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On the premise of crop rotation, is there similarly a plant or organism able to provide nutrients into its environment that exists in water biomes?
I know of the simple concept of crop rotation, and being able to use certain plants to replenish soil, and was wondering if there is a plant or organism that can or does function similarly but in water. I also know there are some plants that are more resilient (and even function or thrive) in soils high in certain compounds and metals (or, conversely lacking in certain nutrients or conditions), that are otherwise detrimental for other plants or organisms. I am therefore also wondering which plants or organisms function similarly, but again--in water, rather than on land.
I have a particular interest in saltwater environments, but also would like to know if there is something in freshwater environments that provides this function.

The question isn't worded very clearly. Scientifically you cannot talk about crop rotation for natural ecology. Ecology has mutualism, commencalism, companion plants that grow together, i.e. some lichen that have three organisms together, plant, mushroom and bacteria, in sponges growing on trees and on rocks.
Crop rotation is especially important on land because we do monocultures, and our sewage doesnt go back into the field, there is a net drain on the soil minerals. In forests and the sea, the situation is different, because plants adapted to the soil grow and build up nutrients over time by rotting with organisms, being fertilized by worms, snails, insects birds and so forth. In the sea, fish provide that function and there isn't the same net drain on a sea environment as there is in a crop.
If you study green life inside different pots of water, from river, tap, rain, and pond, from different sources and different geologies, you will learn some things about aquatic ecology and nutrients. It reacts  with different plants and at different speeds.
The sea is physically so different from land, that the matter falling from the top can be transported miles away, that little comparison is made between nitrogen fixing in soil and in seawater. Also, the zone with the most light also has the strongest currents, so less chance for exchange of nutrients in ecology micro-climates and biomes.
crop rotation is mostly for N P K fixation.
On land NPK availability is often due to the acidity of the geology, which is not quite the same in the sea, plants can live on basalt or chalk, but they have endless flowing water and a good detritus layer in either.
In the sea, NPK is mostly brought by algea and cyanobacteria, which fall and bring it to the phito-detritus layer.
There are not the same forest type ecosystems in the sea as on land, where forests create many meters of peat bogs and massive NPK reserves, as in jungles sometimes. Because forests are less complex in the sea, less green stuff exists on the sea bed, we can say that the situation for plants is less profitable than on land and that instead the biomass exists more in floating small algea, Coccolithophores and so forth, which account invisible for most of the algal biomass of the sea. I cant find if there is more phyto biomass in the land or in the sea. I figure it's on land.
In freshwater environmetns, lakes can have an over or under abundance of NPK, and can bloom more or less completely for a given Ph and environment, given specific adaptations that help them to cope with a particular Ph. it's a lot more variable that the sea with PH going from 4 to 10 and beyond, when the sea ph is about 7.5-8.4.


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What is the meaning of deep winter mixing?
I was reading a paper about eutrophication and there was a term "deep winter mixing" in which an abundant supply of phosphorus is released to the surface waters. I searched a lot but nowhere I could find a definition for that.

The winter mixing of stratified layers in lakes and seas due to temperature changes can vary in depth, so scientists sometimes say "deeper winter mixing" and "deep winter mixing". Scientists measure the water arising from 300 or from 800 meters depending on the year, so the deeper winter mixing is a relative term. i.e.:
1992, associated with more stormy weather and higher precipitation than usual. This anomaly was the cause for the deeper winter mixing in the Cyprus Eddy (>500 m) than the typical 350 to 400 m reported by Brenner et al. (1991). Exceptionally deep vertical mixing (>850 m) was reported that winter also in the Gulf of Aqaba https://www.int-res.com/articles/meps/167/m167p047.pdf
Here is basic description of winter mixing:
https://teara.govt.nz/en/diagram/11817/water-circulation-in-a-lake

and here is a science paper:
https://www.jstor.org/stable/2259960?seq=1
A wiki page on lake stratification:
https://en.wikipedia.org/wiki/Lake_stratification

source: Stack Exchange

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Why did the indigenous peoples of northern Asia and America not evolve the same physical characteristics as people of Nordic ancestry?
I was watching DW's documentary on the Arctic the other day, and I was struck by how the indigenous peoples of the far north seemed - visually speaking - to fit into two categories. On the one hand, there are the peoples of northern Europe, with their pale skin and their preponderance of blue-eyed and blond-haired individuals. On the other hand, there are the Yakuts, Inuit, Aleuts and many more, whose physical similarities - they all seem to share an East Asian-looking bone structure, as well as black hair, deep brown eyes and a skin tone akin to white coffee - belie vast differences in language, culture and belief. Why did northern Europeans evolve these distinctive physical traits while other northern peoples did not? It's probably worth noting that the physical and temporal separation between, say, the Finns and the Nenets is much less than that between the Yakuts and Inuit.
It might be helpful to approach this by splitting up the different characteristics:

Pale skin: Of all the physical characteristics, pale skin seems to confer the most obvious advantage: better absorption of sunlight, and the various benefits connected therewith. Although I've not carried out any kind of systematic analysis, non-Nordic northern peoples do not seem to have a lighter skin tone than their southern neighbours (i.e. the Chinese, Japanese, Native American, etc peoples).
Blond hair and blue eyes: These are the most striking physical differences between Nordic and non-Nordic northern peoples, however it's not clear - at least to me! - what advantage they confer in high latitudes. Is it just blind chance that these characteristics evolved in northern Europe, and not in, say, Central America? If it's not blind chance, why did these characteristics evolve in northern Europe, but not in other northern regions?
Other characteristics: I have read that there are other characteristics, e.g. greater height, associated with high latitudes. Do Nordic and non-Nordic northern peoples have any of these characteristics in common? If there is divergence here, how might it be explained?

Regarding eye colour - remember that ecological selection isn't the only form of selection - sexual selection could potentially have played a role in the spread of blue eye colour, which could explain why it occurs in some populations and not others.

I'm also curious as to why this was downvoted - it seems like a reasonable question to me.

I did not downvote, but I'll hypothesize some possible reasons that others did: 1) why questions (especially regarding evolution) tend to be unanswerable outside an opinionated-scope (off-topic here), 2) multiple questions are being asked (posts should limit to a single question), and 3) numerous statements are made as matter of fact without providing support (we ask that all askers explicitly demonstrate adequate prior research on their own part). The current close votes are for too many questions, so I'd suggest the author (@tom) start by editing the post to limit to a single question.

@theforestecologist seems reasonable, thanks for the explanation.

Equatorial people can reach 1m90 average, i.e. regions in Africa. Statement 3 is wrong? ... statement 1 can relate to vitamine D. 2x UV blockage gives half vitamine D input, restricting inland populations and migrations. Statement 2 has many subtleties, blue eyes is a different thesis.

Why do Native Americans, East Asians, and circumpolar groups (i.e. Inuit) look so similar?
A lot of the reasons why Native Americans and east Asians look more similar is that they are more closely related, genetically speaking. Although there's been a lot of intermarriage between east Asian population and the rest of the Old World since then (not to mention the post-Columbian genetic history of the New World), Native Americans all descend from one to three populations of Paleolithic east Asians that migrated east across the Bering Strait. It is perhaps to no one's surprise that most trees of human genotypes typically find New World natives as a whole to form a group sister to East Asian groups.
Blond hair
The reason blonde hair is so common among Europeans and rare among most other places is that the mutation that produce blonde hair originally occurred somewhere in Europe (or possibly the parts of Asia near Europe) and has yet to spread widely. Red hair, in turn, is a mutation of the mutated gene that causes blond hair. Neanderthals had red hair, but it appears to be due to a different gene than the one that causes red hair in humans.
Blonde hair is not unique to Europeans. Solomon Islanders have it too, but it appears to be from a mutation in a different gene than Europeans.
Blue Eyes
As with blond hair, blue eyes are the result of a mutation in the human genome. The gene that causes blue eyes has been linked to a mutation that occurred in an individual that lived nearly 10,000 years ago on the north shore of the Black Sea, hence why the highest concentrations of people with blue eyes live close to that area (e.g., Scandinavia).
The thing is many of these genes may not confer any selective advantage, they may be neutral genes that arose due to genetic drift. For example Harding et al. concluded that the mutation which cause red hair confer no selective advantage in temperate climates, though they increase the risk of skin cancer in tropical latitudes. Similarly, the epicanthial fold may be linked to a gene that promotes hair growth but confers no selective advantage on its own. The same is probably true of other mutations, though I haven't dug through the literature to find precise examples.
This is the reason why pale skin and blonde hair are rare outside of the high latitudes. In temperate to polar latitudes they're harmless novelty genes and may even aid in vitamin D absorption, in subtropical to tropical latitudes they get rapidly removed from the gene pool due to being a one-way ticket to skin cancer.
Notably, part of the reason people from far western and far eastern Europe seem so different is because you aren't looking at the people in between. People in central Russia, central Asia, etc., show a mixture of traits. In fact, the Wikipedia page for red hair shows a young Uyghur girl from western China with both red hair and an epicanthial fold. Epicanthial folds are also increasingly common as you go west to east across Eurasia, they show up to with some frequency in eastern European populations like the Sami.
Height
Actually, normally people at the highest latitudes are shorter than those at lower latitudes (i.e., the Inuit), because shorter bodies help retain heat better.
Height is also highly variable and is often more subject to nutrition than genetics. If you look at a map of which countries are the tallest and shortest it maps more closely to GDP than it does gene flow. I'm reminded of a story of what happened when a large number of Guatemalan Mayans emigrated to the United States between the late 1970s and early 1990s. Guatemalan Mayans are some of the shortest people known, but this turned out to be due to poor nutrition growing up. Children of the original immigrants from Guatemala living on a more calorie-rich Western diet ended up being nearly 10 cm (almost four inches) taller than most Mayan children of that age.
Notably, the average height in Japan, China, and South Korea has skyrocketed over the last fifty years due to the increase in living standards.

Great answer! The only thing you've not quite convinced me on is height. Obviously, a lanky (for want of a better term) individual is going to retain heat less well than a short stocky one. But, if everything is in proportion, then surely a taller individual will retain heat a bit better than a shorter one? Bergmann's rule seems to have some things to say in favour of both sides of our disagreement.

@TomHosker That's the thing. Everything isn't in proportion. People of the far north have shorter limbs and more "barrel-like" torsos than people further south. This tends to make them shorter, but stockier. This difference is more noticeable in humans because we're bipeds, so a change in leg length greatly affects perceptions of size (since height is the unit we use to measure it)

If you look at the Wikipedia image from their lovely article on human migration, you'll notice that after arriving from Africa, some humans went west and others went east.  The ones who went east went on to most of the arctic regions, except in Western Europe.  The physical differences between these groups probably can be explained as random variation, though we may never know what social and environmental factors (such as the behavior of predators or prey) might have driven adaptive changes.
Previously some might have suggested different levels of Neanderthal ancestry could be involved, but this seems even harder to credit in light of recent evidence that all humans have a small but significant degree of Neanderthal heritage.

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How are some plants and trees able to grow and thrive on little to no soil?
I was watching a documentary about abandoned soviet structures and cities. At the beginning of the documentary a piece of drone footage is shown featuring the abandoned flats of pripyat from above. While watching it i noticed something very peculiar, there were several fullgrown shrubs and even a tree growing on top of the roofs of the flats.

The red arrow points at a berch tree that's apparently growing on top of the rooftop as well. How is such a large plant able to grow there? I've seen plants grow in strange places in my own city Groningen as well. Here's an example of small shrubs that managed to grow out of asphalt.

Here are a couple of pictures of 2 seedlings that are growing out of a hole of a rotten piece of wood. The hole does not go all the way through the wood, so the roots are not in contact with the soil.

According to ChatGPT one explanation could be that over time, organic debris like leaves, bird droppings, and dead insects can accumulate on surfaces. This can decompose and form a thin layer of organic matter that serves as a growing medium for plants. But I can't believe that a tree such as the birch tree in the first video still could grow so large using only organic matter that deposited on the rooftop.
So how does this work? Can trees and shrubs use different materials like asphalt or roofpanels to extract nutrients from when there is little to no soil available? If so, how do they do it?

What two main things are plants made of (think of photosynthesis), and where do those things come from?

@BryanKrause, Plants need minerals as well..

Sure, but not in the same quantities. I'm not really sure what you're looking for in an answer: clearly plants you see growing somewhere are getting everything they need there, or you're assuming they need more than they actually do. Exactly how they get it will depend on the exact situation, and the plants will grow just as much as they're capable of in the conditions.

Plants mostly need air, sunlight, water, and the appropriate range of temperature to grow. Growing through asphalt is not uncommon; water seeps through a break in the asphalt, reaching a seed beneath it, which (believe it or not) when it swells with water is able to break up the asphalt. They also need nitrogen, potassium,  phosphorus, and iron, but not in great amounts.

I think the key is gene expression (specifically, plant response to stress). Plants are living organisms whose genetic material gets altered over time to express what is needed to grow in whatever environment they are.

Bromeliads are called air-plants because they don't need soil, just rain and run off from above.
Photo 3/ That is a plant with big cotyledon leaves which comes from a big seed with lots of energy resources. As the seed sprouts it transforms ambient water into a radicle (embryonic root) of 10-20-30cm that is biologically designed to survive challenging conditions, grow straight down and find soil. Wet rotten wood is a perfect medium for propagation of radicles, it has a PH of 4-6 after a few years, which is similar to the humic acid rich leaf humus of the forest, and is easy for the taproot to travel down 20-30cm at a rate of an inch per day, to find regular water.
Photo 2/ A growing root cell's turgor pressure can be up to 0.6 MPa, which is over three times that of a car tire. Roots can search their environment using micron-thin rootlets the width of individual cells that propagate forwards and under patches of wet leaves or moss where they sprout in the spring time. A tree just has to find a hairline crack through the tarmac to establish a lifeline to the soil. Once it is there, the cells can use chemistry to pump water like a hydraulic jack and push new cells upwards through tarmac. Redwood bark cells have 115m of water pressure, equivalent to a hose that ascends a 35 story building. 20m of water pressure in a hose is very difficult to stop manually.
Photo 1/ That roof collects a lot of water when it does rain, which can collect in pools, under cracked asphat roof linings, and can create pools and cool damp zones in the abandoned building interstices which last for some weeks in summer. They are as big as their access to soil permits.
Those trees require a lot of water for the summer and are sized relative to their resources, they are northern plants like birch who's white trunk is white flexible bark which protects from cold and fast temperature changes due to frost and sun, it also reflects summer sun so that the tree stays cooler in arid times.
Trees also meter their growth by available soil and water and make natural bonsais. There are trees in cliffs with a thousand years of narrow growth rings that are just 1-2 meters tall. Bonsai cliff trees are often prized for dendrochronology.

These are highly specific adaptations to an environment with specific traits. Organisms that are pushing their boundaries (pH, amount of needed water and nutrients and specific proportions, etc...) in some direction. This could be plant adaptations to salt stress, heavy metal stress, or to high temperature, low temperature, or even drought conditions.
The key is the regulation of gene expression to produce the gene products necessary for a given environment.


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I already heard filtering the air to get rid of the Virus is not that effective but what about UV radiation?
Why they don't add a chamber to their air conditions and give the air treatment with UV radiation? I'm not a science guy. Please what might be the reason? Wouldn't it be also cheaper because the air conditions don't need to pressure the air through tiny filters?

I’m voting to close this question because this is not a forum or tutorial service; it is a Q&A site where specific questions relating to biology get specific answers. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to [ask] a good question. See also the section on "homework".

UV is highly effective against many viruses and bacteria . It needs to be germidicidal UV, often known as UV-C in the short UV wavelengths, so there is no doubt that this could work (indeed there are a number of people working on it at the moment, and even some devices available). This sort of technology has been in place in healthcare settings for disinfecting patient rooms for immunocompromised cancer patients for example.
The difficulty with this is providing enough UV to the air-flow so that it deactivates the virus during the short time the virus is passing the UV bulbs. There's a good source of information at the Illumination Engineering Society about UV and germicidal activity here (PDF), which specifically discusses SARS-CoV-2 and the mechanics of how to do it. It discusses in terms of air-changes-per-hour (ACH) and dose for a number of situations:

... simpler evidence-based dose that has been developed over many
years for TB control, typically specified as about 17 mW of 254-nm lamp-emission radiant power per cubic meter (m3) of space to disinfect air.

17 milliWatts of power might not seem like much given that your room lights probably use between 5-200 Watts per bulb, but they are putting out a broad range of light (mostly as heat) from about 400 nm to 800 nm, but the UV bulb output that is being measured here is the specific germicidal wavelength of 254 nm, overall the lamps put out much more light than that and are enormously energy hungry.
It also says that disinfecting the volume above people in a room is more effective than irradiating incoming (or presumably outgoing) air because of the risk of person-person transmission with people in the same room:

Upper-room GUV (see Figure 3-1) disinfects large volumes of room air (above occupants’ heads) at once,
resulting in high "equivalent" air changes per hour (ACH) in terms of air disinfection only...
...When UV is used in ducts, although it ensures that recirculated air does not have viable pathogens, it
unfortunately does relatively little to prevent person-to-person transmission in a room where both an
infectious source and other susceptible persons share the same air. For effective interruption of
transmission, air disinfection has to occur in the same room where transmission is occurring


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Eye vision for distant large objects versus small close objects
We often hear that looking at distant objects after staring at screens is good for the eyes to prevent strain.
But from the perspective of eye muscles, what is the difference between small font that is up close on a screen and a poster with large words on it say 30 meters away?
Since if something grows in size as it travels away from you - from your perspective theres no way you could perceive it as moving away from you.
Doesn't the eye still have to focus in the same way, so why then why would looking at objects 30 meters away act as a way to counter strain from looking at smaller font closer up if they are two sides of the same coin?

Welcome to Biology.SE. Please clarify your question. It seems to be about focal length, which is really a physics question. Perhaps you are trying to ask about how the eye changes focal length — if so, please do some research on your own and then ask specific questions about what is still unclear to you. Also, it is unclear what perception of movement (paragraph 3) have to do with the rest of your question. In general, questions on this site must: demonstrate prior research, be clear, be specific, and be about biology as defined in the [tour]. ...

... You will have a better experience on this site if you familiarize yourself with the expectations by consulting the [help] starting with [ask], what is on-topic, and what is not. Thanks.

I don't see how this question does not fit here even after reading those links...its not about focal length in terms of physics its about how the eye perceives distance in order to adjust its focus. How can the eye tell the difference in order to make the statement that looking at long distances relieves eye strain from looking at short distances from the example i gave.

I did but I am not finding any solid answers other than physics equations but thats not really answering how the eyes/brains interpret it. @Laura_Jonees

I suggest you do some background research on optic first because your premise is way off.

@John no idea what you're on about with my "premise" being way off. I have a degree in physics and know full well about lens equations and optics. But that has absolutely nothing to do with what im asking. Since i am asking about biology and neurology - not physics. But thanks for your contribution - which was basically nothing. IF you know something then provide your knowledge or your comments are unwanted here. Thanks.

the size of an object has no effect on its focal length, so review your basic knowledge of optics. A big object at 30m and a small object at 30m has the exact same focal length and needs the exact same lens to be in focus. this may help https://www.stemmer-imaging.com/en/knowledge-base/optics-technical-overview/

Did you read my question, i am not talking about two objects at the same distance... so a big and small object both 30m away is not what i'm asking. I'm asking about a small object close to the person, and a large object far away. I don't need your physics answer this is a biology question.


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What is the difference between apoptosis caused by the release of enzymes from the electron transport chain vs that from the lysosome?
I know that the mitochondria is responsible for regulating apoptosis via release of enzymes from the electron transport chain. I believe that the release of hydrolytic enzymes from a lysosome is how apoptosis occurs due to lysosomes. According to my book, the difference is that in the case of lysosomes, it leads directly to degradation. I’m just wondering how the process of apoptosis differs in each case.
Here is some info for context:
“The mitochondria are also capable of killing the cell by release of enzymes from the electron transport chain. This kickstarts a process known as apoptosis”
“Lysosomes are membrane-bound structures containing hydrolytic enzymes that are capable of breaking down many different substrates including substances ingested by endocytosis and cellular waste products... (endosomes are talked about)... The lysosomal membrane sequesters these enzymes to prevent damage to the cell. The release of these enzymes can occur in a process known as autolysis. Like mitochondria, when lysosomes released their hydrolytic enzymes, it results in apoptosis. In this case, the released enzymes directly lead to the degradation of cellular components
The reason I’m unsure if the release of hydrolytic enzymes is involved in apoptosis is because when it says “the lysosomal membrane sequesters these enzymes”, the previous text talked about how endosomes package and transport materials so I wasn’t sure if the enzymes are those materials or if it was referencing the hydrolytic enzymes.
TL;DR version: these are my two questions:

Is the release of hydrolytic enzymes from lysosomes responsible for apoptosis?

What is the difference between the processes mitochondrial and lysosomal apoptosis?


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How do peroxisomes work?
I have this question from my book:
A child is diagnosed with an enzyme deficiency that prevents the production of hydrogen peroxide. What would the likely outcome be of such deficiency?
H2O2 is crucial to the function of peroxisomes and if h2o2 can’t be produced, peroxisomes can’t carry out their function. The functions of peroxisomes are:

lipid synthesis
role in pentose phosphate pathway
breakdown (digestion) of fatty acid chains

I would think all of these would be effected but according to the answer key, the only one that is considered is fatty acids. The logic is that fatty acids would build up and eventually apoptosis occurs. So my question is this, is h2o2 only necessary for peroxisomes to break down fatty acids and not synthesize lipids nor is it involved in the pentose phosphate pathway?
If that’s not the case, would I be able to know what would happen if the cell stops synthesizing lipids and how would the functional absence of peroxisomes impact the pentose phosphate pathway?

Welcome to SE Biology. We expect you to do some research as well as apply logic before posting here. There are two things you might check out. 1. Which of the three processes you mention require hydrogen peroxide? (Hint: two do not). 2. Which of the three processes only occur in peroxisomes?

I did do research but I’m still confused. I know peroxisomes’ primary function is breaking down fatty acid chains. I’m still unclear about the role of hydrogen peroxide. All I see is that the peroxides are have a part in the pentose phosphate pathway and lipid synthesis but don’t understand how they are involved. I thought given the name peroxisome, it is crucial for the peroxisome to function, but that doesn’t seem to be the case

OK. The pentose phosphate pathway does not involve hydrogen peroxide directly and occurs mainly in the cytoplasm. I gather it may have an indirect effect via the balance of oxidized and reduced NADP. An answer to your question would consider the actual chemistry involved. If nobody else does I’ll try to (but I’m still trying to find time to work on another question).

Thanks for your help. Please take all the time you need

1. Let's first look into the relation of lipid biosynthesis and peroxisomes -
According to this article, the main functions of peroxisomes are-

As you can see most of the pathways that occur are oxidative in nature. That is,     the main function is breaking down lipids and not their synthesis. The reason why peroxisomes are also known as Oxidative organelle. Even though peroxisome is involved in the synthesis of plasmalogens, and it has no requirement of hydrogen peroxide for the same.
Endoplasmic Reticulum is the organelle that synthesizes majorly lipids. So, the deficiency of hydrogen peroxide won't affect lipid synthesis.
2. Next is the role in the pentose phosphate pathway-
The major pathway for glucose catabolism is glycolysis. The location of the glycolytic pathway is the cytoplasm of the cell. Parallelly to glycolysis, PPP also runs in the cytoplasm. However, the major role of PPP is anabolic and not catabolic. The PPP is generally studied in 2 phases -

The oxidative Phase (Generation of NADPH when Glucose is converted to 6-phosphogluconate)
The non-oxidative phase (Synthesis of 5-carbon sugars)

As this article states

The glycolysis and pentose phosphate pathways (PPP) are tightly connected. The glucose entering the in cell membrane is rapidly phosphorylated by HK and converted to G-6-P. The G-6-P is metabolized either by the glycolytic pathway, generating pyruvate and lactate, or by PPP to produce NADPH. The F-6-P and G-3-P generated from the non-oxidative branch of PPP can enter glycolysis

Also,

The R-5-P, a product of oxidative PPP, is converted into G-3-P and F-6-P by transketolase (TKT) and transaldolase (TALDO1), creating a reversible metabolic link between PPP and glycolysis

Since, both of these metabolic pathways are highly connected to each other. The major location for PPP is the cytoplasm. However, PPP also do occurs in plastids and peroxisomes.
Again, if there is a deficiency of hydrogen peroxide in peroxisome it won't affect the PPP.

Role in the breakdown of fatty acids

As this article states -

Oxidation of fatty acids occurs in multiple regions of the cell within the human body; the mitochondria, in which only Beta-oxidation occurs; the peroxisome, where alpha- and beta-oxidation occur; and omega-oxidation, which occurs in the endoplasmic reticulum.

Also, as mentioned above peroxisomes are the main location for fatty acid oxidation.
Let's take a look at how hydrogen peroxide has a role in this catabolism.
From Lehninger's Principles of Biochemistry(7th edition) -

In the very first oxidative step (for mitochondria), the H-electron is transferred to oxygen, and water is produced.
In the case of the first oxidative step (for peroxisome), the H-electrons are first transferred to FAD, making it  FADH2 then to oxygen, generating a hydrogen peroxide molecule. This biochemical reaction is catalyzed by H2O2 producing enzymes. This H2O2 is further broken into water and 1/2Oxygen by catalase, thus canceling out the reactivity chances of H2O2 with any other molecules.
If there is a deficiency of H2O2 in peroxisomes, that means any of the enzymes catalyzing the formation of H2O2 is deficient. In such a scenario, the first oxidative step of fatty acids breakdown won't take place in peroxisomes. This will eventually lead to the accumulation of long fatty acids chains in peroxisomes and further apoptosis.
Mitochondria's main role is in energy production and not fatty acid oxidation, though it will help in fatty acid oxidation but the number of fatty acids oxidized only by mitochondria will be very very less and the net result will be an accumulation of fatty acids.

Wow this is a lot of information but it explains everything very well. Thank you so much


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Can you identify this species name?

I found this animal in Thanjavur.. It is millipede.. But I don't find out this species name..

Consider this: Orthomorpha coarcata
That's the closest I got, yes this millipede is found here in Odisha too
! Black and yellow millipede


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Protein rafts over the Phospholipidic bi-layer
Does any of you know the specific name of the protein rafts that allow proteins to float over a double layer of phospholipids, (cell membrane)?
I just feel there should be another name rather than simply "protein raft".

These conglomerations of proteins, glycolipids, and cholesterol are usually called lipid rafts.  (Google Scholar shows 84,000 hits for that term, vs. 400 hits for "protein raft".)   Here is a diagram of a lipid raft:

(Key: A: Intracellular space or cytosol, B: Extracellular space or vesicle/Golgi apparatus lumen. 1: Non-raft membrane. 2: Lipid raft. 3: Lipid raft associated transmembrane protein. 4: Non-raft membrane protein. 5: Glycosylation modifications (on glycoproteins and glycolipids). 6: GPI-anchored protein. 7: Cholesterol. 8: Glycolipid)  [from Wikimedia Commons]

As this illustrates, lipid rafts float within the membrane lipid bilayer, not "over" or "above" it. The raft is a part of the membrane, not something outside it or on just one side of it.  The raft is free to move in the surrounding two dimensions of the membrane.
One could argue that "protein raft" might be a better name than "lipid raft" since we would call a common raft a "wood raft" or "papyrus raft", but usually not a "water raft".  Whatever the worth of such an argument, "lipid raft" is the term in use.

I was under impression defferent lipid composition (i.e. more cholesterol and shingolipids than in surrounding membrane) is the defining property of lipid raft. Therefore, I find your argument for "protein raft" being a better name misleading.

I agree with @BagiM. Since the lipid composition is altered and that causes the change in rigidity, I think "lipid raft" is a nice name. The raft in your water analogy is made out of a water solution? Perhaps it is a stretched metahpore at that point... Purely semantic though. This is a good answer that clears up the confusion.

There aren't protein rafts that "float" over a bilayer. There are proteins that insert domains into bilayers, or pass through them, or bind to lipid headgroups. There are also other proteins that bind to these proteins.


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Why are basophils and eosinophils considered granulocytes?
I have read that granulocytes are a type of leukocytes that have granules (hence the name) visible by microscopy. But then there is something called a granulocyte/monocyte progenitor cell, which I thought would give rise to these structures. From this progenitor cell neutrophils and monocytes are created, but not eosinophils nor basophils. Furthermore, monocytes are agranulocytes. I believe my questions are all related:

Based on what I’ve read (stated above), I can only assume there is a difference between granulocytes and granulocyte progenitor cells. So is there a difference? And if is what is the purpose of differentiating between a granulocyte and a granulocyte progenitor cell?

Why are monocytes not considered a granulocyte, when they arise from the granulocyte progenitor cell?

Why are basophils and eosinophils considered granulocytes?

granulocytes are a type of leukocytes that have granules (hence the name) visible by microscopy

Yep, that's it; like you said, that's where they get the name: their appearance. Not their function or progenitor, just their appearance, and they were named long before the other factors were understood. That history goes back to at least the mid 1800s:

Paul Ehrlich's techniques, published between 1879 and 1880, for staining blood films using coal tar dyes, and his method of differential blood cell counting, ended years of speculation regarding the classification of white cells.
...
In 1846, Thomas Wharton Jones (1808-1891) described "granule blood-cells" in several species including humans. The term "granule cell" had also been used by Julius Vogel (1814-1880), who had previously observed similar cells in inflammatory exudates. Vogel, in turn, was aware of the work of Gottlieb Gluge (1812-1898), who had observed "compound inflammatory globules" in pus and serum that resembled eosinophils. Almost 20 years before Ehrlich developed his staining methods, Max Johann Schultze (1825-1874) performed functional experiments on fine and coarse granular cells using a warm stage microscopic technique and showed they had amoeboid movement and phagocytic abilities. Despite these earlier observations, it was Ehrlich's use of stains that heralded the modern era of studies of leukocyte biology and pathology.

Progenitor cells are cells that haven't yet matured into functional fully differentiated cells; usually the name "progenitor cell" is reserved for cell populations that are nearly differentiated and won't result in more than a couple/few final cell types. So, no, a "XYZ progenitor cell" is not the same as an "XYZ cell".
It seems like there is not a settled terminology for various classifications of immune cell progenitor cells, with different publications using different terms. For example, a figure on Wikipedia uses "myeloblasts" to describe cells that undergo either granulopoiesis to become some granulocyte, or they become monocytes:

(from https://en.wikipedia.org/wiki/Granulopoiesis#/media/File:Hematopoiesis_(human)_diagram_en.svg)
They don't really name any general granulocyte progenitor, instead showing them all splitting off together. Others refer to "myeloid progenitors", "granulocyte/monocyte progenitor"/"GMPs", "granulocyte/macrophage progenitor" (as monocytes become either dendritic cells or macrophages), and others.
I don't see any source where a "granulocyte progenitor cell" becomes a monocyte, only that a "granulocyte/monocyte progenitor cell" does; the "granulocyte/monocyte" label seems most clearly interpreted as "granulocyte and monocyte" progenitors, so I see nothing conflicting with these cells giving rise to both granulocytes and monocytes. I also do not see evidence that there is a stage of differentiation in which a particular cell will possibly become a monocyte or neutrophil, yet will not become eosinophil nor basophil; every textbook-style reference I find shares the pattern from the Wikipedia image above or discusses a stage of differentiation in which a cell is either fated to become a monocyte or any of the granulocytes. Given the complexity of differentiation, it's certainly possible some paper has made that claim, but I see no evidence for it.

Thank you for your in detailed response. I was reading the kaplan book and they had a figure but it wasn’t really discussed. However, this does explain the trouble I ran into with other related content.


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Why/How can Hydrophobic things pass the lipid bilayer?
I’m just looking for a simple answer for this question. I’m in Bio 10, and don’t know the in depth stuff. So the lipid bilayer is hydrophilic and the ends, but hydrophobic in the middle; so how can the hydrophobic substance pass through the phosphate head in the first place? If hydrophobic substances can pass through, shouldn’t hydrophilic substances be able to pass through as well? TIA


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Can enzymes be externally administered?
I was reading about Tay Sachs disease - it is essentially the deficiency of the enzyme hexosaminidase. Why can't the disease be treated by administering the enzyme (prepared artificially/extracted from other living things)to the patient?

A good start for your research is to look at where the enzyme normally acts, and how a replacement enzyme might get there.

The idea of using enzyme replacement therapy for Tay-Sachs has been around for a long time (here, for example). I don't know what the present status is, but a quick look at New Approaches to Tay-Sachs Disease Therapy seems to suggest that things haven't changed that much.  One problem is that an enzyme administered in the periphery will not cross the blood-brain barrier.

In general, yes, administration of enzymes in some form or another can be used to treat a deficiency. A common example of this is the use of lactase to treat lactose intolerance. Since lactose intolerance results from the body not producing enough (or any) lactase, you can take oral lactase to alleviate the symptoms:

Lactase products are tablets or drops that contain lactase, the enzyme that breaks down lactose. You can take lactase tablets before you eat or drink milk products. You can also add lactase drops to milk before you drink it. The lactase breaks down the lactose in foods and drinks, lowering your chances of having lactose intolerance symptoms. - NIDDK

For some deficiencies, a general strategy used is gene therapy, which provides a functional copy of a gene to an affected person's cells. The advantage of gene therapy is that, rather than repeatedly dosing with enzyme, you give the cells the ability to make the enzyme/protein that is lacking, which results in a longer-lasting therapy. This can also facilitate delivery to hard-to-reach places (e.g. you might not want to repeatedly inject enzyme into the liver, or brain, but if there's a vector that can target that tissue you can just inject it intravenously).
I'm not overly familiar with Tay-Sachs, but there is some good information in the comments that one of the commenters will hopefully expand into an answer.


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Pathogens vs Microbes and the Immune System
I hope my question isn't too basic or silly. I am currently learning about infectious diseases in Year 11 Biology right now, and I'm stuck at the concept of pathogens and micro-organisms. Whenever I search online, I get the definition for a pathogen as "a micro-organism that causes disease" but I also see other definitions that say it is just an "organism that causes disease." I asked my teacher and she said that it is an organism that causes disease, but especially a micro-organism.
Assuming that my teacher's definition is correct, why are most pathogens micro-organisms? I was also wondering, in regards to the immune system's three lines of defence, does it also apply to pathogens that are not micro-organisms, like tapeworms?

Not all microorganisms are pathogens
Firstly, not all microorganisms are pathogens - some can be harmless and some can be even essential for the host organism functioning (e.g., many microorganisms that are a part of our microbiote).
Many pathogens are not microorganisms
Here one have to mention viruses and subviral entities (prions, viroids) which are not technically organisms, although they fall itno the category micro-.
Then one has to mention pathogens other than bacteria: funghi, parasitic worms, various kinds of larvae, parasitic plants feeding on their host, etc. There are many interactions between two organisms that can be characterized as parasitism, i.e., they benefit one organism but detrimental to the other.
Disease is an ambiguous term as well
Now, even when we talk about multicellular parasites, they are usually smaller than their host. It has to do with what we call disease - indeed, this term focuses on the condition of the host organism which may or may not be due to a pathogen. In addition, a pathogen is usually understood to be in a parasitic relationship with its host, that is - it takes advantage of the host without killing the latter. This again implies smaller energy consumption which typically means smaller size. If a "pathogen" killed a host and consumed it as a whole (or most of it), we would not be calling it a disease/parasitism, but rather a predator-pray interaction.

Just a note that plenty of pathogens are deadly (ebola and rabies spring to mind) even if they don't consume the whole organism.

Most diseases that cause death don't do it by consuming the host, but by causing gradual decline in their metabolic functions or damage to crucial organs.

@Armand This is a good point. But their energy needs are still much smaller than those of the host, which is related to their size - the reason why they are deadly is because they locally disrupt vital functions in teh host, as Barmar has pointed above.

@Barmar Thanks for this precision. See my comment above.

Terminology in biology often gets a little fuzzy around the edges, sometimes as a result of overlapping definitions, or the desire to avoid overlap. For whatever reason, many eukaryotic pathogens are more commonly referred to as parasites. This seems to be more common with (though not exclusive to) multicellular parasites, like tapeworms, possibly leading to some definitions which exclude them as pathogens (even though they are clearly causing infectious disease). A more generalized technical term for pathogens, often used in biosafety protocols and research regulations is 'infectious agent.' This covers the whole gamut of infectious parasites, protozoa, fungi, bacteria, viruses, and non-living agents (like prions) with less potential for ambiguity.
But, the hard truth is that many biological terms lack a rigid and universally agreed upon definition. Conflicting or even ambiguous definitions can persist because such definitions aren't always necessary for biologists to perform productive research. I don't need to know if guinea worms are technically considered parasites or pathogens or both in order to study their transmission and pathology. I don't need to know if prions are living or not to study the infectious diseases they cause. What's more important is to have working definitions that don't cause confusion when used consistently in a given context (in your case, that context is learning year 11 biology).
In response to your second question:

Assuming that my teacher's definition is correct, why are most pathogens micro-organisms?

This answer is a bit of speculation, but, the vast majority of biological diversity on Earth is microscopic. Given how outmatched we multicellular organisms are, both in numbers and diversity, it's a wonder of nature that we persist at all. Eukaryotes are a small branch on the tree of life, and multicellular organisms are only a small minority of that branch. Plus, the most abundant and diverse biological entities on the planet, viruses, don't even have a permanent home on that tree.

I love this idea: "Given how outmatched we multicellular organisms are, both in numbers and diversity, it's a wonder of nature that we persist at all."


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Geometric Interpretations of the DNA Double Helix
In mathematics, a helix is a shape which has constant curvature and constant torque (see Wikipedia here. What are the biological implications of the DNA double helix having constant curvature and torque, or is there none?

Note that the helix has local variability due to local concentrations of ions which have small effects on the curvature, which is therefore not mathematically constant. The DNA can vary from completely curved to completely straight... Using a statistical-mechanical model of DNA bending and protein-DNA looping, recent revised estimates for curvature variations are 1.6-fold and 3-fold, respectively (Zhang et al., 2006a).https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190679/

The standard text-book answer to this question is illustrated by the cover illustration of one edition of, well, the standard text book which I reproduce alongside an image taken from a teaching site of my own in which you can view several different aspects of the double-helix in 3D.

[Views of DNA looking ‘down’ the axis of the helix. On the book cover the bases are black filled shapes of purine and pyrimidine structures, in the image on the right the purines and pyrimidines are red and blue outlines, respectively, with the sugar–phosphate backbone shown in white.]
The regularity of the helix (constant curvature and torque) maximizes base stacking, which involves the π–π interactions of the purine and pyrimidine rings. This is important for maintaining the structure of the double-helix and hence facilitating its function. Base stacking is discussed in another question on Stack Exchange Biology, in that standard text, Berg et al. , and in a chemical article in Wikipedia.
Although concerning a single-stranded RNA rather than a double-stranded DNA, I take this opportunity to illustrate the biological significance of base stacking by considering the anti-codon loop of transfer-RNA. As is well-known (see e.g. this StackExchange Biology answer), there is frequently ‘wobble’ at the 5′ position of the anticodon loop, allowing certain non-standard base-pairs at the third (3′) position of the mRNA codon. As the image below shows, this can be partly attributed to the poorer base-stacking at this position in the anti-codon loop (G-34 in the illustration) compared to the other two positions, allowing greater flexibility.

[Anticodon loop of yeast phe-tRNA, created by the author from 1ehz.pdb]

One is tempted to answer that the helicity confirms a higher stabilty in respect to possible forces trying to separate the two strands. However, the logic of teh question (and such answer) is faulty, as it implies that there is a non-helical alternative to double helix, and that the helical form was evolutionarily selected. I doubt that this is the case (let me know that I am wrong).
So more correct way to see this is to say that DNA just happens to have torque. (Note that it is not exactly constant, as the DNA istelf is not straight, but folded, wrapped around the histones, etc.) One could even say that all linear polymers have torque, except that for some of them the torwue is zero.
Remark
One could compare double helix with the allophorms of carbon, which can adopt forms continuous in all three dimensions (diamond, graphite), two-dimensional (graphene), one-dimensional/helical (carbon nanotubes), and zero-dimensional (fullerenes/buckyballs). Are there any similar candidates for storing genetic information?


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Caudex vs Xylopodium difference
I live in Brazil and many plants from the brazilian grasslands/prairies exhibit an structure called, by the brazilian literature, "xylopodium" (or "xilopódio" in portuguese) - which are tickened, underground, lignified structures (root or stem) to store water and nutrients. I couldn't really find any work outside Brazil that mentions this kind of strucutre, and as far as I know, the structure known as "caudex" fits the very same definition. That being said, are these two terms synonyms?

The New York Botanic Garden gives the definition of xylopodium as:

An underground, woody, storage organ derived from stems or roots and common in cerrado vegetation.

And the definition of caudex as:

A short, vertical, usually woody and persistent stem at or just below the surface of the ground.

I think the main difference here is the focus on the xylopodium as a storage organ, as well as the fact that it is fully underground and can be derived from either the stem or root. A caudex doesn't necessarily primarily provide storage, and as a modified stem, is at or above the surface.

*There is also a definition of xylopodium meaning the type of fruit found in Anacardium (cashews).


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Differentiating molecules based on peptide sequence? How to annotate?
I want to differentiate between classical class I and non classical class I MHC molecules in a model organism using well conserved structural features within classical MHC I molecules (eg intradomain disulfide bridges within class I a1 domain). To do this I need to align the peptide sequences of transcripts of that model organism with transcripts of classical MHC I human genes and see which genes from those transcripts have those structural features. So I am looking for a tool to align and annotate those structural features in a replicable manner
Additionally if you have any other bioinformatic ideas /computational analyses on how to find classical MHC Class I molecules on an organism which is poorly annotated that would highly appreciated!

Check out http://www.bioinf.jku.at/software/msa/ You can do the alignment in R and annotate there in a very replicable manner once you learn the package. You can also align it in Clustal Omega (use the protein option to align), or unitprot.org/align


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What is prochromosome?
My textbook says that prochromosome is a false chromosome present in the nucleoid of prokaryotes.
I looked up Wikipedia and all over internet and this word is kinda sus. So I'm asking about it here. It doesn't seem legit. Wikipedia has just mentioned that the DNA like thing is present in nucleoid but never calls it prochromosome.

It would help a bit to get the exact quote from the text. That definition doesn't seem to agree with what I find when I research the term. For prokaryotes, I find the term here but it is poorly defined and does not agree with what you write. It is described as a "naked" chromosome that is only DNA, but that also doesn't make sense as bacterial chromosomes are bound by proteins. There is no page on wikipedia, as you note, supporting your "sus" designation.
There are current definitions available from online resources. It basically corresponds to condensed pieces of chromosomes (heterochromatin) that are apparent under a microscope under certain conditions. But it is not very well defined biologically, it is a name that humans give to something they see that they don't totally understand.
The term itself appears to be archaic. An early usage in reference to plant genetics is here. I think that it was probably a label that someone put on observations made microscopically before people knew what they were seeing. It looks to have become mostly outdated as cytology matured as a scientific field, here is an example quote from that paper:

Rosenberg (i8) was the first to show that the number of
prochromosomes is approximately the same as the number of
chromosomes. Prochromosomes have been considered as
structures identical with chromosomes (Malte, I3; Stout, 28;
Eichhorn, 2), as centers about which chromosomes form
during the prophases (Laibach, 9; Overton, 17; Rosenberg, 20) and as portions of chromosomes which persist through
the telophases (Heitz, 5; Gregoire, 3; Doutreligne, i). It
has also been considered that prochromosomes bear no direct
relation to chromosomes (Lundegardh, 12; Tischler, 30) or
that they are not directly concerned in the formation of
prophase chromosomes (Kuhn, 8). De Smet (24) stated
that prochromosomes may not be present in meristematic
nuclei.

This does not really correspond to any structure I can think of in the nucleus or nucleoid. It also doesn't correspond to the current heterochromatin definition.
Looking through search results, I am inclined to believe that the term as you have found it is an archaism that has somehow remained in some textbooks through bad editing. Very little current scholarly work is using the term. The scholarly work that does use it recently is using it in the more obscure cytological observational sense (heterochromatin), not in the prokaryotic sense that you have pointed to.
So it makes sense that you were confused given the inconsistent usage and the lack of current rigorous work on it. I would recommend sticking to recent scholarly work or definitions that come from traditional publishers (e.g. here). I would more or less entirely ignore question and answer sites that don't directly cite the scholarly literature.

Interphase chromatin can be divided into "chromosome territories" by chromosome painting probes.  It does seem like people a century ago without these probes may have been able to track these from telophase to prophase to a certain extent (see Figure 4).

@MikeSerfas I'm a little confused; the later reference has no reference to prochromosomes. Are you just speculating that well-known nuclear compartmentalizations are what such terms referred to? This seems uncontroversial, I guess, for the heterochromatic/eukaryotic definition of the term. But it doesn't seem to bear on the asker's question?

See Figure 2 / page 80, for example

@MikeSerfas The PLOS paper (the later reference) has only 1 figure? The other paper is relevant to eukaryotes but not prokaryotes.

Sorry - I had read "latter" for "later" in your comment.  The eukaryotic definition is by far the most prevalent.  Its extension to prokaryotes, however, is logical -- if a chromosome is defined only as a condensed, distinct structure, and "prochromosome" refers to the diffuse chromatin, then a bacterium should not be said to have a "chromosome" throughout its cell cycle, but rather a "prochromosome".  But I think that most people, rather sensibly, have not attempted to keep track of this distinction.  It relies on a uniform morphological distinction made in very different situations.

@MikeSerfas "...if a chromosome is defined only as a condensed, distinct structure, and "prochromosome" refers to the diffuse chromatin..." I guess that I find this a deeply confusing distinction (as do students apparently!). It really makes no sense once the chromosome is understood as anything other than a cytomorphological observation. But the bigger issue is that it doesn't even track with the present-day definition ("Heterochromatic blocks detected during interphase.") linked in my answer. According to that, only the most condensed regions should be prochromosomes (?am I crazy?).


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What do we mean by MHC molecule diversity? Does each human have a variety of MHC molecule isoforms?
I'm going to try and explain what I think I know
From what I understand, MHC/HLA molecules present peptides to T cells. To be able to present peptides from a wide variety of pathogens, they need to have diversity in their peptide binding domains.
My lecture handout tell me that MHC diversity comes due to polygeny and polymorphism.
Polygeny refers to there being 3/6 (handout says 3, textbook says 6) MHC class I loci leading to 3/6 class I isotypes, and 3/5 MHC class II loci leading to 3/5 class II isotypes.
Polymorphism refers to multiple alleles of each gene, meaning a variety of allotypes produced from each gene.
These processes lead to the generation of a wide variety of isoforms of MHC proteins in the human population.
The textbook also states that there is no rearrangement or structural change of the genes encoding the MHC proteins.
So I get that in the population, there is huge diversity of MHC molecules. But in each human, since there is no rearrangement of genes as in the case of antibodies to generate antibody diversity, is there therefore only one type of MHC protein being encoded? So by MHC diversity, we are not referring to diversity in each human, rather in the entire population? And if so, how do our MHC molecules become capable of binding to any antigen from any pathogen?
Please could someone clarify for me if I've misunderstood something, and also if my above explanation is factually correct, with the appropriate use of terminology?

You're right that both polygeny and polymorphism contribute to the diversity of a given gene in the population correctly described what they mean individually.
However, you missed that the polygeny of MHC means that the human genome has 3 different loci/genes (called MHC-I A,B & C) in the haploid genome, meaning that any given human as actually 6 copies of the gene (i.e. 3 copies from each parent). All of these copies perform the same function of presenting peptides to CD8+ cells, but will have slightly different binding preferences for the peptides that they load. This is where the MHC diversity in a single human comes from.
Additionally each of the 3 MHC-I loci/isoforms is polymorphic, meaning that for each of them multiple alleles/variants exist in the human population. Since the number of these variants is pretty big (hundreds to thousands), most humans have different alleles on their paternal & maternal chromosomes and end up with 6 unique MHC-I genes.

Ah yes, okay. So is the diversity produced from just those 6 genes enough to allow peptides from potentially any pathogen to be recognised and bound, and then presented to T cells? And does that mean the variation in MHC alleles between individuals produces only a very small difference in phenotype? I.e. are there large or only small differences in the types of antigen/peptide that each individual's MHC molecules can recognise? I just can't get my head around how such a few number of MHC molecule isoforms can bind such a wide variety of peptides

@Alex Yes, individual diversity just comes from having 6 different MHC-I genes. Generally they all bind broadly ~8-12aa pepdites with a few additional requirements, but still a big variety. Discussing the specificities, differences etc of peptide binding between the different subtypes & alleles is outside of the scope of this question/comment though - I'd recommend you read up about that in a proper textbook.


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Sharks, alligators and Gould's "random walk" theory
I was thinking about Stephen Jay Gould's view on evolution as pure "random walk" / Drunkard's Walk, increasing or decreasing complexity in basically random fashion, just limited by death if an organism becomes too simple and so increasing complexity without meaning that it somehow confers survival / fitness advantage.
Now, I've read elsewhere that at least some of the shark species (subspecies?) have existed in about unchanged forms for at least 100 million years (correct me if that's wrong) and alligators for 37 million years. 100M years or 37M years is pretty long even for evolution, so wouldn't it create pretty high chance that such long-running species would die out and/or evolve into species even more complex (per Gould's claim of complexity systematically increasing for purely random reasons)? Why would then what seems like about optimum fitness for particular environment persist so long?
Note: obviously I'm not a biologist or even student of biology, evolutionary biology is just my occasional interest. Apologies if I made basic mistakes in premises to this question.

You may be making a very common mistake in reasoning about probabilities. Yes, it is very unlikely that a particular species, picked at random,  would persist largely unchanged for 37 million years, but at the same time it might be almost certain that some species would follow that course. The error is that you didn't pick a species at random, you picked it precisely because it showed that high degree of conservation. It's equivalent to accusing the winner of the lottery of cheating, because winning is so unlikely. Yet the lottery is designed so that somebody wins almost every time.

You're also ignoring the optimization factor.  Living in water puts some severe constraints on creatures, particularly on their shapes, due to hydrodynamics.  Sharks in general have converged around a local optimum - and ichthyosaurs, dolphins, and tuna have converged around the same one.  It takes a large evolutionary jump to get out of that optimum.  And since what we see of fossils is mostly their shape, we don't see much change in general "sharkness".

@CharlesE.Grant Well... it's a different lottery winner almost every time, isn't it? Let's say we calculate the probability of alligators staying almost exactly the same over 37M years using binomial probability formula.

@CharlesE.Grant: Calculation: p = 0.999999 (probability that gator species will stay the same over all generations), q is the usual complement, n = r = 37^6. Since n = r, Newton's binomial in the formula = 1, q^(n-r) = q^0 = 1 and so the whole formula boils down to p^r, presuming simplistically that 1 gator generation takes 1 year. Hence, the value is 0.999999^37000000. This probability is so low that my Gnome calculator doesn't even display the actual value, rounding it down to zero.

@jamesqf: "You're also ignoring the optimization factor. Living in water puts some severe constraints on creatures, particularly on their shapes, due to hydrodynamics. Sharks in general have converged around a local optimum" - well... that's my point. Had constant selection pressure not kept shark's complexity pretty much the way it is, sharks would have evolved into something else, by Gould's argument evolution increasing complexity "mindlessly" via random walk, which is not happening.

@CharlesE.Grant: although I think what you may have meant: in a large number of random trials some individual species will be winning systematically more than others due to sheer chance, kind of like if you see stock market as a random walk, some traders will win more than others due to sheer chance and not because they're better. Still, "more than others" does not meand scoring every time better than others. Probability for scoring r successes in n trials with n = r is like I calculated for everyone, which means that basically no trader  or species will "succeed" every time.

@CharlesE.Grant: oops, there's a typo in my initial reply: I meant p = 0.999999 is probability that the gator species will stay the same over one generation, not all generations, obviously.

Assuming there's an upper bound and a lower bound to complexity, e.g. it hopefully can't get simpler, physically, than an atom/quark and there are I'm sure, physical limitations to complexity (one is Galileo's square cube law). If evolution is truly random, we have a yin-yang effect. After evolution (whether complexification or simplification) hits the boundary walls, the random walk will reverse direction and move towards the other limit. However, in the simple simulations I've conducted, sometimes the random walk stays steady at max/min i.e. plateaus at the upper/lower bound, for some time, and then, "having nowhere else to go", proceeds in the opposite direction, towards the other limit.
In the diagram below of a 1D random walk, look at the region circled in purple. A tendency, albeit brief, to remain at minimum.


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Is there vascular supply to cartilage
According to Gray's anatomy, cartilage is avascular but in a recent class, my teacher told me that there is vascular supply but it is confined to upper surface only. So, I'm confused that who is correct.

How do you define "upper"? My suspicion, however, is that there is no conflict: avascular tissue can still be supported by a blood supply, avascular just means there are no vessels in the tissue itself. It's probably best to just clarify this with your teacher.

I think that by upper, he meant surface region.

Then I think most likely there is no conflict and just misunderstanding. A tissue that is supplied only from its surface is equivalent to one that is avascular.

Thank you for the clarification.

This depends on what kind of cartilage you are examining and where it is located. Cartilage is not all the same depending on where it is located and it's intended purpose. Cartilage also generally exists as a continuum with the bone that it is attached to where you will see transitional changes from bone tissue to cartilage without specific delineation. Depending on the cartilage location and its function it may of may not be vascular. Hyaline cartilage existing closest to synovial joint spaces is pretty much entirely avascular. This has some advantages and disadvantages. Damage to cartilage is very difficult for you body to repair for myriad reasons one being avascularity, but also the avascularity allows for you to transplant live cartilage to any person regardless of what tissue type the donor or recipient is.


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What is this ? Found under my bed

Found under my bed. Looked and there was nothing else like it or eggs of any kind.

It was dead. Looked to be dead for a while but I’m not sure

Hi welcoem to Bio. SE. Please provide your location and the approximate size of the specimen. Additional clearer pictures would also be helpful for anyone trying to help you identify this organism. In general, we have a list of expectations for [tag:species-identification] questions here that should be met to avoid having your question closed (and, more importantly, to help you get a correct answer!!). Please [edit] your post to add more of this information. Thanks!

At a glance it looks like a flattened perfectly ordinary dead woodlouse to me.


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Bioenergetics book
I already asked this question on the physics SE but redirected here:
In the field of biophysics, it seems there is a subfield called "bioenergetics" about the processes of generating energy by biology. I am looking for a book to be introduced to the physics aspects of bioenergetics. I checked up on Springer and there seem to be quite some books on the topic, but the problem is that I fear that they would require heavy biology basics.

Whether you are talking about generating heat energy, kinetic energy, or releasing chemical energy, you'll certainly need an understanding of the underlying molecular biology and/or biochemistry. It depends on what you mean by "heavy biology basics". For instance, understanding oxidative phosphorylation would require you to understand that mitochondria have a double membrane and are equipped with an electron transporting machinery within one of the membranes. That certainly is biology.

@SPr Understood, but is there a book that is "self-contained" in some way that the biology basics like "mitochondria" are explained?

Ok so the vital force seems to be oriented towards biochemistry, right? And what is the purpose on Harold on the Peter Michell Nobel prize? I didn't understand the purpose of it in the question. Do you, by any chance, have the list of chapters of The Vital Force?

Sounds a bit too advanced, but a good reference nonetheless :)


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Mathematics for genetics
What types of mathematics are useful for studying genetics? Of course, statistics is, and I'm guessing set theory and group theory, but anything else? What about ordinary and partial differential equations?

Calculus is used pretty extensively in population biology. This can often overlap with genetics (modelling change in allele frequency over time for instance).

Genetics is a very wide field of knowledge and many different areas of mathematics are being applied to genetics. Here is a probably not exhaustive list of the fields of mathematics that I have encountered in genetics (you will note that the elements of the list are not mutually exclusive)

diffusion equations
differential equations
markov processes
birth-death process
probability theory (a lot of it)
Bayesian probabilities
statistics
Math related to MCMC processes as well as HMC processes
Many fields of theoretical computer science are being applied and I guess theoretical computer science is a field of mathematics.
Graph theory
numerical integration
Analysis of dynamic systems

You say

set theory

Yes of course

group theory

Probably not so much or maybe I jsut don't really know what it is

ordinary and partial differential equations

I think pretty much any field of science applying mathematics will use differential equations.

But of course, not all geneticists are good mathematicians. Each geneticist specialize in a particular subfield. Some of them do a lot of mathematical modelling, others don't do any. Statistics and everything related to data science will always be useful though.

Your answer is very intersting, however I'd find it even greater with a short explanation of how each  area is used for genetics. For example, it is not obvious to me how diffusion equations are applied to genetics.

From my understanding, it depends a lot on the sub-field you're in.
Data science, statistics and machine learning follow a different paradigm than calculus. Whereas data driven approaches to problem solving are generally concerned with developing predictive models of the underlying system, differential equation based approaches describe a mechanistic model.
These 'top down' and 'bottom up' approaches both have their benefits and drawbacks. On the data science side, it is very difficult to get a low-level understanding of the system. An oversimplification would be:
"The cell is a black box, so let's figure out the output for a given input to get a better understanding of what's going on inside."
On the calculus side, although mechanistic descriptions are a mathematical formalism of what's going on inside the system (and thus imply a complete understanding of the system - in theory), there is still so much that is unknown about most biological systems you'd care to model. This kind of modelling (from the discussions I've had) will be important in the future, when more is known about these biological systems, but for now it is constrained to small sub-systems. A good analogy might be:
"It's hard to figure out how an engine works when we don't know what half of the parts do."
Of course, there are many projects that bridge the gap between the above two methodologies.
So, to answer your question, statistics, computer science, machine learning, linear algebra, calculus, graph theory, set theory, optimization and combinatorics are all useful.

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What scorpion is this and is it lethal?

Found indoors in Florianopolis, Brazil.
Is able to hang from a web like something inside the jar.

I have another photo of the underside but cannot add because of reputation.

It's it a spider? Had it been a scorpion it would have been armed with a  sting.

It is a spider. Note the spinnerets at the caudal end of the abdomen, and the absence of claws. An eye pattern would be really nice; I think it's a jumping spider of some kind.

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What are the ploidy levels in major groups of organisms?
If total number of chromosome in the cell is x, then for-example;
Are all animals diploid (x= 2n) ?
Are all fungi haploid (x= n) ?
Are all plants diploid (x= 2n) ?
Are all Protists diploid (x= 2n) ?
Also, what is the ploidy of archaea and bacteria?
Thank you very much.

Is diploid = 2n your example for polyploidy in humans?

@AlwaysConfused I think the OP is referring to total number of chromosome (not pairs) as x.

Are all animals haploid (n=x) ?

No

Are all fungi haploid (n=x) ?

No

Are all plants diploid (2n=x) ?

No

Are all Protists diploid (2n=x) ?

No

Also, what is the ploidy of archaea and bacteria?

Generally speaking, Bacteria and Archaea don't have chromosomes (but have circular DNA). As such the question of ploidy does not really apply to them.
You might want to read about Biological life cycle to understand the terms haplontic, diplontic, haplodiplontic (and other similar terms).
Ploidy level can easily varies among species of the same family (typically in plants for which hybridization is common). There is no reason to expect that a taxon as big as "fungi" (for example) would all have the same level of ploidy.
Note that your question that all animals are haploids is surprising as you just described that humans are diploids.

Just want to add that it's certainly possible to talk about bacterial ploidy -- in fact there's a huge amount of variation in how many copies of their chromosome they maintain.

@VictorChubukov Thanks. I don't know much about that. Do you know a good reference for further investigations?

In animal, reproductive cells are haploid for human
Male bees, wasps, and ants are haploid because of the way they develop: from unfertilized, haploid eggs
some fungi are also haploid

bhakti - can you add some references to your answer? we appreciate that very much on BiologySE and it will strengthen your answer greatly


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Is dandelion a sporophyte or gametophyte?
My text book claims all land plants undergo alternation of generation. However, I don't see how it could be with dandelion. The flower head gets pollinated and then turn back on itself. After a while it opens back as a seed head ready to blow seed in the wind. What would be the spores then? And the gametophyte organism? All seeds are a result of sperm and ovula so it would mean the dandelion flower is a sporophyte?

See Alternation of generations - Life cycles of different plant groups

Dandelions are sporothytes. In Wikipedia you can read (Alternation of generations):

"In the spermatophytes, the seed plants, the sporophyte is the
  dominant multicellular phase; the gametophytes are strongly reduced in
  size and very different in morphology. The entire gametophyte
  generation, with the sole exception of pollen grains
  (microgametophytes), is contained within the sporophyte. The life
  cycle of a dioecious flowering plant (angiosperm), the willow, has
  been outlined in some detail in an earlier section (A complex life
  cycle). The life cycle of a gymnosperm is similar. However, flowering
  plants have in addition a phenomenon called 'double fertilization'.
  Two sperm nuclei from a pollen grain (the microgametophyte), rather
  than a single sperm, enter the archegonium of the megagametophyte; one
  fuses with the egg nucleus to form the zygote, the other fuses with
  two other nuclei of the gametophyte to form 'endosperm', which
  nourishes the developing embryo. For further information, see Double
  fertilization"

Hi @Olga. Welcome, and thanks for contributing to Bio.SE! Generally, we ask that answers don't simply include large quoted blocks of text, and instead we hope that those that answer expand upon the resources (quotes, pictures, links) that they provide with additional context, backround, etc. Your post will likely garner more positive attention if you expand upon it further. Additionally, if you reference or quote something specifically, please provide a direct link to where the quote arises so interested users may explore the topic further. Thanks!

Hey! Thank you for constructive comments (my English is not very well and that's why I decided to take such a long quote). For the future I will try to try harder :-). Have a nice day..


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What is the meaning of the following: " completion of open rounds of DNA replication"?
I am studying a paper about the relation between polyP granule and cell cycle exit. As the author explained the four general steps for cell cycle exit, the second step is" the completion of open rounds of DNA replication". But I really can't figure out the meaning of this sentence. I hope that someone can explain this to me. Thank you!

From the context of the article I found from an internet search:

Cell cycle exit in bacteria encompass four general steps:
(i) inhibition of inappropriate reinitiation of DNA replication,
(ii) completion of open rounds of DNA replication,
(iii) segregation and compaction of daughter chromosomes, and
(iv) septation.

I would assume that ‘open rounds’ means ‘DNA replication that has already been started’ (‘open’ signifying already started, and a ‘round’ has the sense of one event of a series). ‘Completion’ is obviously ‘finishing’, ‘ending’ — the cell cycle doesn’t end until all the replication that has started has finished.
I have not seen the adjective ‘open’ used in this way previously, and suspect it is uncommon, but as this is not my field I stand to be corrected.

Oh, I see. So, I may translate it into  the last round of DNA replication before entering the cell cycle exit?


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How do biologists estimate that there is 8% of protein coding genes in human genome?
In class, the professor said that there is about 8% of protein-coding genes in human. I wonder how biologists estimate this without annotating all of human genes. Thank you!

What do you mean by "without annotating"?  Without a minimal annotation of the transcriptional and translational features this is obviously not possible. After they got the sequence they had to read it. What is your question exactly?

S/he's off by about 6 - 7%.
As per the national human genome research institute approximately 1% of the human genome encodes proteins. We can tell this by looking at the sequence (which we're now able to do quite quickly) and identifying those portions of the sequence can be translated to protein using the genetic code.

Scientists have been able to identify approximately 21,000 protein-coding genes, in large part by using the long-ago established genetic code. But these protein-coding regions make up only approximately 1 percent of the human genome...

You are taking some wrong assumptions. There are plenty of regions that contain open reading frames in the human genome and a high fraction of them are translated into "proteins". This was recently seen in ribosome profiling experiments. That does not mean that these translated ORF are proteins in the sense that they perform a function. Most of them are noise as they are transcribed and translated in small quantities.
Additional evidence to consider a translated region as a true protein is usually conservation. However very recent proteins will not appear even in closely related species.

@biojl This is a statement by the NHGRI, the institute at the NIH that oversees genomics research. It represents consensus in the field. There is, of course, more to that goes into it, but you find out how much of the genome codes proteins "in large part by using the long-ago established genetic code". We use conservation of these ORFs as well, but recent work suggests we should be a little more liberal with what we consider a functional protein.

The consensus in the field of genomics (where I belong) has changed quite a lot since 2012... Those statements were true back then but the beauty of science is that it changes when new data or new ways of looking at it appear.

@biojl personally, my time in the lab is remote, but I like to think I'm still on top of things, and current research is relevant to me. Do we really not think that 1-2% of genome encodes proteins anymore? Do we not start that estimation by looking for ORFs?

It is important to remember that protein-coding genes have a start and an end, exons and introns, and identifiable promotors. Knowing that these factors exist and how to identify them (usually by their unique DNA sequences, the frequency they occur and their sequence lengths) we can identify these sequences as part of whole genome analyses.
Next-generation sequencing made it possible to sequence the entire genome of a human in a matter of days, if not hours. This massive database makes it possible to identify it's variable elements. Now, knowing where a promotor is, the following start codon of a gene can be found along with its stop codon. This leads to identifying open reading frames (ORFs).
Now it is simple, in that simply counting all the ORFs in relation to the other structural and "nonsense" DNA and the percentage of protein coding sequences can be determined. Remember that this is the norm, however there is still much we do not know about the human genome. There may be more protein-coding genes with unknown promotors that we do not know of. So always keep on asking!


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Why this fish is accompanying stingray?
During snorkelling a couple of months ago on Canary Islands I've been watching stingrays which I think are "Roughtail stingrays". Often this fish (on pic) was accompanying those stingrays. So what kind of fish is this and why it's hanging around stingrays?

Stingray:

I've seen this behaviour many times so I'm sure it's not a coincidence.

Welcome to Biology.SE! Interesting question — did you observe any interactions between the fish and the ray? For example, did you ever see the ray feeding and how did the fish react? My suspicion would be that the fish is hoping to benefit from the ray's foraging. ——— You may also want to take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome thanks for the hint. No unfortunately I haven't seen any interactions between them. This fish is kinda just hanging around. If you come closer to the stingray the fish will flee and leave the stingray. Also I haven't seen other species of fish hanging around stingrays, it was always the same. I was thinking maybe it's looking for protection? This is completely sandy coast with no cover for fish, maybe hanging around stingray is safer, meaning if it flees the fish will know that danger is around. Maybe stingray sensing danger much better than this fish.

The fish it seems is one of weevers

Curious — the only thing I've been able to find about stingray symbiotic relationships  are mutualistic relationships with cleaner wrasses and commensal relationships with fish and coastal birds that capture small animals disturbed by foraging by the stingray.  In the absence of any observed interactions the latter still seems like the most likely explanation to me, but I guess you'll just have to go back and make more observations to be sure!

@tyersome Probably in a few years :) Though it's not easy to get close to them because they are flee fast. There's some sort of interaction can be seen on this video https://youtu.be/Gjz52RtPakA if you increase size. It seems fish just swim close to stingray and wait nearby for something.


text:
Is reverse tonotopical organisation possible?
In human cochlea tonotopical organisation is that higher frequency sounds are detected near the entrance whereas lower frequency sounds are deep inside the cochlea. Is this tonotopical organisation (high frequencies at the entrance, low - deep inside) justified by some physical or biological constraints or it doesn't matter and we could in principle have cochlea where low frequency sounds are detected at the entrance?

There are indeed constraints: in principle, low-frequency sound waves travel better in viscous media (look here for a simple explanation). The idea behind that is that being sound a vibration in the medium, it causes its molecules to move. The faster the movement (that is, the higher the frequency) induced by the wave, the more the particles will disperse their energy by crashing into each other. This leads to more loss of energy for high-frequency waves compared to low-frequency ones when travelling in a medium.
Now, all of this leads to the detection of high frequencies being better at the beginning of the canal. However, here is the law that quantifies the loss of amplitude of the wave with distance. As you can see, the damping is higher for high frequencies, as well as high viscosities. However, plugging in some sensible numbers (20 kHz for very high-frequencies heard by humans, 1500 m/s for the speed of sound in endolymph, 1 centipoise for its dynamic viscosity, 1 kg/liter for density) gives a negligible loss of intensity (something like 0.0001. I'm sorry for the poor formatting, but I'm on my phone right now and I hope you will try to run the calculation yourself).
Now, a possible need for the accurate detection of even higher frequency sound waves in water for the fish in which the cochlea appeared is possible. However, I neither know if that is the case, nor if the difference would be a significant one.


text:
How do we know that selective agonists are indeed selective?
Suppose we know that compound X is a selective agonist of receptor Y, meaning that it binds only this receptor Y and no other. But how do we know this that it doesn't bind some another receptor? I suppose that screening for the binding strength of a given ligand to all known receptors would be very tedious and not feasible.

Unfortunately, it's really hard in the general sense. Even for FDA-approved drugs with well-characterized mechanisms of action, the binding profiles are incomplete.
For GPCRs, it's you can run your compound(s) against a full panel of many GPCRs. For example, the PDSP (Roth Lab) can test for binding against multiple GPRCs using radioligand binding assays. See: https://pubmed.ncbi.nlm.nih.gov/23235874/, Figure 2 in particular. Most receptor binding assays are competitive, meaning they detect the displacement of known ligands. This is inherently limited because your compound could bind to a different site -- even a novel site.
You'll notice that in Figure 2, the GABA A receptor was conspicuously missing. One of the reasons is that binding is subunit-specific, which is another complication -- many receptors are oligomers, and it's often hard to prepare them for the assays.
For many well-known enzymes, there are specific activity assays available. These measure the level of a reaction product (often by fluoresence). This of course doesn't rule out binding without activity, and these assays are not available for all enzymes.
Another class of assays measure changes in potential across a membrane. For example, the FLIPR assay for GABA A receptors (https://pubmed.ncbi.nlm.nih.gov/31127604/). These tend to be very time-intensive and expensive, they're limited in the number of receptors, and of course they can't detect binding without activity.
As a last resort, you can use pull-down assays. One of the popular methods is immunoprecipitation (IP). You make an antibody that's selective for your compound and use to cross-link to any protein your compound might be binding to. Then these proteins get pulled out with your compound. These are generally very time-intensive and expensive, and they can need a lot of tweaking. And, of course, they won't detect all proteins your compound might bind to.
It's currently impossible to show that a compound is completely selective. To show that it's "likely" to be very selective, you can expect to invest a year or more for one compound.
But! To take a first stab, you can check out commercial assays offered by Eurofin (ex https://www.eurofinsdiscoveryservices.com/cms/cms-content/services/in-vitro-assays/gpcrs/binding/). They have a GPCR panel and a number of activity assays. Unfortunately their services are quite expensive.

Probably also worth noting that selectivity is always relative. Even research compounds that are used specifically for their high selectivity have some off-target binding, one just hopes that it is negligible at the concentrations used.


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Why don't we use hybridization instead of PCR?
So, I would like to ask, why don't we use just DNA hybridization instead of PCR primer amplification to diagnise some illness?
I know, when you have a really small amount of DNA from virus or cell you need to amplifie it, so you can do some hybridizations. But I cannot find out, why you need to amplifie it when you have like 10 ml of substance, where the amount of cells or viruses can be really high.
For instance, when you are trying to diagnose some chromosomal aberation you don't amplifie the DNA, so you do just hybridization, but when you are trying to detect coronavirus you use PCR, why?
I have all the information from Genetics by Eduard Kočárek (Scientina 2008) - so now you know the literature my question is based on.

Could you be more specific about what you mean by "hybridization", e.g. Southern blot? I can assure you that Southern blots are extremely slow and laborious compared to PCR (1-2 days vs. 1-2 hours), more of the time is hands-on work, the technique is more difficult, and Southerns generally involve radioisotopes, which are complex to work with. https://blog.addgene.org/evolution-of-lab-techniques#:~:text=Whereas%20Southern%20blotting%20is%20labor,time%20and%20resources%20(3).

I’m afraid you really need to do some more reading and then edit your question so that it addresses the use of PCR in the diagnosis a specific disease or disease agent. Without that we can’t answer sensibly, as different diseases are diagnosed in different ways.

To add to the other excellent comments, think about what exactly you mean by "diagnose some illness". For example, looking for a genomic chromosomal aberration is very different than trying to determine what bacterium is present. What factors might vary between different types of diagnoses?

From comment.
Could you be more specific about what you mean by "hybridization", e.g. Southern blot? This is the old-fashioned technique that I believe is closest to what you mean. Slot blots are also possible but somewhat less interpretable.
Both are still used occasionally for various reasons but each is much, much more work than PCR. Southern blots specifically are extremely slow and laborious compared to PCR (1-2 days vs. 1-2 hours), more of the time is hands-on work, the technique is more difficult, and Southerns (also slot blots) generally involve radioisotopes, which are complex to work with.


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Reasons behind the sticky substances are used by poplar in buds
It is well known that sticky poplar buds falling on a car can seriously damage the paint. Also these scales from poplar stick to the paws and fur of animals like Velcro. Personally I don’t think the mentioned examples of sricky ‘cases’ explain the puprpose of the sticky buds. Indeed, what the reasons the sticky substances are used by poplar in buds.
I guess the bees could be a reason to collect the sticky substances. However, I can hardly see bees on poplars. Also, the sticky substances could prevent buds to be frozen in early spring (creating a time-delay in growth of buds). What is the right explanation?

See this question: "Why do some bad traits evolve, and good ones don't?" https://biology.stackexchange.com/questions/35532/


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Can viruses grow?
Hey there everybody !
I know that viruses show only one living feature - Reproduction. However they cannot reproduce by themselves so on this basis they cannot be classified as living organisms. They need a host cell to reproduce.
When a virus infects a host cell... and injects the DNA into the host cell... and the DNA merges with the nucleus of the host cell and the host cell starts creating new viruses.
Now my question is, when a new virus is 'made' will it be made in its full size ?
Like- will the virus which is made by a host cell be an 'adult'/mature virus ?
In other words will a newborn virus be like a newborn human baby, where the baby has to grow up to become an adult. Does a newborn virus have to grow ?
I assume NOT, since Viruses don't have any organelles to do any growth and development.
But can somebody confirm this ?
Because there is a weird image in my textbook where we have a virus infecting a bacteria cell and the next image there are 'baby' viruses inside the bacterial cell.
Thanks in advance

Not all viruses are DNA, and not all DNA viruses integrate their DNA into the host cell.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Viruses do not grow. Instead, their components self-assemble inside of a cell to form complete new viruses, which are then released to go and infect more cells.
Here is a fairly accessible review on the subject: Mechanisms of Virus Assembly.  Basically, when the virus reproduces, it manufactures a bunch of parts.  A typical virus may be thought of as having three types of part:

The genome (RNA or DNA) that encodes for the virus
Structural proteins ("SPs"), which form the packaging for the viral genome
Non-structural proteins ("NSPs"), which handle operations within the cell such as replication, packaging, and suppression of host cell anti-viral responses.

In the replication process, the virus makes a bunch of copies of each of these independently. The SPs and genome come together to form new viral particles, and the NSPs get left behind.  Consider for example, this Sindbis virus genome:

Bases 79..7635 encode a "non-structural polyprotein": a collection of four protein elements that assemble in various different configurations to build a "viral factory" out of membranes within the cell and then copy the genome.
Bases 7681..11418 encode a "structural polyprotein" collecting together the five elements that form the capsid that self-assembles around the genome to make a new particle.

Now, this is biology, so there are exceptions and blurry boundaries, but this covers the typical cases pretty well, and even in the non-typical cases I have never heard of a virus that "grew" in a meaningful way.

I agree with the answers given by @jakebeal and @Armand. However, the analogy between a newborn virus and a newborn baby, suggested by the OP, is not without its merits. Indeed the virions released by a cell, in which the virus has replicated, are not always ready viruses. They need to undergo the process called maturation. E.g., see here and here.

Short answer - no, they don't grow once they are released from the cell.
I like to think of it as a factory production process. The widgets coming out of the factory assembly line don't grow, they just get sent out.  Sometimes the assembly line makes mistakes and a virus might be missing something (or most things) or might even be just an empty shell and so be smaller. Some viruses are contained in "bags" (enveloped viruses), so sometimes the bag might be defective instead, or even empty. Some viruses (like TMV) "self-assemble" with their protein coat automatically "growing/assembling" around their nucleic acid (RNA in this case), but that's a one-time process in the cell and doesn't continue once the virion is released.