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Does epigenetics suggest there is at least some element of truth to Lamarckism?
I am not a biologist. But googling "epigenetics lamarck", I find many different opinions:

For: Lamarck rises from his grave, Epigenetics: Lamarck’s Revenge?, Darwin’s theory ... is incomplete without input from evolution’s anti-hero: Lamarck;
Against: One more time: no, epigenetics is not Lamarckism, Why epigenetics is not a vindication of Lamarckism.

This is highly confusing to laypersons such as myself and I'm hoping an expert here can explain to me why there seem to be such vehement disagreements on this matter.
Here's my simplistic layperson understanding of the matter:

Lamarck: Variations transmitted from parent to child can be influenced by the experiences of the parent.
Darwin: Lamarck is wrong, variations transmitted from parent to child are purely random and cannot be influenced by the experiences of the parent.

Based on my above simplistic understanding (correct me if I've made any errors), it seems to me that epigenetics suggests that there is at least some element of truth to Lamarckism. Am I mistaken?

This post is similar to [https://biology.stackexchange.com/questions/3789/can-epigenetic-changes-affect-reproductive-success].

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular note that questions likely to generate opinions rather than facts are against site guidelines — please [edit] your question accordingly. Please also take the time to search for "Lamark" and "epigenetics" on this site as similar questions have come up before. — Thanks!


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Will ammonia continue to accumulate in an aquarium tank if a strong antibacterial or chlorine is added to the water?
I've always wondered what would happen if dead plants and fecal matter lay in chlorinated waters and/or waters treated with strong antibacterials or antibiotics.
I've heard that aquarium tanks owners warn against using strong antibiotics as it can kill nitrifying bacteria which convert toxic ammonia to a safer form of nitrate. Otherwise, ammonia levels can buildup and be toxic to the aquatic life in the tank.
However, that doesn't make sense to me. Even if the nitrifying bacteria die, wouldn't the ammonifying bacteria which produce ammonia in the first place also die? Would there be greater amounts of ammonia in the water after these agents are repeatedly used, or would ammonia levels with nitrate levels together fall significantly?

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A very large part of the bacteria and fungi will die so very few biological processes will continue in the tank if you add chlorine or antibacterial chemicals.
Ammonia will slowly outgas from the water oxygen and CO2 will reach equilibrium in the water as little oxygen is used and little CO2 is produced, it is the same with the other atmospheric gasses.
Life in the tank will simply stop until the toxins are broken down or removed,by toxins i mean chlorine and/or antibacterial chemicals.
Nitrate level will not change as little is produced and little is used, any denitrification will stop too.
Denitrification can only happen in an anaerobic environment but denitrfying bacteria too are killed by chlorine and antibacterial chemicals.

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Is it possible for a invertebrate to evolve features like that of a vertebrate or BECOME a being similar to that of a vertebrate?
Could a invertebrate, for this lets say, a centipede/millipede, evolve into something like that of Pikaia? or something similar? Just an invertebrate turning into something similar or what would look like a vertebrate. Is that even possible in the first place? I was thinking maybe tagmosis could do some of the magic but other than that, I hit rock bottom.

Define similar.  Or consider the hummingbird and the hawk moth: https://en.wikipedia.org/wiki/Sphingidae

Your question is very vague because it covers 100 million years of evolution that happened 500 million years ago, and asks if a centipede can develop many complex features like: bones, endoskeleton, spine,red blood cells, lungs/gills, and lose all the features that define arthropods. best to read up about "earliest vertebrate fossil" and "earliest terrestrial vertebrate"

This is a very complicated question to answer. evolution of that extent might take many millions of years and nobody can say for sure whether something like that would actually happen.
If we look back in time (https://socratic.org/questions/how-did-vertebrates-evolve), organisms with exoskeletons such as ostracoderms appeared before vertebrates. So, perhaps arthropods like centipedes and millipedes could evolve into a vertebrate if it benefits the species in their particular environment.

Thank you! Mad respect

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Why does exposure to a smell for some time reduce the electrical response of receptor neurons in the olfactory system?
In what way does exposure to a certain smell for some time causes them to loose sensitivity and have a lesser electrical response

You may find providing a little more research/context will help net more useful answers? For example, is there research that shows reduced olfactoy sensitivity is a peripheral phenomenon occurring at the receptors, as opposed to sensory filtering that happens in the CNS? I'm also curious about time scales. Are you interested in long-term exposure and/or chronic loss of sensitivity or more short-term/transient phenomena, like when you get in a funky smelling car but stop noticing after a few minutes?

Both, long term exposure as in you cant tell if you smell bad because ur used to ur smell and short term as in u keep smelling a perfume and u stop smelling it for a short period of time

in what way is that different to any neural adaptation?  https://en.wikipedia.org/wiki/Neural_adaptation


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Is there any record of an Albino (Not leucistic) peacock
Wikipedia says there are, however gives no source to one. Does anyone know if an albino peacock was ever recorded?

There is a breed of White Peacock. I could not find any record of 'Albino' Peafowls (the gender neutral term for peacock is peafowl (females are peahens). This white variety of peafowl is similar to how there are white chicken which have been bred over many years.
Albino animals do not produce the pigment 'melanin'. Albinism can be a dangerous trait in some organisms such as birds. The lack of melanin makes albino animals very sensitive to the sun's UV rays which can cause their vision to become impaired. Therefore most birds that are adult and white are usually either a variety of bird that is naturally white or is suffering leucism which is similar to albinism but does not remove melanin from organs such as the eyes.
But not all white birds are albino and not all albino birds are white. Just because the melanin pigment is non-existent in albino birds, doesn't mean other pigments couldn't still exist. Some animals don't even need pigments to achieve a certain color and do so instead by reflecting light in interesting ways.
It must also be noted that sometimes, white varieties of birds (or birds with leucism) are interpreted as albino and mistakenly presented that way online. This goes for other animals as well.

The rate of albinoism in mammals is roughly 1/10,000 births. However, for birds this rate is around 1/1764.
Abinoism has been reported in modern-day peacocks here: https://www.treehugger.com/albino-and-half-albino-peacocks-are-simply-stunning-photos-4858413
However, I did find a 1965 paper that has documented at least 99 peacocks from 8 different species being albino: https://sora.unm.edu/sites/default/files/journals/jfo/v036n02/p0067-p0071.pdf
So based off of the tree hugger photography post, the rate of albinoism in birds, and the 1965 paper looking at albino birds in North America, I would say albino peacocks do exist and are probably occurring more often than albino mammals.

Actually, the 1965 paper is about North American birds, and the 99 cases are of albinism are in the family Phasianidae, which is described as containing "Quail, Pheasants, and Peacocks".  Since Peacocks are not North American, probably none of those 99 cases were Peafowl.


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Why are lungfish cartilaginous?
Lungfish have a cartilaginous notochord, and a reduced cartilaginous skull. Is this feature to improve flexibility, or is there another reason?

Your question is interesting and relevant to here, but it's expected that you show you have researched and tried to find answers to your question before you post, rather than expect others to do it all. Could you include it in your post?


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Which factors dictate the mineral composition in plants\vegetables?
Here's a table of vegetables mineral composition (one of many), just as an example. Each vegetable contains different amounts of minerals, and my question is why is that, or in other words: Which factors dictate the mineral composition of different vegetables, since the diffusion process by which the minerals are absorbed from the ground into the root is essentially the same for all plants\vegetables?

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Do all body organs grow in proportion during the period of physical development?
It is obvious that during childhood and puberty, the human body grows uniformly or proportionally so that a child's arm length, for example, is shorter than an adult's arm length but is proportional to a child's leg length.
What I'd like to know is whether the same is true for internal organs, or are there any organs (even external but perhaps less obvious) that do not grow in dimensions when the rest of the body grows and develops (I am talking about physical growth).

I suggest reading this wikipedia article Allometry

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What could be the reason for the large difference between sodium and potassium blood concentrations?
Reference values for sodium and potassium concentrations in blood tests are usually in the range of 135-145 mEq/L and 3.5-5.1 mEq/L, respectively.
My question is what could be the reason for this (relatively) large difference in the blood concentrations of these two ions which are together responsible for cells function and communication? What other roles does sodium play outside of cells that require it to be a lot more abundant in the blood than potassium?
Also, a follow-up question: is this proportion more-or-less maintained in other animal species?

This is much too broad. Some reading on your part about homeostasis is in order. If you still have a question then, and can explain why it is unclear from your reading, that would be a narrower question. The short answer is because it's necessary for life. When we die, equilibration occurs (more or less).

Although this is a fairly broad question, I think it could still be given an appropriately-scoped answer. One bit of information missing from the question that would make it more interesting is the imbalance between extra- and intra-cellular concentrations: not just that Na+ concentrations are greater than K+ in the blood but that the opposite is true in a typical cell.

@anongoodnurse, I have studied some basic physiology, including nervous system physiology, and I am aware of electrical activity in the cell, membrane potential, ion pumps etc. This question focuses on a very narrow (in my opinion) aspect of this very broad subject, which is merely the quantities. Actually, it came up when I was reviewing a patient's blood tests - I looked at the normal ranges and asked myself: "how come sodium blood concentration is 30-40 times greater than potassium?", or in other words, why did evolution settle on this proportion? Perhaps no one knows, but worth a try.

@Don_S - Sorry, the question read like a beginner's. In that case, God only knows, but it is still too broad. (I was a Molecular Biologist before I became a physician.)

Wait, here's an idea: nothing else lived long enough to reproduce. That answer is probably as accurate as any.

Well, thanks for sharing your thoughts. For me, this is the place to come before giving up... I hope the question won't be closed, at least 3 people liked it...

Sorry that this is an extremely simplified answer, but basically, cells make use of the concentration gradients (and some cells the electrical gradients) produced by pumping sodium out of cells and pumping potassium in. A lot of that functionality would be achieved by simply pumping sodium out, but something has to go in its place or else you would have osmotic effects. The "choice" of sodium/potassium is reasonable because those ions are freely available where life evolved, but are probably still used because a shift would be an enormous challenge to overcome.

I hope someone will come along with an actual full answer but in the meantime I just hope the question isn't closed, I think it's a good one for people at many levels of understanding. As far as other animal species, to my knowledge yes the general pattern is maintained. It likely originates from "extracellular" ion concentrations being seawater, so it is very old.


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Why is it advised to avoid bubble formation during mixing?
I have been told not to vortex solution containing protein. The reason I was given is bubble formation. Here I am interested in the effect of bubble formation in general.

A "bubble" per se would do no harm unless you have cells (without walls like mammalian cells) in the suspension. If you agitate the protein mixture vigourously then it may lead to denaturation of proteins by extensive intermolecular collisions. The "froth" formation is an indication of denaturation as denatured proteins stabilize these foams [1, 2].

References:

Zayas, Joseph F. "Foaming properties of proteins." Functionality of proteins in food. Springer Berlin Heidelberg, 1997. 260-309.
Schmidt, Isabelle, et al. "Foaming properties of protein/pectin electrostatic complexes and foam structure at nanoscale." Journal of colloid and interface science 345.2 (2010): 316-324.

would you not agree that denaturation because of "extensive intermolecular collisions" depends on whether there is a low or high concentration? Because low concentration = few collisions and high concentrations = more collisions. So is the rate/process of denaturation (therefore creation of bubbles)  depended on the solution which is agitated?

@JordiZambrino Yes concentration of the solute and other fluid properties of the solution such as viscosity etc also have a role. You do see more froth with higher concentrations. It also depends on the molecular nature of the protein. But my point is that froth is an effect of denatured proteins and not the cause.

I want to point out about undergrad labs: People vortex SDS mixtures and small volumes, and advertently the pipettes can't get everything out of the tube reasonably sometimes due to bubbles. You could try to centrifuge it, but if there are still bubbles, trying to pipette 50µL of bubbles is annoying. I can remember one lab where we had to pellet E. coli in 4 tubes and consolidate the pellets. The resulting solution was very viscous, and if you formed bubbles while pipetting it made things a lot harder to work with.


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What is a genome?
By genome do we mean a consensus sequence of DNA or a set of sequences that ideally captures all possible variations?

Like with everything, people mean different things in different contexts when talking about the genome.
You can see this in different levels:

genome of a cell: the entire genetic material contained within a cell
genome of an organism: the entire genetic material contained in an organism. For an multicellular organism, this could refer to the average genome between cells. However, technology does not allow us to access this average of all cells. In more practical situations, this could refer to the reconstructed genome taken from cells in the mouth or blood.
genome of a species: the genome of an individual taken to be representative of a species. In more practical terms, this can be the genome of an individual that was captured and sequenced by humans. In the case of humans, several individuals donated their DNA towards the sequencing of THE human genome
metagenome of an environment: the set of genetic information found in an environment, e.g. the metagenome of a human intestine, the metagenome of a river, etc.

Graph genomes are on the rise for species genomes and they will allow for the inclusion of genetic variability between individuals.


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Why cooking make foods , e.g rice, vegetable etc, soft?
My initial guess was it is due to absorption of water during cooking (role of heat is probably to accelerate this process). So to verify this I have left uncooked rice  in water for two days but so far it hasn't softened noticably. May be for sufficient absorption of water for softening I have to leave it longer. Or may be my initial hypothesis is wrong altogether.

It is a nice question, but it probably better suited for cooking.SE. So I am voting to close this one here.

Heat is definitely involved in speeding up the water absorption. In general, every 10 degrees C roughly doubles the reaction rate, so a reaction in 100°C water would be expected to run about 256 times faster than in 20°C water. It's not a perfect estimate, but it's probably good enough for cooking. I suspect that the exterior of your cold rice will turn mushy before the interior is soft though.

@another'Homosapien' chemistry might be even better.

Short answer Hydrolysis
Cooking shortens many molecules, particularly carbohydrates and proteins although almost anything long is affected. By heating them in a aqueous environment (many foods supply their own water) we are inducing billions of hydrolysis reactions. This chops up long polymers into shorter ones.For proteins heat also causes them to unwind which makes them easier to digest.  In effect we are outsourcing a major portion of the digestion. This is why cooking is believed to have evolved as a behavior in the first place – it greatly increases the nutrient availability of the food by putting it in a much more easily digested state. Without heat the number of hydrolysis reactions is negligible, although a few things like extreme PH or infusion of enzymes can be substituted for heat.
For most edible molecules shortening them also makes them softer (most macronutrients are polymers, after all) which is an additional benefit. This is also why there is a balance in cooking, cook too long or at too high a temprature and you start to get lots of other kinds of reactions that produce new indigestible molecules. Cook too short or too low a temp and you get few hydrolysis reactions and it essentially does nothing. Hydrolysis is one of the reasons cooking will also dry out foods, since water is being used up in hydrolysis.


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Help me identify this animal from Bangladesh
I have come across this animal in a facebook group. After one group member identified it as Asian palm civet, I looked at some google images, I am not convinced. Judging from google images, this animal doesn't look like any of the common civet species found in Bangladesh.
Location: Noakhali, Bangladesh

Looks like the Large Indian civet. Notice the size and the fur coloration pattern on the neck.
From wikipedia:

The large Indian civet ranges from Nepal, northeast India, Bhutan,
  Bangladesh to Myanmar, Thailand, the Malay peninsula and Singapore to
  Cambodia, Laos, Vietnam and China.[1]

Looks like it is found in eastern parts of Bangladesh including Noakhali district – the place where the picture was taken.


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Are these structures real petals?
I don't know the name of the plant. It's a common house plant in Bangladesh. What interests me about its flower is the colorful leaflike structure that probably functions as a petal. What is this structure homologous to? Petal, sepal, bract or leaf?

The plant looks like something in the genus Bougainvillea. These plants are native to South America, but found as introduced ornamentals in many places.
The colored petal-like organs are bracts (see the Wikipedia link above). The entire structure is an inflorescence with the flower buds growing out from the surface of the colored bracts — you should eventually see those flowers open and you could then dissect them confirm that the usual flower structures are present.
This is a well labeled diagram:


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Are there viruses that show definite enzymatic activity?
Perhaps due to outer coat protein individually or collectively.

Yes even the smallest viruses have enzymes. like reverse transcriptase/integrase in retroviruses. Your question is unclear.

I think he's talking about the intact virus particle. I suspect the answer is no, as the initial aim of the virus particle on infection is to get into the cell, and until it does that substrates will be thin on the ground. But Nature's always full of weird oddities, so who knows?

@David Influenza virus, for example, has neuraminidase on its coat.

@WYSWYG Not even weird. I'd forgotten that the virus particle needs to get out of the cell as well as get in (which I gather is the function of neuramidase).

@WYSIWYG I add a chemical with virus particles, without the help of cellular machinery will the virus be able to transform the chemical? Are there such virus? That was the question. You have answered affirmative with an example. Thanks. Is this common?

@AhmedAbdullah You should edit your question to add all relevant details. From the question it is not clear what you mean to ask. If you clarify the question then it can be reopened.

As some of the comments mention, this question could use some clarification.
First, assuming you're asking in general about enzymatic activity in viruses:
A few classes of "non-autonomous" viruses (particularly endogenous retrotransposons) don't encode any enzymatic functions and sometimes don't even encode their own structural proteins - they rely on the structural proteins and/or enzymatic functions of the "autonomous" viruses.
With the exception of those non-autonomous viruses, all retroviruses encode the reverse transcriptase and integrase functions, while many non-retroviruses (those which don't have a step in their lifecycle where they convert RNA into DNA) also have RNA-dependent RNA polymerase activities.
Now, assuming you meant to limit your question to the viral coat (AKA capsid) proteins of an intact virus-like particle (VLP):
Most do not have any "enzymatic" activity per se - they do not catalyze the formation or breakage of any covalent bonds. However, many viral coat proteins have membrane associated domains which undergo conformational changes essential for uncoating and trafficking of the virus across the membrane:
Gao, D., Lin, X., Zhang, Z., Li, W., Men, D., Zhang, X., & Cui, Z. (2016). Original Article: Intracellular cargo delivery by virus capsid protein-based vehicles: From nano to micro. Nanomedicine: Nanotechnology, Biology, And Medicine, 12365-376. doi:10.1016/j.nano.2015.10.023
This membrane translocating (aka cell penetrating) activity sometimes does depend on the "collective" action of oligomeric complexes of capsid proteins, but it is not an enzymatic activity.
However, the parvoviruses do encode a phospholipase enzymatic activity in their coat proteins which serves to disrupt cellular membranes and allow viral entry:
Kobiler, O., Drayman, N., Butin-Israeli, V., & Oppenheim, A. (n.d). Virus strategies for passing the nuclear envelope barrier. Nucleus-Austin, 3(6), 526-539.
I don't know of any other classes of coat proteins with bona fide enzymatic activity, but I wouldn't be surprised if some exist, and I've only touched on a few of the multitude of enzymatic activities exhibited by other viral components.

There are other examples of enzymatic activity in the capsid such as the neuraminidase of influenza virus.


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Size distribution of all known species in the domain bacteria
I have found the smallest bacteria are around 200nm (e.g Mycoplasma genitalium an ultramicrobacterium) and largest are around 700um (Thiomargarita namibiensis). I am looking for a graph that illustrate the size distribution of all bacteria species. I have googled with no luck.

You can find the average size of all characterized bacteria. That information is documented but perhaps nobody thought that a plotting a size distribution is useful (especially if you consider all bacteria and ignore the habitat and demographics).

You say you are looking for a graph. I assume size is the variable you require on one axis. What is the other?

@David in x-axis average size and in y-axis number of species

Sorry if I gave you false hope of an answer. I had forgotten you wanted physical size rather than genome size. You certainly will be out of luck for "all" bacterial species, because in recent years the number has increased vastly from genome sequencing of uncultured species (e.g. in the gut) which have not been characterized physically. You might like to take a look at the abstracts of this recent Nature paper and this one to get an idea of the scale of this.


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Identification of huge larva in South Tyrol
On a sunny autumn day (19.09.2021) i saw a huge green larva crossing the street facing a wineyard. The picture was taken near Bozen, South Tyrol (22 °C that day). It is at least 14 cm long and 2 cm thick. It is entirely green, besides black and yellow stripes at each "segment" and with black spots at the lower part of the body. Additionally there is an red/black anal spine.
I would have guessed it is some kind of Acherontia atropos, but i am not entirely sure.

Is that a green horn catepillar? Don't know anything about them or if that is even what they are called but when I saw that photo that name came into my memory somehow. Google seems to correct that term to hornworm catepillar. 4 inches. Similar pattern too.

Sure looks like tomato hornworm, Manduca quinquemaculata or similar tobacco hornworm M. sexta, but Manduca is an American genus.  Agrius convolvuli is European and similar larva, but seems to have a stripe connecting the slashes of the segments.

After some additional research, i would agreelso conclude its one of the larval stages of Agrius convolvuli , which looks pretty similar. So i guess mgkrebbs was right. A friend of mine, working as an agricultural entomologist said, that especially the black stripes of the larva can change during the developement.


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Why do I see purple stripes when moving a small source of light (flashlight) quickly in a dark room?
I was playing with my phone's flashlight (white) in a dark room, Just moving it around quickly when I noticed that I could see thin stripes of purple in the same shape as my hand moved, they didn't disappear instantly rather I could see them like a net of thin purple strips, but vanished when I looked at them for more than 2 seconds. I don't understand why it happened and was curious.

This phenomenon is called afterimage and happens because of adaptations of the photoreceptors in the retina of your eye to the stimulation by light and adaptations by your neurons in the visual processing in your brain.


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Permission for Figure Reuse
I was wondering how I can go about gaining permission for reuse of a figure in this post. I was hoping to reuse the image that is exemplifying the cross section of the retina. If anyone know please let me know I appreciate the help!

This question is off-topic here, because it is not about biology. It is on-topic in academia.stackexchange. I can migrate it if you want.

I’m voting to close this question because it is about figure reuse and not biology.


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Which animals do bait hunting?
By bait hunting I mean some predator which first collects or finds some bait (food of its prey) and then uses the bait to lure and catch its prey. This question is inspired by this video showing an orca using a small fish to catch a bird.
To me this looks like it requires an amazing amount of intelligence from the orca to pull off. Note that the orca in the video is in captivity so I don't know whether this is something that wild orcas can do or whether this is a human trained behavior. More generally, is this something that some smart predators can do?

Intelligence? Ehhhhh...insects can use bait hunting too. I seem to recall I once saw in a book when I was a child that some assassin bugs wave around dead ant corpses to attract more ants (though most Google searches only end up with assassin bugs covering their body with dead ants which is not what I had in mind). Assassin bugs also pluck spider web strings to simulate caught  insects to lure the spider out.

Well,  Crocodylus palustris do this using sticks that birds want for nesting.

(Photo from below article, copyright)
Behind a paywall is:
Crocodilians use tools for hunting.
V. Dinets, J.C. Brueggen & J.D. Brueggen
Published online: 29 Nov 2013
https://doi.org/10.1080/03949370.2013.858276
It is also known that Crocodylus porosus caches uneaten food; and unproven suspicions that they use the cached food to bait-hunt aquatic animals.


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Why are microtubules absent in and around the nucleus?

I was going through fluorescence microscopy and found these four images. The top left corner shows the actin cytoskeleton (rhodamin phalloidin) and the bottom left image shows the microtubule cytoskeleton (Alexa 488). One thing I noticed is that the actin cytoskeleton is continuous throughout the cell as seen in the top right image (rhodamin phalloidin + DAPI composite), but in case of the microtubules, the nuclear position and microtubule localization seem to be mutually exclusive. I can't seem to figure out why this might be the case, and it definitely does not look like a coincidence.

Welcome to Biology.SE! Please provide a citation/source for the images you are using — images should be credited to their creators just like quotes are to their authors. This is generally considered good practice in scientific communication and will help other users understand by providing context. ——— Please see the [tour] and the [help] pages starting with [Ask] questions for information about this site . Thanks!

tl;dr Cells are 3D and the cytoskeleton does not exist within the nucleus.
There are several things you have to be aware of when looking at such pictures. Remember, you are looking at a 3D object which is not homogeneous and uniform in depth.
Shape of a plated HeLa cells
You are looking at HeLa cells. When plated like in your case, they adhere to the plate and make a generally thin, 2D-ish shape with lamellipodia (the extruded parts that look like they are grasping the plate on the sides of each cell). The nucleus is the most prominent vertically bulging part of the cell - the nucleus takes up most of the depth of the cell and there is little space around it. You have to appreciate the vertical dimension of the cell around the nucleus especially. The shape is a little like an egg cooked sunny side up; the yolk makes a bulge and the egg white is thinner around the yolk and there is little space for large filaments like microtubules. Remember, cytoskeletal filaments are so in size: small (actin) filaments < intermediate filaments < microtubules. This is exactly why you see more actin, a little less intermediate filaments, and even fewer microtubules exactly on top or below the nucleus in these 2D plated cells. Also, please remember that these cells are not representative of most cells.
The nucleus is a separate compartment
The nucleus is also a separate compartment, within which the actin and microtubule cytoskeleton system do not exist. The nucleus performs its own structure-keeping in the form of the nuclear lamina, which is composed of protein meshes that sit on the inner membrane of the nucleus.
You are not seeing the small actin filaments inside the nucleus, only around it. The microtubules are too large to see above and below the nucleus in most cases, since they are much larger filaments. In some cases though, you would see microtubules in HeLa cells above and below the nucleus.
See picture below: microtubule stain shown in green.

Other images for a more wholesome appreciation of the cytoskeleton.
Here follow a few micrographs of HeLa cells.
In green, actin.
In red, intermediate filaments stained with vimentin:

And now here you can see a microtubule stain in HeLa cells, in pink. Notice that some microtubules do actually make it around and across the nucleus.

Just to make this point a bit clearer: There are neither actin nor MTs inside the nucleus, but both of them may be on top of the nucleus (and thus appear in the same location in an image). The explanation for the difference between actin and MTs in OP's image is the same as in the ones posted here: it looks like actin is quite uniformly distiributed also on top of the nucleus, while MTs do seem to prefer not to sit right on top of it. Judging just from these images, it seems as though the nucleus creates what looks like an "exclusion zone" for MTs but not for actin in the imaging plane.

@S Pr that sunny side up eggs analogy was spot on. Great answer, Everything's crystal clear for me now.

@MasterOfGalaxy one of the roles of the microtubule cytoskeleton is the mechanical support of the cell. The nucleus has its own specific skeleton. The nuclear lamina is a proteinaceous meshwork located on the nucleoplasmic side of the inner nuclear membrane. On the other hand, microtubule filaments allow for water and minerals transport to organelles including the nucleus from exoplasmic surface while the nucleus has not independent accessibility to exoplasmic leaflet because of its topological position. There is no function for microtubules in the nucleus.


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What are the common dental traits of fungivorous mammals?
What are the dental adaptations for eating mushrooms that are commonly found amongst fungivorous mammals?


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What is a lamprey's tongue derived from?
Tetrapods have tongues derived from the 2nd gill arch and nearby muscles. Lampreys are not tetrapods, and lack jaws, yet they have a tongue. What structure was this tongue adapted from?

Are tongues older than jaws? Because jawed fish came from jawless fish. Could have the same origin.

the tetrapod jaw is just the first gill arch.

the "tongue" is just the bottom of the throat. Its not related to the tetrapod tongue nor are their "teeth" related to tetrapod teeth.
https://www.nature.com/articles/nature11794


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Why are apes so poorly adapted for walking upright?
Non-human apes are quite poorly adapted for walking upright, in terms of their anatomy. I have found many sources that explain how their anatomy is so unsuitable for an upright life, yet none have given reasons why they evolved like this in the first place
It seems like most adaptations for bipedalism would work well enough in other apes, and there should be at least some pressure to move well on the ground
Given this, why are the other apes so poorly adapted for walking upright?

You could ask 'why are humans so well adapted for walking upright' or 'what was the benefit to humans for walking up right' and then consider why those reasons may not apply to apes

@user438383 I get that humans had more reason to be upright, but it still seems like these reasons would apply to the other apes, at least to some degree

Maybe in a few million years given the right environmental pressures... yes. But what're their habitats like at present? Admirably suited to them being how they are (barring loggers cutting down the local trees).

This might be a useful starting point for thinking about comparisons between humans and other apes: https://nationalhumanitiescenter.org/on-the-human/2010/02/the-challenge-of-comparisons-in-primatology/

You don't understand why forest dwelling climbers are well adapted for climbing?

When you write:

It seems like most adaptations for bipedalism would work well enough in other apes, and there should be at least some pressure to move well on the ground

Based on our understanding of how bipedalism arose in ape-like human ancestors, I don't believe that this is true.

There are significant constraints that can make bipedalism disadvantageous (at least in the case of humans, see below), and thus apes would have to either find a substantially different bipedal strategy (likely difficult, given the path taken by human ancestors), or accept the tradeoffs of the human approach to bipedalism.
Do we know that moving around on the ground on all fours is a poor strategy for these primates, to the extent that they need to do so?

Constraints of human approach to bipedalism
Pelvic adaptations to bipedalism significantly restrict the size of the birth canal (see image), among other changes. This imposes a significant tradeoff between walking upright, maternal/neonatal mortality, and other parameters.
Quote from the linked article:

Pelvic anatomy impacts human performance. To walk upright in an energetically efficient manner with a minimal risk of injury, the pelvis must be robust and have a shape that maximizes muscle lever arms and minimizes load [5–11]. The ability to regulate body temperature is affected by the width and depth of the pelvis, which plays a crucial role in determining overall body proportions and the body's surface area-to-mass ratio, thereby influencing heat loss through the body's surface [12,13]. Finally, and most critically from a selective standpoint, pelvic shape must allow the delivery of a healthy infant without harm to the mother [14]. These goals are not all achieved by the same pelvic morphology, yet all three demands must be met. Therefore, selection has favoured compromises between these often contradictory pressures [15–17].

I think this is more about HOW humans are adapted to walking upright, while the question asks why apes aren't so adapted.

@jamesqf that is fair, I will update to directly address this (to the limited extent possible given the vagaries of evolutionary reasoning).


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What do spider digestive fluids look like?
What is the general appearance of the fluids that spiders use to digest their prey before they ingest it into the body?

In most species of spiders, this liquid is thick and brownish (Brown)
This digestive juice helps spiders to feed of prey even larger than spiders.


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If calcium ions and cholesterols are found on the surface of the skin, would it be possible for Vitamin D to be synthesised on the skin?
Calcium ions are abundantly found in the extracellular space of the stratum corneum area, the top most layer of the skin (Skin Barrier and Calcium; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5929942/). Isn't it very probable that it can also be found on the surface? Calcium ions are also actively involved in regulating the water gradient of the stratum cornuem. However, they may be easily washed off from the surface of the skin through the regular use of water and surfactants. Plus, the use or over-use of moisturizers also interfere with natural sebum production and the Calcium ion gradient of the stratum corneum ( The Changes of Epidermal Calcium Gradient and Transitional Cells after Prolonged Occlusion Following Tape Stripping in the Murine Epidermis; https://www.sciencedirect.com/science/article/pii/S0022202X15405603) If calcium is found on the surface of the skin, and sebum plus intercelular lipids (which also eventually make their way to the surface of the skin and mix with sebum and sweat to form the acid mantle) contain cholesterol, wouldn't it be possible then Vitamin D could be synthesised on the skin through irradiation?

Welcome to SE Biology. Please finish the Tour. My first reaction to your question was "What is this all about?". You provide no context to your question. Why are you asking a hypothetical question about a tissue, the structure and metabolism of which is very specialized? One is suspicious that you are engaging in an argument with someone and are trying to get support for a point of view. Is your question any more than will the conversion of 7-dehydrocholesterol to cholecalciferol by UV occur in vitro? Tell us why you want to know.

Long ago I read that vitamin D is made on the skin and absorbed. Not an answer because I have no idea where I read it.


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How do asexually reproductive organisms mutate?
In accordance to my limited knowledge of biology, asexual organisms exactly copy their DNA as there is no "contaminant", which in sexual reproduction is the other organism's DNA.

Your understanding is wrong; you have confused the mutation process with the process of genetic recombination.  The two are not related.

Mutation is mutation, a wrong nucleotide substituted (etc.) for the correct one. The mechanisms don't vary from organism to organism. It is, after death, the great equalizer.

It is not necessary that no mutation occurs in the system where no gene recombination or "contaminant" takes place. There are mutations (which are sudden abrupt inheritable changes)
There can be errors in genome which can cause mutations.
Take example of replication of DNA-:
There are many enzymes linked with it : DNA polymerases ( I, II,III) in prokaryotes where asexual reproduction occurs which add nucleotides to make replicas of DNA of parent ( you can check the complete process at wikipedia)
Come to the point : DNA polymerase III, after synthesising dna chains has ability of proof reading. It can correct the mismatches ( hope you know that adenine bonds with thymine and cytosine with guanine, they are nitrogen bases of dna)
DNA polymerase III can correct the mismatches but it is not error proof- it can't distinguish between thymine and uracil (another nitrogen base ; thymine is methylated uracil)
This is only one possible error, there can be many such hence asexual reproduction isn't error proof

@ collin is that right with you


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Is pathlength correction vital to be included while quantifying protein
I am trying to quantify protein in serum/plasma samples. I have carried out biuret assay for my samples using microplate reader. While performing I encountered the doubt whether I should include pathlength correction, blank subtraction steps to get accurate value. Why and how to use these factors for quantifying using microplate?

The exact way to take pathlength into account would probably depend on your platereader, though if you kept all wells at the same volume the pathlength should not be a problem. If you include blanks and a standard calibration curve on the plate, you should be able to work up the protein concentrations in your unknowns ok just using the absorption data directly from the plate reader. Just be sure to write down what well has what solution so you can do your spreadsheet correctly.


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Degenerate primer designing software
Can any one provide online free degenerate primer designing software. I have tried couple of them like CODEHOP is one where BLOCK formatting step finding difficulty, can anyone help me out....

Benchling is a lab notebook with full DNA tools suite. You can check out a tutorial for the primer design tool her: https://benchling.com/tutorials/25/creating-and-analyzing-primers It's totally free to use for academics, and you can sign up via: https://benchling.com


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Evolutionary Midways
Given that the mechanism of natural selection is sensitive, how do species survive in an evolutionary midway? The ability to breath in air requires complex protein systems. An animal that is developing these organs would not be able to utilize its function until it fully evolves. While it doesn't, wouldn't the wasted resources used in growing half-developed lungs be.. wasted? Or is all evolution continuous?

I have this very question in my mind as I take H2 biology. It is not from homework.

It is a common question
Statements of the kind "Evolution is impossible because of intermediate state" are common from religious extremists literature. There is therefore a lot of resource online that already debunk this type of statement but I guess, I'll just quickly write one more! Of course, I am not suggesting that you are taking an opinion-based position, you might well be genuily seeking for an understanding of the world.

Quickly speaking there are a series of concepts that are necessary to understand in order to answer this question.
Fitness landscape and fitness valley
The term "evolutionary midways" is not used in biology but one can rephrase it with the concept of fitness landscape and fitness valley.

Fitness landscape

The fitness landscape is the function that maps fitness (generally represented in y-axis) to phenotypic trait value (typically multi-dimensional but often represented on a single axis for simplicity). Fitness landscape may also refer to the mapping from genotype to fitness but we will not be concerned with that for this answer.

Fitness valley

A fitness valley refers to a region of low fitness on the fitness landscape. The movement from one locally high fitness state to another locally high fitness peak might well get through a region of low fitness. This is what you call fitness valley and on the fitness landscape and this is what you are interested in.

Is there always a fitness valley?
Let's first consider reasons for which a population might not experience such fitness valley

Logical Fallacy: Argument to ignorance

It is common for a layman to assume that intermediate states ought to be associated with low fitness. In reality the intermediate states might well be neutral or only slightly deleterious (and therefore be mainly affect by genetic drift) or might even be directly beneficial. It appears to be a mistake to assume such fitness valley are more common than they are in reality just because you fail to imagine how a trait may have evolved. In philosophy of logic, this is called an argument to ignorance. Of course, fitness valleys do exist. So, when they exist, do populations ever manage to get over them?

Assuming there is a fitness valley (for a given trait), can populations just "jump over it"?

Do populations need to get through an intermediate state?

Darwin framed his theory into the idea that evolution is a very gradual process. As we know today, this is far from being true. Evolution can actually occur through a big steps. There are single mutations that double the amount of genetic material, there are single mutations that completely affect the physiology or anatomy of an individual. There are cases of horizontal gene transfer (transfer of genetic material between species) as well that can cause sudden important change without having to get through intermediate stages. It is sometimes wrong to assume that there must be intermediate steps.

If there is a fitness valley and the population will not "jump over it"...
Let's assume a fitness valley (for a given trait, for a given population) and let's assume that the population will not "jump over it" thanks to a mutation of big effect.

Shifting Balance Theory

There are a number of different forces that affect evolutionary processes. Layman often think of natural selection as being the only force causing evolution but this is wrong. Genetic drift is another very important process that affect evolutionary process. Genetic drift refers to the random sampling of individual at one generation to build up the successive generation. The relative importance of drift to natural selection in driving evolution of a population depends on the effective population size. Have a look at Why is the strength of genetic drift inversely proportional to the population size?. Genetic drift can typically randomly yield a population toward a fitness valley, from which natural selection will yield the population to either come back or start climbing the opposite fitness peak. This concept is called shifting balance theory. There has been a lot of work on shifting balance theory suggesting that it well be much more common than previously thought.

Phenotypic flexibility

One may wrongly assumed that if a mutation occurs to make, say, a bone a big longer, then one organism would simultaneously need mutations that would make muscles, nerves and other tissues longer accordingly. In reality our developmental process is very flexible to an environmental change or to a mutational change. This flexibility is very much used in medicine and agriculture. If a bone gets a bit longer, muscle might just stretch a little more and end up developing in accordance to the new mutation. It would therefore be wrong to assume that because we are made of a complex interaction of traits, that a mutation cannot bring anything that would not be beneficial. If you are interested in the evolution of complex system you might want to have a look at the post How did the cardiovascular system evolve? for example.

Source of information
I would recommend that you have a look at a very short and introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example and you will be able to understand much more about what evolution is and how it occurs.

https://en.wikipedia.org/wiki/Irreducible_complexity Seems to be what I was writing about. (Just found this out). Thanks for your answer too.

No, I am not at all writing about Irreducible Complexity. Irreducible Complexity has nothing to do with science. It is a fallacy (or set of fallacies) build by creationists. As the wikipedia article you link says: Irreducible complexity [..] is rejected by the scientific community, which regards intelligent design as pseudoscience. If your aim is to learn about evolution, I would recommend reading from the popular science literature (and not pseudo-science and other sources of unjustified arguments). There are many good sources of knowledge, one of them being linked in the post.

Yes you weren't writing about it but I was asking about it. I had thought that complex systems are irreducible, therefore midways are impossible. But I was wrong.


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Reverse evolution to gain back lost traits
Many animals return to shapes similar to their ancestors like mammals and reptiles growing fins and fish tails or animals losing limbs they just grew and so on.
But I notice that once an animal loses a feature it doesn't actually grow back... they con only mimic it, no reptile or mammal has fins but only limbs that look like fins... and no aquatic mammal or reptile seems to regrow back their lost legs or arms.
No animal seems to regrew its ancestral gills even though they live 100% of their lives inside deep waters.
If some organs can be so useful to have back, with evolutionary pressure at maximum, why don't they ever return?
What blocks animals from re-evolving something they lost?

I suggest that you check out the answers provided here: http://biology.stackexchange.com/questions/1754/can-species-back-evolve?rq=1  The main points are that there is no forward and backward in evolution, just a constant adaptation to one's environment.

@Forest, I am not sure that Koume is under that impression that there is a forward or backward in evolution. Instead, I think that Koume is under the impression that an organism is unable to re-attain a trait previously lost due to selective pressure, possibly partly because of the examples being somewhat scarce or inaccessible to the layman.

@niobe From what I understand, the idea of backwards evolution comprises the reacquisition of a lost trait, such as a previous form of some organ. In either case, selective pressures drive the evolution of that trait, whether it's something entirely new, or a return to something previously seen.

@Forest, It seems we are in agreement then.

Back evolution
Evolution do not strictly keep a history of how they were before. There is no way for a population to specifically produce mutations to reverse previously fixed mutations in order to evolve back in time. This has sometimes been called Dollo's law but very few people actually use this term today.
Note however that a population may have kept pseudogenes or specific developmental pathway or case of atavism that make the evolution of some traits similar to previously existing trait "easier". A very nice example of such mechanism is the case of Membracidae (treehoper).
Example of Membracidae
insects have evolved flight once. The first flying insect had 3 pairs of wings, one pair on each of the 3 segments of the thorax. Today, there exist no insects with 3 pairs of wings. In all lineages descendent of this flying ancestor many have no wings and many have 2 pairs of wings only. Here is a schema showing a typical insect with 2 pairs of wings.

As you can see there is no pair of wings on the first segment of the thorax (called prothorax) as it has been lost through evolution. Note that the diptera (true flies) have lost a second pair of wings (the one on the metathorax which has been replaced by halters).
Membracidae (treehoper) is a family of wingless insects. They use previously existing developmental pathways and previously existing genes (Prud'homme et al. 2011) for developing wings on the protothorax but instead of making wings, they make all kind of funny shape for defense purpose. Here are a few examples

I don't remember why I didn't accept this answer back in 2016

May I suggest 2 keywords that might help you get started. Atavism and Dollo's Law
Attempting to answer your question:
In fact there are examples of where animals "re-evolve" a previously lost trait. There is a hypothesis called Dollo's law which posits that the evolution of an organism is not reversible, but as you can see there are exceptions.
Speaking to the likelihood of rediscovering a trait previously lost, assuming it is favorable. From what I can gather, when a trait is deemed to be impossible to rediscover, it would be because the genetic information that expressed that trait has been subject to sufficient mutation and selection so that it has very little resemblance to its previous underlying genetic information. Put differently, it is because the genetic "distance" between what currently is and what used to be is sufficiently great to make rediscovery by mutation and selection very unlikely.
Full disclosure: I am not a biologist and I draw most of my knowledge from studying genetic algorithms in computer science. So let me know if there are any glaring errors that I need to correct.


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How fast does a mole move its claws into soil?
I was watching this video which reports on studies of the force involved when moles dig in soil.
At around 0:30 seconds into the video you can see the mole typically pulls its paws back into the space which has been created by making a tunnel and then thrusts them forwards into the soil before pulling to the side, does anyone have an estimate for the speed at which its thrusts its claws forwards into the soil in the initial part of the digging motion?

Welcome to SE Biology. Questions on this site should be self-contained and not require anyone to go to some other site to watch a video. Please try to rephrase the question so that the video link is suplementary to a full explanation of what you require. Also, provide info on the attempts you have made to answer the question yourself.


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Little owl as decoy for skylark
I read that hunters used (now is forbidden) little owls tethered to attract skylarks.
They say this is due to their magnetic look of the eyes.
I didn't find any scientific documentation of this. Any one knows a scientific explanation of this, if any? Why, if true, should the skylark be attracted by the owl?

Found the reference. Skylarks react to the presence of the owl to mob it.
Van Nieuwenhuyse, Dries; Genot, Jean-Claude; Johnson, David H. (2008). The Little Owl: Conservation, Ecology and Behavior of Athene noctua. Cambridge University Press. p. 6. ISBN 978-0-521-71420-4.


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What is the effect of an acidic solution on hydrolytic enzymes?
I'm working on a school research project and my research question is "What is the effect of increasing concentrations of Acid X on hydrolytic enzymes, measured through the loss of mass of leaf litter after 30 minutes?"
Note that the acid to be used will be chosen later and the time of the reaction can be altered. I plan to use at least one of these hydrolytic enzymes: endoglucanase, cellobiohydrolase, and β-Glucosidase.
I have spent days on end searching for information on hydrolytic enzymes and acids (their relationship). I have been unable to find anything. Do hydrolytic enzymes follow the normal trend of denaturation under a change in pH?

There is a good amount of information about this online, I was able to find information in one google search, for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4875970/

Welcome to Biology.SE. Not all enzymes behave the same way so, in addition to being under-researched, this is also too broad. Thank you for taking the tour, but please also consult the [help] staring with [ask] effectively on this site, what is on-topic, and what is not. You should also search for and read the "homework" policy for this site. Thanks.


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Could the problem of overfishing be solved by throwing fertilized fish eggs at the right place and deepness into the sea?
I hear sometimes about over fishing and I wonder if the following idea could help to solve the problem.
My idea is to throw fertilized fish eggs at the right place and deepness into the sea. These eggs would then grow by themselves and be the fish to catch sometimes later on.
Instead of the fertilized fish eggs a few days old fish could be used. This should increase the chance of survival by a multitude.
My question is: Could it be done?
In case the answer is yes the next question would be how could it be achieved?
In case the answer is no I am curious: Why would it not work?
Just to be on the save side. The idea is meant to produce more "baby" fish. The "baby" fish should grow in its natural way. Just as if the "baby" fish would have been born in the natural way.
The person putting the eggs into the sea would not be the owner of the grown fish. No monitoring of the way from "baby" fish to grown fish would be done. Anybody could catch the grown fish. Just as it is now the case for natural born fish.
I am looking forward to your answers.

Apparently it works better with young fish ( fingerlings ) rather than eggs . Fingerling stocking is very widely used.

Please read the [Tour] to find out what kind of questions are acceptable here. Floating ideas that are only answerable by subjective opinions are not.

Most fish produce extremely large numbers of eggs anyway.  (Google says tuna can produce 10 million eggs/year!)  Most are, of course, eaten by something before they grow to maturity.

and where do you get enough fertilized eggs on a renewable basis?

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Arguably, there's an easy answer to this one: "No!" As Roger points out, there are many complicating factors implicit in your question, but I can't think of any fish species off the top of my head where we could do anything similar to your solution that'd be successful. Consider, for example, Chinook salmon on the west coast of N America. We've been trying to supplement wild populations for decades by releasing juveniles that were spawned and raised to varying ages in hatcheries. There's a legitimate argument to made that this has been successful in that the fisheries for several runs are largely supplied by hatchery-produced fish, but this has come at multiple, complex costs (eg loss of genetic diversity). Perhaps more importantly, many if not most of these runs are still threatened, less due to over-fishing (US fisheries are heavily regulated) than to the loss of spawning habitat and climate change. Ultimately, the "answer" to your question (I'd say) is that the biological and ecological complexities of what you propose are far more than what we can over-come given our state of knowledge and our resources for most species. There are definitely on-going efforts to use hatcheries to supplement or restore wild populations, some of which have had a measure of success, but this is just one (expensive and difficult) tool we can use to address 'over-fishing'. By far the easiest solution (though not without consequences) is to regulate those fisheries--essentially, restrict the quantity of fish caught.

Welcome to Biology.SE. Please take the [tour] and go through the [help] starting with [answer] and [ask] questions effectively on this site. In particular, this was not a good question for this site since it is soliciting opinions and discussion. It is also multiple questions rather than a single one. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Answering such questions encourages more inappropriate posts so please delete your post. Thanks.

The answer is a lot more complex than simple yes or no: it depends on the environment, the type of fish in question, the aspects of fishing, etc. Just to list a few points:

availability of food, shelter and other resources necessary for the eggs to grow - I suppose that this was implied by the phrase at the right place and deepness into the sea, but it is more complicated than it seems.
the preferences of predators/parasites relevant to this species of fish: do they prey on the eggs, the babies or the grown-up individuals?
the competition for resources with other similar species of fish
the life history strategy of the species: are they investing in the massive reproduction with high mortality rate of the young? or do the specimen produce relatively small offspring, but live for many years? Do the parents care for their young?
is this more economically efficient than enforcing fishing quotas? How soon these fish become big enough to be of practical interest for fisheries? Do we expect them to reproduce naturally?

These are all questions that may be answered by conservation ecologists, familiar with the particular kind of fish, environment and the economic situation. But there is no one-fits-all-sizes answer.

References
L. Rockwood, Introduction to Population Ecology


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How do absorbance readings indicate diauxic growth of bacteria?
How is growth rate an indicator of carbohydrate use? How do absorbance readings from a spectrophotometer show growth of bacteria if the absorbance readings are taken several times over the course of a day [and plotted on a graph]? If the second absorbance reading of a sample with bacteria and particular substrate is lower than its initial absorbance reading is there less bacteria present or more? Do the presence of substrates affect the absorbance reading in other words do carbohydrates have any turbidity?
context if needed - experiment determines if a species tested in the presence of a carbohydrate and combination of carbohydrates is able to use each as its sole carbon& energy source and if any are used preferentially to others

How is growth rate an indicator of carbohydrate use?

Carbohydrates are the carbon and energy source available for the microbes, and their assimilation is correlated to biomass production. The relationship between microbial growth rates in an aqueous environment and the concentration of a limiting nutrient or carbon source is given by the Monod equation 1 :
$$
\mu = \mu_{max} \frac{[S]}{K_M + [S]}
$$
This relation is linear when the substrate concentration is lower than the constant $K_M$, this is when it is not saturating.
Now, when the culture is in the log phase of growth biomass ($X$) can be described with the simple growth equation:
$$
\frac{dX}{dt} = \mu X
$$
where $\mu$ is the growth rate of the culture, and it can be interpreted as the biomass production speed. So the fastest carbohydrate use is, the highest the growth rate will be.

How do absorbance readings from a spectrophotometer show growth of bacteria if the absorbance readings are taken several times over the course of a day [and plotted on a graph]?

This is explained by the Beer-Lambert law. Simply put: the absorbance ($A$) of an entity is proportional to its concentration ($c$) - all else being equal.
$$
A = \varepsilon \ell c
$$
where $\varepsilon$ is the molar attenuation coefficient or absorptivity of the attenuating species, $\ell$ is the optical path length in cm, and $c$ is the concentration of the attenuating species.
So, the changes in the concentration of your bacterial population (its growth) are reflected in an increase in its absorbance.
If you find a lower absorbance value at time $t+1$ in comparison to time $t$, yes it could mean that the bacterial cell number at time $t+1$ is lower than at time $t$. However, we know neither the protocol you have been following, nor the values you have been obtaining, so there could be other explanations, such as error of measurement.

Do the presence of substrates affect the absorbance reading in other words do carbohydrates have any turbidity?

Yes, molecules in the medium can impact your Optical Density (OD) values. However, that would only be true if these molecules absorb light at the wavelength you are using to measure the absorbance (eg $600$ nm). This is why you should always blank with some filtered medium (or at least with some fresh medium).


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databases for plant growth temperature and altitude
Does anyone know databases which have info for plant growth temperature.It could be specific numbers or categorization as 'cold, warm,tropical and etc' ?

You might find these maps useful. I am not sure where you live, but most plants will list what region they will grow in on their seed packet or online.
You might also find luck by searching ESRI or ArcGIS maps to find more information.
http://www.ahs.org/gardening-resources/gardening-maps


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How to know which residues belong to the variable or constant regions of a Fab (fragment antibody)?
I have a fragment of antibody (Fab) structure, and I know its amino acid sequences of its heavy chain and light chain. As each chain of Fab can be divided into variable and constant regions, how can I know which residues belong to the variable or constant regions?
I can of course look at its 3-D structure in pymol, but it is difficult to know the belonging of residues between the variable and constant regions.

This link clearly shows how to identify the CDR regions based on its amino acid sequence. Is there a similar way to differentiate variable and constant regions?

The CDR is the variable region. I'm not quite sure what you're asking.

The CDR is only part of the variable region, i.e. the CDR is only part of the VH, VL. Could you please remove the downvote? Complementarity-determining regions (CDRs) are part of the variable chains

I stand corrected. I did not downvote, but I will upvote.

thank you! It is really frustrating to be downvoted without knowing the reason....


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Complementary DNA synthesis
Does the reverse transcriptase enzyme recognize thymine to synthesize the complementary strand of cDNA?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

One reason we do it as @theforestecologist suggests is that it avoids us repeating stuff at you that you already know or have already looked up.


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Why does mold grow on silicone caulk?
I notice mold likes to grow on silicone caulk. I find it odd since silicone is mostly inorganic and doesn't contain any nutrients for mold to grow on unlike soil and clothing. Can mold metabolize silicon?

Can you please post a picture?

The EPA has outlawed certain fungicides from time to time ; it takes time for manufacturers to develop new ones. I have caulk around some windows that has turned black with mold but a nearby window with different caulk is still white . The windows are about 10 years old . 25 year old original caulk is still white . (These are all exterior exposures). It depends on the mold inhibitors available at the time.

This product brochure seems to give a reasonable explanation:

The following conditions help to form mould on sealants:

High air humidity with little movement of air, eg: in bathrooms, showers, kitchens etc.
Warmth
Nutrients in the form of organic deposits. e.g. residues from body care materials
  such as soap, shower gel etc.

Since elastic silicone joints have low thermal conductivity they are the warmest part of a tiled surface and where mould thrives best, in combination with organic residues and moisture.


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Do some flowers excrete urea or uric acid?
Sometimes when I sniff a flower up close, I can't but help smelling a faint urine like odor. From my layperson's understanding, uric acid and urea both are responsible for giving urine its characteristic smell. Do flowers excrete either of these chemicals?

are you just smelling ammonia?

It's very faint. It's the same smell you get in some cigars too, except they call it floral.

May I know, is it for all flowers or only a few? Can you identify those flowers ?

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure.

For example, did you try searching for "flower smell urine"? This gives multiple results including an article in Scientific American.


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Why does X inactivation happen?
Is X inactivation really important? Why don’t the dominant genes on one chromosome mask the recessive on the other chromosome? This happens in other sets of chromosomes so why exactly does this happen in the sex chromosomes of a female?
And during x inactivation in the blastula isn’t there a heightened possibility of getting a disorder since you might be inactivating the normal genes and allowing the x linked recessive disorder to show up?

Welcome to SE Biology. Please read the Tour and consult the Help on asking questions. You will see that you are expected to do some research before posting. Where have you looked for articles about X-inactivation? I imagine any account would explain why it is necessary and perhaps even mention alternative positive compensation mechanisms in other species, eg Drosophila. If this is still unsatisfactory come back and tell us why.

Out of frustration I have to say to all downvoters, that I found this question, particularly the last sentence, helpful. I understand that we are supposed to do the research first but it is not helpful when the first thing you do is downvote us.

If both X's are active gene expression is doubled which causes all sorts of abnormalities. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1686009/
a good and short explanation of X inactivation - https://www.youtube.com/watch?v=Y9vXhmI5FXM
Not all cells have the same X inactivated. It happens randomly so women are mosaics of lineage cells with different Xs. If there is a disorder due to bad mutation in one X, it's not present in all cells. This is the reason why boys with MECP2 gene mutation die shortly after birth while girls can live with Rett syndrome. Because not all cells carry the mutation so it's not as bad compared to when boys inherit it

Hi Retardi Grade, I see your profile says you are an independent researcher. Is there any way I can get in touch with you?


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Name for fluid that leaks out of phyllid (non-vascular) plants?
As Wikipedia says (https://en.wikipedia.org/wiki/Non-vascular_plant):

Consequently, phyllids are unable to control the rate of water loss from their tissues and are said to be poikilohydric.

And indeed, if you've touched these types of plants, they can feel wet and sometimes even slimy. Sometimes the liquid leaking out can look like dew drops, too.
Is there a proper term for this fluid? I thought sap at first, but it seems that term is reserved for vascular plants.

They often feel wet because they grow in damp environments, but you can absolutely dry a moss and re-hydrate it. Slimy texture might be external such as algae or it might be a product of the plant.

I don't know of a name for the external water, but the process of plant water loss is called "transpiration", the evaporation of water from the tissues of a plant.
Note that the phenomena you describe, slimy plants or "dew drops", are not due to transpiration, as transpiration doesn't leave liquid water on the leaves. The sliminess you describe sounds more like plant mucus (mucilage).
The dew drops could be just that, external water. It also sounds like a something called "guttation," a process in vascular plants where transpiration is decreased (such as at night) but water pressure in the roots is high, basically pushing the water out of the leaf. This water is, essentially, sap, since it comes from the plant xylem. The composition of guttation fluid is mainly glucose and some amino acids, which would give more of a sticky texture, while mucilage is composed of a mixture of highly branched carbohydrates and glycoproteins.
I'm not aware of guttation occurring in non-vascular plants, and it may be unlikely since they lack xylem and don't have many ways of slowing transpiration. However, guttation occurs in some mushrooms, so roots and xylem are not an absolute requirement.


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Can primers for PCR be duplicated?
Complete beginner question here, don't laugh:
If I have some primers that have been synthesized, and I am close to running out of them, is there any way to duplicate them / amplify them / synthesize more of them myself? I don't know the sequences.
Or is my only option to buy more?
Thanks

Short answer: You need to buy some more, but you need the sequence also for ordering.
Long answer: The Taq polymerase needs a piece of DNA (or RNA) to prime the reaction and be able to enlarge the DNA chain, this is why we use primers in the first place (also to ensure reaction specificity to the region we want to amplify). To enable the reaction you would need a primer complimentary to the one you used of about the same length (or at least not much shorter), so this actually doesn't really make sense, because you would have to have a primer to make your primer. Since primers are cheap today, order some more.

Thank you for your help


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What is the need of mucilagenous coating in pollen grains of aquatic plants?
I'm a high school student from India and here in our prescribed biology book(NCERT), it is written that pollen grains of aquatic plants have a mucilagenous coating to protect them from wetting.
My doubt is that they already have the most resistant chemical, the sporopollenin, on their exine to protect them. It cannot be degraded by acids, enzymes, high temperature, alkalis. Then what is the need of another layer of mucus to protect even the most resistant of nature's chemical? Or is it that sporopollenin is absent in aquatic plants? I cannot find anything good to satisfy my doubt out there on Google.


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Is the plant-human relationship a form of parasitism or commensalism?
We all know that mankind gets a lot of useful products for satisfying its needs from plants. They can be in the form of timber, fruits, oils, resins whatever. The plants don't seem to be benefitted from these actions in anyways rather in some cases, they might instead get hurt(as for wood and timber). Some tribes even live on trees to stay clear from predators.
So, is this relationship a form of parasitism or commensalism?

This appears to meet this sites criteria for a [homework] question — as such you must demonstrate that you have made a significant effort towards answering the question.  In addition, there are ecological relationships that don't fall into a subcategory of symbiosis ... ———— You might find the material on a site like Khan Academy worth reviewing.

No, this isn't a homework question. I was reading articles on various ecological relationships and this thought crossed my mind.

Questions don't have to be homework assigned for a class to be considered homework on this site — please consult the help pages on [Ask] questions effectively on this site, I suggest starting with the page about homework.

It's a complex study because there are different relationships: wild harvests (mahogany), forestry harvests(douglas fir), agriculture harvests(apples), garden plants (poppies), invasive species.
https://www.agclassroom.org/ok/lessons/upper/symbiosis.pdf
example of how to dial in GOOGLE searches properly to research narrow topics.. time taken? 2 searches, 35 seconds. "commensalism paratism mutualism in forestry human agriculture"

will answer the same next time.


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What is the Icosahedral Matrices?
This website introduces the "Icosahedral Matrices".

What are the locations of the other half?

It only shows around 30 numbers of the 60 facets. So how to know the other 30 numbers on the back?

The 60 transformation matrices are shown below in the website. Are they rotational matrices? What are the exact meaning of those 9 numbers for a particular matrix? For example,

Welcome to Biology.SE! I’m voting to close this question because it is much more likely to get answered on other SE sites, like Mathematics.SE. If you want to transfer this question to another site, please request migration instead of reposting. Thanks :)

Thank you for your advice. If possible, can we wait for a few days? It is an interdisciplinary question. And I think the virologists are more likely to answer it.

Sure! Closing a question requires 5 votes; that would give plenty of time for others to see and possibly answer it.


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Can pymol show cartoon (secondary structure) for a pdb of multiple frames?
I am using pymol to visualise the secondary structure of protein using its cartoon representation. The pdb file comes from a simulation, which contains multiple frames. After loading the pdb, its secondary structure (e.g. sheet, helix) could not been recognised. Surprisingly, if only one frame is kept, its secondary structure could be seen. So how to enable secondary structure recognition for a pdb file with multiple frames?
An example of the pdb file with multiple frames is shown below.
REMARK    GENERATED BY TRJCONV
TITLE     Protein in water t=   0.00000
REMARK    THIS IS A SIMULATION BOX
CRYST1  116.453  116.453  116.453  90.00  90.00  90.00 P 1           1
MODEL        1
ATOM      1  N   ASP     1      85.582  59.777  48.367  1.000.0000           N
ATOM      2  H1  ASP     1      84.882  59.067  48.507  1.000.0000           H
ATOM      3  H2  ASP     1      85.162  60.617  48.747  1.000.0000           H
... ...
ATOM   6615  OT  ALA   442      28.032  36.877  69.157  1.000.0000           O
ATOM   6616  O   ALA   442      30.092  36.087  68.677  1.000.0000           O
ATOM   6617  HO  ALA   442      30.072  35.867  69.597  1.000.0000           H
TER
ENDMDL
REMARK    GENERATED BY TRJCONV
TITLE     Protein in water t= 1000.00000
REMARK    THIS IS A SIMULATION BOX
CRYST1  116.384  116.384  116.384  90.00  90.00  90.00 P 1           1
MODEL        2
ATOM      1  N   ASP     1      75.052  41.097  56.132  1.000.0000           N
ATOM      2  H1  ASP     1      75.622  41.407  55.352  1.000.0000           H
ATOM      3  H2  ASP     1      75.602  41.357  56.932  1.000.0000           H
ATOM      4  H3  ASP     1      74.682  40.167  56.272  1.000.0000           H
ATOM      5  CA  ASP     1      74.032  42.157  56.202  1.000.0000           C
... ...
ATOM   6615  OT  ALA   442      45.292  49.247  90.922  1.000.0000           O
ATOM   6616  O   ALA   442      47.102  49.617  89.632  1.000.0000           O
ATOM   6617  HO  ALA   442      47.662  49.327  90.342  1.000.0000           H
TER
ENDMDL

I suspect that the PDB is malformed. Is it available online somewhere so I can take a look at it? Alternatively, could you post and excerpt of the HELIX and/or SHEET records from the file?

I notice that the ATOM records don't contain a chain identifier. I'm not sure if that would prevent PyMol from recognizing the secondary structure elements.

@canadianer the chain ID is not the problem, as it works for a single frame

Okay... Does an NMR model with multiple conformers display correctly (5VKV, for example)?

So it must be this particular PDB. If there's anything wrong with the portion of the file you've posted, I don't know what it is. Does the file with multiple models have HELIX/SHEET records?

Ah okay, I can reproduce this. If you compare the original model with the model with the HELIX records removed, you may notice that the secondary structure assignments are not identical. It seems that if no HELIX record is present, PyMol attempts to assign secondary structure itself. For whatever reason, it does not do this if multiple models are present. You should be able to use the dss command to force PyMol to calculate secondary structure in the PDB with multiple models.

yes, exactly! can you please answer it? (so I can accept your answer)

Sure thing; glad it worked for you.

It seems that if no HELIX record is present in the PDB, PyMol attempts to assign secondary structure itself. For whatever reason, it does not do this if multiple MODELs are present. You should be able to use the dss command to force PyMol to calculate secondary structure in a PDB with multiple MODELs.

Thanks for this, it was so easy to get this "fixed"! Works like charm.

@MarcinMagnus You’re welcome!


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How to filter out the antibody light chains into kappa and lambda types on the PDB website?
The antibody light chains can either be kappa or lambda types. I am searching homologous sequences on the RCSB PDB website. Is there a way to filter out these two types?

The instructions are as follows.

Go to the RCSB PDB Webite.
Under the search bar, click Browse by Annotations.
Click the blue tab labeled SCOP.
Click the white arrow next to the folder titled All Beta Protiens.
Click the white arrow next to the folder titled Immunoglobulin-like beta-sandwich (...).
Click the white arrow next to the folder titled Immunoglobulins (Superfamily).

This is where it splits, based on your specific search.
For Light Chain, Constant Domain:

Click the white arrow next to the folder titled C1 set domains (antibody constant domain-like).
For Kappa Type, Click the folder (not the arrow) titled Immunoglobulin light chain kappa constant domain, CL-kappa.
For Lambda Type, Click the folder (not the arrow) titled Immunoglobulin light chain lambda constant domain, CL-lambda.

For Light Chain, Variable Domain:

Click the white arrow next to the folder titled V set domains (antibody variable domain-like).
For Kappa Type, Click the folder (not the arrow) titled Immunoglobulin light chain kappa variable domain, VL-kappa (...).
For Lambda Type, Click the folder (not the arrow) titled Immunoglobulin light chain lambda variable domain, VL-lambda (...).

This should get you to the list of proteins that you are looking for.

Very very helpful! Just to confirm, would it be possible that some antibody PDB are not fully annotated so not included in this search?

Yes, a lot of them are not included in the above searches. However, you can find most of the rest here -> https://www.rcsb.org/pdb/search/smartSubquery.do?smartSearchSubtype=TreeQuery&t=12&n=1933

@lanselibai Would you like me to add instructions for heavy chain types as well?

Of course, go for it!


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What is the known safety data on phenoxyethanol?
I came across this news article stating that a certain skincare product was declared by FDA to be unsafe for infants due to having chlorphenesin and phenoxyethanol. However, I have been unable to find any claim that phenoxyethanol contributed to any concrete harmful effect at the concentration used in that product. In particular:
  1. I could not find any actual account of harm to infants, and FDA did not report any at that time.
  2. Phenoxyethanol is widely used in many other skincare products with no reports of side effects.
I am aware that chlorphenesin affects the central nervous system, and that seems to be sufficient to explain the FDA warning not to use that product. So why did FDA mention phenoxyethanol as well? What scientific evidence were they relying on, or what biological effect does phenoxyethanol have on infants that can contribute to a risk of "respiratory distress or vomiting and diarrhea in infants" as stated by FDA?

Both of your links are to news articles, not to anything directly from the FDA.

@BryanKrause: I couldn't find the FDA statement in a form I could access, so I did the next-best.

The FDA statement on prohibied and restriced ingredients in cosmetics is here, and it makes clear the limited authority this body has in the US. There is a list of prohibited or restricted ingredients that does not include phenoxyethanol, so it seems strange to me that they would have made a statement about this. But I am neither a US citizen or a toxicologist. A Google search revealed that its use in the EU and Japan is restricted, and there are many articles about whether  it is toxic.

@David: Thanks for finding that! I believe that there may have been unpublished reports of adverse effects on infants of mothers using that product, and FDA decided that the most likely culprits were chlorphenesin and phenoxyethanol in combination, but the problem I have is that I can't find any data at all on how phenoxyethanol contributes to this. I too find this reported statement strange. However it's nearly impossible for both NBC and Reuters to make it up, since otherwise FDA would have easily sued them or at least issued a counter-claim.

@user21820 The health numeral of the fire diamond for 2-phenoxyethanol is a 3 (4 being the most dangerous possible categorization). The SDS from Fischer Scientific lists the LD50 (median lethal dose) in rats at 1850 mg/kg. Wikipedia mentions it is used as a preservative in pharmaceutical products, so my guess would be trace amounts of it under acute conditions would not be particularly harmful. Cyanide and Mercury salts for instance are extremely toxic but you'll still find trace amounts of them in many medications....

@user21820 That being said, if the FDA released a statement advising against administering the product to infants then my advice would be to listen to them. If the statement was restricted to infants then it suggests that an adult would need to be less cautious.

@DavidReed: Thanks for that information! My concern is that phenoxyethanol is used in many skincare products, but the FDA statement only concerns one specific product that gets ingested by infants. So I have no idea about its toxicity in other use cases including sunscreens. Where can I find the Fischer Scientific data that you cited? And do you know about toxicity for long-term daily exposure? By the way, I don't think cyanide and mercury are used in scientifically backed medicines.

@user81820 They are used in the manufacturing process as they are important reagents in organic chemistry. For instance, cyanide is used in the synthesis of ambien. It's impossible to achieve a perfect separation of reactants and products. What matters is that they are within the acceptable tolerance limits.

@DavidReed: Ok, but I don't think phenoxyethanol is merely an intermediate in these skincare products, as it is use as an active ingredient. Anyway do you have answers to the two questions I posed in my last comment? Thanks!

https://www.fishersci.com/store/msds?partNumber=AC130242500&productDescription=2-PHENOXYETHANOL%2C+99%25+250ML&vendorId=VN00032119&countryCode=US&language=en and https://pubmed.ncbi.nlm.nih.gov/31588615/

@DavidReed: Thanks for that! I think in my case (skincare products), the relevant data would be LD50 for dermal contact. I surmise that phenoxyethanol is used at less than 1% concentration in skincare products from reputable brands, and the relevant part of the JEADV article you just cited is "the haematological effects reported in the developmental study conducted in rabbits were observed at a dose approximately 200-fold higher than that used by consumers". Correct?


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Sensory neurons, interneurons and motor neurons - recognizing the type of neuron at microscopy images
Is there a simple way to distinguish between sensory neurons and interneurons and motor neurons at the microscopic images?
I read a little bit about Open Connectome Project. Is there a possibility of automatic (computer - algorithmic) recognition of the aforementioned types of neurons?

Classifications are based on shape, number of connections, projections of axon and such. Thus there is definitely a possibility of automatic recognition if its not already being done.


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Is there a known or quantifiable correlation between capsaicin and its effect on the body's metabolism?
I've often heard that spicy foods can speed up your metabolism, I presume, due to the capsaicin.  Though I'm sure this is a minor effect - I doubt eating a pound of jalapenos a day will help me lose weight - has the medical/nutrition community quantified how various levels of capcaicin affect the body's metabolism?

Capsaicin do affect your metabolism. It affects your Capsacin receptors ( scientifically TRPV1 receptors). These receptor starts calcium influx into various types of tissues. In endothelial cells because of this it mimics stress response (McCarty et al 2015). Quoting from McCarty et al,

Clinically, ingestion of capsaicin-or its less stable non-pungent analogue capsiate-has been shown to boost metabolic rate modestly. opical application of capsaicin via patch was found to increase exercise time to ischaemic threshold in patients with angina

Coming to your question, there are scientific studies which suggest that capsaicin helps in maintaining weight by limiting weight regain after weight loss. Not just this, capsaicin has also shown potential in treatment of obesity. However you should remember that it will required specific amount of dose (you can check details in papers I cited ) to help maintaining your weight. Do not eat pound of jalapenos a day :P

Scoville scale is used by legislators to specify the allowed concentrations on pepper spray used by the police.
Although that is most important for excessive concentrations, you'll find more studies using this scale in relation to the effects you look for (for instance: https://scholar.google.com.br/scholar?q=Scoville+scale+metabolism).
The Wikipedia article cited talks about "sensation of heat", and indeed we sweat a lot when we eat strong peppers. But I think that eat the maximum diversity of food is healthier than seek the "best foods" according to the "public opinion" of the season. You should be worried about living healthier, not just losing weight. Seek the former and you'll reach the latter.


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Will dead cells in culture media have any significant impact on Live cells during incubation?
I am generating stable cell lines and have something like 25+ culture flasks to take care of. Ideally I can let dead cells sit in the media with the live adherent without rushing to change media constantly - Will this affect growth of live cells - I don't want to hinder them as they are already sitting in high[] Hygromycin

I think, you should change the medium in a normal frequency, so every 2-3 days. But I don't think, that you have to change it every day. The cells shall die so in the end you have small populations which fit your purposes.

I'm not sure if this is linked to the actual dead cells, but I've found that not changing the media on plates while trying to generate lines from primary cultures can lead to contamination. Again, I haven't determined if this is because there are dead cells available for contaminants to derive nutrients from, or if it's just because changing media removes contaminants before they can grow too much. You might want to keep that in mind, though. I've found that changing media every 3 days is good enough.
Also, it depends on what you want to use your lines for. If you're hoping to study cell signaling or polarization (like if these are immune cells), it may be a problem, as the dead material will activate immune cells, and alter their signaling patterns. This has less to do with your worry about overall growth and more about you developing a good model for whatever you're doing.
To be fair, these signaling shifts can modulate proliferation in culture, but that's really going to vary from cell type to cell type. Sorry for being a bit vague! It's just that all cells are different- I happen to work with immune cells that are fairly finicky. There are other types that are a lot more robust, however, like fibroblasts, that you could probably spit on and they'd be fine.
If changing the media every 3 days really is too cumbersome, you could try splitting off small subcultures and doing a mini-experiment to see if changing the media vs not impacts confluence after a week or so? That would tell you how flexible your cells are when it comes to this.
Edit: Here are some publications that discuss the effects of dead cells in culture and differences between cell types. I also recommend that if you're using a cell line, looking up information via the ATCC website and reading their datasheet and some of the top references they site that likely describe how the line was isolated and best practices for culture.

"Inhibitory effects of persistent apoptotic cells on monoclonal antibody production in vitro" - a good example of how a lack of dead cell removal in vitro can impact cell function/phenotype and highlights the differences between different cell types.
"Cell death in mammalian cell culture: molecular mechanisms and cell line engineering strategies" - a good review that touches on the actual molecular mechanisms to which I was alluding. I particularly recommend reading the section "Induction of cell death in mammalian cell cultures", as it summarizes and links to several primary resources that show how increases in cell death can affect things like productively, growth, and cell number. It also does a good job of touching on the different kinds of cell death, which is important to understand but may be a bit too in-the-weeds for the original question.
"Links between metabolism and apoptosis in mammalian cells: Applications for anti-apoptosis engineering" - similarly good as the previous source, but looks at it through a more metabolic lense, which I think is helpful when considering the realities of cell culture.

Thanks for the answer... but could you please include some sources?  In biology we can't just take you'r word for it; we'd like to see some peer-reviewed articles / books from which you can defend your response.  Thanks!

Thanks for the hot tip. There's a lot of sources relating to the effects of cell death on different pathways, activities, and functions, so I picked a good primary example and two reviews so that it's easy for OP to get a good overview and find more information if they so wish.


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Problems interpreting gram stain slide
My main question is this: when you interpret gram stain results, does the majority color determine if its pos or neg?
We've been given unknowns and now have to determine what the organism is. I'm having trouble interpreting gram staining results. As far morphology they are all cocci and (sort of) in clusters but (this is the confusing part) they are both purple and pink. I understand that purple indicates gram+ and pink is gram-, but there should be one genus of organism not two. So shouldn't there be only purple or only pink, but not both? Should I be looking for the "majority" color and using that to decide whether I have pos or neg? That is, if its mostly purple, does that mean pos, ...but if so, then why are there still pink cocci on the slide?
I also understand why gram-pos appear purple, --that the crystal violet-iodine complex is retained due to thicker cell walls in gram-pos..... and thinner cell walls in gram-neg, so they are decolorized and appear the color of the counterstain.
Also I definitely did not see any rods in my slide, just cocci.

The only reason that it shows both colors is due to imperfect manipulation while staining. You cannot count on the majority to determine the result of the stain.
In your specific case, rinsing or decoloration with EtoH was probably not done enough and safrainin wasn't completely eliminated.
The best way to be sure of the result would be to redo the coloring.
A good tip while staining is to have duplicates or triplicates.
Secondly, to answer what you said here:

I also understand why gram-pos appear purple, --that the crystal
  violet-iodine complex is retained due to thicker cell walls in
  gram-pos..... and thinner cell walls in gram-neg, so they are
  decolorized and appear the color of the counterstain.

Actually it is not only the thickness of the cell wall that will cause the bacteria to retain or not the crystal-violet. Gram positive bacteria have a plasma membrane then peptidoglycan on top while Gram negative bacteria have a plasma membrane, then peptidoglycan and another outer membrane on top. Crystal violet "sticks" primarily to the peptidoglycan.
Decoloring will remove the stain on the outer membrane of gram negative bacteria. You were right with the fact that Gram positive bacteria will have thicker peptidoglycan.
Gram + vs Gram - cell walls http://www.diffen.com/difference/Gram-negative_Bacteria_vs_Gram-positive_Bacteria

I did 15 seconds of EtoH rinse but I'm hoping I can just do whole test again because it should be all purple , but its not gram neutral its definitely one microorganism