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Are specialized cells considered to have life?
A common definition of life, including the one in Biology SE Life requires physical entitites to have the capability of being able to reproduce.

A process defining organisms that grow and adapt to stimuli while
maintaining a state of organization and energy production and being
capable of reproduction.

Under this definition one could think that a specialized cell like a bone cell or a skin cell doesnt have life. But also, a common definition of cell, including the one here in Biology SE says a cell is

the smallest unit of life.

So, my question is, are specialized cells which dont reproduce supposed to have life? This question came up to me thinking of other living organisms which have tissues which seems to be inert and survive hundreds or thousands of years (ie, wood, bones, etc.)

I'm not sure if this belongs here and hence it might get closed, but 'life' has several meanings and 'a life' usually refers to an entire organism most notably humans, while cells are 'living' things or 'lifeforms', but it's not common to use 'a life'.

Note that your first quote used the word "organisms," while your second one used the term "life." Are specialized cells in the body alive? Yes, by most definitions they are living. Would a culture of skin cells in a petri dish be considered a viable organism? Probably not. But definitions in biology can sometimes get fuzzy around the edges. The Philosophy stack is probably a more suitable place if you're looking for an in-depth discussion of this question.

It has to belong here, because if Biology deals with life, you can't do science over something that doesnt have a definition. The requirement for doing science over something is to be able to test it, and to be able to test it you need a definition

Life is defined in many ways.
Common definitions are usually simplified definitions. Under some definitions it would be "life" under others it would not be. But it doesn't matter. The problem you are having is thinking definitions of life are anything more than artificial categorization. Really there is no difference between living things and the rest of chemistry, or at least there is a smooth gradient connecting them, but we humans can't easily think that way, so we create descriptive but imperfect definitions to help our thought processes. There is a lot of gray area for any definition of life, and you have found one.

If we use definitions to identify similar properties and the common nature of entities, and be able to build knowledge over it, how is it that it doesnt matter? For example, can I expect a wood cell to biological age? How about a skin cell? How about Taxonomy? There are 103 million entries in Google talking about this branch of Biology, it doesnt seem it doesnt matter to classify living things. I think there should be more discussion on the definition of life if some unidentified definitions are being used to build knowledge in Biology

All of those things can be asked without ever deciding whether the thing is "life" many living things do not age and many do. The difference between life and non-life are arbitrary, a hold over from when we though life was special. Its only useful at the most simple level but once you are talking about biology in any detail the definitions become counterproductive, as can be seen in your original question.

The short answer is that Yes, specialized cells are considered to have life, as are sterile ants that serve the colony but do not themselves reproduce. The definitions that are given for life are attempts to characterize a phenomenon that people are already capable of recognizing. Specialized cells arose out of a reproductive process and they do other life-y things like metabolizing. So they are alive.
If the definition given in a book seems to imply that specialized cells aren't alive, then the definition is ill-formulated, misunderstood, or both.


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How does the descending branch of the loop of Henle equilibrate concentration?
I'm learning physiology and I have a hard time figuring out how the cortico-papillary gradient is created.
Most explanations go as follow:
1) Sodium is pumped out the ascending branch into the interstitium until a 200 mOsm/L gradient is established between the tubular fluid and the interstitium.
2) Water passively flows from the descending branch into the interstitium to equilibrate osmolarity between the tubular fluid and the interstitum.
3) The tubular fluid flows, moving everything towards the ascending branch.
1 bis) Sodium is again pumped out until the 200 mOsm/L gradient is established
Reapeating this steps over and over again creates the vertical gradient.
This is illustrated here

Ok, so far, so good; here comes my question :
In step 2, how comes the final concentrations in the interstitium and the tubular fluid in the descending branch are equal to the initial concentration in the interstitium?
I would expect the final concentration to be the mean of the two. In the examples above, starting from 400 mOsm/L in the interstitium and 300 mOsm/L in the descending branch, I would expect 350 mOsm/L at the end, not 400 mOsm/L.
How is that possible? Is this because at every moment, when water flows into the interstitium diluting its content, the ascending branch keeps pumping sodium to maintain the 200 mOsm/L gradient?
Thanks a million to whoever will answer this question!

source: Stack Exchange

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

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Are any genes over a billion years old?
Are there any genes (for any organism) for which we can say with confidence that they are over a billion years old?

Ribosomal RNA (rRNA) genes are shared among all living organisms, including lineages that have diverged from one-another well before a billion years. Bacteria, Archaea, and Eukaryotes diverged over 3 billion years ago, and their rRNAs are virtually identical to one-another. http://www.biologyreference.com/Ar-Bi/Archaea.html
Any genes that are shared between plants, animals and fungi would also be over a billion years old.

"…their rRNAs are virtually identical to one-another." No. Just counting the bases, typical examples are ssRNA: bacteria 1542 nt, eukaryotes 1869 nt; lsRNA: bacteria 2906 nt, eukaryotes 5070 nt. They are certainly related, but a nuanced explanation of how is required. See e.g. R. Brimacombe (1984) TIBS  9  273–277.

Counting the bases is meaningless. Eukaryotes possess non-conserved expansion segments that account for virtually all the variations in length. You can take ribosomes from a prokaryote, and insert them into eukaryotes, and they still function. I stand by the fact that they are virtually identical. Saying that they are related is obvious, but seems to indicate a lack of understanding for how genes evolve following their divergence after speciation. At the time lineages split, the genes are identical. Then the nucleotides change over time, but the structure remains.

I didn't want to answer myself and inevitably overlap with yours, so I suggested you edit it to clarify the point. But I have no wish to argue the point, I'll just write one of my own when I have the time.

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Are there any studies on the solar latitude limits of different plant species, beyond which they wouldn't thrive even with suitable weather?
Not sure whether this belongs here or in the Gardening & Landscaping StackExchange, but here goes...
According to maps provided in the paper Present and future Köppen-Geiger climate classification maps at 1-km resolution which assumes no reduction in greenhouse gas emissions, by the end of the century climates (for example) suitable for Theobroma cacao (with rigorous irrigation) and Cocos nucifera may extend at least to Porto Santo Island (33.08(3)°), the latter possibly to the Azores (38°) given that they are more tolerant of anemic winter heat than frost, for Carnegiea gigantea Northeast Kazakhstan (43.208(3)°), for Olea europaea North-Central Iceland (66.525°), for Malus domesticus Knivskjellodden (71.18(5)°), for Trachycarpus takil Knivskjellodden (71.18(5)°) or potentially even Southwestern Svalbard (77.5(3)°), and for trees in general the Eureka area on Ellesmere Island (79.48(3)°).
However, even though poleward areas may become suitable for species previously restricted to areas closer to the equator in terms of their thermal and precipitation profile, they may not in terms of their solar profile. I mean, while a Windmill palm would be able to accept the mid-10s °C summers and slightly-above-freezing winters of future Finnmark, would it accept the month of darkness and low solar angle except in mid-summer? Would olives tolerate the midnight sun? Would coconuts withstand the sub-30° zenith angles of the mid-latitude winter? This question could also apply to the extreme low latitude limits of species; for example, could hemiboreal Hol/Nearctic winter-deciduous trees live in the modern Southern Altiplano where average monthly temperatures are vaguely similar but the latitude is inside the tropics?
So... Have there been any studies on the potential latitudinal limits for different plant species? They don't have to be for the species I've mentioned, those were just examples.


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Can motor neurons in the brain stem start movements?
Supposedly (consciouss) movement is started in the cerebral cortex. But some time ago I've read a research which stated it might be possible some movements (not specified which ones, probably mean automated ones) start in the brain stem. That research was in one of those research file websites, it wasnt an article and it didnt have any mainstream visibility. Then I didnt hear anything more in this line, but you hear many times about these babies "born without a brain" who lacks most of its brain, 80% of its brain or who lacks cerebral cortex yet they move. Where are those movements started? Can motor neurons in the brain stem start movements?

Yes, movements (including fairly complex ones) can start in or be driven by the brainstem (and spinal cord).
Central pattern generators are key to producing coordinated rhythmic movements, including those for locomotion, chewing, and breathing: these are also located in the brainstem and spinal cord.
There have been many experiments done to study brainstem control of locomotion (see Shik and Orlovsky, 1976), particularly in decerebrate cats. You can induce a walking motion independent of cerebral control in these animals just by moving the floor (e.g., using a treadmill).
More generally, voluntary motor commands from cortex are mostly just a "suggested plan" - the specific patterns of muscle activation are determined in the brainstem and spinal cord, with input from proprioception and modulation by the cerebellum and brainstem nuclei such as the red nucleus.
In humans, spontaneous movements are also common in ~50% of brain-dead patients (Saposnik et al. 2005), although definitions of brain death typically include the brainstem, so these should be thought of as spinal rather than brainstem movements.

Saposnik, G., Maurino, J., Saizar, R., & Bueri, J. A. (2005). Spontaneous and reflex movements in 107 patients with brain death. The American journal of medicine, 118(3), 311-314.
Shik, M. L., & Orlovsky, G. N. (1976). Neurophysiology of locomotor automatism. Physiological reviews, 56(3), 465-501.


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Where can I find a video of human cells reacting to cold water vs warm?
I have the following lists:
Hot Water Effects on Human Cells:
When human cells are exposed to hot water:

   Denaturation of Proteins:
   The proteins within cells denature,
   losing their normal three-dimensional structure.

   Cell Membrane Damage:
   The cell membrane can be damaged by heat.
   The lipids in the membrane become more fluid.

   Increased Metabolic Activity:
   Increase the metabolic activity of cells.
   Can lead to cellular stress and even cell death.

vs.
Cold Water Effects on Human Cells:

    Reduced Metabolic Activity:
    Slow down the metabolic activity of cells.
    This is one reason why hypothermia can be life-threatening.

    Cell Membrane Changes:
    Cell membrane to become less fluid,
    potentially affecting its permeability and functionality.

    Ice Formation:
    Extreme cold can cause ice crystals to form
    within and around the cells.

But I really want to see these up close under a microscope.
The temperatures don't have to be extreme. Just like mildly cold ice water vs. a warm shower. When the cold water hits a cell do you see it like bounce off? When the warm water hits a cell do you see it enter the cell?

You can't see these changes easily under a microscope.  It is a challenge to add heat or cold to cells on a microscope in a manner that you might see, unless you have the right equipment.
You might see protein denaturation - it's like an egg cooking, but because the cells are so small, it happens very fast and you aren't left with a residue, the cells detach before this happens or just disintegrate. For this to happen you need to be heating above about 55 - 65 C (131 - 149 F) for observable denaturation - this is about the same temp as egg white denatures (IIRC 61 C/141 F), but some proteins denature much earlier. Part of the reason it is so difficult to see is the range of temperatures it happens over, so the process is spread out.
Membrane fluidity is not something you will see at all unless you are making specific measurements of it - the cells just don't move enough for you to notice the difference between warm and cold. Water doesn't "bounce off" or enter cells because of membrane fluidity - it enters through protein channels called aquaporins - you can't see these either, far far far too small for light microscopy.
Adding water to the cells (note - cells don't like water in general, mammalian cells need isoosmotic conditions with some salt to keep them happy or they undergo osmotic stress and pop, which you might see, but it isn't dramatic at all). As they are already in a liquid - Have you ever added hot water to cold - how much difference do you see? How would you know when the cold/hot water reached the cells?


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Measures of animal intelligence
What is a good cross-species measure of intelligence?
I want to use this information to decide which animals to eat, so preferably it would have been measured for most commonly eaten animals.
I read about the Encephalization Quotient. Would EQ be a good choice?  Is there somewhere I can find a list of animals and their EQ?

The EQ is not a good measurement of animal intelligence. Note octopuses are highly intelligent but their nervous system is like an alien organism's. Also, note which animals are commonly eaten is country specific. Which country are you posting from?

@anongoodnurse I live in the United States

This might be opinion-based to some degree depending on how one defines intelligence. To get a reasonably reliable answer, I think you first need to define intelligence in your question. For myself (who also struggles with that question), I cannot bring myself to eat pork (even bacon), because they are highly intelligent and self aware. To me, to me, it's murder. I won't eat octopus. I'm glad dogs aren't on the menu in the US. It's not an easy question, but it's an honest one, and important.

We're getting a bit into philosophy, but you'd need to figure what counts as intelligence before that, and we're not yet sure what that is.
There's no singular measure for intelligence that you could really apply..

Have you tried the wiki on it It has a lot pf helpful information https://en.wikipedia.org/wiki/Encephalization_quotient

EQ or EZ can be helpful with several qualifiers.

you should account for differences among groups, birds for instance have smaller brains than mammals for what most would consider similar intelligence, bird brains have higher synaptic density than mammals likely due to weight constraints during evolution. the brain has evolved along sperate paths with different mass efficiencies. EQ gets less and less useful the further you get from mammals and primates. invertebrates in particular become very problematic since the brain is not extremally centralized like it is in vertebrates, so even estimating what is and is not the brain runs into issues.

Improvements have been done to EQ by using the only the parts of the brain responsible things we associate with intelligence, this helps account for drastic difference in sensory parts of the brain which affect overall brain size, but again this breaks down when you get away from mammals because the brains works differently in those groups. You also run into the issue that folding of the brain increases neuron density faster than mass so it can deflate EQ scores while making the animal more intelligent.

If you really want to estimate intelligence, then just like in humans,  behavior is your best metric, but this is not going to be a easy to research number. I have a similar issue to your conundrum and I won't eat anything that appears to understand the concept of death : elephants, great apes and some other primates, dolphins including orca and, grey parrots. I generally iffy on eating anything that has complex problem solving and tool use. I won't eat any primate at all for other reasons (disease). But this requires knowledge of animal behavior. You will never get a nice easy number to look at, intelligence is just too complex a thing.

If you lead a pig (pet or laboratory) to an area facing a mirror, if the pig sees an interesting object in the mirror, they will turn around and go to it without hesitation, i.e. they understand that a mirror is a trustworthy reflection of physical reality. Even dogs can't do that. I had a superintelligent dog that would watch TV with me, but he never figured out that it wasn't real. As he was a shepherd variety, if there were horses running, he'd try to nip at their fetlocks. I can't imagine eating dog, let alone pig.

There isn't really a good answer, since we don't have a singular quantifiable measure of intelligence for humans, let alone other species.
Any human measures of intelligence might not apply properly to an animal, because it's based on either human behaviours, or specific human cultures/context. An animal that does not confirm to either might not complete the test as expected, or not recognise it as one at all.

Yeah intelligence is not a single thing so there is no single way to measure it. Even the most conservative definition of intelligence still has several separate aspects. Then you run into the sensory and manipulation limitations.

There is no easy way to quantify intelligence because it's poorly defined. I would suggest narrowing your focus on measurable behaviour as a proxy for intelligence, and looking at the many behavioral research studies on commonly consumed animals.

Would you eat an animal that has social bonds?
Would you eat an animal that is able to be taught new skills?
Would you eat an animal that demonstrates problem solving?

There is good evidence that chickens, pigs, cows, sheep, fish, all form social bonds, can learn new skills, and solve novel problems. All of those things are a key part in survival and reproduction in many animal species.
You might find the mirror self-recognition test worth looking into, particularly as something that highlights the absurdity of trying to design a test across species.
Here's a list of animals by number of neurons which may help you on your quest - if you can find evidence that number of neurons is an adequate proxy to intelligence for your purposes. There is another on that page about number in the cerebrum. Not a lot of fish on there though.


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Is there an ISO code for animal reproduction method?
Is there an ISO that can represent animals' reproduction method such as:
Oviparity, Ovoviviparous, Viviparous, and others?
Note: If the ISO term is not clear, here an example of an ISO: https://en.wikipedia.org/wiki/List_of_ISO_639-1_codes

I don't know the answer to your question, but aren't ISO standards relating to created things. I believe there are terms defined, but not a specific standard for something that occurs naturally. You can also do a site search in google for example type (without quotes): "oviparous site:iso.org" into your search bar.

From the ISO website https://www.iso.org/developing-standards.html: "ISO does not decide when to develop a new standard, but responds to a request from industry or other stakeholders such as consumer groups. Typically, an industry sector or group communicates the need for a standard to its national member who then contacts ISO." I can't think of anyone with both the financial incentive and resources to fund an effort to develop animal reproduction terminology.


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For wide trees such as Alerce Milenario, can't a longer core just be made (according to web sources the tree is too wide for standard corers)
The Alerce Milenario is only a candidate for the oldest tree. The verified oldest is a bristlecone pine. Trees like Giant Sequoia and Alerce grow both tall and wide, some others stay low to the ground but have massive trunk widths. Bristlecone pines do not grow that wide, they are more modest in size. This means that in the smaller trees complete cores can be taken. In the case of the Alerce Milenario, it's been commonly said that standard corers cannot reach the tree's centre so computer simulations were needed to extrapolate the age of the tree. But why not just make a longer corer? Why wouldn't that work? I haven't found any explanation for this.

It sounds like the centre of the tree is rotten so you can't get a meaningful complete core.

The dead wood is filled with tannins so it will not rot easily.

Rest assured that it will rot - otherwise the forest floor would be totally covered in branches and dead trunks would be standing everywhere. It's also possible that hitting the exact core is difficult, not because of length, but not knowing where it is exactly - trees don't grow as perfect cylinders, they shape themselves to dominant wind direction, ground slope etc. Cores also are fragile - they can break, and getting the rest out can be difficult. Without knowing the exact problem from the (unpublished) study in question, we can only make guesses as to the problem.


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Does Dr. Sinclair's Epigenome Resetting in ICE Mice Also Repair Telomere Length?"
Dr. Sinclair's team at Harvard University has published a paper this year on rejuvenating ICE mice by reprogramming cells to reset the epigenome. Does this cellular reprogramming also repair the length of telomeres?

Welcome to SE Biology. Please finish reading the [Tour] and the Help on asking questions. Regardless of who was the captain of the team and where they play, without a link to the paper, most list members will ignore your question. You can't expect us to go searching for it. The second point is whether you are asking if the information is in the paper, in which case you should point out where this isn't clear, or whether you really expect someone on this list to know about the group's unpublished work.

Thank you very much, it was very informative. I will take measures from now on.


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Why does harper states that aldehyde dehydrogenase is a oxidase? Is it a misnomer then?
Oxidases are those which uses O2, but dehrydrogenases doesn’t? Then is my book wrong ? Is it a misnomer that aldehyde dehydrogenase is correctly a oxidase?

Can you quote from your book?

Nevermind, I dug it up for you. But please, in the future, if you're asking about something written in your book and you want to know if it's right or wrong, quote from your source. Otherwise, we don't know if the book is wrong or if you're misinterpreting what the book says.

In Harper's Illustrated Biochemistry 32nd edition Chapter 12 in the section "Other Oxidases Are Flavoproteins" there are several enzymes listed and described. Quoting from that paragraph:

and aldehyde dehydrogenase, an FAD-linked enzyme present in mammalian livers, which contains molybdenum and nonheme iron and acts on aldehydes and N-heterocyclic substrates

The "FAD-linked enzyme present in mammalian livers, which contains molybdenum and nonheme iron" is aldehyde oxidase. This is a different enzyme than aldehyde dehydrogenase. It appears to be a typo in the textbook.

Seems worth noting that oxidase and dehydrogenase are both used in common nomenclature, but not in systematic names. The IUBMB guidelines for enzyme classification and nomenclature suggest that 'dehydrogenase' could be used in the common name of any oxidoreductase, while oxidase may only be used for the special cases where oxygen is the final acceptor. (https://iubmb.qmul.ac.uk/enzyme/rules.html)
The author of that chapter still should have known that the commonly accepted name for this particular enzyme is aldehyde oxidase. So, yes, likely a mistake.

@MikeyC Systematic naming conventions and nomenclature tendencies aside, there are two separate enzymes commonly called "aldehyde oxidase" and "aldehyde dehydrogenase".  The description given is clearly consistent with one of them, and it isn't the one called dehydrogenase.

I agree with you, @Bryan. Just thought that a little more context about the relationship between oxidase and dehydrogenase classifications might be useful to the reader.


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Compliance lung chest wall together
I do not understand compliance better why do the lung chestwall together system compliance is less than the individual compliance of lung and chest wall? shouldn’t it lie in middle? Please clear it.

Can you provide the source of this information?

Guyton and hall

The compliance can be represented by the change in cavity volume caused by the change in unit transmural pressure. It is determined by the equation "compliance = ΔV/ΔP", which ΔV refers to the change of volume and ΔP is the change of transmural pressure.
The transmural pressure mainly counteracts the effect of elastic resistance while enlarging the volume of lung/chestwall. So as we can see from the equation, compliance is inversely proportional to elastic resistance（which determines the pressure required for inhalation）.
The total elastic resistance is the sum of (also is larger than) the individual elastic resistance of lung and chest wall. So according to the equation, the total compliance is less than the individual compliance of lung and chest wall.


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Could an animal have a developed Broca's area but no Wernicke's area?
Broca's area's function is for speech production, specifically, the control of muscular movement for speech, and Wernicke's area's function is the comprehend language or communication, Communication being the keyword here. Communication includes the physical gestures and movement of an organism such as the Waggle Dance of honey bees.
Would this mean that honeybees (although they have very small brains) wouldn't have Broca's area as they cannot produce speech but have a slightly developed Wernicke's area?

These are terms used for the very particular organization of human cortex. No animal except humans has a Broca's area or a Wernicke's area. I would leave those words out of the question.

Remember that you're asking about a creature that has had a radically different evolutionary pathway from humans. Remember also  the network-wide requirement to show your research when asking a question. Perhaps start by looking at the different structures and their functions in apes melifera, comparing them with the human brain, then take the [tour], read-up in the [help] especially about [ask], then you can [edit]  your question into shape.

Thank you, will do


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Why did Darwin say "the misfortune to undertake"?
Why did Darwin say "the misfortune to undertake"?
"Every naturalist who has had the misfortune to undertake the description of a group of highly varying organisms, has encountered cases (I speak after experience) precisely like that of man; and if of a cautious disposition, he will end by uniting all the forms which graduate into each other, under a single species; for he will say to himself that he has no right to give names to objects which he cannot define."
One reason, is that he was challenged with a difficult task.
Another is that he is unhappy because he could not name more than one species and had to say they are all one species because they graduate into each other.

This would perhaps be better suited the the English Language and Usage site.  It's simply a literary device, a way of saying that he was faced with a difficult, frustrating task.

I'm voting to close this question as off-topic because it is a question of literature, not biology.

If you read the subsequent paragraph it is clear that he is speaking of the difficulty in drawing borders between species.
It is not possible to draw definitive species boundaries, especially if you follow species over time  rather than classifying organisms with a snapshot in time: these issues come up time and time again on this Stack. Some examples:
How could humans have interbred with Neanderthals if we're a different species?
Usage of "lineage" over "species"
Transitivity of Species Definitions
Because all species descend from common ancestors, there is a time at which any two organisms shared an ancestor. For related organisms, you can recognize that shared history, emphasize the similarity and at some point group two subspecies together as one species, or you can focus on differences and separate them. Whichever you choose, someone can argue that the species should instead be separated or grouped.
Ultimately, the distinctions are based on somewhat arbitrary decisions, and counterexamples are abundant whichever rule you try to use (for example, a rule that organisms that have viable offspring should be considered species renders many examples that one would argue should be separate species, and examples of individuals that should be one species that are nonetheless not able to produce viable offspring).
It's not so much the misfortune of the task being difficult but rather of it being not possible to come to a definitive answer.


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Alternative to Lotka Volterra
Would you guys know any kind of differential equations that would dictate population growth without relying on Lotka Volterra ? Thanks ^^

I'm voting to close this question as off-topic because equations for population growth are not biology.

I think this question could use some improvement and background to make sure it's clear what the goals are; right now it seems overly broad. However, I disagree strongly that discussing equations that are highly relevant to biology is not biology, unless that discussion is not directed at a biologically relevant problem.


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16S sequencing: pooled or individual samples?
I am planning to run 16S sequencing on a set of individuals to explore microbial diversity. The question I am facing is: should I sequence them individually or I pool them (for example 5 individuals = 1 sample)?
I was just thinking on advantages and disadvantages of both methods:
1) individual. I can get the diversity of each individual, in that way I know the proportion of individuals which have a particular species of bacteria. The cost are higher since I need more samples with respect to the pooled way, but the reads/sample needed should be lower (since this number increases with the microbial diversity).
2) pooled. I have only a general proportion of diversity in the pool (I can't assess how many individuals have a peculiar becterium). The cost are lower due to small amount of samples, but reads/sample should be higher due to more than one individual pooled (?).
Can someone help me? Are my assumptions right or I am missing something?

It would help if you shared more about the type of questions you are interested in answering, types of samples you're working with, and sequencing platform. Generally speaking, there's no scientific reason for pooling samples if sequencing them individually is an option. Most next-gen sequencing platforms generate enough reads that pooling is almost never necessary, especially for 16s amplicon sequencing.

Sure, so I have to sequence insects from 5 countries to explore their microbiome. I will use MiSeq sequencing to sequence V3-V4 region. I would like like to know if my thoughts are right and why I should use individual instead of pooled. or viceversa

By pooling samples one loses a lot of information (it excludes any possible analysis of beta-diversity)... but, yes, it is cheaper.

Ultimately, it depends on what insights you are trying to glean from your sequencing data, but from a purely scientific perspective, there's almost never a reason to pool samples in the the way you described. You pro-con list is not far off, in terms of information lost or gained, but I think it overlooks some of the down-stream consequences of losing that information on your analysis. For one thing, pooling limits your ability to make biologically or statistically meaningful comparisons. For example, if your individual samples are pooled by country of origin prior to sequencing, you have no way to estimate varation within those pooled samples. Because of that, not much can be said about any observed difference between countries beyond simple descriptions of richness and taxonomy. Treated as individual communities, you can look for differing trends, make meaningful beta-diversity comparisons, and actually analyze them with statistics. If you have environmental data, you might even be able to do some meaningful ecological analyses.
Second, as you mentioned, a pooled sample should theoretically have more diversity than the individual samples it was pooled from (at least it should have no fewer unique sequence variants than the richest of the pooled communities), but pooling could also mask community diversity. If one of the pooled samples has a particularly high abundance community that is dominated by just one or two organisms, it could create the appearance that some organisms at moderate abundance in other more diverse communities are actually vary rare, or non-existant. Even at a much greater depth of sequencing, diversity metrics accounting for abundance lose value, since any outlier sample could skew pooled results, creating a false impression of overall community profile.
Lastly, all of the cost-savings assumptions in your post are going to depend on the sequencing center you use and how they bill samples, so there isn't really a straight answer to give. But I will say that the per-sample cost of Illumina 16s amplicon sequencing is pretty cheap (especially compared to the cost of collecting insects from 5 different countries). And because of how sequencing is performed, pooling samples might not even save you much money. Sequencing is often billed per sequencing kit or per lane of sequencing used, not per individual sample you send. So, unless you have someone to share your sequencing run, it's possible that you'd pay roughly the same amount for 5 samples as you would for 95, with only minimal cost savings on library prep and extraction kits.
To summarize, pooling samples reduces your effective sampling effort and limits your potential scope of inferrence. The only valid reason I can think of for pooling samples in such a way would be if you cannont isolate enough bacterial DNA for sequencing from any one individual (which could be the case, depending on what type of insects you're working with). Like I said at the start, though, it really depends on what you want to learn from your 16s data. If the microbiome comparison is crucial to the outcome of your study, I'd suggest sequencing as many individual communities as possible, or at least a subset of individuals from each country (depending on how many you collected). If you don't plan on doing much analysis beyond describing microbial richness and maybe some taxonomic classifications, maybe pooled samples are sufficient for you needs.

Thank you so much MikeyC for your very clear answer!


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Does severing the Corpus callosum, effect the brain's communicating ability?
With serious epileptic seizures, a treatment is to sever the corpus callosum, which stops the seizures. However, does this affect the communicating ability between the two hemispheres? Or how does this affect the brain differently? What are the consequences in the brain?
Thank you in advance! (If I've got this all wrong, please let me know.)

Yes, it does; the corpus callosum is a major communication pathway between the hemispheres. Severing the corpus callosum is only done when seizures are severe enough to warrant it, and other options are ruled out for various reasons.
The condition of having a severed corpus callosum is often referred to as being a split-brain patient. There are some individual differences between patients, but hopefully searches using the keyword "split-brain" can help you find tons more information (summarizing it all here would give much too long of an answer).
One thing that is important to keep in mind is that although the corpus callosum is a very substantial connecting pathway between the hemispheres, it is not the only one, so the hemispheres are not completely severed. The cortex also communicates substantially with other brain structures that are not directly impacted by severing the corpus callosum.

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


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Gene copies vs. gene paralogs - what's the difference?
I'm trying to get into the theory and practice of gene copy number variation (CNV) analysis, but there is something basic confusing me, which I couldn't yet figure out. Sorry if this is a dumb/trivial question - would appreciate your help anyway.
My confusion is regarding the terms 'gene copy' and 'paralogs'. As far as I understand, paralogs are created when a gene undergoes duplication (never mind by what molecular mechanism), and then starts accumulating mutations as evolution proceeds. So, if gene X was duplicated to create another X, and then X changed to become X', are X and X' considered copies of the same gene, or are they paralogs? Is it a matter of applying some threshold on the sequence similarity between X and X', so they are considered copies up to the point where they diversify enough? Or maybe gene copies are expected to be perfect duplicates? If so, I'd guess that finding such gene pairs is very rare... Maybe it's a matter of function, so once X' gets a different function from X (neo-functionalization), it is considered a paralog? This is a rather complex and difficult to measure definition...
To make things less theoretical and more practical, lets limit the conversation to the context of whole genome sequencing analysis. Let's say that I am annotating a newly-assembled genome, and let's assume that the assembly is good enough so gene copies are not collapsed, but rather are located in their respective genomic positions. How would you look for gene copies and paralogs, and how do you make the classification?
Could anyone clarify this point for me, or refer me to relevant literature?
 Thanks a lot!

The general term "copies" has multiple meaning with reference to genes. In diploid organisms for example, we have two copies of each gene (except those on the Y chromosome). However, these copies are called alleles. Copies that are due to duplication are called parlalogs. There is no distance criterion for differentiating copies or parlalogs. Once duplicated, there are two copies. But the consequences of paralogy would depend on differences, so the question is interesting. At the first generation after duplication, if both copies included all of the upstream regulatory elements, it would be hard to identify which of the copies was the original, since they would both be identical. But over time, if one were to evolve a new function or (more likely) accumulate frameshift substitutions, the altered one would be called the paralogous copy (relative to comparisons across species).

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


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Can I column purify instead of gel extract?
I'm digesting a plasmid for assembly. In my experience, I always have low yields when gel extracting and purifying. Since I am only making one cut in my vector, could I just purify with a column? Any advice would be greatly appreciated, thanks!.

Yes, this is perfectly possible. There are a few small caveats though:

do not overload the column with too much DNA, as this will result in lower yields
also do not load an amount of DNA which is too small, this may result in loss of your sample. In my experience it worked better cleaning small samples from a gel.
also carryover of salts or Ethanol can cause problems
look up the exclusion size of the column from the manual. They can typically on purify DNA above a certain size and sometimes only work efficiently up to a certain DNA size
they are quick and convenient, but more expensive than a gel


text:
What kind of spider is this (from Bangladesh)?
I just saw this spider in my bathroom. I was wondering what kind of spider is this and if it is venomous.
Country: Bangladesh

Only three Sparassidae (huntsman spider) species have been observed in Bangladesh on iNaturalist. Only one looks anything like the individual in your photo: Heteropoda venatoria. I venture it's a male based on the dark brown patterns on its prosoma and the overall body's lighter brown color. Most spiders are venomous, but according to a University of Florida IFAS publication, this spider isn't dangerous to humans. Hopefully this helps.

Thank you. This is the answer I was looking for.

Glad I could help!

This is a huntsman spider , which is venomous but it's affect on humans is not so reactive , it's not can cause several symptom like itching, swelling,in more severe vomitting and nausea like ,
It was a coincidence to identify it because my cockroach also have the same upper structure like it so. I thought it should have some relation and the results were **these are cockroach eating ** I didn't know the exact reason behind this unique relation


text:
How does the area under the curve mean the total exposure to the drug?
I was wondering how the area under the curve in the case of a conc against time plot would be equal to the total exposure in the body? I know that this area is integrated using

AUC = ∫C dt

However wouldn't that mean - according to my understanding - that the product of this is the sum between the total conc of the drug and the time as the latter is a part of the calculation? And if it's the case, wouldn't that mean the AUC isn't just the total exposure?

can you post a reference for this, whatever the materials you're looking at? a diagram might also be helpful if you can post one. It also isn't clear to me what your logic is. To me, it makes sense that if I've had 10µM drug at time 0, 8µM at time 1, 2µM at time 2, that overall my body has experienced 20µM of the drug if those are the 3 (hypothetical, infinitesimally short) times that we care about. Can you be more specific why this doesn't make sense to you?

I would think of this as a definition: the definition of "total exposure" is the product of concentration and time, in other words, the area under the curve if the curve is time versus concentration.

Welcome to SE Biology. Please finish reading the [Tour] and edit your title so it has some meaning. Referring to “the curve” just will not do. You need to say what the curve plots, and if that seems too long-winded, give a title that expresses the concept involved. In any case the curve should be described in full (preferably as an illustration) in the question itself.

Wikipedia has an article on [AUC] (https://en.m.wikipedia.org/wiki/Area_under_the_curve_(pharmacokinetics). You should read it. It represents the total drug concentration the body was exposed to. Per the Wiki article, it can be used to compare tissue exposure to different formulations (capsules/tablets) of drugs.

If by you, you mean me, there is no obligation on me to read an article that some anonymous person has written on Wikipedia to clarify a phrase in plain English that is so vague as to be useless in a title. In your actual question, where you use the abbreviation AUC (the codon for isoleucine, I presume) you do not define it. You still have not done us the courtesy to finish reading the [Tour] of this site which explains how it works, but presume to tell us what we should do. Read it, then you will learn what you should do.


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Can a person have different sex at cellular level?
I mean like every cell has a sex chromosome.So does a male with XY chromosomes has all the cells in all the organs inside his body of XY chromosomes only? And vice versa.....

Same as comment on Aurelius' answer: "sex" isn't a property of a cell. At best, it is a property of a whole organism related to its reproductive plumbing. I think that you are interested in the idea of "karyotype" and "aneuploidy", and more specifically the idea of sex chromosome mosaicism is well known.

@MaximilianPress but doesn't sex chromosome mosaicism affect the entire organism? I guess OP is asking for that but in some cells only

@Aurelius It seems like OP is talking about whether all cells always have identical sex chromosomes within an organism- OP should feel free to update if it's otherwise. Mosaicism means exactly that not all cells have identical karyotype. Mosaicism will be apparent in any collection of cells greater than 1 if any two of them differ in karyotype.

there are biological males with no Y and instead XX chromosomes. there are biological females with XY chromosomes.

Every organism(sexually reproducing) starts life from a single cell zygote formed by union of sperm and ovum.
Since all cells are formed by mitotic divisions and differentiation of the zygote, the number and type of chromosomes remain same in every cell of the body.
In rare cases however there maybe chances of aneuoploidy of the chromosomes during cleavage or later mitotic divisions. As given in the article, post-implantation mitotic aneuploidy is rare and is checked. Should it escape:

Mitotic aneuploidies have been suggested to affect the developmental potential of human preimplantation embryos, possibly leading to developmental arrest or embryo loss at later stages of development. Mitotic aneuploidies may contribute to implantation failure or when compatible with implantation, may result in fetal or confined placental mosaicism. It might also cause serious fetal complications like intrauterine growth delay, congenital malformations, mental retardation, and uniparental disomy.

If chromosomal abnormalities occur after immune system has started working, it can be taken care of.
It's rare to have mitotic aneuploidy in a  person. To have it in two chromosomes(the allosomes) is even rarer
In conclusion it will be extremely rare for a living cell to have different sex than that of the person
For plants though it is much more common.
Edit: As @BryanKrause has pointed out. Chimera are another cause. If chimera  due to organ transplant is also considered makes it not so rare as I mentioned

I don't think that "sex" is a property of a cell. At best, it is a property of a whole organism related to its reproductive plumbing. Karyotype != sex (!= gender).

Chimeras are also rare but it happens.

All women who have been given birth (or maybe past some point of a pregnancy) are effectively chimeras.  Most (if not all, haven't bothered to search for exceptions) such mothers have cells containing the DNA of their children in their bodies for years (if not forever) after the birth.


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What is the part between the eyebrow tail and above the eyelid called?
I need to know that anatomical name of the portion of the face between the eyebrow tail and the eyelid, as highlighted in red in the image below, as I need to refer to that particular area in writing succinctly and specifically and without any ambiguity or elaborate description. Upon thorough digging, I have found out that the lacrimal glands (responsible for producing tears) are present underneath the skin of the highlighted part but I fear that lacrimal fossa (where the aforementioned gland is contained) is not the correct term for the highlighted portion as refers to the specific part of the human skull and definitely not the highlighted skin-area pertaining to facial anatomy.
Further brainstorming has got me to the conclusion that the best way to denote these areas in a succinct, unambiguous way without being too "technical" is through "left/right brow bone" but I feel that there is a better/more-specific term for this.
Thanks in advance.

The answer to this question can be found buried deep in the occuloplastic surgery literature.*
It's called... the upper eyelid. (!) Nowhere was it listed in numerous facial surface anatomy illustrations. I first encountered the name of the specific area here. It refers to how facial tissue ages.

The drooping brow and inelastic skin combine to cause upper eyelid tissue to drape over the lid margin, often obstructing the superior visual field.

The "eyelids" in common medical parlance usually refer to the structures that (normally) glide over the eye when blinking. The "eye" normally refers to the actual eyeball.
The occuloplastic literature, though, is necessarily more specific. The upper eyelid is the area between the eyebrow and the eyelid, the lower eyelid is the area that gets saggy in the elderly. The "eye" is the whole kit and kaboodle limited by the forehead above and the cheek below.
Droopy upper eyelid:

This is a YouTube video of a Beverly Hills oculoplastic surgeon who, along with another plastic surgeon, has a show about botched plastic surgery (I believe it is called Botched.) In the video, you see him run his index finger over the area you asked about repeatedly, calling it the upper eyebrow (oops) eyelid.
*Seriously. It took me a while to find it.

This area could be referred to technically as the zygomatic process of the frontal bone. The frontal bone is the top/front part of your skull that comes down to the orbits of your eyes. It connects to the cheekbone (or zygomatic bone) via a protrusion (or process) forming the orbit of the eye. This is also a name for the skeletal anatomy rather than the skin you actually see, but I'm not sure there will be another specific term that doesn't refer to the anatomy of the skull itself.
For a less technical term, you could call it the upper/outer orbit of the eye. That will also refer to the bone, however, and may refer to a location above or below the eyebrow depending on if you're furrowing or arching your brow.

Regarding your suggestion to call it the "upper/outer orbit of the eye", would calling it the "brow ridge" or "supraorbital ridge" pinpoint to the area without making it too technical and avoiding ambiguity caused by your suggested term? Would really love your further inputs and suggestions on this!

@hecate Both of those would refer to the ridge over the eyes, but wouldn't be specific about lateral location. The brow ridge would span from temple to temple going over the nose, but wouldn't specifically refer to the outer parts of it. "Outer brow ridge" might be close enough without being too technical.

No one refers to it that way ("zygomatic process of the frontal bone"). It's also not referred to as any part of the orbit. Link to a reasonable source, please.

@anongoodnurse It is a technical anatomical term. https://en.wikipedia.org/wiki/Zygomatic_process

Also, please note that on this site, we request that folks support their answers with reliable sources. Otherwise the answer is subject to deletion.


text:
static versus dynamic equilibrium when bending over
When a person stoops/bends over, is the equilibrium functioning static equilibrium or dynamic equilibrium? I am not sure, because on the one hand the person is not moving (static), however, his/her head is moving (dynamic).
Thank you!


text:
Effect of angle of light on flowering of plants
I understand that the angle of light changes the direction of growth in plants (phototropism), but would the angle of light have any effect as such on the flowering of plants?
Thank you!


text:
Infectious diseases spread by insects
if blood feeding insects can transmit many diseases(west nile,...,etc.),why cannot all infectious diseases like AIDS,Ebola be vectored by insects?

Regarding AIDS, you can find some answers in this paper : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352396/

Possible duplicate of Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?

A critical point is that mosquitoes and ticks inject saliva into their host, not the contents of their stomach.

Arboviruses, including dengue and West Nile virus, are injected into vertebrates within mosquito saliva during mosquito feeding. Mosquito saliva contains anti-haemostatic, anti-inflammatory and immunomodulatory molecules that facilitate the acquisition of a blood meal.

http://ncbi.nlm.nih.gov/pubmed/18342898
So for a virus carried by an earlier host of the arthropod to infect a later host of that arthropod, it's not enough to survive in the gut, the salivary glands must be infected. This isn't possible for viruses that aren't adapted to arthropod cells.

Diseases that are spread by arthropods (I'm including things like ticks here as well as insects) are generally highly adapted for that lifestyle, and there are many specific adaptations that are needed to make this efficient. They're not simply passively carried by the arthropod; they actually replicate in the arthropod as well as in their vertebrate host, and since there is an enormous evolutionary gap between arthropods and vertebrates, the pathogen basically needs to have two, parallel and separate, lifestyles prepared.
If they don't undergo these adaptations, they'll be rapidly destroyed in the arthropod by being digested, or simply because the volume of blood is so small that unless they actively replicate there wouldn't be enough pathogen to transmit.
To give a sense of the double specialization an arthropod/vertebrate pathogen needs to undergo, here's a brief summary for tick-borne viruses:

Arboviruses differ from other viruses in their need to replicate in both vertebrate and invertebrate hosts. ... Arboviruses transmitted by ticks must adapt to the peculiar physiological and behavioral characteristics of ticks, particularly with regard to blood feeding, bloodmeal digestion, and molting. Virus imbibed with the blood meal first infects cells of the midgut wall. ... After infection of midgut cells, tick-borne viruses pass to the salivary glands for transmission during the next blood-feeding episode. To do this, the virus must survive molting by establishing an infection in at least one cell type that does not undergo histolysis. ... The infection can then persist for the life span of the tick with little evidence of any detrimental effects on the tick.

--Adaptations of Arboviruses to Ticks
So to be a tick-borne virus, these pathogens have to survive being eaten by the tick and avoid being digested. They infect at least three distinct types of cells, and have to survive the tick molting period. In the second set of cells they set up a life-long infection. And they need to do this without making the tick unhealthy, so that it can go and bite more vertebrates.
The question specifically asks about West Nile virus, which goes through a similar path of infection in mosquitos, first infecting midgut cells and then spreading to the salivary glands where it replicates to high levels (West Nile Virus: Biology, Transmission, and Human Infection).
And then after the tick bites a deer, they have to go through the whole thing again, in a brand new host that's completely different from the tick in just about every way.


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What are reasons we know insects evolved on land rather than water
I am reading up on the evolution of insects, and insects supposedly evolved on land rather than water. How do people know?What evidence is there that insects evolved on land and not water?

The sister group of hexapods (Insects plus Collembola, Protura, and Diplura) are thought to be Remipedes. Remipedes are cave-dwelling aquatic pancrustaceans. The most recent common ancestor of Hexapoda and Remipedia was likely aquatic. But somewhere along the pathway to becoming modern hexapods, after they split from the lineage leading to modern remipedes, the ancestors of modern hexapods developed tracheal respiratory systems that function on land. So the evidence comes from the fact that the extant lineages of insects, close to their most recent common ancestor, including Collembola, Protura, Diplura, Archeaognatha, and Zygentoma are all terrestrial.


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Why was the precipitation-streamflow correlation greater in the intact catchment at Hubbard BrookI
I gave an assignment and ran a class on this data last year.
https://lifediscoveryed.org/r290/hubbard_brook_streamflow_response_to_deforestation
Its a classic small watershed experiment where streamflows and precipitation are compared for two catchment areas, one with intact tree cover, the other deforested.
Streamflow and precipitation are, unsurprisingly correlated, but this correlation is apparently much greater for intact (0.91) than deforested (0.72) watershed.
I had no explanation to offer students for this, (I'd expect the opposite) which is OK, but if I run it again I'd like to have one up my sleave.


text:
Gaba and Magnesium
I read read that magnesium divalent ion binds to gaba receptors and induces the same effects as if gaba has binded. Does anyone know what happens to the gaba that would have been synthesised and otherwise bind to the gaba receptor if the magnesium divalent ion wasn't there. E.g is the gaba broken down, does it wait till the magnesium unbinds from the gaba receptor and then attaches itself to the gaba receptor?

Please give a reference/link/full citation of what “you read”. That way we can identify possible misunderstanding you may have of what you have read, which is suggested your writing “if the magnesium divalent ion wasn’t there, and renders the question unclear, at least to me.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


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Which lipoprotein has the highest protein content?
I know that HDLs have the highest protein/lipid ratio but know that the HDLs are very small molecules too and I couldn’t find the exact answer for this question. I mean, by amounts which of these lipoproteins have the most protein?

Please do not use the title of a question in lieu of the question itself. You need to carefully define numerically your concept of “highest protein content” and explain how it differs from protein/lipid ratio. At the moment it is completely unclear, at least to me.

LDL has the higher protein content than HDL. LDL consists of Apo B48 and Apo B100. These are proteins with higher molecular weights between 250 kDa to 550 kDa as compared to other apoproteins. And these apoproteins are not present in HDL.
And if lipoprotein (a) is included in comparison then it has highest protein content.
(Via:  https://lipidmaps.org/resources/lipidweb/index.php?page=lipids/simple/lipoprot/index.htm)


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Is the Mycetozoa phylum part of Amoebozoa or Protozoa kingdom?
I'm not sure if the two kingdoms are essentially the same thing. I was looking at mushroom data collected by citizen scientists, and a lot of the data is labeled as belonging to one of three kingdoms: fungi, protozoa, and amoebozoa. However I don't really understand the difference between protozoa and amoebozoa.


text:
How can I determine statistical significance in seed length and width measurements?
I am researching seed size variation in cereals. I used ImageJ to measure the seeds and generated arbitrary values. Later I converted the measurements to micrometers. I took length and width measurements of 151 unique accessions of single cereal species. I measured ten seeds per accession and generated a mean. I have summarized the mean values by length and width of the ten smallest, medium, and largest seeds. I have calculated SD and SE. In GraphPad, I have grouped these into three data tables and summarized them into one summary figure. I would like to determine if there is any significant difference between the different accessions.
I am unsure of how to best conduct this analysis. I am looking for any suggestions!
Thanks!

If this question is more about statistics (which I strongly suspect), it would probably be a good idea to migrate it over to statics.stackexchange: https://stats.stackexchange.com/.

I’m voting to close this question because it belongs on Cross Validated

I will repost in stats.stackexchange. Thanks.


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Why UniRef representative sequences in UniProt are so long?

I found that some sequences in UniRef90 database are tens of thousands amino acids long. I read UniProt official documentation and figured out that these sequences are the representative sequences of clustered known protein sequences. That is, they are sequences of real proteins that do exist in nature.
I know that some giant proteins like Titin have the length of tens of thousands a.a. However, when I visualized the lengths of protein sequences in uniref90.fasta, I got the plot below.

It seems that at least thousand of proteins are longer that 10,000 a.a. and average protein sequence length is around 5,000. So far, I have thought that proteins are hundreds a.a. long. Do natural proteins are usually composed of thousands of a.a?
Thank you.

This is a good question, but there are a few things going on. There is a subtlety about what you're asking: do you want to know the average length of a protein sampled from a cell, or the average length of a sequence sampled from this specific database? Because the plot you use relates to the second question, while you seem to want to know the first one.
The whole Uniref is also probably not the best set of sequences to test this with. The clustering would tend to amplify the proportion of outliers caused by missing stops, skipped exons, pseudogenes, or duplications, since they will form their own cluster. Also, each isoform can form its own cluster. From a quick look at the first ~100 Uniref90 sequences, maybe 80 of them are annotated as titin isoforms. Plotting and comparing the distributions of Uniref50, 90, and 100 might be a good exercise. At the very least, median is better than mean here.
This is a good relevant paper: Protein length distribution is remarkably uniform across the tree of life
Also, this from the always-excellent bionumbers is good: https://book.bionumbers.org/how-big-is-the-average-protein/

Now I understand. The plot I made shows only the representative sequences of UniRef90 clusters. It doesn't consider about the other members in each cluster. Therefore the average length must differ from that of proteins sampled from a cell, which considers any sequences whether it is representative sequence or not. Also, such representative sequences contain may outliers due to the reasons you've mentioned. I will analyze the data again keeping your advice in mind. Thank you so much.

There's something odd about your numbers:
I took a quick look at the database and just used the (LENGTH:[X TO Y]) command to filter by lengths. This gives you numbers of entries for each size bracket (see numbers on left of image under the Clusters heading).

These are the numbers for clusters I get in the UniRef90 database (Yes, there's some overlap in the brackets 'cause I used 0-1000, 1000-2000 etc, but it doesn't matter in the final analysis, all it did was save some typing time for me):

Size bracket
Number of clusters

0 - 1K
173,209,693

1K - 2K
5,303,314

2K - 3K
658,504

3K - 4K
161,999

4K - 5K
80,517

5K - 6K
32,742

6K - 7K
12,207

7K - 8K
7,076

8K - 9K
4,995

9K - 10K
2,616

10K - 11K
1,603

11K - 12K
900

12K - 13K
792

13K - 14K
476

14K - 15K
519

15K - 50K
3902

From this you can see that the first two brackets (even the first one alone) are vastly more than all the others summed together, which means that there's no way that the average cluster can be 5000 aa in length
This tells me that you have some real problems in your analysis or in your data, but what that problem might be, I don't know. I thought it might have been that you had substituted size for length, but even there cluster size of 5K-6K is only in the 400 range and vastly outweighed by the 1-1000 clusters.
Rest assured, the average protein size is between 50 and 2000 amino acids in length (see 4th para in link).
Edited to add:
I did some analysis of my own using R and ggplot. I downloaded a dataset specifying 90% identity and lengths to be between 2000 and 8000, to keep the file smallish. This makes it a fairly small dataset of 952,569 entries and using the following code (yes, poor coding style, but it's literally a 4 line code including loading the file and library (left out here), so don't need anything fancy). The binwidth of 200 means that the counts for each category are "binned" in lengths of 200 aa, meaning there are 5 bars per 1000 aa.
plot <- ggplot(file, mapping = aes(x = Length))
plot + geom_histogram(binwidth = 200)

This shows me that there is a peak number of entries between 2000 and 3000, not the ~5000-6000 peak in yours (I note that your bins don't line up with nice groupings, so it makes it hard to work out what they are, but something like 910 aa per bin I think, so it should be about 5400 at the peak). This peak has about 200,000 entries, which is massive compared to the ~45,000 peak in your plot, and if you pool my numbers into brackets of ~1000, you get an even more telling picture:

These plots, together with the numbers in my table above, tells me that there is a problem with your dataset or the code you used to generate the plot, probably the data table.  You might wish to explore your data more - look at the number of entries in the table. I think, from your plot, that you have vastly too few entries to be a full UniRef90 dataset, as they should total somewhere close to 180 million not the (very rough) <200,000 entries you have.

Thank you for your answer. I downloaded UniRef90 dataset again from the official UniProt website but got the same result. I think there must be some errors in my own Python script which I used to analyze the data. So currently I'm trying to debug it. (It might take some time since I have bad coding skills.) And thanks to you, I became aware of the existence of Uniprot query syntax and was able to learn it. Thank you again, I’m really grateful for your help.

@dearname You are welcome. If you think either of the answers is the correct one, then you should hit the checkmark below the voting arrows to tell people that it is the accepted answer. Stick at the programming, it's a steep learning curve, but is a very rewarding and looks great on your CV. Data science is hard, but it always pays to do some exploratory things (like looking at number of entries, quick distribution plots etc) before jumping in to a full analysis.


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How exactly are the eye color genes related?
How exactly are the gey (maybe aka EYCL1?), bey(2?) (aka EYCL3?), HERC2, and OCA2 genes related to each other? There are numerous sources that explain eye color in terms of OCA2's role in the creation of melanin and the probable role of HERC2 in regulating its expression, and many Punnett squares invoking the gey and bey genes to explain inheritance (with the appropriate caveats regarding evidence of numerous other genes that also play lesser roles), but the relationship between the two is never really clarified.
Is the bey2 gene an alias for OCA2, or is it merely an unphysical phenotype that is likely coded (in part?) by OCA2 genotypes, or a pairing of specific HERC2 and OCA2 codings? What about gey?

There is polygenic inheritance of eye color as well.


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The split in Boroeutheria into Euarchontoglires and Laurasiatheria. Was this due to the opening up of the Atlantic Ocean?
I'm asking this question as a cat owner. I've seen a figure like 94 MA for the most recent ancestor of both cats and humans (this from, I guess, molecular clock arguments), and it kind of lines up with the geologic timescale of the Atlantic ocean opening up south to north. Moreover, Laurasiatheria literally means "beasts from Laurasia", and Boreoeutheria is "true northern beasts".

I'm starting to think I'm asking this question in the wrong community. Maybe geology is closer to home?

I disagree, this is the right site for phylogeny questions.

It would seem the answer is "No" at the current understanding of this issue.
You should understand that this is a very complex topic, which is based on both molecular (i.e. DNA sequences or protein sequences derived from DNA or by protein sequencing) and morphology. These are both hamstrung to some extent by the lack of mammalian fossils from this period to confirm any tree, but there are a fair number of early mammalian fossils for this period in particularly in North America but also from Eurasia. Most of the implied phylogeny analyses have been done using DNA from existing species and these results don't always agree depending on which sequences are used. To quote one paper from 20081, where segments are the different DNA sequences they analyzed:

Laurasiatheria was generally not well resolved in any of our analyses, and orders within Laurasiatheria did not have a consistent relationship among the different segments.

It would seem that the Laurasiatheria2 and the Euarchontoglires3 are fairly widely supported as "real" clades, both based on DNA sequences, but there is some dispute as to whether Boreoeutheria is real, with some saying yes, others no.
A 2007 paper from Wildman et al., 20074, had this to say:

The mode of diversification between Laurasiatheria and Euarchontoglires remains murky, and it is unclear whether this was primarily because of vicariance between North America and Eurasia, some other vicariant event, or dispersal.

I found a paper by Springer et al. from 2011, which seems to be the current authority on the question, and is free to read on PubMed Central (see last link in reference; it might also be free to read at the DOI link, which takes you to the publication in the Philosophical Transactions journal)5.
In the section titled Placental Biogeography, they state (with my emphasis), that Eurasia, not North America is the likely origin:

The remaining placental orders are placed in Laurasiatheria (Eulipotyphla, Chiroptera, Perissodactyla, Cetartiodactyla, Carnivora, Pholidota) and Euarchontoglires (Primates, Dermoptera, Scandentia, Rodentia, Lagomorpha). With the exception of bats, these orders have first fossil occurrences that are exclusively Laurasian. Our reconstructions provide support for Eurasia, but not North America, as the ancestral area for these clades...
...Further, the fossil record suggests that Eutheria were dominant in Eurasia throughout the Cretaceous, but were absent from North America through much of the Late Cretaceous and only attained appreciable diversity there during the last approximately 10 Myr of the period

More recent papers seem to take this information as understood and I can't see any more recent papers that dispute it.
Refs:

Prasad AB, Allard MW; NISC Comparative Sequencing Program; Green ED. Confirming the phylogeny of mammals by use of large comparative sequence data sets. Mol Biol Evol. 2008 Sep;25(9):1795-808. doi: https://doi.org/10.1093/molbev/msn104. Epub 2008 May 2. PMID: 18453548; PMCID: PMC2515873.

Waddell PJ, Okada N, Hasegawa M. Towards resolving the interordinal relationships of placental mammals. Syst Biol. 1999 Mar;48(1):1-5. PMID: 12078634.

Murphy WJ, Eizirik E, Johnson WE, Zhang YP, Ryder OA, O'Brien SJ. Molecular phylogenetics and the origins of placental mammals. Nature. 2001 Feb 1;409(6820):614-8. doi: https://doi.org/10.1038/35054550. PMID: 11214319.

Wildman DE, Uddin M, Opazo JC, Liu G, Lefort V, Guindon S, Gascuel O, Grossman LI, Romero R, Goodman M. Genomics, biogeography, and the diversification of placental mammals. Proc Natl Acad Sci U S A. 2007 Sep 4;104(36):14395-400. doi: https://doi.org/10.1073/pnas.0704342104. Epub 2007 Aug 29. PMID: 17728403; PMCID: PMC1958817.

Springer MS, Meredith RW, Janecka JE, Murphy WJ. The historical biogeography of Mammalia. Philos Trans R Soc Lond B Biol Sci. 2011 Sep 12;366(1577):2478-502. doi: https://doi.org/10.1098/rstb.2011.0023. PMID: 21807730; PMCID: PMC3138613.

Hat's off to you! This is an amazing answer to what was basically a shower thought of mine. Thanks!

@EmanuelLandeholm No problem, I'm a total nerd so learning things outside of my sphere of expertise and putting my search skills to use is always fun.


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What does it mean that the transcript is enriched?
I think I don't get the meaning of "enriched" in the context of genes.
What's the difference of gene being "enriched" and "expressed" in the cell?

Welcome to SE Biology. It would be far better if you cite an actual example of the use of "enriched in the context of genes" that is unclear to you (with a link if possible). That way we would be able to clear up any misunderstanding, for example whether it is the gene that is enriched or its transcript. See the Help on Asking Good Questions.  (In general when one has a problem it is good to explain it in detail: often that helps one see logical flaws or questionable assumptions.)

In the context of transcriptomics the term 'enrichment' is usually connected to differential analysis:

If a transcript (or some/all transcripts of a gene) are detected in a given sample that transcript is expressed
If a transcript is detected at (statistically significant) higher levels in sample  (or condition) A compared to another sample B, that transcript is enriched in sample A.

In some cases one might compare two cell types, where only one expresses a given transcript, in this expression and enrichment in that cell line (compared to the other one) would be almost the same.

Thank you so much! Totally makes sens now.

In most cases (i.e. assuming there is no aneuploidy) a gene won't be enriched, however, the transcript from a gene may be enriched. A synonym in this case would be overrepresented. In other words, you find relatively more of the transcript compared to other transcripts.
Since you seem to confused about the difference between transcripts and genes, I highly recommend working through the material on a site like Khan Academy. This will help you understand the basic vocabulary and concepts of molecular biology. There are also a number free online textbooks available at NCBI where you can get more in depth information.


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Why does the cervical vertebrae contain more white matter than the more lower parts of the spinal cord?
Why does the cervical vertebrae contain more white matter than the more lower parts of the spinal cord, like the lumar vertebrae?
In white matter are the axons of interneurons.
Anyone know this?

This is true according to my book, but why?

Try thinking about where those axons are going and where they are coming from, does that help?

They signals come from the receptors and go to the brain and then they get back to the muscles/glands. But I dont see why you would need more axons around your neck, instead of your trunk, because thats where most body parts are.

Try drawing a simple diagram where you connect the brain to muscles in the body with wires, and in another color from the peripheral receptors to the brain, and see what it looks like.

Btw I am Dutch. Peripheral means in the non-central nerve system right?

Yes - for this exercise it doesn't really matter though. You will get the same answer even if you just draw the axons going to muscles.

Still dont get it, could you just give the reason?

The neck part has more receptors?

I think I know it: there is more white matter upwards because there all the axons meet up, causing it to be more white, due to myelinated cells of Schwann?

Yep, pretty much. There are more axons in the neck because it has to contain all the fibers from all the rest of the body heading to the brain. Axons in the spinal cord make up "white matter" because they are mostly myelinated, and myelin is white. Since you've figured it out you could write it up as an answer and answer your own question here.

There is more white matter upwards because there all the axons meet up, causing it to be more white, due to myelinated cells of Schwann.

Welcome to Biology.SE! I'm sorry you're not receiving a more positive response to your first posts, but I encourage you to persevere — as a first step please take the [tour] and then consult the help pages for additional advice on [Answer] and [Ask] questions effectively on this site. ——— Specifically, this answer sounds reasonable, but it is much more likely to receive a favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). Thanks!


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Can Darkling Beetles Fly?
I searched the internet on the question whether darkling beetles can fly, and I read mixed results to it. Some say they can, there are even videos about it, but then again they say that they cannot, due to fused wings or the like.
I am currently interested in mealworms, and plan to farm some myself, and some people show their containers without covers, even though the beetles should be able to fly out then, shouldnt they?
This is really confusing to me, thanks for the awnsers.

Short answer; It depends. Darkling beetles is a very large family of beetles (Tenebrionidae) where some species can fly and some do not. Looking more narrowly at the genus Tribolium (i.e. mealworms), which many people refer to when they talk about darkling beetles, it also differs. The common Tribolium castaneum (red flour beetle) as well as T. molitor are good fliers, while T. destructor does not fly. The same goes for the confused flour beetle (T. confusum), which is not know to fly from what I know.

Ah I see, I really gotta start using the Latin-Names, that makes life easier..


text:
Reference Request: Human visual system takes in $10^7$ bits/sec at the periphery and compresses it down to 50 bits/sec deep inside
In Sparse Components of Images and Optimal Atomic Decompositions by Donoho, 1998, the author claims that

The human visual system is thought to do a tremendous job in achieving sparse representation of image data, taking $10^7$ bits/sec at the periphery of the visual pathway and winnowing it down to about 50 bits/sec deep inside.

Can somebody please point me to the source of that claim, as it is not mentioned in the paper, at least to my knowledge.

Good to ask for such a reference, because these sorts of claims are usually based on some truly silly assumptions when taken too literally.

How about this:
https://www.springerprofessional.de/data-compression-and-data-selection-in-human-vision/3218014
The original link in the Abstract referenced (https://link.springer.com/content/pdf/10.1007%2F978-3-642-04954-5_7.pdf) above isn't available anymore, but I found a repository:
https://webdav.tuebingen.mpg.de/u/zli/prints/ZhaopingNReview2006.pdf
I don't think the review is peer reviewed, but maybe you find a reference in there (it's not my field, so I guess you know more on where to look ;-)
She's now in Germany:
https://www.researchgate.net/profile/Li_Zhaoping
If you don't find anything, maybe you can ask her on researchgate directly.


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According to an online course, ribose and adenine can bond to make ATP. Is this true?
I recently came across this question in the MIT Open Learning Library Pre-7.01 Biology Course. It is question 2d in Problem Set 1 (archived link).
The question, as well as the correct answers and explanation from the answer key, is shown below:

The following is adenine base, which can covalently bond, through condensation reaction with ribose sugar to form a nucleotide (ATP).

Which carbon atom of the ribose sugar would covalently bond with the circled region of adenine to form Adenosine triphoshphate (ATP)?
 C1' ← correct answer
Ⓑ C2'
Ⓒ C3'
Ⓓ C4'
Ⓔ C5'
Would you classify this base as purine or pyrimidine?
 purine ← correct answer
Ⓑ pyrimidine
Explanation:
Bases bond to the 1' carbon (C1') in the formation of nucleotides. Other key carbons are the C5', which binds to the phosphate groups, and C3', where new bases are added in nucleic acid synthesis.
Purines have two rings, a hexagon and pentagon, while pyrimidines have only one (hexagonal) ring.

The question, answer, and explanation are confusing to me:

It looks like the molecule shown in the picture (labeled adenine) is actually guanine. Is this a mistake in the question?
I know that a nucleotide is formed when adenine bonds to (deoxy)ribose which bonds to a phosphate group, but the question says that adenine covalently bonds with ribose to form adenosine triphosphate, which it calls a nucleotide.

Is ATP a nucleotide?
Ribose ($\text{C}_5\text{H}_{10}\text{O}_5$) and adenine ($\text{C}_5\text{H}_{5}\text{N}_5$)—or ribose and guanine ($\text{C}_5\text{H}_{5}\text{N}_5\text{O}$)—do not contain any phosphorus atoms, so it doesn't make sense that they would be able to bond to form ATP ($\text{C}_{10}\text{H}_{16}\text{N}_5\text{O}_{13}\mathbf{\text{P}_3}$). Furthermore, the reactions would not balanced in either case without using multiple molecules. Am I missing something?

Creative Commons Attribution Notice
The image above and the text of the question discussed are licensed by the Massachusetts Institute of Technology under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

The structure shown is indeed of guanine, not adenine.

A nucleotide is defined as being composed of a nitrogenous base, a pentose sugar and phosphate (see, e.g. the Wikipedia entry). So the simplest nucleotide based on adenine would be AMP. However ATP is also considered a nucleotide, as can be inferred from this IUPAC entry. Often we refer to it as a nucleoside triphosphate. (A nucleoside is just the base–sugar combination.)

I think you misinterpret the wording as describing the formation of these compounds. The wording — which is poor — is meant to describe the components and bonds in the chemical structures, not laboratory chemical reactions or the mechanism of the formation of the compounds in the cell (which is different, complex, but well documented). The use of bond and bind as verbs is bad, as it implies an active process. If I were writing this (and I am an educator and an author), I would write something like “In this structure there is a covalent bond between…”

If you paid for this course, I would ask for a refund. If it is free, “You get what you pay for.”

With all due respect, but if MIT out of all places is hosting this I think it's much more prudent to make them aware of the mistake so they can fix it instead of taking a "You get what you pay for" stance.

@David Thank you for the excellent response! Can you please clarify your third point? Are you referring to the question "Which carbon atom … Adenosine triphosphate (ATP)?" If so, I'm afraid that I don't understand your explanation of how you interpret the question.

If only the synthesis pathways were as simple as that text you linked makes it sound...

@IanCampbell — Metabolism is not simple. However it can be understood if it broken up appropriately, and learned in an appropriate order. If one starts learning the central pathways of metabolism (as organized in a text book) one becomes familiar with the building blocks that are available. One will learn how ribose is made in the pentose phosphate shunt, and how phosphate is present in the cell and is introduced into sugars. Finally one can consult a text to see what constituents are used to assemble the more complex purines and pyrimidines. The overall balance between these follows.

@BenZelnick — The key statements I am criticizing in point 3 are "Bases bond to the 1' carbon…" and "…C5', which binds to the phosphate groups…". I should also add that "…C3', where new bases are added in nucleic acid synthesis." All of these suggest that the actual biological synthesis of nucleotides is being described, which is clearly NOT the case. It looks as if the author was just trying to describe where the components of the structure are connected by chemical bonds, but lacked the appropriate vocabulary or was following the road to hell known as "elegant variation".

@Mast — I am judging the material as I see it. Anyone can copy and paste the structure of the wrong compound. However the ambiguous use of the verbs "bond" and "bind" indicate to me that the material is poor. If the poster wishes to make the producers of the course aware of this, that is his concern, not mine.


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Question regarding statistical testing for fractions in low N paired samples
I am unsure about how to analyze some data of my PhD project and could use some input. I am analyzing data from a Phase I clinical trial where we have scRNAseq + Histology of paired PRE and POST biopsies. However, as the clinical trial was stopped early due to outside reasons (adverse effects in a different trial in a different condition), I am left with "only" 5 paired samples. Now, I want to compare fractions (e.g. Number of CD8+ T cells/mm2, or %of stromal coverage, or % of total population) between PRE and POST to see where the treatment induced changes. In some cases, it seems quite clear as there is a strong difference, however I don't know which statistical test to apply.
Normally I would say the Wilcoxon matched-pairs signed rank test, since I don't think I can assume normality for fractions. However, with 5 paired samples, the power is too low to reach significance threshold (lowest attainable p value with wilcoxon with N=5 is 0.0625), which in principle I don't care about since I think there is still a pretty strong message when I see the same effect in scRNAseq and histology, but I am worried that it will make submission more difficult.
I have also seen people use the paired t-test for these kinds of fractions in the literature in good journals (e.g. Cell), but I think that would be cheating (but I'm hoping to be wrong here - please tell me).
If you have other ideas, feel free to let me know. If there's some special test for low N paired samples not assuming normality that is not available in Graphpad, I am fine with R as well.
Thank you all!!

You don't have enough data for traditional statistical hypothesis testing. No statistical test will get you around this fact.
I'd recommend just reporting the raw data when there are so few numbers. Let your audience decide what they want to believe or not regarding the data.

Thank you, I guess I needed a bit of tough love so to speak. I had hoped that maybe there's some more advanced statistics that can make sense of the situation but I guess not.


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How to keep primary human cancer cells alive in vitro and derive a cell line?
I am studying a human cohort of patients treated with neoadjuvant immunotherapy before surgery, of whom we have pre- and post-treatment biopsies as well as the resection. In one patient's resection, we discovered a population of less differentiated resistant cancer cells, which excluded immune cells (even though the rest of the lesion was extremely infiltrated). We profiled these by spatial transcriptomics and indeed do find similar cells in our scRNAseq samples of both the pre- and post-treatment biopsies. All very interesting stuff. I'm super curious to figure out how these cancer cells manage to exclude immune cells. The scRNAseq data gives a hundred interesting leads that /could/ reasonably contribute. However, in the end it's lacking experimental support.
Here's the kicker: We still have primary dissociated cells from the pre- and post-treatment biopsy. All cells that weren't used for scRNAseq were frozen in standard freezing media (1 PRE vial, 2 POST). Thus, I essentially have three shots at thawing these cells (pre- and post-treatment biopsy, unless somebody has a tip on how to safely split frozen vials), and attempting to culture and immortalize them. Here comes the issue: Nobody at my institute has experience with this, everybody says that it's hard and with a low chance of success (I somewhat agree). I still think that it's worth a try and that preparation is key here to increase the chance of success.
I am trying to read online resources about primary cancer cell culture (which does seem hard) and also do find various commercial offers of companies that claim good successes with their numbers, but also wanted to turn to the labrats here and ask for advice or hints on where to look/who to ask. So thank you for any and all suggestions!

Way too broad; there are entire book chapters about this.

I'd highly recommend finding an experienced collaborator.

@BryanKrause Thanks for the suggestion. It crossed my mind before but brings additional complications (which might be too much with the current time constraints)

It is very hard - you have a tiny chance of success normally. It's been many years since I last did something similar, but IIRC about 1/10^6 cancer cells will grow, but the vast majority of these will not make it to cell line transformation stage. You also have to consider removal of other non-cancer cells from this process; fibroblasts will grow very well under most conditions.

@immunoLogical My expectation is that the alternative to dealing with those complications, whatever they are, is failure of the attempt at best, and embarrassing or fraudulent results otherwise (e.g., you'll think you were successful but actually you only succeeded in growing some contaminant instead). See bob1's comment as well.


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Ladybug: Number of spots
I'm interested in Ladybugs. I read a lot about the number of spots of ladybugs. The number seems to be between 0 and 24, but as far as I can see, not every number in between exist. Up to now, I found ladybugs species with 0, 2, 4, 5, 7, 10, 11, 13, 14, 16, 17, 18, 19, 22 and 24 spots. Do more exist? Is there a scientifique site in the net with exactly that subject?
Thanks for your answers!
Ladybug


text:
Does columnar epithelium always have microvilli or cilia?
Is there any example of columnar epithelium in any part of our body that do not have cilia or microvilli?


text:
If the very first codon of an mRNA strand is a start codon (ie, AUG) does no 5' UTR exist?
Apologies if this is too basic of a question, but from what I've learned all mature mRNA strands have both a 5' and 3' UTR. Normally this is just because the start codon has not appeared yet. However, I was given a complete strand of mRNA where the very first sequence was the AUG codon. Does the translation skip this codon to form a UTR and wait for the second, or does it immediately start translating with no UTR?

Welcome to SE Biology. Please take the time to finish the [Tour. You write “I was given”. By whom? What was it — a real mRNA or just something invented for a student question?  I suspect the latter. But you need to provide us with this context if we are to help you. There are questions about the initiation of eukaryotic (I assume it was this — it’s important to know) protein synthesis on this site. You should check them out. I wonder whether your question should be “are there eukaryotic mRNAs without a 5’ UTR?” Personally I doubt it, but I may be wrong.

It would be a student problem, yes.
The entire (very small) mRNA sequence encoded by the human XAM gene is given
below. The stop codon is capitalized.
5’-augucccauccuuuucaccaggaugggagagguugcuucccucccacauccggcaugcgcauuaUAAaagaugauaauauaaag-3’
The problem looks like this, and as it starts with AUG, I am wondering whether to skip that one to leave a 5' UTR. I apologize for the lack of clarity.

@FK18 There are a few ways of dealing with this - You could look up the gene and decide for yourself; you could BLAST the sequences and various translations and see what turns up.

If it is a student problem then it is just on interpreting the genetic code. I cannot find a human XAM gene and suspect it is entirely fictitious. In any case there can be no justification for missing the first AUG. Real bacterial mRNAs always have at least a ribosomal binding sequence preceding a start AUG, and eukaryotic mRNAs almost always have a cap sequence at the 5' end, where the ribosome binds and scans along to either the first AUG (generally) or a subsequent one. But clearly the question is not about this. This is often the problem with this type of contrived problem.


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Live birth versus eggs
Would it be right to say that animals or birds that have ears visible outside, including say holes in the head, give birth, and those that have ears concealed inside the head, lay eggs? The point is not to go to minute biological terminology, and if we can resist that urge of vengeance, would the above be an OK statement?
Thank you

Welcome to Biology.SE. I am afraid the terminology might matter more than you'd hope. Maybe you could give specific examples that pushed you to think that such correlation would exist. I don't know much about hearing (and I am not a very good naturalist) but when I think of lizards and birds, I think of many species that 1) lay eggs and 2) have holes in the head for hearing.

You might want to read a little bit about phylogenetic signal to avoid the misinterpretation of such correlation as being the result of selection. You might typically want to have a look at the post Why don't mammals have more than 4 limbs?.

Thank you  nothing pushed me  simply, please tell me  three species that have holes in the head for hearing which are visible from outside, and also lay eggs?

You said "holes in the head", not "visible from the outside" in your question. By saying "visible from the outside", I don't really know how visible they need to be but these details probably won't matter much. Consider any owls (pics) or many lizards such as for example this alligator lizard.

you might want to accept LinuxBlanker answer just so that the question is marked as answer.

No.
Animals without noticeable outer ear that give birth: cetaceans (dolphins, whales and such), lots of pinnipeds (sea lions, seals and such).
Animals with noticeable outer ear that lay eggs (as suggested in @Remi.b's comment): owls, lizards.

No
Vivipary and ovovivipary have evolved multiple times in multiple lineages, laying eggs is the ancestral/basal condition for tetrapods but it has been lost multiple times.


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If I receive dopamine only from doing difficult things will I eventually enjoy them?
I've recently read a post from reddit about how dopamine affects our motivation. Author states:

Dopamine is pleasure. Your brain craves more pleasure. You get too
much pleasure and your brain adapts to feel like tons of pleasure is
less pleasure then everything else becomes more boring. Cut those big
pleasure spikes out and everything else becomes more pleasurable. Your
dopamine receptors change to interact with less dopamine when you have
too much and when you cut down on dopamine, your dopamine receptors
change to interact with more dopamine. This makes boring stuff fun. Do
boring things long enough and endure until it becomes pleasurable via
dopamine receptors. And remember, think in terms of dopamine the next
time you feel like not doing what you need to do!

He advises to stop listening music, playing video games, watching porn, digital entertainment intake. He says:

This will make your dopamine receptors less dull over time and more receptive to lower levels of dopamine so doing things that are boring now will eventually feel not-boring if you can cut out big dopamine spikes.
Then, you keep doing the things you know you need to do but don't feel like doing long enough until your dopamine receptors become used to less dopamine and those things will feel good to do.

Some people accused author because of bro-science in his post. Can someone prove the theory or debunk it?
Will I enjoy doing difficult things which don't give me pleasure now if it's my only dopamine source?

Reddit is not always a reliable source. Have you done any research into this? What have you found?

Perhaps it's just a language issue, but 'difficult' and 'boring' are vastly different.  Backcountry skiing, flying your plane into short mountain strips, or playing a musical instrument can be difficult, but not boring - at least to me.  OTOH, video games, porn, and digital entertainment are boring to me.  And though I've scrubbed my toilet regularly for all my adult life, it's never become pleasurable.  So it seems that there's a major flaw in the argument :-)

I recall times when I found anything boring except activities which author advises to give up. Since the moment I quit playing video games I became interested in many things which previously seemed to me very boring and uninteresting.
For clarification, by difficult things I mean things you [have to]/[need to]/[should to] do but they seem boring and uninteresting and you don't enjoy them. Interesting things can be challenging, but if I enjoy them they aren't difficult to me. So difficult - hard to bear.