and you could use this to your advantage using spectral photometry.
Photometry + correcting for absorbance due to cell growth
Another approach is to quantify over time how your bacteria affect absorbance as a function of time and then subtract this from your experimental values.  For example, in a wellplate, place the following adjacently: use a (i) well without cells, and only arsenite in solution, (ii) cells without arsenite, and (iii) cells with arsenite. This should allow you to quantify quite accurately how much the arsenite, the cells, and how much both affect absorbance.
Of course as you say there may be an interaction between the cells and the arsenite slowing or speeding up cell growth, so that would be a pickle to disentangle. You could try, perhaps in the wellplates (this would be best!), to find out what effect arsenite has on growth and correct your final data this way.
Periodically sampling the solution; removing bacteria from the measurement
Another idea would be to culture your cells in arsenite, and take samples to obtain time-points. For each sample, you filter using small syringe filters (these are cheap and are typically used for sterilizing solutions, i.e. getting rid of bacteria but keeping the solution, given their pore size of ~.1 microns) and then perform photometry for the molybdenum-blue complex. This is typical practice in microbiology.
PCR? An idea.
Last but not least, it's good to remember this is an indirect readout of transgenic gene expression. Similarly, you could use quantitative PCR to quantify the expression of any transgenes - here, you use housekeeping genes as controls for cell number, and the mRNA expression of your transgene as the readout. You would be reading out the expression of mRNA, but I personally don't think it would be more 'indirect' than measuring arsenate concentrations in solution, especially when there are confounding factors and awkwardness in getting a clean measurement. The PCR approach would be quite accurate and likely more reliable.
These are just some initial thoughts - perhaps you could add a comment or we could chat about this if you think it could spark up some concrete ideas!

Thanks for the advice! I will be collecting data hopefully over a 3 hour course. For the amount of time I have to complete experimentation, I might go with the periodic sampling method that you mentioned. I could try to grow multiple culture tubes on a shaker, and at 10 minute intervals filter out the solutions into the wells (containing LB, amp, sodium arsenite, and potassium phosphate dibasic). Also, I would create several stock solutions with known concentrations of arsenate and arsenite while accounting for absorbance values of LB and amp. I could just calculate all needed concentrations.

Also, I dont have any arsenate on hand to make a stock solution; I just have arsenite. I know if I have stock solutions, I can calculate the amount of arsenate based on absorbance, but would it be scientifically "acceptable" to have my measurements in absorbance instead of concentration?

Depends on what you are trying to demonstrate. If it is not feasible to measure arsenate concentration, you can use absorbance as a relative unit! Twice as absorbant doesn't mean you have twice the concentration, but you can compare different bacterial strains; you'll know which one oxidizes arsenite more. Very often in biology (and science generally) we don't have absolute measurements; we can only compare to a control, for instance. PS. It's good to check whether arsenite oxidizes by itself over time (it might not, I have no idea) - you'll have to correct for this if you want solid data.


text:
What chemical test can be used to tell apart meat and plant-based meat?
Long story short, I thought about this question and simple Google searches weren't enough. I know there must be some nutrient that can only be found in one of the meats but not the other, but I can't seem to search for it.
For this scenario, just assume that the 2 meats are exactly the same in terms of texture, color, consistency, taste, etc., to the point where only chemical tests can tell one apart from the other.

Testing for cellulose seems like an obvious choice; unfortunately, cellulose (sometimes loving referred to as "wood pulp" in a food setting) is a common additive to processed foods, including meat. Ex: Is there wood pulp in your burger or taco?

@theforestecologist good point, though for balance, I might mention that the article you linked makes it sound like a bad thing that there be cellulose in your food, which is not the case.

@rotaredom ha, right! Thanks for "balancing out" my link! Good follow-up :)

There are a lot of things you could test for.  The thing that come to mind off the top of my head is cholesterol.  This will be present in all animal meat, since all animals muscles contain cholesterol, whereas meat substitutes usually do not.
That said, there are other options as well (such as starch vs. glycogen levels, for example), and even molecules such as collagen differ between plants and animals, so a careful analysis (provided the proteins have not been too altered by the commercial production process) should be able to reveal thousands of differences, even in molecules found in both plants and animals.
Further reading

Marzetta CA, Rudel LL. 1986. A species comparison of low density lipoprotein heterogeneity in nonhuman primates fed atherogenic diets. Journal of Lipid Research.  27: pp. 753-762

Sorry for responding so late. Nevertheless, based on the research linked, it seems that significant effort would be required to make meat substitutes taste like actual meat.


text:
Can an animal evolve after birth?
I am wondering if animals do evolve even after birth and gain DNA changes that give them advantages and make them more suitable to the environment while they are alive, then pass these "enhancements" to their children
UPDATE
After all, cell do split and multiply when the animal is alive, and it could end up with a totally different cells than the one born with, so if a mutation happened during this period that led for it to be the dominant "property", what stops it from being passed on?
Is there a research on this?

I would encourage you to look at this question, and maybe clarify in your question what you understand evolution to mean. I would note that typically, in the general sense, evolution is understood refer to changes in a population of organisms, but in some domains it can refer to changes in a cell population. This circumstance, though, doesn't involve passing on to the offspring of the organism, but the offspring of the cell.

No.  Certainly not.  There is only a very limited number of cells in the body of any creature which pass on genetic material to the offspring generation; these are referred to as gametes.  Mutations to these cells, however, do not affect the parent in the least, as their sole function is to produce offspring.
One gamete from the father & one gamete from the mother fuse to produce a child with a combination of genetic code, which means that mutations in those gametes (which did not affect the parent) will be present in every cell of the child's body, and affect the child.
Furthermore, do remember that most mutations are not "enhancements"; rather the vast majority of mutations are harmful.
After birth (and really, long before birth) mutations acquired in the organism are unable to be passed on to the offspring, unless they happen in the gametes, in which case they do not affect the parent carrying those mutations.

But doesn't gametes have the DNA of the animal?

Yes.  But the gametes rarely (if ever) express the portions of that DNA which will effect the rest of the animal.

Sorry but I don't understand, which portion and why it won't carry it?

Each cell in the body of an animal has a copy of the entire genome (all the DNA).  Some parts of that DNA only affect the cell it's in, whereas other parts of that DNA code for molecules which could effect the entire body.  Because of the function of gametes, they are specialized to express only parts of the DNA which allow them to grow and perform their function, which is to reproduce.  Consequently, they are kind of resident aliens with little / no effect on the parent until fertilization, when you have two distinct animals (distinct genetic code), one residing and depending on the other.

OK, so let us assume that while multiplying/reproducing, a bone cell mutated and gained DNA information that makes the leg bones longer, you are saying that this info won't be passed to any other types of cells in the body other than bone cells?

Correct.  There's a process known as differentiation which sets in stone early on in the development process what kind of cell a cell will be, which in turn defines what its function will be.  In your simplified example (obviously it's more complicated than just "gaining information for longer legs"), the bone cell will be utterly incapable of passing that genetic material on to the gametes, so although the parent has longer bones, the offspring will have normal length bones.

@Mocas FYI, a cell mutating and migrating its mutated form to other tissue is basically a cancer that has metastasized (though it would not be infecting other cells with its mutations; only invading their tissue).


text:
Why are dietary recommendations for methionine consumption combined with cysteine?
I want to understand the amino acids missing in certain vegetables. I looked up the US recommendations for amino acids
(source: wikipedia).
I don’t understand why they pair

Methionine + Cysteine: 25 mg/g protein
Phenylalanine + Tyrosine: 47 mg/g protein

I searched for a justification but I cannot find one. While I acknowledge the chemical and structural similarities between them, they are separate amino acids. If these pairs could simply be transformed from one to another, then why bother considering methionine and phenylalanine to be essential? If you could easily convert cysteine to methionine, then methionine could be manufactured by the body. Similarly, so could phenylalanine. But it is commonly assumed this does not occur. Thus, an answer based on the idea that they can be "easily transformed into one another", if true, needs to address these issues.
Here are references for methionine:

The intimate relation between amino acids and protein and nitrogen requirements is well recognized. Nutrition research has focused on the capacity of food to meet the need for nitrogen and indispensable amino acids (IAA) and led to the conclusion that the quality, not just the quantity, of protein is critical. This is especially relevant in regard to the sulfur amino acids (SAA) methionine and cysteine because of the increased understanding of their relation to chronic diseases (e.g., cardiovascular disease, dementia, cirrhosis), immunomodulation, DNA transcription, and RNA translation. Considerable effort has been expended to determine whether and to what extent cysteine can spare the requirement for the IAA methionine. In vivo studies in humans generally concur that the dietary requirement of the SAA ranges between 13 and 16 mg/kg/d, but how much can be met by cysteine relative to methionine remains controversial.
Using the indicator amino acid oxidation (IAAO) approach to further examine this issue, Di Buono et al. (9–11) confirmed the mean requirement for methionine as 12.6 mg/kg/d in the absence of exogenous cysteine but noted that a safe level of intake of total SAA for the population was substantially higher at 21 mg/kg/d.

Naomi K. Fukagawa; Sparing of Methionine Requirements: Evaluation of Human Data Takes Sulfur Amino Acids Beyond Protein, The Journal of Nutrition, Volume 136, Issue 6, 1 June 2006, Pages 1676S–1681S
...and phenylalanine:

Conclusion: On the basis of the 24-h IAAO and 24-h IAAB methods, a mean phenylalanine requirement of 38 mg/kg/d is proposed for healthy well-nourished Indian adults in the absence of tyrosine intake. This finding is similar to that in Western adults.

Anura V Kurpad, Meredith M Regan, Tony DS Raj, Vidya N Rao, Justin Gnanou, Vernon R Young; The daily phenylalanine requirement of healthy Indian adults, The American Journal of Clinical Nutrition, Volume 83, Issue 6, 1 June 2006, Pages 1331–1336
Questions:

Why would amino acid requirements be grouped together?
If methionine is considered an essential amino acid, wouldn't grouping it with cysteine allow a food high in cysteine to appear as though it is satisfying your methionine requirement?
Suppose I consume 12.6 mg/kg/d of methionine, would this affect my ability to consume cysteine?
If the recommended level of methionine and cysteine is 19 mg/kg/d and this article proposes 12.6 mg/kg/d, then is it logical to consume approximately 6.4mg/kg/d of cysteine?
If true, would the same logic apply to phenylalanine and tyrosine?

In humans, cysteine can be synthesized from methionine and tyrosine from phenylalanine (note that the reverse pathways do not occur). Because their synthesis requires essential amino acids and the biosynthetic capacity of the organism does not always meet its need, they have been labelled conditionally essential. Under normal circumstances, an adult human can live with no dietary source of cysteine so long as dietary methionine is adequately supplied since the dietary deficiency can be compensated for by biosynthesis. Because of this, though, less dietary methionine is required when the diet is also supplemented with cysteine since less methionine is required to synthesize cysteine. This effect is known as cysteine sparing and a similar effect is observed with tyrosine/phenylalanine.
The data you cite are the reference values for PDCAAS, which is an indicative tool to evaluate the essential amino acid composition of protein sources. This system was introduced in 1991 by the WHO, and in this report they give the following rationale for their combined scoring of methionine and cysteine as sulfur amino acids:

The total of methionine and cystine [is] used for scoring purposes... Cystine is not an essential amino acid but can be synthesized from methionine. Cystine in a diet can thus "spare" methionine, and the total of the two has been found more satisfactory for scoring purposes than methionine alone.

They also recognize and somewhat address the weakness in this methodology that inspired your question:

While it is known that cystine can spare part of the requirement for methionine, FAO/WHO/UNU 1985 does not give any indication of the proportion of total sulphur amino acids which can be met by cystine. For the rat, chick and pig, the proportion is about 50%. Most animal proteins are low in cystine; in contrast, many vegetable proteins, especially the legumes, contain substantially more cystine than methionine. Thus, for animal protein diets or mixed diets containing animal protein, cystine is unlikely to contribute more than 50% of the total sulphur amino acids and scores calculated using cystine plus methionine will be appropriate. However, in certain all vegetable combinations, e.g. wheat and legumes, part of the cystine value may not be realized. Because of insufficient data on human requirements, however, the total of the two sulphur amino acids should, for the present, remain the recommended approach for computing amino acid scores.
...
A further complication arises from our lack of knowledge of the proportion of the total sulphur amino acid requirement which can be met by cystine. Without that knowledge, expression of protein values in terms of the sum total of methionine and cystine has both theoretical and practical limitations.

It's because of their structural similarity.  Here are some quick pics of the molecules:
Phenylalanine:

Compare with tyrosine:

You can see that the only difference is the methyl group in para position on the benzyl group in the tyrosine.
Similarly, take a look at cysteine and methionine:
Cysteine:

Compare with methionine:

These two look somewhat less similar; you have an extra methyl group on the methionine, a butyl chain instead of a propyl chain, and the alpha carbon bearing the amino group is in R position instead of S.  Nonetheless, they are the only amino acids bearing sulfur  Also, if you go back to the original paper, they say,

While RDAs are provided for each age group for the nine indispensable amino acids, histidine, isoleucine, leucine, lysine, sulfur amino acids (methionine + cysteine), aromatic amino acids (phenylalanine + tyrosine), threonine, tryptophan, and valine, the requirements for these amino acids are used to develop the FNB/IOM Protein Scoring Pattern.

Because of their similarities, some of them can be fairly easily transformed one from the one to the other in the body.  For instance, cysteine can be produced from L-methionine. This results in it being easier to classify them together, since if they can be produced one from another, they become virtually indistinguishable between the intake and usage pathways.

Sources:

Trumbo, Paula, Sandra Schlicker, Allison A. Yates, and Mary Poos. "Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids. (Commentary)." Journal of the American Dietetic Association 102, no. 11 (2002): 1621+.

Institute of Medicine of the National Academies. 2003. Dietary Reference Intakes. p. 138.

U.S. National Library of Medicine. Toxicology Data Network: HSDB: (L)-Tryptophan.

Bin P, Huang R, Zhou X. 2017. Oxidation resistance of the sulfur amino acids: Methionine and cysteine. BioMed Research International 2017 : 9584932-6.

I’m afraid a bland statement “some of them can fairly easily transformed…” is not an adequate answer. You need to present and reference the precise pathways for this interconversion in humans. This is the crux of the answer. How do I know if it’s true?

Are you sure that the grouping is based on the metabolic transformation in humen? Maybe the chemical analysis is done that way: the total amount of Met+Cys or Phe+Tyr was measured without distinguishing both compounds. This might be easier (cheaper) due to certain chemical similarities of each pair.

I agree with @David. I take issue with "can be transformed easily enough" as I think that erodes the idea of essential vs non-essential.  I made an edit with pointing out issues I have with your argument.

@Arsak there's definitely something to what you're saying; check out Standardised methods for amino acid analysis of food by Otter DE in the Journal of Nutrition.  The feeling I was getting from my research was that there was the understanding that it's not extremely critical to distinguish them since cysteine can be synthesized from methionine (see The Sulfur-Containing Amino Acids: An Overview by Bronson JT & EB) and similarly for the aromatic amino acids (see The conversion of phenylalanine to tyrosine in man [shortened title] by Clark JTR & Bier DM.)


text:
Are viruses ever manufactured directly from viral DNA embedded in the genome?
Some viruses can cause their genetic material to be pemanently stored in the human genome -- even getting passed on to offspring.
Endogenous Retroviruses, for example are thought to make up between 5~8% of the human genome.
Does stored viral DNA present in an otherwise uninfected human being's (a newborn baby for example) genome ever get used to spontaneously manufacture new virus bodies, thus infecting the host, and causing them to suddenly become contagious without ever having encountered an actual virus?
Put differently, is it possible that a human being harboring viral DNA and quarantined in a sterile enclosed environment (bubble, etc) preventing any contact with external contaminants (viruses), could ever spontaneously become infected with a virus, due to the stored viral DNA getting expressed?

It sounds like you're referring to the transition from the lysogenic cycle to the lytic cycle. The lysogenic cycle involves the viruses' DNA being integrated into the host's genome, such that the host has a dormant infection, the lytic cycle involves the virus' DNA being transcribed and translated to make the components of viruses, like capsid proteins, which then self-assemble to form many viruses which then leave the cell. The fact that this transition can occur means someone can experience an active viral infection, with proliferating virus particles, without exposure to additional viral contaminants. If it couldn't, then would there be much point (from a virus' perspective) to the storage of viral DNA in the genome which, as you've noted, retroviruses can do?
Transitioning from integrated DNA to phage particles:

To use the lambda phage (which is a bacteriophage and thus infects bacteria, not humans, but the underlying principles are the same) as an example, the expression of the viral DNA is controlled. But, the viral DNA is not a monolith - parts of the viral DNA of a prophage (the genetic material of the bacteriophage integrated into the bacterial host genome) are expressed but their expression prevents the expression of those parts of the viral DNA which would cause a transition from prophage an active infection, i.e a switch from lysogeny to the lytic cycle.
The lambda phage genome is shown below:

But an easier to deal with version which focuses more on the elements required for regulation would be:

There's lots of stuff going on here, but the key point is that lambda repressor, a protein coded for by the yellow cI gene, represses any transition to the lytic cycle. Aside: cI stands for clear I, because virus mutants which don't have c1 go straight into the lytic cycle and so produce clear spots on agar plates of bacteria since the bacteria are straight out killed rather than hosting the virus in the prophage form.
The lambda repressor prevents the transcription of the genes under those arrows in the top part of the diagram, and it's those genes which code for the things required for active virus particles, such as enzymes required to rupture the host cell's wall, and the proteins required to form the virus' coat.
So, to sum up, yes. Viruses existing as viral DNA embedded in the genome can cause infections, even in individuals not exposed to additional contaminants (but contaminants which cause damage to the host's DNA, like mutagens, will trigger the transition from lysogeny to lytic), and some of the viral DNA is always expressed (repressor genes) in order to prevent the expression of the parts of the viral DNA which would cause an active infection, were they to be expressed.

Thank you for taking the time to write such an in-depth and informative answer.


text:
Approximate Cell Doubling Time?
If I know it takes 12 min to occur in mitotic fibroblast cells and I count there are 32 dividing cells in the microscope slide out of a total population of 32034 cells, how do I calculate the approximate doubling time in hours?
My colleague says it should be around 200 hours. But I don't understand how they reached to this conclusion, can anyone explain this to me please?
Thanks

I figured it out, 32034/32 = ~1000
1000 / 5 = 200 hours
Because 12*5=60 min = 1 hour


text:
Is there any explaination to homeopathies in modern biology sciences?
I'd like to know if there is any sort of explaination from rigurous biological arguments which could potentially explain how homeopathies could work?
I'm not talking about placebo effects (psychological) or "water memory" (purely hypothetic), but really about the immune system itself.
Usually, there is only 1, or a really insignifiant amount of toxins after the dillutions for the homeopathies.
But does that mean that there is absolutely no effect on the organism, biologically talking?
Or could there be some immune memory taking place here for example (ik it is usually in adaptative reaction with the lymphocytes, but does it happen with the white cells or other stuff)?
I'm just curious about it :), thanks!

I searched for duplicates on my internet browser but not on stack exchange itself. Sorry for the duplicate, i'll try to be more aware, and thanks.


text:
Can environmental pressures affect genes in one generation?
Environmental pressures are the catalyst of evolution. Pushing a species to adapt to changes therein. My question is can these mechanisms cause significant adaptation over one generation(parent-> child). My thinking is the pressure of the equivalent of human trauma in a species(depending on neurological and biochemical makeup of said species) would be enough to induce genetic influence.
If not, what is the minimum theorized timeframe for environmental pressures to act?
Edit: This is not a duplicate, the previous question is about one animal's lifetime

I've tried to answer your question, though I am a little confused about the sentence re: "the equivalent of human trauma".

@DeNovo to clarify further, an event that would cause some sort of psychological ailment as a result(i.e PTSD,GAD) in humans. From what I understand, things like anxiety from social or non-threatening situations are neutered versions of the physiological reactions we had pre-society.

@hisairnessag3  so your point is that if parent in childhood experience some trauma ( for example sexual abuse) if that change genetic information hand over to children?  Am i correct ?

I voted to close as "unclear what you're asking", because the question, though unclear, is certainly not asking if an individual animal can evolve after birth. It is asking evolution can occur in one generation. Indeed it can, and only ever does.

Don’t think that this is a duplicate as the main question (ignore speculation on trauma)  can be answered with a definitive YES. This was demonstrated recently for first time: Rowan D. H. Barrett et al., “Linking a mutation to survival in wild mice.” Science 363, no. 6426. (February 1, 2019). doi: 10.1126/science.aav3824

@tsttst I believe the first time it was demonstrated was 160 years ago...

The formal link between going from environmental pressure to change in frequency of a naturally occurring variant of a gene within one generation for non-laboratory condition is new. Given everything else known about evolution and molecular mechanisms of inheritance this is expected. The above shows it explicitly within one generation. 160 years ago they did not study genes.

Can environmental pressures affect genes in one generation?

Yes. Environmental pressures that cause a change in allele frequency will always produce changes in a single generation. If the environmental pressure is present for more than one generation, it will affect changes in allele frequency over a longer time span.
I'd encourage you to look at this set of case studies from UC Berkeley's Understanding Evolution
To clarify what "pressure" means in the context of evolution. Selective pressure, or evolutionary pressure, as wikipedia describes it, is anything that changes the reproductive success of an organism. It is, by definition, something that has an effect in one generation. Selective pressure causes organisms with certain heritable characteristics (and certain alleles) to reproduce at a different rate from organisms with other heritable characteristics (other alleles). The pressure selects for certain alleles.
Considering the comments, it sounds like you're describing a disorder (psychological ailment, e.g., PTSD, GAD), which may have a heritable diathesis, and an environment (trauma) that causes the expression of that disorder. To consider that environment to be selective pressure, it would need to be present at a population level and cause individuals with that heritable diathesis to reproduce at a different rate than individuals without it. If it did, you would see changes in allele frequency over one generation. Indeed there is no way for selective pressure to cause a change in allele frequency without it occurring in a single generation.  I'm not aware of any study that has demonstrated this to be the case for any anxiety disorder.


text:
Why are Chloride Anions necessary for gastric acid functioning?
Why do parietal cells of the gastric mucosa release Chloride anions along the H+-ions, which are pumped into the lumen by the proton-pump. Wouldn't the presence of protons alone be enough to denature proteins?

Mebrane divide basicly enviroment to two disimular sections. This sections differ in lots of chemical/ phycical properties. One of those is electrochemical potential which it can be in the very simple way describe as whole charge of disimular section divided by biomembrane.

So if cell  pariental cells pumped into stomach that section will have too much positive value of electrochemical potencial which can repulse pumping more hydrogen ions back to the pariental cell. This lead to freeze hydrogen pumping to  the stomach area. Than chloride aniont came to the scene basicly to reduse positive charge and enable to pump tremendous amount of hydrogen to the stomach.

I tried to make it simple as possible. I hope this still can help you.


text:
Is it possible for a sex chromosome to be homologous?
I am following a great introductory biology course online, MITx: 7.00x on edX.
A question in the course assumes a cross between a pure-breeding male fly and a pure-breeding female fly:

You are studying genetics in a hypothetical fly and you find a fly
  that has purple eyes. Assume that the purple eye phenotype is due to a
  mutation at a single locus. Use the notation E and e, where the upper
  case letter is used for the allele associated with the dominant
  phenotype and the lower case letter for the allele associated with the
  recessive phenotype.
You cross a pure-breeding male fly with purple eyes to a pure-breeding
  female fly with normal eyes. All of the F1 offspring have normal eyes.
  From this experiment you determine that the purple eye phenotype is
  ______________ to the normal eye phenotype.

My question is this: how can a male fly be pure-breeding? The reason I wonder is that as far as I understand, pure-breeding implies a homozygote gene, yet the sex chromosome can not be homozygote because the Y chromosome is not homologous to the X chromosome. In other words, does it make sense to speak of homologous sex chromosomes?

How can a male fly be pure-breeding?

A fly or any organism can only be pure-breeding for a certain trait, not all traits at once. If the trait-determinant allele is found on an autosomal chromosome, this is not a problem. If it's on a sex-chromosome (chr1 in flies), it is sex-linked, and therefore cannot be pure-breeding because it may depend on the sex of the offspring whether the trait is expressed. For instance, you may have a male carrying an allele on its X chromosome; its female offspring will inherit the X, but male offspring will not (those inherit the Y chromosome), i.e. it is not pure-breeding. Male flies cannot be pure-breeding for traits determined by loci on their sex chromosomes. Similarly, you may have a heterozygous female carrying an allele on one of its X chromosomes (A/a); its female offspring will only inherit one allele, either A or a, so it is not pure-breeding either. A female fly must be homozygous for an allele on its sex chromosomes to be pure-breeding for that trait.
Male flies can be pure-breeds for traits determined by alleles on autosomes.
Also, cool and useful funfact, Drosophila sp. male flies do not experience homologous recombination during meiosis. This is called achiasmy! This is useful to know when designing complicated crosses when there is a difficulty in balancing a genotype.

Does it make sense to speak of homologous sex chromosomes?

The X chromosomes in females (X + X) are homologous, but the male Y chromosome is not homologous to the X. They are vastly different, just like the X and Y sex chromosomes in humans.

Pure-breeding implies a homozygote gene

Correct. Pure-breeds are allele homozygous so that all offspring, regardless of recombination, inherit the allele.

Thank you so much! It all makes more sense now.

To add to @S Pr's answer and provide another cool and useful fact, in some organisms, like birds, the males are the  homomorphic sex (their sex chromosomes are the same size and haven't decayed like the Y has in human males), not the females (who are ZW, with the W being the analogue of the mammalian Y chromosome).
So more generally, sex chromosomes can be homologous only in those organisms which are members of the homomorphic sex, which otherwise phrased means they're homogametic organisms. This sex is female (for mammals).


text:
What species is this cocoon?
I found this cocoon outside my house and I want to know what insect might be inside it and it’s species. Please help!
I found it a day ago when it was a worm, now its a cocoon, it’s like outside the main entrance (which is like 2 metres high) and the cocoon was half way on the left, and it was out in the sun, to be honest I’m surprised little kids didn’t kill it yet.
I live in Kuwait in a town called Hadiya.
I don’t see many worms in Kuwait, I’ve only seen like 4 in my whole life.

Hi, and welcome to the site!  In order to be able to identify it, we'll probably need more information - where do you live?  You found it recently, I presume?  Also, a more precise description of the environment in which you found it could be helpful: "outside my house" leaves a lot of unanswered questions: how high? it looks like a painted surface?  Is it in the shade or in full sun?  Please [edit] to include more detail.  Thanks!


text:
Are all genetic disorders inherited?
I know that genetic diseases such as cystic fibrosis are often passed down through generations and are therefore classified as genetic disorders, but if a mutation occurs spontaneously, which for example leads to cancer, is this then classified as a genetic disorder?

Are all genetic disorders inherited?

Not all individuals with a genetic disorder inherited that disorder. Some genetic disorders are caused by spontaneous mutations.

Is cancer a genetic disorder?

Yes. The seminal paper by Hanahan and Weinberg, the Hallmarks of Cancer, is a good place to go to get a sense of what we understand cancer to be. This paper is quite influential and has its own wikipedia page. These authors wrote an updated review in 2011. Re: your question as it relates to cancer, yes, genetic changes result in tumorigenesis. Cancer is a genetic disorder of cell populations. One can view cancer diagnosis and treatment from the framework of cancer as a metabolic disease, but this adds to, rather than subtracts from the framework of cancer as a genetic disease.

Are other diseases caused by spontaneous mutations genetic disorders?

Yes. Achondrodysplasia is one illuminating example. It is a form of dwarfism caused by a mutation in the FGFR3 gene. It does follow mendelian autosomal dominant inheritance patterns, but in 80% of cases, the mutation is, in fact, acquired spontaneously (that is, not present in either parent). As noted by @Eff in the comments, Down syndrome, Trisomy 21 (and other chromosomal abnormalities, e.g., Turner, Kleinfelter, Patau, Edwards) are other common examples.

Down syndrome is a similar genetic disorder that isn't inherited right?

Yes, there are many examples

Down syndrome can be heritable, but most cases are spontaneous.

@swbarnes2 yes, cancer, down syndrome, and achondrodysplasia are three examples of genetic disease that can be heritable but are spontaneous in most cases.

Great answer, though I'd personally recommend expanding the "yes" you start off the answer with, since the question in the title and the question in the body lead to different conclusions from a simple "yes."  Just a bit confusing.

@rotaredom good note. Done.


text:
How did sneezing evolve?
Did we develop the sneezing mechanism to get rid of pathogens like bacteria and viruses in our nose?
Or did pathogens develop a way to make us sneeze to propagate themselves?
Or did we develop the sneezing mechanism, and then pathogens hijacked this pathway to benefit themselves?
I'm trying to understand why we sneeze so much when we get sick - is it our bodies trying to help us, or is it something the pathogen is causing to help itself spread? And if it's both, how did that happen?

Although your question is quite interesting, it appears to be very broad; you can possibly find entire books/reviews dedicated to this topic (if there is already an answer).

By "we" do you mean humans? Because sneezing is shared at least across tetrapods.

Sneezing is a response to an irritant, any irritant, including pepper, pollen, dust, someone sticking a hair up your nose, etc. No pathogens necessary. That should answer the question.

@kmm I meant all organisms that sneeze. But the point that we sneeze in response to any irritant answers my question - I guess it's just lucky for pathogens that the sneezing response propagates them. Thanks for your answers!

Sneezing itself is a part of long story of human evolution.
Sneezing for early humans was as common as eating is for us. Early humans lived in caves which were full of dust and insects so whenever they wake up from sleep they sneezed intentionally to remove the dust and small insects from their nose, slowly this behaviour of early humans was proved to be beneficial and muscle memories remembered the Activity as a daily routine work and performed it to remove dust and any irritant in their nose or nasal cavity.
As they evolved they passed on their daily routine works to their descendants and this was also passed on , this way sneezing was slowly incorporated into the muscle memories and it exists till now as a way to relax is from external allergens.
There are several other theories too about evolution of sneezing and it itself demands great research .
 There is also a video on Veritasium on YouTube regarding the Sneezing whenever one sees light , this video too discusses this theory.
You should check that out too.

This answer needs citations and an explanation of why my dog also sneezes.


text:
Is Protein-to-DNA ratio a good estimate of cell size?
I need help interpreting the result of an experiment. My class performed an experiment measuring protein concentration between heart, liver, and kidney tissue samples. The results were:

Heart: 4.714 mg/ml
Liver: 10.586 mg/ml
Kidney: 9.140 mg/ml

The DNA concentration was given to us and they were:

Heart: 8.6 ug/ml
Liver: 57.6 ug/ml
Kidney: 28 ug/ml

Computing the Protein:DNA ratio:

Heart: 0.548
Liver: 0.184
Kidney: 0.326

Doesn't this mean that the protein-to-DNA ratio has an inverse relationship with cell size as the results show that the liver tissue has the highest protein concentration and DNA concentration, yet has the lowest protein:DNA ratio. Also, why does DNA concentration differ so significantly between each tissue sample? My understanding is that genome remains the same between different cell types. So why does DNA size change?

Is this DNA concentration nuclear DNA only or does it also contain mitochondrial DNA? The amount of mitochindrial DNA will scale with cell size but also energy consumption rates, so it could influence an experiment like this. The nuclear-DNA/protein ratio for sure depends on cell size (and surface area) but also a lot of other factors like general protein expression levels and potentially multiple nuclei (this shouldn't apply to these organs though).

@Nicolai - there can be multiple nuclei in liver. It is quite known for its paritial polyploidy: "Cell and nuclear size varied between hepatocytes, as well as the number of nuclei per cell."

Regarding your last question: ignoring polyploidy, if a cell has the same genome packed into a smaller volume, it will have a higher DNA concebtration.

@bleubambooglu I am not sure from your question what are your thoughts on number of cells per sample (ml of sample). Your first question appears as if you think: more DNA in 1ml -> implies -> more cells in 1ml -> implies -> cells are smaller.
However, your second question appears as if you think: there is equal number of cells in 1 ml -> implies -> there should be equal amount of DNA.

@BagiM I had overlooked that simple aspect of the data, thank you!

So after discussing my concerns with my professor, I have found out that I overlooked the simple fact that the DNA concentration is not measured based on a single cell of tissue type.
Protein-to-DNA ratio is directly proportional to cell size and the reason why liver cells has the highest DNA concentration at 57.6 ug/ml is because they have a smaller cellular size compared to the other two. So a single ml of liver homogenate is going to present with a significantly higher cell count and thus, a higher DNA concentration. This is also why a single ml of heart muscle DNA concentration is only 8.6 ug/ml due to there much larger cellular size.
This finding can be confirmed from calculating the Protein:DNA ratio as the liver homogenate with its smaller cellular size is only 0.184 and the heart homogenate with its larger cellular size is the highest at 0.548.
Thank you everyone for trying to help me with this problem!


text:
protein size range for ultrafiltration or nanofiltration
I am hoping to concentrate mixed proteins in homogenized leafy vegetables such as kale, spinach etc (after removing pulp and fibers) as a first step in further investigations (second step using size exclusion to isolate frations), but am unsure what pore size is appropriate for ultrafiltration membrane as I do not know the dalton range of the mixture.
Is there a typical range of protein molecular sizes in Daltons found in plant matter?
Would appreciate any pointers.

Why not do SDS-PAGE and determine the size range?

Mind that protein isolation goes beyond size exclusion.

apologies for the abbreviated terms, edited question. I am a chem eng and fairly ignorant about biochemistry laboratory techniques. So, is it sensible to perform electrophoresis on the raw extract to determine the MW range? Can I do that without concentrating and "cleaning up" the raw extract? I was going do that as a later step.


text:
Have there been new discoveries concerning the perception of taste for the last 10 years?
What are the last discoveries concerning the perception of taste for the last 10 years?
We discovered the 5th flavour: umami.
Also the 6th and 7th: oleogustus and starchy.
Anything else?
Maybe in genetics, as we all have genetic predisposition?
Or concerning the creation of the systems in charge of the perception of taste during the embryo-genesis?

We welcome new users to SE Biology, but ask that they bear in mind that this is "a question and answer site", not a discussion site. "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do." This question does not fall into that category, but is a broad question about a field, inviting subjective answers. Furthermore, you provide no evidence of having searched the literature for reviews on this topic. Sorry, but I have voted to close.

The field of chemosensation is an active field of research. The answer to all your questions is yes. So, so much has been discovered in the last decade, both regarding detection by sensory neurons, genetics, behavior, the (embryological) development of these systems, and the coding of tastes and odors in the brain. What's more, there are many model organisms used to study this (insects [flies, moths, locusts, mosquitoes, etc.], worms, mice, zebrafish as well as in vitro methods (e.g. electrophysiology) currently in use.  Sadly you'll have to narrow down your questions to get concrete answers.

I'm not quite clear on exactly what you're interested in, but the short answer is yes, there have been discoveries related to the perception within the last 10 years.
The example that comes to mind is the role of the cannabinoid 1 receptor in the sense of taste of lipids.  The full text of a good article is available online here.

Source:
Brissard L et al. 2018. Orosensory Detection of Dietary Fatty Acids Is Altered in CB1R−/− Mice. Nutrients 10(10): 1347.


text:
What makes an E.coli an E.coli, genotype or phenotype?
According to this paper, among 61 strains of E. coli they studied only 6% of the genes are common in all. Which means that the overwhelming majority of the genes are not shared.
And wikipedia defines E. coli like this:

... is a Gram-negative, facultative anaerobic, rod-shaped, coliform bacterium of the genus Escherichia that is commonly found in the lower intestine of warm-blooded organisms (endotherms).

Which is a phenotypic  definition. My question is: what defines E. coli as a species: its genotype or its phenotype?

This is actually a very good and frustratingly obfuscated question.

That's more like a morphological description. Pre-genomic microbiological classification relied a lot on serological and biochemical tests.

Related, but possibly not a duplicate: https://biology.stackexchange.com/q/68853/36466

"Which means that overwhelming majority of the genes are not shared." You forgot to say "by all". The vast majority of genes are shared by the vast majority of E.coli. Also, phenotype and genotype are the wrong terms for talking about a genome — they are used for individual genes, not whole genomes. So, obviously, before whole genome sequencing bacterial strains were defined by general characteristics as @WYSIWYG says. Your question doesn't seem to me to address a real problem. Rather it concerns semantics, which in biology are best ignored.

I think there's more than just a semantic question here, although indeed species definitions are a bit of an arbitrary construct to begin with, decisions have been made to call certain organisms E. coli and others not.

@David in my experience, genotype can refer to an entire genome, most often with regard to a virus, as in HIV genotype, HCV genotype, etc.

@WYSIWYG serological and biochemical tests were used, but definitive identification included morphological description, at least during my infectious disease training

@DeNovo — Sloppy usage. One should encourage the use of plain English when this suffices. I would add that the genotype/phenotype is/was used and useful in relation to mutation of individual genes.

@David it's not sloppy usage. It's usage you're not familiar with :)

Interesting paper.
"... This is because the molecular cutoffs for demarcating species have been calibrated to yield the species groupings already determined by pheno-typic clustering. The 70% cutoff for DNA-DNA hybridization was calibrated to yield the phenotypic clusters previously recognized as separate species, and the 3% cutoff for 16S rRNA divergence was calibrated to yield the species previously determined by DNA-DNA hybridization and phenotypic clustering. "
--What are bacterial species? , Frederick M. Cohan 2002

@AhmedAbdullah Can you please add the additional refinements to you question by [edit]ing it? It would be clear to everyone without having to scroll through the comments :)

The context for identifying E. coli is primarily clinical Microbiology, and in the clinical lab the identification is primarily phenotypic, based on various properties such as growth and morphology on selective media, Gram stain appearance, biochemical characteristics, etc - only under unusual circumstances is genetic testing done. The latter is problematic because of extreme genetic diversity within the species and some overlap with others (even other genera).
The problems with the notion of "species" in E. coli in the context of 16s sequencing, horizontal gene transfer, mobile genetic elements, plasmids, etc is discussed at some length in Quammen's recent book The Tangled Tree.
For now, phenotypic species identification is the norm, as illustrated by the "Nomenclature" guidance to authors of the Journal of Bacteriology, a publication of the American Society for Microbiology.

Surely both. Nowadays, with molecular technics avaiable with low effort, the typing is mainly done with genotyping. This can be done using the 16S rRNA gene, which is composed by hyper-variable regions, as reported in picture. This choice is justified because this gene is highly conserved into the bacterial phylum, giving perhaphs variation into some regions due to evolution. This concept is explained by the term "molecular clock" in evolutionary biology.

By designing specific primers (they already exists for more species) you could obtain only amplification by E.coli cells. This is just an example, exportable also to other bacterial species: by analyzing other conserved phenotypes for every strains of this species, is possible to do also some real-time PCR using other regions of the genome. Remember always that isolation and, by so, phenotyping is required while doing bacterial identification; the genotyping is the fastest and most accurate way to the first recognition step.

I happened to encounter a related problem recently in answering a question regarding a paper on virus classification. I am not a microbiologist, so this answer may be flawed, however it raises a point that I don’t think has been made in the other answers. I welcome corrections.
First, however, it is obvious that bacteria were identified many, many years before their sequences were available, and, as indicated in the answer by @Argalatyr, classification could only be on phenotypic characteristics. The imprecision of this is acknowledged in a statement in a 2000 review article by Dijkshoorn et al. ‘Strain, clone and species: comments on three basic concepts of bacteriology’:

“A species consists of strains of common origin which are more similar to each other than they are to any other strain.”

The paper I came across previously was by Bobay and Ochman (2018) in which they state:

“Members of a biological species are defined by their ability to exchange genetic material”

This definition — by its nature genotypic — clearly predates the DNA sequencing era. (In asexual organisms like bacteria, exchange of genetic material can occur by recombination of DNA.)
It should also be mentioned that this definition applied to bacteria does not require members of the same species to have the same number of genes (the concern of the question), only that they can recombine.
In their paper Dijkshoorn et al. go on to discuss current efforts to correlate what, I assume, is this accepted definition with DNA-based comparisons — 16S rRNA sequencing and overall DNA percentage identity.

“Recently, a comparison of DNA–DNA pairing data and 16S rRNA similarity data showed that strains with rRNA similarity less than c. 97% generally showed no significant DNA–DNA reassociation and thus belong to different species. Similarity >97% may or may not indicate close relationship. The use of this percentage as a rule of thumb has in many cases made rRNA sequencing replace the more cumbersome DNA–DNA pairing technique for the creation of new species. At present, either the 70% or the 97% rule is used to underpin most proposals for new species.”

The moral would seem to be that we have reached a stage where it is cheaper and easier to try to define species from DNA sequencing that to go into the laboratory and perform experiments to see whether they can exchange genetic material.

Recombination and other genomic information exchange is arbitrary as a criterion; apart from the dichotomy of sexual vs asexual reproduction, recombination is often a biological not species characteristic. For example, HIV packages 2 copies of its genome - perhaps explaining its rampant recombination, whereas hepatitis C virus (HCV) recombination is a remarkably rare event.
Ultimately, sequence similarity thresholds are arbitrary as well. Species definition is largely a convenience for humans, not an intrinsic biological grouping.

@Argalatyr — I thought it was evident from my answer that I regarded taxonomic distinctions as arbitrary human constructs. Perhaps we should both make this explicit. Both answers addressed the question of practice. Your answer stated that the ‘norm’ for species identification was phenotypic. I have never studied taxonomy (or indeed organismal biology) but my answer drew attention to papers that implied that a different — genotypic — criterion constituted the ‘norm’. I did not, and do not, claim that this or any other classification is absolute, only that it appears to be in use.

I think we're in agreement that genotypic classification is rapidly getting cheaper, but the criteria for discuss definition remain somewhat nebulous. I don't think that exchange or genetic information will stand up as a species definition for the reasons that I provided.

@Argalatyr — I think that is generally recognized. The original virology paper Of the other question was concerned with the problem of horizontal transfer of individual genes. And I’m the last person to wish to be involved in controversies regarding what is or isn’t a species.


text:
How can inbreeding be used for selecting mutations?
I understand that inbreeding, after a number of generations of crossing genetically related individuals eventually yields homozygotes, however I can't seem to understand how it can be used for selecting mutations.

What particular allele is retained in the homozygote?  Where did that particular allele originally come from?

Consider a sibling-sibling mating system, the simplest inbreeding situation, with a simple Mendelian trait.
Step 0:
Let's start with heterozygotes, Aa x Aa.
Step 1:
Their offspring will be a collection of AA, Aa, Aa, aa, in roughly those ratios assuming equal survival.
Step 2:
Now we breed siblings. If we happen to breed Aa x Aa, we are back to the original starting point. Return to Step 1.
If we happen to breed AA x AA or aa x aa, and then continue to breed those offspring with their siblings, all of the following generations will be homozygous unless there is a mutation. Stop here, you have homozygotes.
If we happen to breed AA x Aa or Aa x aa, the next offspring will match those parents: AA, Aa or Aa, aa. If we breed Aa x Aa, return to Step 1. If we breed AA x AA or aa x aa, stop here, you have homozygotes.
Of course, theoretically you could end up with heterozygotes doing this forever, but the odds get lower and lower the more generations you breed.

For selecting a particular mutation, it is often simpler to genotype for presence of an allele rather than zygosity (i.e., just use simple RT-PCR). For example, if you want to eventually produce aa, you can test for the 'a' allele, and not breed any offspring that do not have any 'a', therefore they are AA. If you do this, you will always eventually end in a path with aa homozygotes.
If you have an easily produced model organism, you can also do this simply by phenotype (depending on the trait): once a strain settles into a consistent phenotype, you know you have a homozygote of one type or the other. If your model organism is easy to produce, it's okay if some don't end up carrying the mutation.
For selecting a random mutation, the same is true, except you have many genes instead of just gene "A". Any random mutation in just one individual early in the breeding could potentially be fixed in the inbred population somewhere down the line, following the steps above. If you breed BB x Bb, where Bb has a random mutation, you have a chance to breed a Bb x Bb pair in the next generation, which starts you at Step 0 for that particular random mutation.


text:
Can a less fit species evolve from a more fit species, by living at separate places?
[EDIT] if the genetic mechanism responsible for bringing about evolution is random, and if the environmental favoritism of some heritable traits over others is non-purposeful (like in the example of the black peppered moth during the era of industrial revolution: see here), then one would expect to see some examples of evolution that results in emergence of species the members of which has lower fitness than those of its immediate ancestor species. What I mean by that is that the genetic material in the gametes of some members of some species undergo changes that results in the emergence of a NEW SPECIES the members of which has lower fitness, that can go live in a separate environment.
Are there such examples? if not then why?
I'm not asking here about examples of an offspring having lesser reproductive rate than its parents and yet that offspring belonging into the same species of the parents. Of course that is well known to occur, since many hereditary disorders clearly affects the reproductive rate and survival of the affected individuals. No I'm asking about the emergence of a NEW SPECIES the members of which has lower fitness than those of its immediate ancestor species. The reason why I've mentioned that members belonging to the new species go live in a separate place from that of its immediate ancestor species, is because if they live in the same place, then clearly members of the ancestor species having more fitness would overcome members of the newly emerging species, to result in their extinction by natural selection, that's why I'm asking if it is possible for members of the new species to travel to another environment where it can live, albeit being less fit than members of the ancestor species from which it emerged. I call that backward evolution, though the term is odd, to mean that the direction in that particular case of evolution was towards lesser fitness rather than toward increasing fitness of members of the newly evolved species.
Are there such examples in the history of Evolution.
I'm not asking if the mechanism of such a step in evolution is due to Natural Selection, I'm asking if that evolution step can occur? and if it had occurred? And what are possible mechanisms behind such a step?
With the founder effect, what I'm understanding is that migration is the cause of lessening in genetic variation of the original population, and that this can possibly further lead to emergency of a new less fit species.
What I'm asking about here is a little bit different, I'm asking if the emergence of the new species caused the emerging (less fit) population to migrate as to avoid competition with members of the more fit original species. And because of this separation in place both populations need not compete each other for available resources, since they live at distant places. In other words, if some mechanism caused the birth of some less fit individuals that belongs to a distinct species form its ancestor, and such that those less fit individuals migrated as to avoid competition with the more fit ancestors, and that by this migration they managed to survive and reproduce. So it is not that migration caused at the end the less fitness, as in the founder effect, No its the opposite, its the less fitness that caused the migration.
I hope the question became clear now.

Comments are not for extended discussion; this conversation has been moved to chat.

Frankly your edited question is still unclear, although it does add more emphasis on sub-populations traveling to new environments. Please explain how the founder effect (which has been mentioned already) doesn't answer your question.

And your question still has major terminology issues that make it hard to answer (despite all the efforts of commenters to make you clarify what you mean), chiefly your usage of species instead of populations and perhaps your confusion of evolution with natural selection,

@Fizz, thanks about reference to "founder effect", I've updated my question, I hope its understandable now. I'm not familiar with the founder effect, I'm not sure if what I'm asking is an example of it, but from the reference you've linked it appears to be 'change due to migration' while here what I'm asking is "migration due to change", i.e. that some genetic mechanism caused the emergence of individuals that has different genetic material from the original population, such that those individuals belongs to a different species that are less fit than the original population, that caused them

.. to migrate, in order to avoid natural selection, selecting against them in favor of the original species which is more fit then them.

its a kind of evolution avoiding natural selection, thereby produce emergence of less fit species from more fit ones. Can this happen? actually did this happen? and if yes, by what mechanism?

Your updated question sound a bit like shifting balance theory, which is itself hard to test, except that in your question you insist on some poorly defined lower fitness... Fitness depends on the environment; if geographic division occurs, the environment is not the same for the sub-populations (and eventual species) so it makes little sense to compare population/species fitnesses that way. In that regard see "is evolution progressive?"

@Fizz the fitness I'm speaking about is the average number of reproductions per individual in the population. So its not poorly defined. That's beside the two geographic locations might have similar environments yet be distinct in place. So comparisons can be allowed.

Ok, so compare the average number of reproduction per individual between coyotes and humans. And conclude what from that? (Your definition of fitness is another idiosyncrasy.)

And since my last comment was probably not educational/detailed enough on that confusion: http://gregladen.com/blog/2013/07/19/reproductive-success-and-fitness-are-not-the-same-thing/ That was also discussed here, in less detail: https://biology.stackexchange.com/questions/45248/whats-the-difference-between-evolution-fitness-and-reproductive-success

@Fizz, that's not my definition that's what's written in the introductory reference that was cited to me here including Wikipedia article on natural selection. second I'm speaking about the relative fitness of members of a species and those of its immediate ancestor, neither coyotes came from humans nor humans from coyotes. also see your references.

You have a lot of individual questions together, you may have better luck asking them individually. Generally only one question per question is accepted.

The question contains a fair number of issues as explained in the comments. I won't go through them here. I will phrase some specific questions which might be of interest to you and very quickly answer them

Can an offspring have a lower fitness than its parent?

Yes, of course. There is a whole load of environmental reasons for that but leaving them aside, the offspring might have inherited some new deleterious mutations

Can the offspring population have a lower mean fitness than a parent population?

Yes. Under constant environment, with an population of infinite size, without migration, without mutations, it would not be possible (unless some fancy linkage disequilibrium and epistasis) as, in such circumstance, the mean fitness of a population increases exactly by the additive genetic variance of the parent population.
However, populations are never infinite. Hence genetic drift is in play and can cause the mean fitness to randomly vary which may cause a drop from any generation to any next generation. Other things such as an environmental change or an extreme mutation rate may also cause the mean fitness to decrease.

Can an offspring have fewer offspring than its parents

Yes. Fitness is an expectation. There is variation from it. Whether or not the fitness of the offspring is higher or lower than the one of the parent, it still remain that there is variation from the expectation.

Can a mutation undo a previous mutation.

Yes.

Can an entire population back to the exact same stage it was a few generations back.

If by exact same stage, you mean "exact same genome of the entire population", then this would be so fantastically unlikely that I will just say no.
Edit

I think you need to post that as an answer explaining why NS will "by definition" always acts to increase the frequency of more fit individuals,

NS is defined as the fitness differential among different genotypes in a populations. The change in allele frequency that results from this fitness differential. Individuals with higher fitness leave more offspring than those with lower fitness leading to a change in allele frequency, alleles associated increase in frequency.

I think you need to post that as an answer explaining why NS will "by definition" always acts to increase the frequency of more fit individuals, so that there cannot be an instance of speciation whereby a less fit species evolved from a more fit species.

You misunderstand the concept of speciation. Your sentences are so non-sensical that it is really hard to be of help to you. Really, you should just have a look at an intro course to evolutionary biology.

I find some difficulty in understanding how NS is "not purposeful", it seems to have a purpose to me, namely "producing more fit species from earlier ones", this is a kind of purpose.

The term "purposeful" is never used in science as it is very much undefined. The term feels to me that to have a purpose you need a conscience or a will. Obviously NS is not a small green creature hidden somewhere with the goal of making life evolve. It is just a natural phenomenon like many others.
You should just follow an intro course to evolutionary biology to understand what the terms natural selection, evolution, mutation, genetic drift and speciation mean.

By then if fossil evidence or laboratory evidence documents an event of what I'm saying here, it means that NS is false. right

I don't understand what you refer to by "what I'm saying here" either.
I highly recommend that you follow a short intro course to evolutionary biology (such as evo101 for example). It will take you a few hours and you will learn a lot. Also, you will be able to ask questions that don't give a headache to whoever is reading it :) Good luck!

Comments are not for extended discussion; this conversation has been moved to chat.


text:
Is it possible to determine if it is the 5’-a 3’ strand or the 3’-5’ strand?
DNA is constructed in an antiparallel manner.  This means if you number each of the 5 carbons in the sugar deoxyribose the 3rd carbon will be connected to one phosphate group and the 5th carbon will be attached to another phosphate group of another nucleotide.  One strand will go from the 5th carbon atom to the 3rd carbon atom in one direction(5’ -3’).  and the complementary strand will go in the direction of the 3rd carbon to the 5th carbon in the same direction(3’-5’). Essentially they are made in opposite directions.  If I tell you the nucleotide base sequence of one strand is ACGGACTA.

I'm not clear what you are asking. If you are asking about convention, convention is to write sequences 5' to 3' (https://biology.stackexchange.com/questions/71530/what-direction-is-a-sequence-in-databases-written). If you are asking "which strand is the 5'-3' strand" the answer is both and neither: it would be like asking which side of a street is the forward side, they are both forward sides and reverse sides, it depends which direction you are traveling. Can you clarify your question?

Are you asking whether there is a convention for writing polynucleotide sequences? If so, the answer is yes, 5’ to 3’. But you might have researched that yourself.

Good analogy, @Bryan.


text:
Are there known counterexamples to Hennman's size principle for muscle unit recruitment?
It is known that generally muscle units are recruited from small to large, and that typically also means slow to fast twitch.  This principle is called Hennman's size principle.
I've seen many articles backing this claim up.  However, I'm curious if there are any known situations where this principle is known to fail.  (Perhaps when there is a known impulse arriving shortly and it needs to be opposed by large fast-twitch muscle).
All I have found so far are articles which agree with the principle, but it seems surprisingly simple for a biological system.


text:
Where does the proton come in the reduction of NAD?
In our curriculum biology textbook the reduction of NAD+ is depicted as follows:
NAD+ + 2 H+ → NADH + H+
If this proton in the products was not present in the reactants, then where does it come from? Alternatively, if it does not take part in the reaction, then why is it depicted?

Can you reference the book? It's a bit weird, usually, NAD reduction is written simply like NAD+ + H+  >>  NADH, you don't need the extra proton. Having some more info from the book paragraph you have found this reaction may help.

In a very simple way the equation describes the reaction. NAD is reduced using 2 hydrogen atoms. The two hydrogen atoms can come from one reactant (lactic acid fermentation) or from two (in a reaction of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate; as shown in the figure below).

First of all, I will pick a particular example from glycolysis, catalyzed by glyceraldehyde-3-phosphate dehydrogenase.

Phosphate by its own has one hydrogen at cytosolic pH (because of the pKA). Thus in this reaction, there are two hydrogen atoms. One hydrogen atom is in the form of a hydride (a proton and two electrons) from the aldehyde group. This hydrogen atom is used to reduce NAD+ to NADH. A second hydrogen atom (in the form of a proton) comes from the phosphate. In the bisphosphoglycerate form, the proton dissociates from the phosphate group and is in solution.
The eventual fate of the electrons that were used to reduce NAD+ to NADH is the electron transport chain (in the mitochondria). In some cases, though, for example muscle cells in an anaerobic environment, or other species that don't have an electron transport chain, the electrons are used in fermentation of pyruvate to alcohol or lactic acid. When NADH donates its electrons in either case, it is then oxidized back to NAD+.

References:

Glycolysis
NAD
Lactic acid
fermentation
HPO4

Hi LDiago. I've edited your post to make it a little more readable, and added a little more explanation in a few parts. I hope you find it helpful! Please feel free to rollback if I've inadvertently changed the meaning, or you disagree with me on style.

A quick search on Wikipedia showed the same reaction you book is presenting.

In metabolism, the compound accepts or donates electrons in redox
reactions.[2] Such reactions (summarized in the formula below) involve
the removal of two hydrogen atoms from the reactant (R), in the form
of a hydride ion (H−), and a proton (H+). The proton is released into
solution, while the reductant RH2 is oxidized and NAD+ reduced to NADH
by transfer of the hydride to the nicotinamide ring.
RH2 + NAD+ → NADH + H+ + R

This should answer your question.


text:
What does the difference between GPP - NPP represent?
Overview
Researchers have been studying a temperate grassland ecosystem with the view to understand it's current status with regard to carbon inputs and outputs and to identify whether the grassland is currently a sink or source of carbon.
The aim of this self-study is to become more familiar with different energy fluxes within the terrestrial carbon ecosystems.
The idea is to calculate energy fluxes in various scenarios, and I am feeling a little confused about the scientific theory of gross primary productivity (GPP), net primary productivity (NPP), net ecosystem production (NEP), net ecosystem exchange (NEE), RT = Total respiration, RA = animal respiration, and RS = soil respiration,
If anyone can help, I would be deeply appreciative.
The relationship between production fluxes and other fluxes summarised by these key equations:

NPP = GPP - (plant respiration)
NEE = NPP - (heterotrophic respiration)
NEP = NEE - (carbon losses from leaching, disturbance, and other inputs, and outputs)

Table of flux values

Questions:
What does the difference between GPP - NPP represent? In other words, what is GPP-NPP equal to (see table for values)? Is the value of 800 equal to respiration?
GPP - NPP = R
1400 - 600 = 800
I understand that GPP is the overall rate of biomass production by producers at the rate at which solar energy is captured as carbohydrate molecules during photosynthesis and NPP (energy captured per unit error per unit time). Producers such as plants use this energy respiration and growth.
I also understand NPP is the rate of energy lost to metabolism or maintenance or the energy stored as biomass by plants or primary producers in the ecosystem.
I am making the assumption that this value of 800 is associated with the respiration of plants; although, I am still confused with what this value represents. From my way of thinking, the difference between GPP-NPP equals the extent of CO2 lost from plant respiration within the ecosystem. Since the value of GPP (1400) is larger than the value for NPP (600), more energy has been used during the intake of carbon during photosynthesis rather than plants using glucose or the energy stored in the system to photosynthesise for the emission of CO2.
Therefore, this value represents the amount of CO2 that is lost from plant respiration or from metabolic activity.
Am I on the right track? Do I have the right ideas about energy fluxes?
Diagram

I'm going to answer your question, but could you say where your table of values comes from?

Hey Oosaka, the table values in the table come from a study on a temperate grassland ecosystem. The values are part of an assignment question without a reference, so I am not sure if they come from an authentic study. I think the idea is to manipulate values to obtain an understanding in the theory, which I am finding very confusing the more I read. Many thanks for your help, I am extremely grateful.

I'm mostly confused by how the respiration rates don't add up, but I'm going to guess it's because Rs (soil respiration) includes respiration from the roots of plants, meaning it includes some plant respiration.

Me too! That's the next question. What is included in total respiration (RT). I’ve been sitting here for 2 hours trying to figure this out

Total respiration is all of the respiration happening in the ecosystem; it can be broken down in many different ways. For example your schematic breaks it down into "heterotrophic respiration" and "plant respiration" (i.e. plant respiration, and respiration by all other organisms in the ecosystem). Your table of values doesn't so much break it down as give some different subsets; soil respiration is respiration by everything underground, which includes both plants and heterotrophs. Hence why you can't add Rs+Ra to plant respiration to get total respiration because you double-count plant roots.

I am glad you said that because I was thinking along the same lines; RS + RA = 950; RP = 800. However, this still does not make any sense because the values put into different combinations do not seem to RT=1300

I don't think you're supposed to combine them to get total respiration. Did the assignment suggest you were? I'm guessing those values are given because they're those that were measured; some quantities are easier to measure than others. Soil respiration for example can be measured by finding how much CO2 comes out of a patch of soil; simple enough.

It just says: The researchers have meaured the total ecosystem respiration as RT=1300 g/C/m-2/yr-1. What is included is included in this total respiration? Then researchers have calculated soil respiration as 900 g/C/m-2/yr-1, and animal respiration above groundas RA = 50g/C/m-2/yr-1. The values for plant shoots (R,P-S), plant roots (R, P-R), and microbial activity (RM). I am just making a power point diagram now to add boxes and values to get the + and - parts right

What does the difference between GPP - NPP represent?

The answer is in your overview: it's plant respiration.

Is the value of 800 equal to respiration?

That is the unavoidable consequence of the equation you presented and the numbers you plug in, yes.

I understand that GPP is the overall rate of biomass production by producers at the rate at which solar energy is captured as carbohydrate molecules during photosynthesis and NPP (energy captured per unit error per unit time).

That sentence was fine until "and NPP". What is it doing there? Did you misquote something or are you thinking NPP is a process like photosynthesis?

Producers such as plants use this energy respiration and growth.

Yes.

I also understand NPP is the rate of energy lost to metabolism or maintenance or the energy stored as biomass by plants or primary producers in the ecosystem.

No. NPP is the energy stored as biomass by plants or primary producers in the ecosystem (or rather the rate at which such energy is stored, if it's productivity you're talking about and it's in gC/m-2/yr-1). Respiration is the energy lost to metabolism or maintenance. GPP is what that sentence seems to be describing, as it's the total carbon captured by plants, i.e. whether it's used to build up the plant's biomass or used by the plant in its metabolism (i.e. respired).

I am making the assumption that this value of 800 is associated with the respiration of plants;

Correct.

although, I am still confused with what this value represents.

Maybe you should study the metabolic processes of plants and life in general to better understand this. All life consists of chemical reactions that build up structures; in order to build them up you need energy (because of the second law of thermodynamics), and all living things create that energy by breaking down complex molecules into simpler ones. (as such it would be more accurate to say that all life consists of chemical reactions that build up and break down various structures). You might be wondering "but what about the difference between autotrophs and heterotrophs I heard about"; the difference between those is where they get the complex molecules from in the first place. Autotrophs use a different source of energy to build them up while heterotrophs get them from their environment. As such, you can think of every living thing as being made of two kind of molecules: those that actually form their structure (in humans, the molecules that make up cell membranes, bones, muscles, etc) and those that are stored in order to be broken down to power the whole system (in humans that's fat, glycogen, glucose, etc). Of course a molecule can do both; if you're starving your body may start to break down structural molecules for power. There are many different ways of breaking down those big molecules for power; the most efficient one, that starts with a big chain of carbon atoms and cuts it down into individual CO2 molecules using O2 molecules, is called aerobic respiration (i.e. respiration that uses oxygen).
Because those complex molecules are required to power all life, autotrophs (the organisms that actually make them) are very important, and the processes they use to make them are very important too. The process that makes almost all of the molecules that power almost all life on earth is photosynthesis, which uses the energy from the sun to power a reaction that converts CO2 from the atmosphere into big carbon-based molecules we'll call carbohydrates. This is called "fixing carbon", since the carbon atom is the most important one; measuring how much photosynthesis is happening is another way of measuring how many carbon atoms move from being part of a CO2 molecule to being part of a plant.
GPP is the measure of that exact process: how many grams of carbon per square meter per second (or year in your graph) move from being in a CO2 molecule to being part of a plant via the process of photosynthesis.
You might think this is also a measure of how much the plant grows, but it ignores the fact that as I said, all living things contain molecules that make them up and molecules they break down for power; obviously the plant's growth will involve the former, and the latter just goes back to being CO2 through the process of respiration. Another way of putting it is that in the flow of carbon, there is a huge flow of CO2 to plant molecules via photosynthesis (GPP), but a huge proportion of that flow goes right back the other way (the plant molecules are broken back down into CO2 via the plant's respiration); the remaining flow that's actually still in plant molecules at any given time is NPP.
NPP is the proxy for plant growth; it's basically how much of the carbon the plant fixed via photosynthesis it actually contains in its body, while R (respiration) is how much of the carbon it fixed it broke back down for energy, releasing it as CO2 into the atmosphere. Hence, GPP = NPP + R, and GPP - NPP = R.

From my way of thinking, the difference between GPP-NPP equals the extent of CO2 lost from plant respiration within the ecosystem.

Indeed.

Since the value of GPP (1400) is larger than the value for NPP (600), more energy has been used during the intake of carbon during photosynthesis rather than plants using glucose or the energy stored in the system to photosynthesise for the emission of CO2.

I don't understand this sentence at all. The fact that GPP is larger than NPP shows that plants don't keep all of the carbon they convert from the atmosphere to make up their physical structure; they also use a lot of this carbon to power their metabolism through the process of respiration, which results in said carbon turning back into CO2 and being released back into the atmosphere (as opposed to staying in the form of wood, leaves, starch, etc).

Therefore, this value represents the amount of CO2 that is lost from plant respiration or from metabolic activity.

That is correct, with the two caveats that it's the amount of carbon fixed in organic molecules that is lost by being released into the atmosphere under the form of CO2, and that there is no "or" - all plant metabolism is fuelled by respiration, and the only metabolic activity that releases CO2 is respiration.