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Does Glycolysis produce lactate, or pyruvate?
EDIT- Somebody suggested that this is the same question as this, it isn't. This one is asking about the definition of glycolysis. That one was asking about the definition of fermentation.
Does Glycolysis produce lactate, or pyruvate?
I'm aware that ultimately in the human body, after sugar is converted into pyruvate, then if fermentation happens it will be converted into lactate, or if aerobic respiration happens then it won't.
My question is on the term Glycolysis
I notice that most sources seem to say glycolysis ends with pyruvate
e.g.
Glycolysis.. is the metabolic pathway that converts glucose.. into pyruvate
The only time lactate comes into it is After glycolysis.
(so in this wikipedia page on Glycolysis, in the Post Glycolysis part it mentions this)
https://en.wikipedia.org/wiki/Glycolysis#Post-glycolysis_processes
"pyruvate is converted to lactate "
However, on the other hand, I see some sources, even another wikipedia article titled "anaerobic glycolysis", which the page says isn't well sourced, it has glycolysis as ending in lactate.
https://en.wikipedia.org/wiki/Anaerobic_glycolysis
"Anaerobic glycolysis is the transformation of glucose to lactate when limited amounts of oxygen (O2) are available"
Also here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4343186/
"we contend that La− is always the end product of glycolysis"
(putting aside their controversial claim that it is always the end product, i'm interested here in the idea of theirs that it is ever an end product, so, their use of the term glycolysis)
So it seems that there are those two positions
For the purposes of this question i'll call one position the lactate position and the other position the pyruvate position.
One position, call it the lactate position, which is those sources that place lactate,  as the end product of glycolysis.. thus counting not just sugar->pyruvate, but sugar->pyruvate + the whole fermentation process, as glycolysis.
While others, call this the Pyruvate position,  count purely sugar->pyruvate those sources count just that, as Glycolysis.
I'm wondering if both definitions are correct.. / both usages are valid.. Or if one of those e.g. if the lactate one, is an odd one out and if most academic texts wouldn't use that definition, and would use the pyruvate position for their definition of Glycolysis.
Note- I had written that glycolysis ends with pyruvate {or pyruvic acid which dissociates into pyruvate}, and the lactic acid fermentation ends in lactate {or lactic acid which dissociates into lactate}. But what is in those curly braces there is wrong and I have been corrected on that one. Glycolysis produces pyruvate, and Lactic Acid Fermentation produces lactate.  The reason (answerer David explains), why Lactic acid fermentation bears that name, is it is named after what are called "lactic acid bacteria" "Lactic acid bacteria are named for their effect on the medium in which such bacteria grow, not for the ionization state of lactic acid in the cell and when bound to enzymes (about which the namers could have had no knowledge)." and they do that type of fermentation that produces lactate.  There are two types of "lactic acid fermentation", https://en.wikipedia.org/wiki/Lactic_acid_fermentation  homolactic fermentation, and heretolactic fermentation. Humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol https://www.onlinebiologynotes.com/different-fermentation-pathway-bacteria/
Also, note that Muscle cells do what is called "lactic acid fermentation", but the idea that they produce lactic acid is a myth that has been commonly propagated in sports science(I guess perhaps partly as a result of what I think is biology's poor nomenclature, the fact that the process is called lactic acid fermentation). Muscles don't produce lactic acid, in fact, it's not lactic acid and they don't produce it. Muscle cells use lactate, they don't produce lactic acid. This is verifiable from googling humans produce lactate not lactic acid eg the first line here mentions that myth and calls it out as a myth.  The  body of the following question and its answers here are related and very interesting.

Possible duplicate of Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?

@bpedit No it isn't. That question you linked to is asking about the definition of fermentation. This is asking about the definition of glycolysis. I shall edit my question and make that point

"or pyruvic acid which dissociates into pyruvate" No. Pyruvic acid is not the product of pyruvate kinase reaction. The substrate (PEP) is ionized at cellular pH and I imagine the enzyme will bind its negative charges. That part of the molecule is not changed.

@David ok is this similar statement correct? "or lactic acid which dissociates into lactate"

No. It's lactate. The pKa is ca. 3.9.

Yea. Pyruvate is formed.. No chance of formation of lactate
... Thats glycolysis. The synthesis of glucose into pyruvate by the use of several enzymes

@David So why is that fermentation sometimes called lactic acid fermentation  and not a name like lactate fermentation https://en.wikipedia.org/wiki/Lactic_acid_fermentation  (i'm assuming lactic acid fermentation is the same fermentation that produces lactate?)

Lactic acid bacteria are named for their effect on the medium in which such bacteria grow, not for the ionization state of lactic acid in the cell and when bound to enzymes (about which the namers could have had no knowledge). Anaerobic oxidation of glucose to lactate also produces a hydrogen ion which would cause the pH in the cell to drop if this, and the counter-ion lactate were not excreted from the bacteria (or from the mammalian muscle), Thus it is the external medium (or blood) that becomes acid.The LDH structure shows lactate bound by +ve counter-ions, as expected at this pH.

@David and to clarify, when you say " the ionization state of lactic acid in the cell and when bound to enzymes "  Do you mean that in the cell and when bound to enzymes or anywhere in the body, it's lactate, not lactic acid?

I mean when bound to enzymes or immediately on generation in a reaction. (The latter is covering my back for the remote possibility that a reaction mechanism might actually generate -COOH, e.g. by the oxidation of an aldehyde. But this certainly does not happen as the acidic residue in pyruvate and lactate is generated way back in glycolysis as 3-phosphoglycerate.) However, without wishing to patronize you, I wonder how familiar you are with the ionization properties of weak acids. Do we need a question relating to this material?

A key term in the study is "anaerobic" glycolysis, glycolysis is part of aerobic metabolism as well.

I think you will find all text books (e.g. Berg et al. Ch 16) describe glycolysis as the conversion of glucose to pyruvate, as this is how it has been defined and considered in countless biochemical papers. The subsequent reactions of pyruvate  are regarded as separate metabolic steps or pathways.
The title of the short review article you cite (“Lactate is always the end product of glycolysis”) has mislead you — it was obviously meant to be controversial. It is the ambiguous term “end product” that is the (deliberate?) cause of the problem. What the article suggest is that the product of glycolysis — pyruvate — is always, at least partially, converted to lactate in animal cells. It would have been better entitled “Lactate is always produced from the pyruvate generated in glycolysis”. Whether or not that is true (and that is not your question as I understand it), the conversion of pyruvate to lactate is not considered to be part of glycolysis any more than its conversion to acetate.
There may be ambiguity in the use of the ancient term ‘fermentation’, but not with glycolysis and other metabolic pathways established in the twentieth century.

Thanks. What is your view regarding this source I mention in my question https://en.wikipedia.org/wiki/Anaerobic_glycolysis "Anaerobic glycolysis is the transformation of glucose to lactate when limited amounts of oxygen (O2) are available"

As a stickler for correct nomenclature I liked this answer, +1.

@barlop — This entry relates to Anaerobic Glycolysis and is obviously incorrect as anaerobic glycolysis in brewer's yeast leads to the production of ethanol. You or I could edit it to correct it if we felt like it. The Wikipedia entry on Glycolysis is much more detailed and documented. The first illustration shows the conversion of glucose to pyruvate.

@David funnily enough I see that the more comprehensive Glycolysis page says https://en.wikipedia.org/wiki/Glycolysis  "Fermention of pyruvate to lactate is sometimes also called "anaerobic glycolysis", however, glycolysis ends with the production of pyruvate regardless of the presence or absence of oxygen."

@user1136 Could you give me a page ref. because I suspect your quotation is taken out of context. Figure 16.3, Table 16.3, and the separate discussion of different fates of pyruvate (Figure 16.10) all indicate that Berg et al. regard glycolysis as the conversion of glucose to pyruvate.

@user1136 I am afraid the paper you cite uses a definition of glycolysis that differs from that in general use, perhaps because the authors appear to be chemists, rather than biochemists. The Greek root of a word does not constitute a definition of its English meaning, but, in any case, glucose is split in the formation of pyruvate which is then reduced, rather than being split further, if it goes on to form lactate. Berg is careful to refer to "the pathway", not "glycolysis", and immediately goes on to say that "the fate of pyruvate is variable" and "three reactions are of prime importance".

@user1136 — I replied to your comment out of courtesy, however I now see that you have your own answer and were involved in long series of comments which was moved to chat. I was not involved in the criticism of your answer, and I really think it better if you desist from commenting on mine now. Just let the answers stand on their own for people to decide. This is not an undergraduate debate about what Berg did or did not mean.

Lactate, not pyruvate, is the end-product of glycolysis. If pyruvate was the end-product, there would be a major problem: glycolysis would stop.
I am talking here about how cells 'obtain' ATP from the splitting of glucose under strict anaerobic conditions (glycolysis).
Glycolysis is the splitting of glucose, and occurs anaerobically without any net oxidation or reduction, and the free energy sequestered in the form of ATP is derived from the splitting reaction.  In thermodynamic terms, we can envisage that entropy makes a contribution to the overall (favorable) Gibbs free energy change: splitting a molecule into two parts makes the system more disordered (to take a crude view of what entropy means). But of course the rearrangement of chemical bonds will also make a (major?) contribution.
Let's be blunt about the role of oxidation and reduction: as stated, there is no net oxidation or reduction in glycolysis.  But in this last statement lies a major paradox, and  therein is the reason why we must consider lactate  (and in alcoholic fermentation, ethanol) the end-product of glycolysis.

Although glycolyis proceeds without net oxidation or reduction, a supply of oxidied NAD (i.e., NAD+) is required in order for the process to continue.

I am of course talking about the glyceraldehyde-3-phosphate dehydrogenase (GAPdh) reaction, that ubiquitous enzyme of glycolysis.
$$ \mathrm{\text{glyceraldehyde-3-phosphate}\,+\,NAD^{+}\,+\,P_i\text{ =  }\text{1,3-bisphosphoglycerate} +\,\,NADH\,+\,H^+}$$
Pyruvate production from glucose is an oxidation - we have 'removed' a pair of electrons (strictly speaking, 2 pairs), but for glycolysis to proceed we (paradoxically) need a reduction - we must (somehow) get rid of the electrons from NADH, and one way (crazily at first sight) is to 'give' the electrons back to the carbon skeleton from whence they came - to pyruvate in the case of muscle (lactate) glycolysis.

One of the key steps to understanding glycolysis is to ask the question: how is the NADH produced in the GAPdh reaction oxidized back to NAD+?

In lactic acid fermentation and in muscle glycolysis, this it done with lactate dehydrogenase (LDH), which catalyzes the NADH -linked reduction of pyruvate to lactate, with concomitant production of NAD+, thus allowing glycolysis to continue. If we could 'knock out' the LDH gene, there would be no glycolysis (a lethal mutation), unless the cell could somehow find another method of regenerating NAD+.
The splitting of glucose into lactate may be represented stoichiometrically as follows (one glucose is split into two lactic acid molecules):
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\text{ = 2 }CH_{3}\,CHOH\,COOH}$$
We may note that there is no oxidation or reduction. In aerobic respiration, glucose yields 12 pairs of electrons to the respiratory chain, and all are 'held' in either carbon-carbon or carbon-hydrogen bonds.  Each lactate acid  molecule (or more precisely, each lactate molecule) has six (C-C and C-H) bonds: they are all there, nothing has changed.
Furthermore, it is the above reaction that yields the free energy, no matter how we view the intricacies of the molecular processes that lead to it. That is, fundamentally, lactic acid fermentation (or muscle glycolysis) is a sequestration of Gibbs free energy, in the form of ATP, obtained by the splitting of glucose into two molecules of lactate.
In the case of pyruvate, we would need to write the equation (balanced in terms of electrons but not hydrogens) as follows:
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\,+\,2\,NAD^{+}\text{ = 2 }CH_{3}\,(C\text{=}O)\,COOH  +\,2\,NADH}$$
If we count the number of (C-C and C-H) bonds in pyruvate, we see there are five: one pair of electrons is 'missing' and is now 'held' by the nicotinamide cofactor.
So what of alcoholic fermentation? How is NADH re-oxidized here? In this case, pyruvate is first decarboxylated to acetaldehyde and CO2 by the enzyme pyruvate decarboxylase, and  NADH is reoxidized by the enzyme alcohol dehydrogenase acting as an aldehyde reductase. That is, the NAD+ necessary for the GAPdh reaction is 'regenerated' by the reduction of acetaldehdye to ethanol. As far as anaerobic fermentation in yeast is concerned, ethanol is a 'waste' product (but very useful to us humans).
$$ \mathrm{CH_{3}CHO\,+\,NADH\,+\,H^{+}\text{ = }CH_{3}CH_{2}OH\,+\,NAD^{+}}$$
If we count the number of (C-H and C-C) bonds in acetaldehyde, there are five, but in ethanol there are six. As two molecules of ethanol are produced for each glucose, the total is twelve and we have accounted for everything: once again there is no net oxidation and reduction, and the stoichiometric splitting of glucose  in alcoholic fermentation may be written as follows (one glucose gives two molecules of ethanol and two molecules of carbon dioxide),
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\text{ = 2 }CH_{3}CH_{2}OH\,+\,2\,CO_2}$$
and it is the Gibbs free energy 'released' in this reaction that is used to 'make' ATP.
NADH produced in glycolysis may also be regenerated 'aerobically', that is by reoxidation in mitochondria via the respiratory redox chain. The problem here is that the inner mitochondrial membrane is impermeable to NAD, and a  shuttle system, such as the aspartate-malate shuttle, is required to get the electrons across the inner membrane. If NADH is regenerated via mitochondrial respiration, this is of course an alternative to the LDH reaction and lactate need not be formed (but we are no longer talking about anaerobic glycolysis). This, I suspect, is where the confusion often arises.
To make one final point about lactate glycolysis in humans. A muscle cell, perhaps obtaining as much energy as possible from glycolysis during vigorous exercise, regards lactate as a waste product. But this is not true of the organism as a whole: the lactate is taken to the liver where it may be converted back to glucose (via pyruvate) as part of the Cori cycle (which is way beyond the scope of this answer).
So why the apparent paradox of NAD oxidoreduction during glycolysis? And why oxidize a carbon skeleton with NAD+ and then regenerate the oxidizing agent by reducing the carbon skeleton at a later step? I have no explanation, but this is surely a great example of what Albert Lehninger called the molecular logic of living organisms.

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What is this insect in Southern California?
I saw this insect flying around in Southern California, USA during the summer. It is about 1.25 cm in length. When it flies, it opens up its wings like a ladybug's.  What is this?

You want to add the species-identification tag to your question, and say something about size; this will bring your question to the attention of those most likely to be able to answer it.  If you have better photographs, adding the best of them will also help

The observation about the way it opens the wings, like a ladybug, is a good one. Both are Coleoptera: https://en.wikipedia.org/wiki/Beetle. "Coleoptera" means something like "with shielded wings". Like most insects, they have two pairs of wings, but the front one is hardened and has a protecting role. The animal has to open this "shield" to allow the rear pair of wings to do the flying job.

It appears to be a type of beetle, most likely a May beetle (genus: Phyllophaga).

This is a scarab beetle that belongs to the genus Cyclocephala, and has the nickname of "masked shafer" (gallery). There are over 300 different species within this genus, however, the species most common to southern California is C. hirta and C. pasadenae, with me leaning more towards the former.

C. hirta; San Diego County, CA (source)

C. hirta; San Leandro, CA. (source)

C. pasadenae; Vail, AZ (source)

When it flies, it opens up its wings like a ladybug's.

Ladybug, left; masked chafer, right.

I have seen that bug for years, I know its a type of beetle and you are not suppose to smash em. This is just coming from my own research and talking with friends. I think they are called June Bugs.
Heres a descriptor I found.
mahogany-colored beetle of the scarab beetle family, widely distributed in North America and especially abundant in the NE United States and the adjacent parts of Canada. It is also known as June bug, although true bugs belong to a different insect order. The adults, which may swarm in great numbers in early summer and are attracted to lights, feed by night on the foliage of deciduous trees and hide during the day. The eggs are laid in the soil, where the larvae, called white grubs, remain for two or three years, eating the roots and other underground parts of grasses, grains, and trees. The grubs cause great destruction to lawns and fir trees. Many birds and small mammals, such as skunks and pigs, root out the grubs and eat them. The insects pupate underground in the fall and emerge as adults the following spring. June beetles are sometimes called cockchafers, a name used primarily for some of their close relatives in the Old World. They are closely allied to the leaf chafers, including the rose chafer. June beetles are classified in the phylum Arthropoda , class Insecta, order Coleoptera, family Scarabaeidae.

For the people down voting my response, its better than nothing.  If you know what this is then post otherwise stop being a keyboard warrior troll.

It would seem that your response was accurate to the family. And to speculate as to your incurred downvotes.. I believe that people generally expect a [brief] response that contains an image of two, and at least one source. Even though your response was somewhat correct, your presentation is what kept it from being better received.

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Is water released when a phosphodiester bond is made between two nucleotides during DNA replication?
I know that when two sugar molecules (like glucose) connect to each other, H2O is released because of the -OH and -H groups in both of the molecules. I want to know if the same thing happens when two nucleotides connect to each other during DNA replication.

Welcome to Biology.SE! What research have you done before asking it here?

yes there is no water release during phosphodiester linkages because the 3'OH of the growing daughter strand exerts a nucleophilic attack on the phosphodiester linkage between the alpha phosphate with the beta & gamma phoshate of the deoxyribonucleoside triphosphate.
During such formation there is no hydrolysis rather it would precisely be a transesterification type of organic reaction.
REFERENCES:TEXT BOOK OF BIOCHEMISTRY(T.M. DEVLIN)
https://en.m.wikipedia.org/wiki/Transesterification

No, nucleophillic attack by the activated 3'-hydroxyl on the α-phosphate of the incoming nucleoside triphosphate results in the formation of a new phosphodiester bond and release of pyrophosphate (PPi), which is subsequently hydrolyzed.

[image source]

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Extreme or just rare: evolution of complex life in extreme environments
Many environments are considered "extreme" (boiling hot springs, acidic/basic water, etc) and those tend to be dominated by Archaea instead of the "usual" mixture of bacteria along with complex plants and animals. But "extreme" is in-part in the eye of the beholder.
Very little of earth (in terms of total energy available) is at 100C or pH 0, etc. Broadly speaking, the more organisms in parallel trying out various mutations the higher the chance there is to come up with something useful. We can't expect a 1km^2 hot-spring cluster or the energy-starved layer of groundwater at the 100C geotherm (about 3km below ground) to evolve as much as a 1000000km^2 rainforest exposed to direct sunlight.
There are large extreme environments. There is plenty of energy available in deserts such as the Sahara or the open surface ocean (an iron desert) but the primary productivity is very low. This means that the environment is harsh enough to stop life from adapting "effectively". Here "effectively" means how much of the available energy is used, i.e. what fraction of the sunlight is absorbed by the plant/algae (the conversion efficiency into glucose is very low, at most 7% and often ~1%, but we are ignoring that). Note that in many cases a desert is actually more hostile to microbial life because larger organisms can store water/nutriants/etc more easily.
On the other hand, there is one example of an "extreme" environment that became widespread and in which life thrived: Oxygen. O2 forms reactive species in a wide variety of biochemistry, which makes it a pretty universal poison. But life found a way around with enzymes such as superoxide-dismutase and was able harness the high energy or these reactions.
To the best of our understanding, to what extent would life have evolved and thrived if the entire Earth's ocean were an extreme environment, such as 100C, pH 0, or 34% salinity?

We cannot have any "understanding" of the outcome of a hypothetical postulate. Whereas discussion of this may be of interest to you and possibly others, there can only be subjective opinions on the question and therefore I am afraid that it is off-topic for SE Biology. (see: https://biology.stackexchange.com/help/dont-ask)


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How can the melting temperature of PCR primers be so far below the extension temperature?
Since our primer TM is lower than the extension temperature by design, (and often by a significant amount) shouldn't the primers be released from the template at extension temperatures?
Now, I have done PCR experiments and know they work. I just want to justify what's actually going on molecularly to be at peace. The only thing I can think of is that as the temperature ramps up to the extension temp, the polymerase has already begun adding nucleotides, thus raising the effective TM, preventing dissociation.

That will happen in some cases, but by the time you are ready to extend, the annealing step will have mean that primers formed double helix stretches with you template, and the polymerase will have bound to both, stabilising it, thus it isn't free to be released from the strand.

Note that 'melting temperature' is actually about POPULATIONS--it's generally the temperature at which 1/2 of all of the millions of copies of 2 things will be stuck together and 1/2 apart. Once stuck, not all primers will leap off the template simultaneously even at much higher temperature... As you indicate, there's nothing to stop the polymerase from starting its work (extending the primer) before the extension temperature.
And, as in another answer, polymerase can add stability to the pairing.


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What is this black and white worm in a white case?
The case is very small and it's an off white color.
The thing living inside can come out of either end. It's a black and white looking worm. It will poke its head out and move everywhere!

They are all over my back porch and some are even coming in my house!

Could you link more (and clearer) pictures please?

Related: https://biology.stackexchange.com/questions/15845/what-insect-is-this-india/15856#15856

@arboviral I also thought it was a duplicate... however, the answerer in that question mentions several families, but not Tineidae.

Related Question.

Related: Identifying a creature that appears to be a worm wrapped in a cocoon, What is this black and white worm in a white case?,  Help in identifying an unknown arthropod, What insect is this? (India), Identify this smooth-cocoon worm from Southern India, Small worm living in some kind of cocoon......

Related:  What is this animal that hides in dustlike structure?, What in the world is this critter?, What is this hard shelled insect in my house?, What is this insect found commonly in coastal India?, Insect identification - pantry moth vs clothes moth

Does this answer your question? Identifying a creature that appears to be a worm wrapped in a cocoon

This is just a larva of a moth from the Family Tineidae, most probably Phereoeca uterella (known as plaster bagworm or household casebearer), or Tinea pellionella (known as case-bearing clothes moth).
As you can see, the larva of this moth...

... constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings. (from Wikipedia)

Here is a better picture of Phereoeca uterella, from the entomology deptartment of the University of Florida:

Here is the imago (adult), for comparison:

@Lynn If this answer helped you, consider "Accepting" it (hit the check mark under the down-vote icon). Glad you got what you were looking for!


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properties of lamps for indoor plant growth
Ikea has a brand of hydrophonic start kits called vaxer. Part of their offering consists of lamps that aid in the cultivation of the plants (example1, example2 and example3). There are other companies offering lamps that should help plants grow. Here is an example on ali-express.
When I compare the lamps from ikea as well as others I find it hard to figure out what lamp may be preferable for my hobby projects at home. I recall seeing a documentary where it was suggested that plants prefer red and blue light because that is the colour they themselves do not emit back. This makes me wonder why the ikea lamps don't have these colors.
I'm new at this field but I may be interested in investing in some lights for some indoor hobbying. When considering this though, what are properties of these growth lights that are important as far as plant growth goes?
In my particular situation I am not concerned with heat but more the correct type of light and the costs of electricity.

You might find more people with expertise in this area at Gardening.SE

I am not a biologist, but I have read up on this a little bit. I recommend that you do a bit of research online at your library or online because it can get somewhat technical. There are several variables to consider. You are correct that the bulbs emit different colors of light. Plants species may have different needs for different colors during their growth stage & their flowering /fruiting stage. You should investigate what your plant needs. The amount of the light emitted by the bulb is measured in a unit called lumens- this is usually on the package. More lumens= brighter light. For indoor hydroponic, there are expensive lighting systems using a variety of bulbs & lamps, like fluorescent, halide & sodium, each with specific uses & (dis)advantages. One recent development are LED grow lamps. The LED's advantage is that instead of having 1 large heavy & hot light bulb like with a halide or sodium lamp, you have many little LED light that can come in different colors, allowing flexibility in different life stages. The LED lamps also consume much less electricity & don't create a lot of heat- but they are more expensive. OK, good luck with your project. Also, if you like hydroponics, learn about aquaponics, an offshoot of hydroponics that incorporates an aquarium into the system. The water flowing through the plant's roots circulates down into the aquarium and back up again, so that the fish poop helps to nourish the plants and the plants' roots act as a filter for the aquarium water, creating a type of symbiotic ecosystem between the plants & fish.

Vaxer is a total gimmick apparently. it's just cheap 1cents chinese LED's branded as IKEA grow lights at 15 euros... it's about 10w for 55w equivalent, 800 lumens,
Phillips currently sells 11w 100w equivalents for the same price. for 1520 lumens. Cree has a19 lamps which are less intense and which are 13w for 100w equivalent. in terms of money you can also buy red-blue 20w vac cob chips for 2.50USD and 50w vac cob chips for 3.00USD, to 50w dont last as long and are hotter.
Many home experiment comparisons have whites beating red/blue leds. There are no clear figures and research papers on the topic. it's all about efficiency for producing a PAR plant spectrum. Photosynthetically active radiation
You need penetrating LED's too, reflected PAR (Parabolic alu reflector) and unclouded diffuser to get best penetration into the plants.
Your best bet for efficiency is to get a white 120 lumens per watt light. Its a good way to achieve the PAR spectrum for plants. The plants may benefit from Green light for other pigments like Anthocyanin.


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Do plants need sleep?
Turns out that you can do indoor farming these days via hydroponics and specialised LED lights. My mother, who has a large garden, warns me from exploring this as a hobby. She mentions that 'plants need to sleep too' and that having a LED light on them 100% of the time might be bad for them.
Is there any sense in this? Is it true that plants would grow suboptimally if the sun was on them 100% of the time or would they in fact grow quicker? Is there any research on this?

The quote as phrased is a bit non-sensical really because it mostly hinges on what you define as 'sleep' or 'rest'. Plants, like most living things, including us, are far from dormant at night.
It's true that diurnal patterns govern the behaviour of most, if not all, living things that are exposed to them (1). Plants are no exception to this.
For example, photosynthesis is a 2-component process. With the so called 'dark' and 'light' reactions of photosynthesis (more correctly "light-dependent" and "light-independent"). Though both happen during the day and night, it is at it's peak during peak sunlight.
In CAM plants, to avoid dessication, there is differential carbon fixation because the stomata are kept shut during the hot daylight hours.
Respiration however, where the produced food is converted to energy, primarily happens at night.
The Khan Academy has a great 'walkthrough' of the steps of photosynthesis:
https://www.khanacademy.org/science/biology/photosynthesis-in-plants/the-light-dependent-reactions-of-photosynthesis/a/light-dependent-reactions
(1). The diurnal course of plant water potential, stomatal conductance and transpiration in a papyrus (Cyperus papyrus L.) canopy
https://link.springer.com/article/10.1007/BF00379885

The light-independent (or 'dark') reactions take place in the light, not at night. The production of ATP and NADPH by the light-dependent reactions is not separated in time from the fixation of carbon dioxide. How would the plant store all of the ATP and NADPH?  Also carbon dioxide fixation produces carbohydrate not hydrocarbon.

Right you are. Wrote that answer in a bit of a rush, edited it now.

Yes, as long as there is light there is photosynthesis going on. The light/dark cycle allows your plants to process what they created and rest a bit. It is good for them and encourages adequate growth.
http://www.popsci.com/blog-network/our-modern-plagues/do-plants-sleep

Could you please add some sources for this?

Plants need no rest as long as there is a constant source of nutrients and they are kept in the right environment they will not be damaged or die or get "tired". However Plants can be subjected to the seasons where they rest in the winter ect. due to the lack of resources and essential elements.
You can however make them grow better by subjecting them to blue and red light as this is the light they respond to the best out of the whole spectrum of light.
https://www.popsci.com/blog-network/our-modern-plagues/do-plants-sleep
https://homeguides.sfgate.com/24hour-light-schedule-bad-plants-95954.html

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If a DNA letter is one of A,T,C and G, and there are 3 billion base pairs, why don't we say that there are 6 billion letters in the genome?
A DNA letter is either one of A,T,C or G. Human genome is supposed to have 3 billion base pairs coming from each parent. But these are pairs - a combination of A-T or C-G. So, doesn't that make the total number of DNA letters from a single parent, equal to 6 billion ?

It's more common to say there are ~3.6 Gbp (Giga-basepairs). What you're asking is equivalent. You only need to know one of the letters in a given strand to know what the other is too.

A, T, G and C are abbreviations for the deoxynucleosides of DNA and often, more loosely, for corresponding bases. They are not letters. 'We' presumably refers to the scientific community, which includes me, and I certainly never talk about 'letters' in relation to DNA. This may appear technical pedantry, but it is important in science to refer to things precisely without adding unnecessary implications. The implication of letter is that it helps to spell a word — presumably in relation to a protein. In many cases that is not so. If you use the correct terminology, your question does not arise.

For all those who have voted to close this question as off-topic (or are willing to do so), please at least read the reason you are chosing. This is certainly not a homework question, and does not show lack of research either, IMO. This is just misunderstanding of the terminology, as @david says. This is what downvotes are for, there is no need to vote-to-close this question.

In response to the comment from @another'Homosapien', I should explain that when questions are voted off-topic under the category ‘homework’ it is not necessarily because they are considered homework in a literal sense. As I pointed out in a post on meta, ‘homework’ includes “A question that addresses a basic biology concept that may seem trivial to biology professionals”. I argued there that it would be better if this were separate category because of the ambiguity. Any takers now?

If a DNA letter is one of A,T,C and G, and there are 3 billion base
  pairs, why don't we say that there are 6 billion letters in the genome?

It is a convention, and stating the actual number of bases would not add any information, but would actually lead to more confusion. It's like saying

I have six pairs of socks

vs.

I have twelve socks.

It means bascially the same, but now one could assume that these twelve socks are not from actual pairs (e.g. twelve left socks). The same goes for DNA. Saying we have pairs of bases emphasizes the redundancy of the DNA double strand.

If a DNA letter is one of A,T,C and G, and there are 3 billion base pairs, why don't we say that there are 6 billion letters in the genome?

We do.
Just like English has 26 letters while this post has 522 letters (not counting numbers and punctuation), the genetic alphabet has 4 "letters" while the human genome has 6 and a half billion. The thing is people tend to stop using the letter analogy after talking about the 4 or 5 naturally available nucleotides. After that, we tend to go back to calling them nucleotides and base-pairs.
Whenever you have a question about something that doesn't seem to make sense, the first thing you should ask is if your premise is even right.

You can refer to the Human genome as haploid or diploid. The haploid genome is around 3Gb, the diploid one is 6Gb. Usually, the bare term "Human genome" refers to the haploid one. The first picture on this Wikipedia article makes it clear.


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Can we measure the rate of mutation in (say) E. coli without gel electrophoresis or genome sequencing?
If so, how? And, what are the pros and cons?

This is pretty broad question so I'm not really sure what the end goal is here, but here goes.
The answer is both: "yes" and "it depends what you mean exactly". I'll explain what I mean.
Firstly, you should clarify in your question whether what you actually mean is the substitution rate, or not. The mutation rate, which is how often a given base pair position changes, cannot be observed with any current technique, even Next Generation Sequencing. This is for 2 reasons (that spring to mind, there may be more).

If you make an observation at time $t$, and another at time $t +1$, but a base mutates (say A $\rightarrow$ C) and then mutates back again between your observations, you would not be able to tell that this had ever happened. Thus there would be 2 mutation events which you would not count in your 'rate'. This is one of the reasons molecular clocks based on SNPs tend to underestimate ancestral distances.
If a mutation occurs that is deleterious (has a negative effect on the organism), the mutation won't be observed because the lineage of the organism won't survive to be sampled. By the way, the chances of a mutation being deleterious are considerably higher than it being advantageous, but lower than it being neutral.

The substitution rate is how many mutations have occurred that persist in the lineage. Now if we assume that when you say mutation rate, you mean substitution rate...

Yes, you can study mutation rate without 'molecular techniques'.
Throughout the history of classical genetics we've studied mutation rate without access to these tools.
My favourite example is basically the one I used in this question, where you can study the emergence of antibiotic resistance in bacteria (since you provided the example of E. coli, this is rather apt).
In the papers I linked however, they will almost certainly have used some molecular techniques to validate their answers.
But, if we set that aside for the moment, the very first indication of antibiotic resistance one might observe in the lab is seeing colonies of a bacteria growing on a petri dish in the presence of an antibiotic they are supposedly susceptible to.
Now, if we consider the 'mutation rate' to be the time taken (perhaps counted in the number of generations), for a spontaneous mutation to appear as a phenotype (observed characteristic), you can assess this purely visually without any molecular techniques. If you repeated this experiment however, you would most likely not be able to verify that resistance arose in exactly the same way twice without use of various molecular technqiues.
As a molecular biologist though, I would not really consider this a very good approach/definition of mutation rate, which leads me on to...

'It depends what you mean exactly'
If you were to stick to what is probably the stricter but more widely accepted definition of mutation rate (.i.e substitution rate), you'd need molecular techniques to determine this, as you'd need to know precisely which bases are changing.
Hand-wavy list of pros and cons:
Phenotyping (pros and cons):

Quick
Cheap
Easy
Low resolution
Possibly not reproducible

Genotyping (pros and cons):

Massive resolution
Can be quick in some circumstances
Functional information
Generally expensive
Requires specialist equipment

Not an exhaustive list by any means.

Here is a classic reference that shows how you can use bacterial mutation rates to test compounds to see if they are carcinogens:
https://www.ncbi.nlm.nih.gov/pubmed/4151811


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Does Ox or Bull Semen have Taurine?
Numerous skeptical communities have debunked the claim that Red Bull has bull semen (including Snopes, and Skeptics.StackExchange. But, none have said whether or not it is even possible.
Taurine, according to Wikipedia, is "widely distributed in animal tissues." But, does it get excreted through semen, and has anyone found it in bull semen?

I'm unsure as to why this question is about to be closed as unclear. I don't think it could possibly be any more clear.

Taurine is widely found in meats and fish. It was named from the Latin word for bull (taurus) because it was first discovered in ox bile.
From http://www.frontresearch.com/news/china-taurine-market-is-fluctuating/

In recent years, the global Taurine consumption has kept growing with an GAGR of 5.5%, more than 50 kilotons in 2014.

I have no idea how much taurine is in bull semen but even if it contains a great deal, do you really think Red Bull will be using that as a source? Can you actually imagine a way of getting bull semen to extract it? The ratio of bulls to cows or steers is very small. The only reason a farmer or breeder keeps a bull is for breeding and many cows are artificially insemination from a limited number (relatively speaking) of bulls with the desired qualities.
All this is to explain to you that your question is  completely inane and pointless. I can't believe anybody would actually think it could happen.

I found a few papers about the function/concentration/localization of taurine/hypotaurine in the male reproductive system of various species:
The taurine and hypotaurine content of human semen:

Hypotaurine, an antioxidant, may play an important role in protecting sperm from reactive oxygen species.

Protective effect of taurine from osmotic stress on chimpanzee spermatozoa:

These results suggest that taurine plays an osmoregulatory role in chimpanzee spermatozoa, which possibly involves stabilization of the cell membrane.

Taurine maintains and stimulates motility of hamster sperm during capacitation in vitro:

These results suggest that in addition to its importance for motility taurine might stimulate capacitation. The mechanism through which taurine supports and stimulates motility is not yet known, but its use results in the first relatively “defined” in vitro capacitation medium for hamster sperm.

Hypotaurine in spermatozoa and genital secretions and its production by oviduct epithelial cells in vitro:

Taurine and/or hypotaurine are necessary compounds for sperm capacitation, fertilization and embryo development. Hypotaurine has a protective role against peroxidative damage... Hypotaurine and taurine were quantified in spermatozoa and seminal and tubal fluid of various species, and in secretions by oviduct epithelial cell layers in vitro. Significant amounts of taurine and hypotaurine were identified.

These are but a few papers I found in a cursory search. You can also see this article for what seems to be a comprehensive overview of the "physiological actions of taurine". Even though I haven't found any direct measurements of bulls, it seems safe to say that, given its function and ubiquitous nature, bull semen contains taurine.

I too don't doubt bull semen contains taurine. As you mention, it's ubiquious, found in most animal tissue. All members of Felidae require taurine in their diet as they're unable to synthesize it as most mammals can. But I can't imagine felines, even a Siberian tiger, relying on bull semen for their source. When I read the OP's question, a mental picture of people trying to collect bull semen came to mind. :D

@Jude Ha! I just read the question as whether or not bull semen contains taurine; the stuff about Red Bull seems ancillary. I only posted this answer because I found that article with a quick search but, truly, I know about as little as is possible about this topic.

Which is why I told him in my answer that his question was both inane and pointless. I was doing my best as being polite as is fitting for a fellow Canadian.

Inanity is quite common in questions here.

I'm beginning to notice that! There are some but much less on Gardening SE and Seasoned Advice SE as people ask for advice or to honestly learn how to do something, for the most part.


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Weed Identification
These are are weeds which grow on the silt of a lake, in India , climate is semi-tropical monsoonal

They dont look native probably exotic species. What are they?
Height is probably 1.5 feet.
Lake is this

Is there any reason you don't believe they're native plants?

@Jude they are not found elsewhere except on lake bed everyear, moreover lake was constructed 50 yrs back ,

Please edit your question with the location (e.g. 1) what the lake name is, 2) what's the name of the river that drains into the lake, 3) the rough height of the plants). This would help a lot along with any other relevant details you can add.

Second one quite strongly  seems to be Xanthium strumarium but the first (and foremost) one is confusing. Take a zoom close up of the inflorescence, if it contains small fruits (few mm) with 3 wedges  (looks like [this]) then it could be Rumex dentatus

@AlwaysConfused make this as answer

The first one looks similar to artemesia vulgaris, which grows in many places opportunistically in the south of europe. If you rub the seeds, do you get a very strange smell? if so it could be an artemesia. The second plant originated in America, the first plant from america to arive in the old world is Datura, for which the importation date is perhaps millenia old as similar to Datura in indian and chinese documents. It is an american solenacea related to tomatoes and datura.

As Always confused already suggested, the second picture is Xanthium strumarium.
This is a very variable species, and there is a lot of debate around splitting this species into (sub)species. There is a possibility this is plant belongs to one of the few accepted species that wikipedia lists, some even native to Eastern Asia. However, I can't verify this because pictures of these are scarce.
But from my personal field expierence, this plant looks exactly like the X. strumarium and the habitat also matches, so I am comfortable to call this X. strumarium.
As to your first plant:
- It will be hard to say without a close-up of the flowers/seeds.
- It would be better to ask only one plant per question, so please remove it here and ask a new question.


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Is genome recurrence possible like in Jupiter Ascending?
I have watched Jupiter Ascending many times now and I was wondering if genome recurrence, like what happened to Jupiter Jones, is possible.
Is it possible to find two unrelated people, possibly several generations apart, that cannot be distinguished between by DNA sequencing?
Taking the example of Jupiter Ascending: in the movie Seraphi Abrasax they show the "genetic recurrence" of Jupiter Jones, which means the same sequence of DNA has repeated after several thousand years from Seraphi to Jupiter.

Could you expand on "genetic code recurrence like what happened to Jupiter Jones". This is new to me. It sounds like you are asking "is it possible for unrelated people to be genetically identical?" Technically possible. Statistically, however, nigh on impossible.

@James I'm directing you to this wikia http://jupiter-ascending.wikia.com/wiki/Recurrence for more information.

I got the gist of it. For all intents and purposes, it's impossible.

I have edited this post, especially the title, to replace "Genetic Code" by "Genome". If you do not understand the difference between the two, follow the links I have provided.

@James if you understood the question, do you think you could try to clarify it by editing the question but I don't understand the question!

@Remi.b It's fantastical and loaded by saying "is it possible" (anything is possible given enough imagination), but I've tried to edit my interpretation into the question. Richeve, if I have changed the meaning of the question, please do roll back.

Various types of genetic variation exist in natural populations. One is the single-nucleotide polymorphism (SNP), which is where different nucleotides are present at the same location in the genome of different individuals in a population (with variation present in a nontrivial number of people; the threshold is usually set arbitrarily at 1%).
Even just considering SNPs and ignoring other types of variation, what you talk about would be effectively impossible.
The human genome is about 3 billion base-pairs long. Along the whole genome, according to Chen et al 2012, between two individuals there is something like 3 million SNPs. Imagine two people flipping a coin and the result is exactly the same every time, 3 million times. Now imagine instead of heads or tails, there are 4 options.
Only 1 result of the series of 3 million 1 in 4 chances is identical to the original series.
$\frac{1}{4^{3000000}}\approx\frac{1}{\infty}$ = 0
Go ahead, try it on your calculator.
Now, there are also variations that are beyond SNPs between individuals that cause much more variation between two people. These can cause even more "unprobability". Since we already require infinite people before this event is likely to happen, I think we can just call this event impossible.

3 Gbp is 3 billion, not 3 million, so the odds are even lower. It's not = to $1/\inf$ though. Its still finite, its just vanishingly small if we are being pedantic :P

That we need infinite people does not make it mathematically impossible (as you state in a comment), but biologically (or generally, practically) impossible.

@JoeHealey I was coming at it from the point of a comparison between 2 people: of the 3 Gbp in their genomes, 3 million bp are likely to be SNPs from one person to the other. The likelihood that those SNPs are the same is an incalculably small number (at least, according to my calculator :P).

Ah I see what you meant, yeah.

It is almost impossible. Considering that the haploid Human genome is around 3 Gb (Giga-basepairs) and that ideally any of those can mutate generation after generation, the chance of having the very same sequence recurring in a population is extremely unlikely. There will be some differences.

I was thinking that your term "population" refers only to Earth, but in the movie, the population refers to their "planet farms" and they have many seeded planets that uses their own genetic code as the base to construct new sets of modified human beings. So with these large set of population it is still not possible?

Still, you have 4^3giga possibilities (roughly speaking). Even having the whole universe and billions of years it will be an "almost-zero" chance of having two identical sequences. Unless you interfere with technology, some cloning-like tech for example. But if we stick to natural reproduction, then the chances are ridiculously low.

I was trying to picture this mathematically, like if you have a finite set of bases and the DNA sequence which is long but non-continuous which means there's a limit to its length then any sequence with finite set of elements and constant length can have a possibility of repetition even if the generation is random. The chances is almost zero but not zero which means there's still a possibility. Since Earth is a closed space and considering we haven't tapped yet to cloning, or haven't introduce synthetic bases to our DNAs then our DNA set is still finite and thus repetition is still possible.

Mathematically possible, practically impossible. That's why my answer states "almost impossible".


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Do ants actually stick better after "licking" their legs?
I found an uncommonly large black ant and put it in a glass cup to observe it. It initially had a lot of trouble climbing vertically by any amount. However, I noticed it paused and when I looked closely, it seemed to run its front legs quickly between its mandibles, and it looked as though it secreted some kind of orange liquid through its mouth. After it did this and climbed again, it climbed a little bit further up the cup, but fell down again.
Then, it repeated the process of pausing and running its front legs between its mandibles. After this, it tried to climb again and I saw it was able to climb a little bit further than it did after the first run before falling down, though I didn't think to measure the exact height on a drinking glass. I saw it repeat this process yet again, and it stuck to the cup even better and climbed even higher before inevitably falling, and I assumed it would continue this process indefinitely until it was able to climb out of the cup, so I threw it back outside.
I would hypothesize that the ant was coating its legs with its own saliva which has evolved to be sticky for situations like this, seeing as how it so quickly exhibited the mental aptitude for recognizing its climbing challenge. But, I'm not biology expert. Perhaps its legs already inherently possess all stickiness ability it needs, and it is only that its legs were dirty or covered with water.

Lots of relevant information at the Wikipedia page for insect adhesion and in this paper. No mention of 'saliva', I suspect that what you saw was grooming to prepare adhesive structures.


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Any references contradicting Hormesis from low dose studies?
I've recently read some papers on Hormesis (the stimulatory effect of low doses of substances toxic at high doses). The papers are all published in respected peer-reviewed journals, here, here, and here for example, but they're pretty much all by one person, Edward Calabrese. I'm struggling to make sense of an issue which is clearly an acceptable enough possibility to appear in peer-reviewed journals, but which seems to have garnered absolutely no further interest beyond the one man. I naturally presumed that the concept had been dismissed by some later study, but I cannot seem to track such a study down.
To be clear, I'm not interested in policy, as the use of linear no threshold models vs Hormetic models for public policy is so highly politicized a topic with unscientific approaches on both sides (the vested interests of polluting industry vs an easily panicked population urging it's legislators). I'm just looking to fill the gap in my reading of the science. Papers showing demonstrable low dose responses which match a LNT model would be good, papers showing contrary results to Calabrese's for the same toxins would be ideal.

Hormesis Defined Nesbitts paradox resolved? Nicotine physiological response changes with dosage I think in general it's accepted that decreasing pollutant concentration is better than increasing it.

He is not the only person. I have come across papers on hormetic effects of heat stress on C. elegans. https://www.nature.com/articles/ncomms14337, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1847401/. See this review for more references.

I'm voting to close this question as off-topic because: 1. it is based on a wrong assumption that the "theory" in question is propagated by just one person 2. it is asking for literature mining for evidences "contradicting" an established phenomenon.


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What are the differences between Trachinotus and Bramidae species?
What are the differences between Trachinotus(Pompanos) and Bramidae(Pomfrets) ?
...like the difference between where they live/can be found, bone structure, etc.

Can you add more context to your question? Simply repeating the title is not acceptable. What do you want to know specifically? There are very broad differences, sufficient for systematists to put them into different families.

Pomfrets comes from the order Perciformes (the largest order of fishes) and are part of the Bramidae family. They strictly live in marine environments, mainly the Atlantic, Indian, and Pacific Oceans. They have a dorsal fin extending over the length of the body in some and anterior dorsal fin spines unbranched.
http://www.fishbase.org/summary/FamilySummary.php?ID=319
Pompano comes also comes from the order Perciforme and are part of the Carangdide family which includes jacks, mackerels, scads, and runners. Most are fast-swimming predatory fish that hunt in the waters above reefs and in the open ocean. They also mainly live in marine environments such as the Atlantic, Indian, and Pacific Oceans, and are rarely found in brackish waters. Their body is generally compressed, although body shape extremely variable from very deep to fusiform.
Quote about Pompanos from Fishbase.org:

Most species with only small cycloid scales. Scales along lateral line often modified into spiny scutes. Detached finlets, as many as nine, sometimes found behind dorsal and anal fins. Large juveniles and adults with 2 dorsal fins. Anterior dorsal fin with 3-9 spines; the second having 1 spine and usually 18-37 soft rays. Anal spines usually 3, the first 2 separate from the rest; soft rays usually 15-31. Widely forked caudal fin. Caudal peduncle slender. Pelvic fins lacking in Parona signata. Vertebrae 24-27 (modally 24).

Unfortunately, I can only post one link due to my rep, but it fairly easy to search fishbase.org for information on both species.


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What is a CAG::ChR2 rat?
I am reading the paper: Pyramidal Cell-Interneuron Interactions Underlie Hippocampal Ripple Oscillations.
The authors use CAG::ChR2 rats (for example in Figure 2) and I don't know what it means.
I understand for example that in PV::ChR2 mice, parvalbumin neurons will be activated by light.
I am also familiar with types of other interneurons (Ivy, Martinotti, OLM, LTS, Bistratified, Mopp, VIP, Somatostatin...)
but I have never encountered CAG cells.
Is CAG represent a type of neuron? or, maybe it represents something else?
Thanks!

CAG is a synthetic, ubiquitous promoter which combines elements of the CMV early enhancer, the chicken β-actin gene, and the splice acceptor of rabbit β-globin. According to the researchers who created it:

The elements which constitute the pABWN vector, the CAG promoter, the weak neo unit, and the BPV fragment have only low specificity to cell types or species. Therefore, this system can be applied not only to L cells or CHO cells, but to a wide variety of cell lines. The pABWN vector should be very useful for producing large amounts of valuable proteins in mammalian cells, for changing the phenotype of host cells by overexpression of some normal or mutated genes, and for disrupting the function of targeted genes by overproduction of anti-sense RNAs.

In the paper you cite, CAG-ChR2 is used to activate all neurons in the vicinity of the light stimulation, for example in Figure 2Ab, where the panel is labeled "PYR+INT activation."


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Do spermatozoa have mitochondria
This is something that I have heard/read so many different contradictory claims about over the years.
In high school I was taught that sperm cells have a lot of mitochondria because they need a lot of energy quickly. This made sense to my adolescent mind.
When I was an undergrad, my one microbiology lecturer swore up, down and sideways that they did not have mitochondria. She never gave any reason or evidence, but I had gotten used to the idea that high school info was often out of date and, sometimes, completely incorrect, so I let it slide.
Then I was reading an article for a paper several years back and it said that, not only did sperm cells have mitochondria, but they did not lose them all. That in fact, some were preserved and engaged in genetic recombination with the mitochondria belonging to the ovum (the maternal ones). This contradicts another rule that so many treat as certain, which is that while nuclear DNA is 50% from each parent, mitochondrial DNA is exclusively maternal.
To sum up: Do spermatozoa contain mitochondria or not? And if so, is the recombination I described above likely?

With all certainty yes, they do have mitochondria. What article are you referring to in the second to last paragraph?

I can't remember in the slightest, and I lost my copy with a crashed computer. It was an off-hand comment in a pretty mediocre article. What I was actually researching was a particular gene on the mitochondrial DNA, I was just struck by that statement and the question bothers me every so often.

Wikipedia paternal mitochondrial DNA transmission

The midpiece has a central filamentous core with many mitochondria spiralled around it, used for ATP production for the journey through the female cervix, uterus and uterine tubes. This is a good article explaining more about this topic: http://genetics.thetech.org/ask-a-geneticist/mtdna-comes-only-mom

Thanks. That helped. Who would have thought that what I learned from a high school biology textbook published in the early '80's would be the right answer.


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What is the role of glucose in plasmid isolation?
My understanding is that glucose is used in the resuspension solution to prevent cells from bursting by maintaining the appropriate osmotic pressure. Why do we even bother doing this? The cells are going to be lysed with the addition of the SDS+NaOH, and we have EDTA in the resuspension solution to chelate Mg, thus inactivating nucleases.

This is a common misconception: in fact, in the alkaline lysis method for plasmid isolation, the glucose does not act as an osmotic stabiliser.

Glucose is present in the resuspension buffer at 50 mM. This concentration is not high enough for osmotic protection of spheroplasts formed by lysozyme treatment: from memory, 0.5 M glucose is typically used for stabilisation. So why is the glucose included?
The original method for plasmid preparation by alkaline lysis was published by Birnboim and Doly in 1979. They explain that the method relies upon achieving a pH of between 12.0 and 12.5 after addition of NaOH so that linear dsDNA (sheared chromosomal DNA) is denatured but closed-circular DNA (plasmid) is not. They state in the paper that:

further pH control is obtained by including glucose as a pH buffer.

According to this site glucose has a pKₐ of 12.3, which aligns nicely with the claim that it helps to keep the pH within the desired range.

This is an interesting bit of information (I really like the explanations of this mechanisms). Thanks for finding it.

@Chris I actually knew the answer, having been around when the Birnboim & Doly paper was published. This technique revolutionised what was possible with plasmid-based cloning at the time and I read it very carefully. At the time of writing (05-07-2017) the paper has 12,877 citations, but most people who use the technique (in kits) won't even know of its existence. Sic transit gloria mundi

The kit problem (as I usually call it with our students) is exactly the reason why I love the information bits. They help in trouble shooting and it is good to know how a method works anyway. Classical biochemistry with finding out exact mechanisms. I thought I would know the lysis method and the steps pretty well, but there is always something to learn. As it turns out, this paper is already in my literature database, I will re-read it sometime later.

Really great answer, but the second link is broken for me.

@canadianer fixed, I hope.


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Please identify this plant
I don't know anything about plants

Welcome!!! to Biology Stack Exchange. You should add [tag:species-identification] tag to your question. And also please provide information about your location and size of the leaf.

Try to use a more descriptive title. Give details about what you observed.

Any fruits ever develop? Looks like Solanaceae to me.

Not my area of expertise... but looking at the pictures, it looks like it has a distinctly square stem. This is a characteristic of the mint family
Lamiaceae; the leaves look reasonable... but that's obviously an incomplete answer and not definitive.
Note that there are some iPhone & Android apps that help; look up 'LeafSnap' for example (I think that one's iPhone only and perhaps limited to trees)

I'm no plant expert, but it looks a lot like a cucumber plant.  We used to have them in our vegetable garden.

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Reasons for a flower type to consume water faster than another?
This is an easy experiment where you put a white flower into a recipient filled with water and liquid watercolor, so that the flower gets dyed.
While doing this experiment for different types of flowers, and assuming equal ambient conditions, what would be the most important characteristics  (e.g. flower size, petal length, stem thickness, number of petals...) and the biological reasons for certain flower type to consume water (and get itself dyed) faster than another? (e.g., does a thicker stem mean the xylem is stronger?)
More specifically, I'm interested in comparing a rose like this and a carnation (like the one shown in comments) as an example to the answer.
(Note: I couldn't show a carnation sample image due to my reputation being lower than 10, but I'll update it as soon as I can).

light levels and temprature will have a large effect, so you should consider this.

@John Experiment was attempted to make under similar light and temperature values, although it wasn't exactly made in perfectly equal conditions (It was a school project). Yet I'd mostly like to know what should happen and why.

The major factor should be how much water each looses and thus needs to be replaced by the dyed water. photosynthesis levels and stomatal count will both effect this.  Stomata count is influenced by both genetics and the environment in which the plant is raised. Hopefully someone with more knowledge about these specific plants can help, but I would not expect the loss/uptake to be the same.

One problem with giving a definitive answer is that there are literally thousands of different varieties of roses, with different flower sizes and number of petals.  I'd guess (perhaps wrongly :-)) that water uptake is related to the area of the petals, so a single-flowered species rose would take up water much slower than something like a centifolia.

related: https://biology.stackexchange.com/questions/48023/do-flowers-transpire

Carnation flower that I'd like to use as an example is something like this.

people are touchy about the scientific qualifications of an answer, so i wont answer even as a fan of flower and gardening. fat stalks, woody stalks, aversion to vase water, waxy/long lasting flowers vs fast wilting ones, all contribute to your result. generally a fast wilting flower which absorbs vase water well by capillarity will go the fastest, if you find a list of flower wilting times from 1-7 days you'll be on the right track.

Don't forget to consider the 'engineering' of the plant, as brought about by evolutionary history. Some plants will build fewer openings in their leaves ('stomata'); others use a strategy that allows them to only open these at night (see 'C4 photosynthesis') or CAM (Crassulacean Acid Metabolism) photosynthesis.

rbrucep is totally right, the engineering of the plant, waxyness, stomata size and frequency, surface area, cils to stop air moving, water reserves within the plant, rigidity and pressure of cell walls, change the plant's responses.


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What chemical conversions are involved , and what's the name for the process, when the muscles use lactate as an energy source?
I understand that muscles do anaerobic metabolism, specifically, "lactic acid fermentation", which I understand produces lactate. I'm not asking about that process.
What chemical conversions are involved , and what's the name for the process, when the muscles use lactate as an energy source?
I'm aware that it can happen as    This paper, is tellingly and usefully titled, "Lactate as a fuel for mitochondrial respiration"   (though I only have the abstract)
And aside from that paper i've also heard

"lactate produced during exercise can be reused as fuel by the muscles
  by turning it into glucose".

But I'm interested in what chemical conversions are involved

Have you read about Cori's cycle? Not sure if it answers your question, but it is relevant to lactate transport and clearance.

@SatwikPasani You can post that as an answer and i'll add my elaboration as an end note.  And if it's wrong hopefully somebody will comment or post a better answer..   actually just needs a formula but should be easier to find now..

@SatwikPasani thanks.  My elaboration Looking at https://en.wikipedia.org/wiki/Cori_cycle shows https://en.wikipedia.org/wiki/Gluconeogenesis   it looks like Gluconeogenesis in the liver converts lactate to glucose. So the muscles wouldn't be fuelled by lactate(the article was unclear to suggest so). Muscles are fuelled by Glucose (not lactate) and they'd do aerobic and anaerobic metabolism..  I'm not expert though but that seems correct. But now I see more where lactate fits in.. The liver takes it in and converts it to glucose which can go back into the muscle.

Just mended the broken link.

I'm answering this as a comment because I think the question is too trivial to survive long and @SatwikPasani is not reading the question or the paper in taking about the Cori cycle. The answer is Lactate -> Pyruvate -> AcetylCoA. This can happen to the extent that the particular muscle in question has mitochondria and can obtain oxygen from the blood. This is not anaerobic metabolism, but the quote and the paper say nothing about it being anaerobic metabolism. The point of the paper is that most of the energy is from glycolysis but some can be obtained by lactate oxidation.

@David  Thanks, I didn't say it was anaerobic metabolism and I know the paper didn't say it was.   Regarding that formula you gave.. Lactate -> Pyruvate -> AcetylCoA   Does that all take place in the muscle, and what is the name for that process?  (If some takes place in the liver and some in the muscle, then it sounds  like the cori cycle though you suggest it isn't that)

@barlop — The reference you cite says it takes place in the muscle. There is no distinct name for the — as people didn't think it occured there was no reason to name it.

@David Is there a wikipedia page on it? I'd like to be able to google about it without just picking up that paper or the Cori cycle which you say isn't it. Also I only have the abstract of that paper not the full paper. I see the abstract says it produces lactate and excretes lactate.. I don't see the abstract saying it converts the lactate.. can you quote where it says that?  is it this " skeletal muscle has a large capacity for lactate oxidation" ?

@David so basically it looks lke cutting edge stuff that you get something like the Cori cycle in muscle.. Lactate dehydrogenase doing a reverse reaction of Lactate to Pyruvate,  in muscle itself.. whereas (that study aside), it's thought to be or was thought to be, particular to the liver

I'd read  of lactate being recycled and used as fuel for the muscles.. but that might've meant recycled by the liver.. and to glucose..eg as said lactate produced during exercise can be “recycled” into glucose and used as fuel by the muscles
Read more at http://running.competitor.com/2014/01/training/six-lies-you-were-taught-about-lactic-acid_29432/6#ZygL5Uh57rWIdzTV.99   But this one is in the muscle itself which is a different reaction.. I see.

@David and importantly, that formula you gave is not in the abstract.. can you give any screenshot of the paper with that formula?

It is not cutting edge, it is backwater. It is not like the Cori cycle in muscle. The Cori cycle is a confusing term for the flow of metabolites from muscle to liver to blood to muscle, without involving the mitochondrion or oxidation. I did not give you a formula, I gave you the names of intermediates in a conversion. A map may give you the route from Glasgow to London and London to Dover, but if you want to go from Manchester to York then you have to buy a map and work it out yourself. The map is the major metabolic pathways in a text or on Kegg. Finally, why do you care about this?

@David i'm curious.. I get curious sometimes.

OK, but it would help us help you if you told us the real reason. I deduce from the other lists you follow that you are computing professional, i.e. not a biological science student. Now your interest could be personal medical or home brewing, but it could also be that you are interested in using computer methods to model pathways. If it were the latter I would tell you you have to buy and study a biochemistry text to do it properly. If you have a specific goal one could give different advice. But if you think you can dabble without learning the language, I can't help.

@David I'm not doing a model, and your comments were very helpful in answering the question.. Thanks

I see you've already got an answer in the comments, so this is rather a collection (with more proper formulation) of comments. As is known, lactate is produced by muscles (generally) during exercise due to absence of oxygen. However, the lactate produced can be used again in following two ways:

Conversion of lactate to glucose in the liver via a process known as Cori's cycle. Basically, the lactate produced from the muscles is released into the bloodstream, through which it reaches liver. There, it is converted back to glucose and again released into the bloodstream, through which muscles can use it again as fuel. The basic cycle looks like:

Conversion of lactate to pyruvate is the one you are concerned about. However, this process does not have a special name, because this reaction can be catalyzed both in forward and reverse direction. In the absence of oxygen, an enzyme lactate dehydrogenase convertes pyruvate into lactate, consuming 2 H+ during the process. However, when the envrionment is rich in oxygen, or the concentration of lactate is high, the same enzyme converts lactate into pyruvate, producing 2 H+ in the process. The reaction can be shown as: $$\ce{CH_3COCOO^- + NADH + H^+ \leftrightharpoons CH_3CH(OH)COO^- + NAD^+}$$
Thus, when the concentration of lactate increases, the enzyme lactate dehydrogenase catalyzes the (above) reaction in the reverse direction. After this, the pyruvate produced can be used in the TCA cycle.

PS: there have been studies which now suggest that indeed lactate, not glucose, is the primary energy source of neurons. As per the lactate-shuttle hypothesis, the glial cells neighboruing neurons convert glucose into lactate, which is then used by the neurons. This fits with the observation that the extracellular fluid immediately surrounding the neurons is richer in lactate as compared with blood and cerebrospinal fluid, as shown in microdialysis studies. These studies suggest that glucose is not the actual primary energy source of neurons.
EDIT: As you see, the first reaction in both the cases is $\ce{lactate \rightarrow pyruvate}$. However, the main difference arises after this reaction. In muscle cells, this pyruvate is used in Krebs cycle, for which the first enzyme is pyruvate dehydrogenase converting pyruvate to acetyl-coA. However, in gluconeogenesis i.e. formation of new glucose molecule (a part of Cori's cycle), the first step is conversion of pyruvate to oxaloacetate, and is catalyzed by the enzyme pyruvate carboxylase. Thus, although the first step in both processes is the same, the end product is quite different.
References:

Lactic Acid - Wikipedia
Lactate Dehydrogenase - Wikipedia
Cori's Cycle - Wikipedia

Thanks. What's your view re what david says about that paper, which is that it's saying that the formula he gave "Lactate -> Pyruvate -> AcetylCoA."  is according to that paper, a reaction that happens in the muscle itself

according to that cori cycle image you've given, which i've seen verified elsewhere too.. it's as you say,  lactate to pyruvate to glucose..  in the liver. So why do you say "lactate to glucose" as one point, and "conversion of lactate to pyruvate" as a separate point..  Isn't lactate to pyruvate just half of that "pyruvate to glucose" reaction.. Also, why do you think that "lactate to pyruvate" is more relevant than "pyruvate to glucose"?

So there's 3 words here then..  Lactate->Glucose is Gluconeogenesis.    So what's the word for the in between reactions of A)Lactate to Pyruvate (the reverse of lactic acid fermentation)   and B)Pyruvate to glucose(the reverse of Glycolysis). (And yeah I understand your image I see the reverse reactions occur in the liver).

Secondly, David wrote in one comment  "the answer is Lactate -> Pyruvate -> AcetylCoA  "  and  another "The reference you cite says it takes place in the muscle. There is no distinct name for the — as people didn't think it occured there was no reason to name it. "    <-- So am I interpreting David's comment correctly there, that he's saying that that process with that formula occurs in the muscle?  And that it's according to that recent study and thus being a recent discovery it has no name.

(note, also I think David isn't talking about the Cori cycle, and the liver eg he said it occurs in the muscle, and he thought that one commenter was
"not reading the question or the paper in taking about the Cori cycle"  ).  I think the Cori cycle is relevant but it's also relevant that there may be this other scenario that David brings up of a process with that formula David gave, occurring purely in the muscle, not the liver.

So Lactate to Pyruvate (reverse lactic acid fermentation), occurs in the muscle.  Would Pyruvate to Glucose(reverse Glycolysis), also occur in the muscle?

Ah, looking at your edit,  so reverse Glycolysis doesn't occur in the muscle.  But reverse lactic acid fermentation does?

Note-  You wrote that David referred to Gluconeogenesis in comment.. David didn't refer to gluconeogenesis and he wasn't talking about the cori cycle.  I was the first and only person to mention Gluconeogenesis  in comments in the context of the cori cycle.  From what I understand.. Gluconeogenesis is  the right term in the case of the liver, but not for the muscle. Also on a related note and in correction to an earlier comment of mine, I have just found out that the pyruvate->glucose reaction in the liver is not reverse glycolysis 'cos the enzymes and pathway is different.

@barlop 1) no gluconeogenesis is mostly restricted to liver and kidney 2) yes "reverse" or "forward" lactic acid formation occurs in muscles, depending on presence of O2 and concentration of reacrants/products 3) seems I got confused with so many comments :P yup the pathway is quite different, but some enzymes involved here are also part of glycolysis. Now, lets delete these comments now ;)

Seems as if the downvoter did not even have a reason for their action this time :/

On a related note,  I have improved my question..(partly in the hope of dissuading any close voters) 'cos it looked a bit like the question was almost answering itself to an extent.  Your answer still applies and doesn't change as a result of that update...

Would you say that After Lactate is converted to Pyruvate, then that Pyruvate could be used for either aerobic metabolism or anaerobic metabolism? And that similarly, (with the other process, so), when Glucose is converted to Pyruvate, then that Pyruvate could be used to fuel either aerobic metabolism, or anaerobic metabolism?

@barlop yup, you're correct. Once pyruvate is formed, then it totally depends on environment where it would be used. As a matter of fact, glycolysis doesn't change; only the reactions following pyruvate production depend on O2 availability.

Thanks David And Homosapien..
HomoSapien has posted an answer which i've accepted.
I have included here a useful diagram showing the conversion of Lactate to Pyruvate to AcetylCoA, and a description how it relates to the question.
As has been mentioned there are two different processes not to be confused. There's the Cori Cycle aka Lactic Acid Cycle, where which involves the liver, blood and muscle. Liver converting  Lactate->Pyruvate->Glucose (that process in the liver is called Gluconeogenesis).    Glucose travels to the muscle..  Muscle performs Glucose->Pyruvate->Lactate  , lactate travels to the liver and in that cycle.  so there Lactate is very indirectly fuelling an anaerobic metabolism in the muscle.    Also note that(I understand from speaking to a biochemist), that when the Pyruvate is converted into Glucose it's technically not the reverse of Glycolysis since different enzymes are used and it's a different pathway.  I see that the conversion of pyruvate to lactate is a reverse of lactic acid fermentation, as the same enzyme, LDH, is used
The other process, which is quite interesting and less spoken about in popular articles,  is one which occurs entirely within the muscle. It's what David explained was Lactate -> Pyruvate -> AcetylCoA   There is no conversion to Glucose there.  And as Bryan has pointed out to me, The lactate metabolism they are talking about in that paper isn't really anything special - all of the reactions except lactate->pyruvate, are exactly the same reactions from standard glucose aerobic metabolism.  That  - Lactate->Pyruvate->Acetyl Coa is the one the paper is talking about. A  main point to make there is that the Lactate->Pyruvate conversion  is performed by the enzyme LDH which can work both ways, and in doing lactate->pyruvate, it is doing the reverse of "lactic acid fermentation". The other part, Pyruvate->AcetylCoA is what happens in aerobic metabolism.
I found a really good picture in that paper which helps explain things related to the answer of my question in regards to the process where muscle converts lactate to pyruvate as fuel for aerobic respiration... (I suppose it could potentially fuel anaerobic metabolism rather than aerobic)
So the picture shows the cell and the mitochondria within it.

The paper itself is titled "Lactate as a fuel for mitochondrial respiration"
We see in that picture the Glycogen which will be converted into Glucose, is converted into Pyruvate (Glycolysis), and some Pyruvate is converted into Lactate by LDH (Lactic Acid Fermentation).  But some Pyruvate can be fed into the Mitochondria which would fuel mitochondrial respiration.  The way that Lactate would fuel mitochrondrial respiration, would be lactate converted to Pyruvate by LDH, and that pyruvate would then go into the mitochondria to fuel aerobic respiration.
So when  this page for example, (to quote what I know to be an accurate part of that article), says "lactate produced during exercise can be 'recycled' into glucose and used as fuel by the muscles"  It's referring to the cori cycle, since it mentions lactate converting to glucose.  Whereas in contrast, that paper, is talking about a process within purely within the muscle. Also the cori cycle is about pyruvate being used for anaerobic metabolism(anaerobic metabolism occurs in the cytoplasm)  and the paper mentions about pyruvate being used for aerobic respiration(a reaction in the mitochondria).

I think that after Lactate is converted to Pyruvate, then that Pyruvate could be used for either aerobic metabolism or anaerobic m And that similarly, (with the other process, so),when Glucose is converted to Pyruvate, then that Pyruvate could be used to fuel either aerobic m, or anaerobic m.  (that is the case though the title of the paper and the concept of the cori cycle don't suggest that, as teh paper is distinguishing itself from the cori cycle by speaking of aerobic, and the cori cycle as a continual cycle is speaking only of anaerobic) I aim to update my answer to make that more clear.


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Watermarks visible during DNA fingerprinting?
Let's say we have a human man that was somewhat genetically modified from the very beginning (conception?) by a team of scientists, and is also a product of careful selective breeding. They did this hoping to produce a specimen that would  certain physical characteristics such as superior size and strength, speed, vision, sense of smell, things like that that would result in a "perfect soldier" type of man.
Is it plausible that the team of scientists, like Craig Venter's team, could have installed Watermarks in this man's DNA that would show up on a DNA fingerprint? A DNA fingerprint done by the American FBI?
A user on this forum suggested this possibility in a former thread, so I mean no disrespect to that user by asking this question. I'm just interested in feedback from others. I am writing a novel and this is research for the story. Without getting too deep into specifics, I'm trying to find a way for the authorities to become alerted to the fact that this man is abnormal from other humans.
Any input greatly appreciated.
EDIT:
Basically, I am dipping my toe into the deep end of the pool. I know only the very basics of DNA fingerprinting and Genetic engineering, so technical language is hard for me to follow. I appreciate the answers very much but I'm still a little in the dark. Another user on this forum suggested that possibly "watermarks" might show up on the test, which is why I'm attempting to rephrase the question.
I have written a scene into my novel wherein my main character, a man that has been genetically engineered, unbeknownst to him, gets into a fracas with some bad guys and he wreaks havoc and escapes. The American FBI gets some of his DNA from the scene and works up a DNA Fingerprint on him, purely for the purposes of identification if they catch him. so, yeah, just like on CSI or whatever on TV. When the technicians complete the fingerprint, they recognize that something is different about this person and they contact the lead investigator to let him know. Perhaps they see some evidence of genetic modification or something that raises their eyebrows and they feel it's worth mentioning.
So, essentially all I'm asking is if that is at all possible, and what could they conceivably have seen in the fingerprint? If it's completely not plausible then I'll either delete the scene or rewrite it.
Thanks.

I'm not sure how this question is different from your other question. Importantly, DNA fingerprinting does not look at the sequence of DNA. Such modifications would only show up if they alter the length of a genetic locus being tested.

As was alluded to in your last question, it is plausible. It would require that the loci that DNA fingerprinting analyses be altered in length as canadianer said above. I would have thought that that would be enough 'support' for the case for a novel. It would be pretty easy to state that the FBI just sequenced the DNA sample though, then you could say much more about what they might find. Bearing in mind this is a science fiction novel, so what is 'plausible' is kinda up to you, and how far in the future the story is set?

It's not really in the future. There are no dates but the entire story takes place in a present day setting. The laboratory technicians notice something in the fingerprint that makes them curious about the suspect. They call the lead investigator to ask who their suspect is because something is odd about the fingerprint. The investigator informs them that he's just a man and asks what the problem is. What does the lab technician tell him?

This would only happen if the FBI was looking for that particular watermark or had some other reason to be suspicious. It would not show up as unusual on a standard DNA fingerprinting test for identification. There isn't really anything unusual that can show up on those tests. It also isn't scientifically sound to use those tests on a general database, this increases the odds for false positives tremendously. Instead, DNA tests are most useful when you already have a suspect and you want to verify that evidence at the scene is from that suspect.

The "watermarks" that you're referring to sound exactly like DNA fingerprints: stretches of DNA that are unique to an individual. These unique stretches occur naturally in all individuals, but specific artificial sequences could theoretically be inserted via techniques such as CRISPR.
Once inserted, these artificial sequences could be searched for specifically through PCR, if the sequence is known, or through traditional enzymatic restriction methods, such as described in the first link.
It's worth mentioning that in order to be easily detected, your watermarks would most likely have to be inserted into the germ line of these genetically modified humans. Otherwise, you'd only be able to get the watermark sequences into a small region of tissue. Once in the germ line, the body's own DNA replication mechanism takes over copying those sequences throughout the organism.
Good luck writing!

In principle, sure--as long as you're not looking in his KIDS (remember 1/2 his DNA goes into kid; 1/2 lost). The technique could still work if the watermark were very close to or part of the 'special' DNA sequences.
Also depends somewhat on your meaning of 'fingerprint'; if you are adding new DNA, then besides the functional sequences, you could add a 'signature' of any sequence you wished. Since we know the sequence of many human genomes, you could pick a stretch that's very different from any known sequence. There are many techniques to ask "Is sequence 'XXXXXXXXXXX' present in this DNA sample?". It would not need to be very long, and for certainty, you could drop 3-4 different, unique 'watermarks'. It's also reasonable that the genetic modifications themselves are unique sequences, so no further signature would be needed.

A "DNA fingerprint" is a set of about 13 loci which consist of repetitive elements, and you look at the size of those repetitive elements.  I guess you could if you could invent your own into someone's genome of unique sizes, there would be no functional purpose.
If you gave a person multiple alleles of those regions, such that it looked like the person had more than 2 alleles at each locus, that would probably get someone's attention, depending on how automated the software that assesses those PCR products is.  But there is no functional reason for someone to alter a genome like that.  You need to find a reason for researchers to go out of their way to do that.
If the researchers wanted the ability to find their creation with a DNA test, they could easily put in a region of sequence which most people would never intend to probe with appropriate PCR primers.  In the future, whole genome sequencing might be cheap enough that you could see everything, and a large section of unexpected sequence could in theory be detected and flagged.  A very small sequence might be ignored by anyone not looking for it as noise.
If your "careful breeding" means "inbreeding", your subject might be homozygous at lots, or all of the standard loci, and that might raise flags.  It wouldn't scream "genetically engineered" but it might be weird enough to get someone's attention.


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Count colonies in the right way
I use Rose bengal agar cloramfenicol for search yeast and molds for inclusion in petri plat. Which is the method correct for count? I'm not sure if i count everything or only the bigger one?

Yes, you have to count every individual colony.
However, in practice the question is more, what is deemed a countable plate and how important is it. In many laboratories you will find that technicians and scientists won't bother to count each and every colony on the plate if you have a visibly high number of colonies. They will for example simply say (with a bit of experience), the count for this plate is greater than 300 (write >300).
Nevertheless, you will of course still need a count, so it is common practice to do one of the following:

Split your plate into sectors of equal size (you can draw lines on the bottom of the plate), count all colonies in one sector and then multiply this number by the number of sectors you have divided in. So, say, you have split your plate into 4 sectors (quadrants) by drawing a big cross on it, you would count the colonies in one quadrant and then multiply by 4. This is obviously an extrapolation.
The other option, is to dilute your sample until you get it within countable range. So you could do a serial dilution, put it onto plates and then once your organisms have grown you can count the entire plate and then multiply by the dilution factor. So, say, for example you have your sample in an enrichment broth and do two 1/10 dilutions (1/100) and then plate out 0.1mL (counts as 1/10), you have a final dilution factor of 1000. So you would need to multiply the count that you get on this imaginary plate by 1000.

In your sample you obviously have a variety of different organisms. It is probably advisable to check official methods for what they recommend. Here is an excerpt from the official BAM method for Yeasts, Molds and Mycotoxins:

Count plates after 5 days of incubation. If there is no growth at 5 days, re-incubate for another 48 h. Do not count colonies before the end of the incubation period because handling of plates could result in secondary growth from dislodged spores, making final counts invalid. Count plates containing 10-150 colonies. If mainly yeasts are present, plates with 150 colonies are usually countable. However, if substantial amounts of mold are present, depending on the type of mold, the upper countable limit may have to be lowered at the discretion of the analyst. Report results in colony forming units (CFU)/g or CFU/ml based on average count of triplicate set. Round off counts to two significant figures. If third digit is 6 or above, round off to digit above (e.g., 456 = 460); if 4 or below, round off to digit below (e.g., 454 = 450). If third digit is 5, round off to digit below if first 2 digits are an even number (e.g., 445 = 440); round off to digit above if first 2 digits are an odd number (e.g., 455 = 460). When plates from all dilutions have no colonies, report mold and yeast counts (MYC) as less than 1 times the lowest dilution used. Isolate individual colonies on PDA or MA, if further analysis and species identification is necessary.

Please see link here.


text:
Can formalin fixed tissue stored in absolute ethanol be used for histology?
Can samples which have been stored in buffered formalin and the moved straight to absolute ethanol be used for histology?
I know that the samples normally need to go through a series of ethanol concentrations (70%, 80%, 90%) for dehydration before they reach absolute ethanol, but can you still use samples that have been immediately immersed in absolute ethanol? Or would the rapid dehydration cause too much distortion?

Can they be used? Sure. How much distortion you get will depend on the tissue type and several other factors. How important that distortion is will depend on what you are trying to measure. "Too much distortion" is a relative term. You can't really know how bad it will be without trying it.
Should this ever be done intentionally? No - there is good reason for using the gradual dehydration steps. I would be really hesitant to do any quantitative analysis or draw any solid conclusions from tissue processed incorrectly, though.


text:
Testosterone level in body with activites
Does ejaculation lower level of testosterone in body, Conflicting reports on internet, a firm answer would help a lot?

There are two studies that shows that level of testosterone is higher during abstinence.
A research on the relationship between ejaculation and serum testosterone level in men:

The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak.
...
The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum.

Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence:

These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.


text:
snake identification
While moving large, old oak logs I'd stacked a year ago to form a terraced garden, I noticed it was very moist under the logs.
I saw 5 kingsnakes, a scarlet snake,  a couple of small brown earth snakes and an unidentified snake:

Thicker body than the King snakes, very skinny head, 3-4 feet long, and  almost all brown.

Can you identify the snake?

  Note: Picture taken from about 10 feet away. The debris on the snake pictured is sawdust and wood pieces.
We catch, picture and release kingsnakes, rat snakes and hog nosed snakes all the time, but this one escaped before capture or a good picture. Only one copperhead in 18 years.
Location: Gasconade County, MO (USA; 1 mile from Rosebud, MO).

We have a 1.5 acre pond about 80 yards from the picture site.