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How does Anabantoideis' labyrinth function? What does it look like?
Anabantoideis are fish with an organ that allows them to take oxygen directly from the air outside of water. However, I cannot find much on how this functions, nor can I find any clear image of what it looks like. Those I do find seems to contradict one another.

This image shows what looks like a bubble flowing into a hollow hole.

This image shows something very different, a mess of flesh, presumably where oxygen is absorbed and expelled from the gills.

This image shows a mess of flesh like before but more similar to intestines, but disconnected to the gills.
What images are most accurate, and how does the labyrinth function?

Welcome to Biology.SE. Have you tried doing an image search and looking for actual images rather than diagrams? ——— You are likely to get a better response if you [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please also take the [tour] and consult the [help] starting with [ask] for details.

@tyersome Yes, I've looked for actual images, but they are even less helpful, usually only showing external anatomy and never the real labyrinth itself.


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What is the ball of jelly on the left eye of this mantis?

This mantis was seen in the wild in north Israel.
It would be great if the Mantis species can be identified too.

source: Stack Exchange

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

sort: votes


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Setup of terrarium for an early life experiment
I'm building a terrarium in which an early life environment will be simulated. Over multiple years a few experiments with different starting molecules/atoms will be held in it. The selected materials will be manipulated through grinding against each other, being mixed, slow temperature change and radical temperature change. Different starting materials with different manipulations will lead to different new molecules being formed. The more diverse and complex the molecules I end up with are, the liklier it is I'm getting closer to simulating the start of life on a planet. I expect to find ways of recognizing certain molecules through how they 'behave'. The thing I'm most interested in, would be to map out what types of changes in environment are required to get over hurdles in which diversity or complexity start to stagnate.
The way I imagine I could set it up:

Get a very big, cleaned transparent plastic bag that's flexible enough for hands to be able to grip objects through it.

Put the bag around the terrarium, the selected prepackaged molecules, gas bottles, a bottle of alcohol and some tools.

Close the bag and install a small pump on its surface.

Pump as much air out of the bag as possible.

Release some gas from the bottles inside the bag to make working easier. (Else the bag sticks to the open terrarium-box)

Cover everything inside the bag with alcohol.

Pump all the gas out again and release new gas from the bottles.

Clean the insides and the lid of the terrarium with towels.

Open each bag of molecules (salts, carbon, water, etc.) and drop the contents into the terrarium.

Seal the terrarium very well.

Are there any better ways of sterilizing an environment to a point where no molecules formed through evolution on earth are inside of it?
E.G. heating it for a long time, drenching it in a base/acid...

I don't want to discourage you from at-home experimentation, but this isn't going to work. Everything that goes into the chamber needs to be sterile, not just clean. Bacterial spores, for example, can be extremely resistant to many forms of cleaning and sterilization - some can survive high doses of radiation, others the vacuum of space. Creating clean rooms is a whole industry in and of itself, and involves everything from the air circulation systems to the water to gasses to the materials of each surface, plus a ton of experience and lots of validation to make sure it actually is clean.

Aside from the extremely difficult mechanics of setting everything up and keeping it sterile, what are your endpoints going to be? You say you're working with "molecules" - how are you going to tell if your experiment is successful? What exactly are you looking for?

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.

See a somewhat related question on Space.SE involving the difficulty in ensuring spacecraft do not accidentally bring organisms to other places: https://space.stackexchange.com/questions/54293/is-there-any-demonstrated-or-even-proposed-technology-that-can-sterilize-a-space

@MattDMo thanks for taking the time. I'll elaborate at the top of the post and make the question at the end of the post more specific.

@Bryan Very interesting. Thanks you!

I suggest you investigate chemical means of cleaning - strong acids (3-5 M nitric, 5 M HCl) neutralized with strong base (NaOH) should work. Note that we don't actually know the conditions in the early earth, but a number of "biological"-like molecules are found in the spectra of stars and in lunar dirt, meteorites etc.

this may save you a lot of trouble, this is not an easy experiment to duplicate in a small school lab but it is doable. https://www.youtube.com/watch?v=Mp9l3LhPLgE

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


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Hardy-Weinberg Equilibrium help
I am currently working on understanding Hardy-Weinberg Equilibrium problems. I have come upon two examples of a problem in two different Youtube videos which got me confused:
Example 1:
19% of a population shows the dominant phenotype. What is the dominant allele frequency?
The instructor in the video says that we should address 19% as a combination of both dominant homozygous and heterozygous, so:
p^2 + 2pq = 0.19
Example 2:
In a given population of velociraptors that assumes Hardy-Winberg principles, brown skin is homozygous dominant, and gray skin is homozygous recessive. If the percentage of brown-skinned Velociraptors is 64%, what percentage of velociraptors are Heterozygous?
In this case, the instructor says that p^2 = 0.64.
What I don't understand is why in this case p^2 = 0.64 and not 2pq + p^2 = 0.64.
Couldn't the heterozygous velociraptors also have brown skin?
Referred videos:
First: (Minute 17)
https://youtube.com/watch?v=NS3BjKWHK1s
Second: (Minute 5:20)
https://youtube.com/watch?v=IVGEusDdJGk

you might want to try and find the video this is a little confusing without it.

First: (Minute 17) https://www.youtube.com/watch?v=NS3BjKWHK1s Second: (Minute 5:20) https://www.youtube.com/watch?v=IVGEusDdJGk

You are correct and the instructor in the second video should have used p^2 + 2pq = 0.64. The only reason I can think of for leaving out the 2pq term is if the heterozygous individuals do not have brown-skin. This would only happen if the gene controlling skin color displayed codominance (heterozygotes would have patches of brown and grey skin) or incomplete dominance (heterozygotes would be a solid greyish-brown color). In either case you would not need Hardy-Weinberg Equilibrium because you can directly count the number of heterozygotes.

I think what question 2 is trying to imply is that only homozygotes for brown alleles are brown skinned.  But if the heterozygote has a different phenotype from the homozygotes, I don't see how it is correct to call brown "dominant" and grey "recessive".


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Why does there have to be two muscles to control the size of the pupil?
In dim light, the circular muscles relax and radial muscles contract to allow more light to enter the eye, and vice versa in bright light.
Why is there the need to have two muscles when probably the circular muscles would do the job itself? Couldn't a single circular muscle be responsible for to enlarge the pupil (muscle relaxation) in dim light and constrict it in bright light (constriction)?

Those aren't biology questions. Those are engineering questions at best and what if questions. Just because something is the way it is in biology doesn't mean it must be that way, but it probably means there are good reasons for it. "Why must DNA have a right-handed helix?" is asking the wrong question to ask.

It's a biomechanical question, and therefore on topic. It can be answered with general knowledge of biomechanics to explain why/how the two muscles are applied in this setting. I'm not a fan of the question given the lack of research effort, but I see no reason to close due to topic choice. @user, please [edit] to show some personal effort to answering the question. Thanks.

Short answer
Agonist / antagonist muscle pairing in the form of the sphincter and dilator muscles in the iris allow for quick and powerful movements of both the constriction and the dilatory response.
Background
Like the (striated) skeletal muscles, the smooth iris muscles come in pairs. Contraction is per definition an active process, and hence it is fast. Take the familiar example of the arm; when the agonist (biceps) contracts, the arm bends. Its antagonist (triceps) relaxes at the same time to give minimal resistance to the motion. The process reverses when the arm is stretched again (Fig. 1).
A similar mechanism operates in the iris to regulate the pupil response (Fig. 2). In this case it is smooth musculature: the sphincter muscle  forms a ring around the pupil and constricts the pupil. The dilator muscles radiate from the pupil such that contraction dilates the pupil. Also here, the action of the dilator is antagonistic to that of the sphincter and the dilator must relax to allow the sphincter to decrease pupil size. Their actions regulate the amount of light that enters the eye as well as the depth of field. The iris sphincter is controlled by the parasympathetic system, whereas the iris dilator is controlled by the sympathetic system (source: University of Texas).
A constriction and relaxation alone cannot do the job, unless some basic tension would exist that would keep the arm continuously bent; in that case a constant muscle tone would be needed to keep the arm fixated somewhere in the middle of its dynamic range. Increased tension would bend it, relaxation would stretch it. However, a decrease in tonus would never allow it to be stretched completely without the assistive force of gravity or another source of power. In addition, it would be a really sluggish process. E.g., using your arms to get up from the ground would be impossible.
In terms of the eye, the pupil response would be fast in the active process, say the constriction, but very sluggish at best in the opposite direction. Viscosity and friction of the tissue might even prevent the antagonistic (dilation in this example) movement altogether, leaving your pupils stuck in a constricted state (in our example), hampering quick adaptation to dark environments.
Reference
- Tudor & Deaconescu, MATEC Web of Conferences (2018); 178(3): 07005

Fig. 1. Arm control. source: (Tudor & Deaconescu, 2018)

Fig. 2 Pupil response. source: Mammoth memory


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How do the hair cells of the inner ear contribute to most of the hypercapnic respiratory response?
https://www.sciencedirect.com/science/article/abs/pii/S0306452210015253
Mice with damaged ears exhibited a significantly suppressed respiratory response to carbon dioxide.
From the study:

The mean respiratory frequency of control mice increased in response to CO2 by more than 100 breaths per minute, an increase of approximately 40–60% over their baseline values. In contrast, the ear-damaged experimental mean values increased by only 2–11%

Question: How do the inner ear hair cells contribute to most of the hypercapnic respiratory response?

Welcome Sarah. There's a related question, though the link may not seem immediately apparent. ;)

I don't know. Does anyone know? Did you try to find an answer? How? Please edit your question to include your research.


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How can "position" be measure by bp unit?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the CNV:

Whole-genome re-sequencing is fast becoming the norm in the field of human comparative genomics. It is sufficient for the accurate detection of single-nucleotide polymorphisms or SNPs (i.e. variations in a single nucleotide position in the genome in members of a population). To a lesser extent it can also identify short insertions and deletions in non-repetitive DNA, as well as reveal copy number variations (CNVs) between target and reference genomes. CNVs are increasingly recognized as being important in human biology and disease; in genomic data, they manifest themselves as differences in the depth of sequence coverage obtained for a specific gene or stretch of DNA. Genomic regions showing a large increase or decrease in the number of individual reads mapping to the reference genome are indicative of changes in copy number in the organism of interest (see Figure 8).

I don't have enough knowledge about this topic, and I don't know how "position" could be measured by "bp" unit, which is mainly a unit of length in similar contexts!

@user438383 So, does "chromosome position" refer to "the position of the chromosome itself" or "position of a specific thing within it"?

The latter - the position within a chromosome.

‘Position’ (or genomic coordinate) in genetics is just a 1-dimensional measurement, as the genome is basically a 1-dimensional object (in most contexts - the genome actually has a 3d structure but that’s usually ignored for simplicity in a majority of case).
‘Chromosom(al) position’ will therefore almost always refer to the position of something like a gene within a chromosome.
Perhaps this is confusing if you assume ‘position’ refers to at least a 2-dimensional coordinate like it does on a map or something.


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Why does oestrogen go from inhibitory to stimulating LH/FSH?
Typically in the menstrual cycle, oestrogen is released from the follicle. The oestrogen goes on to the hypothalamus to have an inhibitory effect on releasing more GnRH and LH/FSH.
However, when all the other follicles in the ovaries have died/atrised, the oestrogen acts as a stimulatory hormone. It increases FSH and LH secretion, to create the LH surge.
Why is this? How can one hormone go from being inhibitory to stimulatory?

"...suddenly the oestrogen acts as a stimulatory hormone. It increases FSH and LH secretion." What estrogen? What causes menopause? Why does FSH increase with menopause? It's easy to google and what you find will show you where you took a wrong turn in your reasoning.


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What is the status of the telomeres in HeLa cells?
I read several times about the hypothesis, also reported on Wikipedia, that ageing is linked to the length of the telomeres. Each time the chromosomes are duplicated during a cell split the telomeres lose a little bit of their length and their ability to drive further duplications declines.
But now I read the story of Henrietta Lacks. Her cancerous cells where harvested 70 years ago and they have been used to create thousands of cell lines. Since she was 30 years old when the cancer was discovered those cells now might be 100 years old. The real age is probably less because most of them were frozen from time to time, but on the other hand they are cancerous cells duplicating at a frantic pace.
I read from this answer that cancer cells can activate telomerase and restore the telomeres, but is it still happening after so many years? In all the cultivations in vitro did were they always provided with the right nutrients to produce telomerase?
Is there a study on the status of the telomeres in those cells? Are they really "eternal" in practice or the definition of eternal is still in theory?

Wow.  I looked this up on PubMed and there are 906 results for HeLa telomerase.  Not all are real, but there's some data to work with here.
I've been reluctant to rely on Russian charity with the Cold War in full swing, so there are a lot of leads I won't follow in the abstracts that came up: Ivankovic, 2007 says "surprisingly, found that the fraction of cells that divided 0-1 time over 6 days in culture have several times higher endogenous telomerase activity than the fastest dividing fraction. Additionally, the non-growing fraction regains an overall high labeling index and low SA-beta-Gal activity when subcultured again."  Varshney, 2014 wrote that "The overexpression of telomerase is not proportionate to telomere length in cancer cells, suggesting that the immortalizing phenotype can be mediated through other factors in addition to telomere length."  Taji, 2017 reports that autophagy reduces the telomerase activity in HeLa cells.  But TERT induces autophagy according to Roh, 2018, which describes the involvement of hexokinase 2 and glucose metabolism and more importantly is actually published in the sense of public.
Anyway, I eventually happened upon Nakashima, 2013 (open access) which says "the telomerase inhibitor BIBR1532 acts together with TEL patch mutations to inhibit the growth of HeLa cell lines and ... apoptosis is a prominent mechanism of death of these cells."  (Without the inhibitor the cells seem to just make more telomerase until it works without the patch)  I'm rather amazed that a veteran "cancer survivor" so to speak like HeLa will still undergo apoptosis if it runs into a telomere problem, but there it is!

What is unclear to me is why HeLa cells are that particular? My understanding is that the permanent based on (supposedly) the telomerase mechanism exists in all cancer cells, as well as in stem cells that are today cultivated. So why are HeLa's cells that important? Because they were the first to be cultivated?

First, I will address your misconception. You can interpret the telomere length of a typical somatic cell as its upper limit of remaining replication-cycles and therefore as an indicator of its age. This describes the fate of a cell, however, the age of a person should be seen as something else; when you are 20 years old, your cells don't have shorter telomeres than when you were half that age. Aging as a person is a complex topic with compound gradual influences e.g. loss of epigenetic memory, i.e. DNA and histone states, worsening of proteome health, i.e. worsening of protein homeostasis that eventually leads to cells not being able to cope with the required protein turnover leading to functionally ineffective proteins and accumulation of waste. DNA damage also plays a role.
To your actual question: HeLa cells can regenerate their telomeres with telomerases. This means that different HeLa cells within a flask will have telomers at different lengths. Most of your bodies cells do not have telomerase activity as it represents a huge risk for cancer. HeLa cells are enteral at least in the sense, that the cell-line will probably be conserved as long as there are humans or it is deliberately destroyed for political reasons. However, individual cells are not immortal, e.g. might die to external damage or mutations.

Thank you for the answer. But I still have a doubt. Those cells line are eternal by observation (because someone observed that at least few cells in the line have full length telomeres after thousands of duplications) or in theory.

@FluidCode Both and neither. Cell lines are considered immortal when they are able to replicate indefinitely in a lab. That doesn't mean they will exist forever, doesn't mean that particular dishes of the cells can't accumulate mutations that make them no longer capable of dividing indefinitely, etc. From the perspective of telomeres only, all you need is to know both empirically and theoretically is that the telomeres do not get any shorter over time to say that telomere length will not be a limiting factor in replication.


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What is this bee-like insect flying above the swallow in Singapore?
Photo was taken within the past week in the Singapore Botanical Garden. The bird is the Pacific swallow Hirundo tahitica, but there is also an unidentified insect flying above the bird, which is sizing up the insect. The insect wandered into the frame of view while attempting to photograph the bird, which was the reason that it is out of focus.
The insect appears to be about 1cm long, and has the black and yellow colouration as well as wing shape of a bee, but the mouthpiece doesn't appear to resemble any species of bee or wasp that I am aware of. What could this insect be?

I think that's some sort of nectar feeding moth. Search for ones that mimic bee or wasps.


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Has electrical activation, rather than mechanical tension been investigated as a direct trigger for hypertrophy?
Three of the most common theories for what induces hypertrophy are mechanical tension, muscle damage and metabolic fatigue.
The prevailing theory at the moment is that mechanical tension is the main mechanism for inducing hypertrophy, with the other two possibly playing a smaller role. [1]
More specifically, activation and mechanical tension in high threshold motor units (type 2 fibres) induces hypertrophy, whereas activation of low threshold motor units (type 1 fibres) induces little to no hypertrophy.
The theory is that the muscle cells have a mechanism whereby they sense being physically stretched, which triggers off the hypertrophic cascade.
It seems that mechanical tension would highly correlate with activation. In that,  when electrical signals from the nervous system are telling the muscle to contract, a stronger electrical signal would result in greater contraction and therefore greater mechanical tension.
My theory is that an alternative mechanism could be that the muscle cells sense high levels of electrical activation in type 2 muscle fibers, and it is this which directly triggers the hypertrophic cascade, rather than the cells sensing being physically stretched.
Has any research been conducted as to whether it is the electrical activity itself which triggers the hypertrophic cascade rather than mechanical tension?

An answer for this should be relatively easy to find. If it were so, repeated electrical stimulation should induce muscle mass increase without mechanical load. Does it?

My theory is that this would only be the case if the electrical stimulation is strong enough, and necessarily occurs in high threshold motor units.

It doesn't matter what your theory is. What does the research say? I gave you ample terms to do an effective search.


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What kind of bug is this? Small, slower than an ant, black head, red body
It is very small but it is slower than an ant. It has a black head and six legs with a red body. I’m in North Carolina.

Welcome to Biology.SE. Please [edit] your post to include as much of the following information as possible to improve your chances of getting a good answer: 0) size estimate; 1) photos from multiple angles if possible; 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information — e.g.s: (the building is) in a forest (conifers vs. deciduous), next to water (lake vs. river vs. ocean), etc.; and 4) any other behavior you observed. See detailed tag info page.

It actually looks like a bug to me - a true bug (Hemiptera) nymph.  Unfortunately, it doesn't resemble anything I am familiar with, but luckily there are lots of bug specialists around - someone should be able to point you in the right direction!


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Autoreceptor control of phasic and postsynaptic control of tonic signalling
I have read the following paragraph : "Whereas tonic DA signaling is affected by postsynaptic stimulation/blockade, phasic (transient) release of DA during dopaminergic cell bursting is modulated by presynaptic drug action (Grace, 1991)" in a paper by Frank & O'Reilly, 2006. Whereas I do find evidence that phasic release of DA is negativeley modulated by presynaptic drug action, I don`t understand why postsynaptic would mainly influence tonic DA signalling (and not phasic?). Can anyone help me out here or point me towards relevant literature?
Thank you

Can you provide some surrounding context? What is the book/paper about, what drugs are we talking about, etc.


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Exhaustion of 'memory' CD8 T cells
I've been reading literature on the exhaustion of cytotoxic CD8 T cells. In many of the papers I read, the authors aim to delineate molecular mechanisms that differ between exhausted and memory phenotypes; one such review on this field is the following from Prof. John Wherry's group.
But unfortunately, I could not find any paper that discusses the possibility of recalled memory cells being prone to exhaustion. If I'm not wrong, exhaustion markers like PD-L1, Tim-3, etc. are present on memory cells at lower levels than exhausted cells. But in response to antigenic stimulation (recall response), do such 'recalled' memory cells also start accumulating exhaustion markers like short-lived effector cells? Can someone help me out, please?


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What kind of spider is this (East Texas)?
My wife has seen this spider in a shower in Texas:

What kind of spider is it?
I could not identify it by comparing it to pictures of common spiders in Texas.
Size: It is sitting on corrugated sheet iron in the picture. The legs span from the "top of one wave to the next". The body is "between" the waves.

Welcome to Biology.SE. Please [edit] your post to include as much of the following essential information as possible to improve your chances of getting a good answer: 0) when observed; 1) size estimate (Is there a standard wave length of corrugated sheet iron and what is it?) 2) clearer photos — ideally from multiple angles; 3) habitat information; and 4) any observed behavior. Detailed tag info page. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

This is a fishing spider, Dolomedes genus, from the tenebrossus group (i.e. not Dolmedes Triton).
The picture is not clear enough to reliably choose a species, but it is probably Dolomedes tenebrosus (dark fishing spider) or Dolomedes vittatus (banded fishing spider), both of which are in Texas.


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What is an apple?
Reader : please consider that I don't know anything about biology, which is the case by the way.
Context :  I am currently preparing a presentation for a research grant application, which I will submit to a jury of mathematicians for their decision. My first slide aims to highlight the fact that human beings have a natural reflex to classify the objects around them, and to do this I consider the case of two objects that are a priori distinct, but which are equivalent by convention: they are just two apples (image). To be clear, I need to say why they are equivalent.
Question : Biologically speaking, what justifies that these two a priori distinct objects are indeed two apples, and therefore biologically equivalent? As a biologist, what is the justification you would give to say these two things are quite the same?

Well, personally I wouldn't. The distinctions made in biology go down to the molecular level, we differentiate between the colour red and the colour green on a macro and micro levels. Also on the differing effect the colour has on a species that likes apples - not just humans, that is we'd be looking at the item in context of the environment too. Then there's the evolution of how the differences came about .... it goes on. Doesn't this more come down to a [philosophy.se] question than a biology one?

I’m voting to close this question because it is about ontology and the philosophy of classification. Replace the apples with any two similar-but-distinct objects and the question remains the same. Perhaps there is an on-topic interpretation of this question regarding taxonomy, but it's not clear to me.

On reflection, you might want to take a look at our [psychology.se] stack. If asking there, you'd need to be sure to frame your question in existing models of perception and language.

I agree this is off topic. However, you got some answers anyway before being closed that you seem to indicate appreciating and wanting to employ in your presentation. Just a reminder, then, that I think you should plan to be citing these users as your original source(s) for these ideas (especially since the answers you got are less biological fact and more ontological discussion).

How do you know they are not snapples?

@user338907 proving yet again that there is a relevant XKCD for just about every question on Stack Exchange.

Biologists aren't the people who decided what an "apple" is, the general population of users of language are.
You could try back-create a definition that is biologically relevant based on descent, for example "fruit of plants in the genus Malus", but that would include a lot of apples that aren't really apples the way English speakers in general use the word.
You could limit it to just fruits of Malus domestica, but that probably wouldn't work great, either, because there are several fruits outside that species that a typical English speaker would still call "apple".
A relevant botanical definition is that an apple is a pome:

A pome is an accessory fruit composed of one or more carpels surrounded by accessory tissue. The accessory tissue is interpreted by some specialists as an extension of the receptacle and is then referred to as "fruit cortex",[2] and by others as a fused hypanthium (floral cup).[2]

...but many botanical fruits of this type are not "apples" in the English use of the word, such as pears or hawthorn.
It happens a lot in language that biology and culinary or other language issues conflict, for example the "is a tomato a fruit?" debate. There are also other popular language classification quirks that people debate on the internet like "is a hotdog a sandwich?". These are all questions about language and how language is used, not about any biological or other scientific essence of things.
Biologically speaking, your brain learning these things is a lot like how an artificial neural network is trained to, say, identify road signs. Just like when you complete "Captcha" tasks to "prove" you are a human when acting online like "select all images with a stop sign in them", and this training data is sent to an AI algorithm, as a developing human the adults around you will hand you things and say "apple". You then assign a little slice of all the features you perceive and associate those with the concept "apple" in your brain. They're also correct you and say "no, that's an orange" if you expand your definition beyond "apple", and you'll learn to break associations between those orange-specific perceptions. In this way, the things you call "apple" are just the things that other people call apple, and that's how we can use language to communicate with each other: as long as we all mean roughly the same thing when we say "apple", it's a useful concept, even if it doesn't make sense biologically.

Thanks a lot for your answer. I accepted this one because it answers my question perfectly !

I think one thing you are overlooking is that humans employ hierarchies of classification. We group things at multiple levels depending on the degree and types of similarities. In the picture you've provided the two images are the same in the sense that they are both examples of the genus Malus:

The fruit is a globose pome, varying in size from 1–4 cm (1⁄2–1+1⁄2
in) in diameter in most of the wild species, to 6 cm (2+1⁄4 in) in M.
sylvestris sieversii, 8 cm (3 in) in M. domestica, and even larger in
certain cultivated orchard apples. The centre of the fruit contains
five carpels arranged star-like, each containing one or two seeds.

They are different in that one is perhaps an example of the variety Delicious, and the other is perhaps of the variety Granny Smith. The two varieties differ in skin color and taste among other attributes, but share many of the attributes associated with the broader category of genus Malus.
They are also different in the most abstract sense because they are two different objects.
Which classification is relevant depends on context. If I'm making a grocery list the variety is the most significant classification. If I'm writing a fairy story the genus may be all that's relevant.

Your answer is very clear and helped me to think about what I should say to introduce this topic. Thanks :)

My answer: based on DNA similarities I can confidently tell you whether two "things" are so similar they merit similar names.
Other points to mention: We might call two things similarly without necessarily implying that they are the same thing (e.g., a giant panda and a red panda). Both of those pictures are apples because they look, taste, and feel like an average apple and we decided on that before we could check their DNA. There's a Stanford lecture on Human Behavioral Biology that discusses how we humans tend to categorize objects into groups to ease information processing that you might want to check out.

That lecture seems really interesting !  Do you have a link ? I didn't found it ...

You can find it here https://www.youtube.com/watch?v=NNnIGh9g6fA&t=3s


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Larval abalone devlopmental times - what does ~ °C.days or °C hr-1 mean
I'm looking a number of papers on abalone larval development and the term °C.days or °C hrs-1 keeps coming up. The numbers before these terms are much larger than they would be if this term actually meant days or hrs. For an example of a publication, see here.
for example one source said larvae are competent to settle at 100 °C.days, however they most likely settle at around 7-10 days
Just wondering if anyone knows what this °C term means in terms of time

Welcome Dr Who Fan. :) Could you find a way to link to a source for this seemingly odd notation, to let us see context in case there's some clue?

From e.g.
Fukazawa, H., Kawamura, T., Takami, H., & Watanabe, Y. (2007). Oogenesis and relevant changes in egg quality of abalone Haliotis discus hannai during a single spawning season. Aquaculture, 270(1-4), 265-275.

Oogenesis of abalone Haliotis discus hannai was examined histologically during a single spawning season using broodstock of various maturation conditions, which were controlled by effective accumulative temperature (EAT)

Once adult abalone have experienced an appropriate EAT, they can release gametes when they are stimulated by environmental spawning cues, such as storm events (Sasaki and Shepherd, 1995)

The units on their figures are given in units of "temperature x time", such as "°C x days". This would be integrated temperature over time. In units of °C x days, you would say that 1 day at 20°C = 2 days at 10°C = 10 °C days.
In this context, we're talking about a mollusc that has a seasonal reproductive pattern where temperature controls reproduction, but not simply via hitting some key temperature one time (which would likely be unreliable and lead to spawning in the wrong season given the possibility for temperature extremes), rather by integrating temperature over time. Once the threshold is reached, other cues trigger the actual spawning behavior.
I presume "°C hrs-1" would be "°C hrs-1" which can also be written "°C/hrs" or read "degrees celsius per hour"; that would be a rate of change of a temperature, but you'd need to provide context to verify.
The authors of the paper I link to write in their methods:

EAT was calculated using the formula defined by Kikuchi and Uki (1974).

...but the paper they refer to is in Japanese. It's not clear to me exactly how EAT is defined, but it's quite possible it involves subtracting a reference temperature that is somewhat above 0°C. Hopefully some of the papers you are reading are more clear about this.

(+1) Things are a little clearer here, maybe.  "EAT (effective accumulative temperature) is expressed in
degree days (◦C-days) and calculated by subtracting the BZP from daily
water temperature and summing this value over the rearing time (in
days).  The effect of temperature on gonadal development is cumulative above a certain
threshold temperature that varies between species. This threshold
temperature is termed as biological zero point (BZP; a theoretical minimum temperature at which gonad growth and development begins)"


text:
How do algal blooms deplete oxygen?
How do algal blooms deplete oxygen and kill marine life? Don't they release, not consume oxygen as seaweed does? Different types of algae function differently in that respect, don't they? If they need the same things as plants (nitrogen, phosphorus), they should function the same way as plants, I thought
See, I'm trying to understand eutrophication. This webpage says it occurs

when night-time respiration of large blooms depletes oxygen from the surrounding water

and

can also occur at blooms termination, during which bacteria break down the dead algal material deplete oxygen from the water

I'm pointing this out so that you don't close this question as a duplicate of this one. It's apparently not only something that happens only as a result of algae decomposition

Is it true? Do growing algae deplete oxygen too, not only bacteria that decompose them after they die?

In case that website is wrong why don't releasing oxygen by algae and consuming oxygen by bacteria as algae decompose balance each other out?

Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your post accordingly. In particular, quotes must be referenced — this is considered good practice in scientific communication and will help other users understand the context for the quote. In addition, each post should have a single clear question that includes: where you've looked for answers, what you do know about the topic (with references to reliable sources), and where exactly you still have questions.

@tyersome I forgot to add the link (I wrote "this", it was indicative of my intention to do so)

@anongoodnurse I specifically addressed that

Why does it not answer your question? Add to that, "What do plants do at night?" You've answered your own question; O2 is consumed in greater quantities than produced.

@anongoodnurse well, at any rate there's no answer that addresses all the raised points, neither here nor there

There is, but you seem to not be able to see ti.

@anongoodnurse See the comment of the user with the nickname Resonating under one of the answers. He asked one of my two questions, but no one replied

Do you know why? I'll be blunt here, and I'll explain. It's because we all know why and you just don't get it. We're trying to help you all by giving you clues without just feeding you the answers like pablum. We're professionals here, and we have a mindset of people doing some thinking for yourselves. There's a saying, "God helps those who help themselves." We aren't Gods, but we do want you to work at it a bit. See those upvotes by my comments? It means someone agrees with me. The answer is right under your nose!


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Anyone able to identify this mite?
Located in a chicken coop crawling on windows. I’m guessing this is a bird mite as I’m only seeing them at night on the coop itself, but want to confirm so that I’m able to treat them effectively. I was able to get this picture by using my microscope with the 10x lens. The size of a grain of salt. Located in Wisconsin.

Welcome to Biology.SE. Please [edit] your post to include as much information as possible to improve your chances of getting a good answer: 1) closeup photos of the organism from multiple angles if possible; 2) how you acquired this image (it looks like you may have used a dissecting scope?) and what magnification you are using; and 3) an estimate of the size of the organism. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

to get rid of bird mites you can use https://en.wikipedia.org/wiki/Diatomaceous_earth i have used it myself in our chicken coop and it is effective against mites.if you take a look at the ceiling where your chickens rest at night you will find a lot more mites.

Thanks! Just dusted with DE tonight. I bought elector PSP so I wouldn’t have to mess around, but here I am messing around. Sprayed yesterday for the second time. They are relentless.

Your Answer : (CM/Red Mite) https://entomology.ca.uky.edu/ef516

Sorry, without actual access to the mite, identification is practically impossible - there's just too many different species it could be to actually choose one. As for control, clean the coop regularly and dust with diatomaceous earth to kill any remaining mites.


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What are some experimental techniques to identify binding partners?
What experimental techniques can be used to identify binding partners for a given protein? I know that if you have some candidates that may bind to a given protein, then you can use techniques such as pull-down or coimmunoprecipitation to determine whether the protein binds to those putative binding partners. But can you screen for its binding partners when basically there is no knowledge on what the given protein might bind to?

Welcome to Biology.SE, Cactus. I think the operative search term is protein-protein interactions. Googling how to detect protein protein interactions gives multiple websites that list and describe many methods.

BioID comes to mind.

I will
(1) obtain antibody of said PROTEIN (search catalog or custom-made).
(2) pull down said PROTEIN with antibody and techniques you mentioned.
(3) identify other proteins in the pulled-down complex with following method:

(From here) There are two main methods of amino acid sequencing:
mass spectrometry and Edman degradation with a protein sequenator.
Automated Edman amino acid sequencers are offer convenient analysis of
polypeptides of up to 50 amino acids long. This process is generally
characterized by seven steps:

Break apart disulphide bridges in the protein with a reducing agent
Separate the protein complex and purify the chain(s)
Determine the amino acid composition and terminal AAs per chain
Fragment each polypeptide chain
Recreate the AA sequence using these fragments
Repeat with different fragment patterns to mitigate errors

Identification via mass spectrometry is increasingly preferred as it
overcomes many of the established limitations of Edman degradation.
But there are various techniques within protein mass spectrometry that
make amino acid sequencing via MS techniques harder to define in
brief.


text:
If Myxozoa is animal, so what is really animal?
I read about the new discovered creature call Myxozoa and it say that Myxozoa is animal because of it possess cnidocysts like other cnidarian. But why doesn't it is a converge evolution ?
Myxozoa doesn't fit one of the most important characteristic of animal kingdom, "Multicellular". I know that all multicellular creatures aren't animals but all animals are multicellular until I read about Myxozoa.
Characteristic is like a rule without even a single exception for any specific group. Something that most of the group have in common, for example, "true tissue"(except sponge), "has limit life span" (except immortal jelly fish) etc. are important property that most of them have in common but not characteristic since some of them don't have.
I know it is hard to find any thing that all animals have in common without even a single exception for any specific group but it is important. We do need a check list to check if any creature is animal or not and to separate it from other eukaryote.
Here is my check list for animals which is from many source and my knowledge of all animal group which I try to separate animal from other eukaryote.

Eukaryotic
Multicellular in all part of the life cycle except zygote state
Heterotroph (No chloroplast but can be symbiosis with other creatures that have chloroplast.)
Motile (relocate entire body) in at least one part of the life cycle
No cell wall
Aerobic respiration (has mitochondria)
Has tissue - Has basic tissue (like sponge) or true tissue
Have at least 5 different type of cell that do different job in at least one part of the life cycle (Sponges, comb jellies, Placozoa, Cnidaria and Xenacoelomorpha have more than 5 different type of cell. All more advanced bilateria animal obviously have more than 5 different type of cell. All Choanoflagellate have less than 5 different type of cell.) and at least 5 different type of cell that can communicate with each other.

I know I might be wrong but we really a check list to separate animal from other eukaryote. This is the best check list that I can make.
Myxozoa will not fit three of these list, "Multicellular", "Have at least 5 different type of cell that do different job in at least one part of the life cycle" and "Aerobic respiration" (A Myxozoa species call Henneguya zschokkei doesn't have mitochondria.). And if these characteristic is removed, we will not unable to separate all other eukaryote from animal.
Myxozoa should be another protist with its own group but not animal. I think it can possess cnidocysts due to the converge evolution or obtain cnidaria cnidocysts gene through horizontal gene transfer in some way in hundreds million years ago.

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

Using the traditional taxonomic approach that contain the familiar kingdoms rank (e.g.animalia), has grown increasingly unpopular due to known inconsistencies in relatedness of lumped species when observed from a genetic and then phylogenetic approach.

A cladistics approach (using Phylogenetic nomenclature)   lacks categorical ranks such as "kingdoms" & instead uses hierarchical group names based on nested ancestral synapomorphies. Generally ~6 informal supergroups (sometimes called "suprakingdoms") have been recognized based on phylogenetic research. 1 such group (i.e., clade) is the Opisthokonts that include animals + fungi. Not so simple anymore...

@theforestecologist please continue in chat.

First multicellular is not always a defining characteristic of animalia, protozoa used to be included in animalia.
Second you are falling for a issue a lot of young biology students run into, Taxon separations are subjective historical artifacts, and don't really make a lot of sense. Taxon do not need to be monophyletic although it is encouraged. Taxonomic rank is becoming more a way of organizing names and less a reflection of evolutionary relationship. This is one of many problems with trying to keep archaic names and taxonomic approaches, it does not fit well with the current understandings of biology and the system is creaking under the weight of historical baggage.
This is one of many reasons cladistic approaches to taxonomy is being used more and more, it is at least internally consistent and reflects the complexity of life.

Yes, the protozoa and very small used to be call animalcule. But once we know more about them, we can separate the protozoa from the animal and get the better characteristic of animalia. I thought that the more knowledge we have, the better characteristic we get. Apparently, I am wrong. It is weird that at some point, the more we know about animal, the fuzzier the boundary between animal and protist is. And at some point, the characteristic doesn't work any more.

@NawatNakhon actually that makes complete sense when you think about evolutionary history, as you go back in time the line between every group is eventually just the fuzzy line between two closely related species. At one time protists and animals  actually WERE the same thing they had not diverged yet.


text:
Is there a good protocol for bilateral decortication in rodents?
I was thinking about using bilateral decortication in rodents (preferentially mice) to study the roles of certain brainstem areas in cognitive tasks in the absence of cortex. However almost all studies I could find with bilaterally decorticate rodents date back to at least the 1980s if not older. Is there a specific reason for this? Also, do you guys know of any relatively recent protocol for bilateral decortication in rodents?

Probably seen as a bit ethically questionable these days, without a particularly keen need/reasoning. Also techniques are preferred to be able to temporarily turn parts of the brain on and off, for example with optogenetics, DREADDs, etc.

@BryanKrause - this is akin to answer in comment. Insert a few links here and there and (at least) I would be happy with this answer. Otherwise you might wish to delete the comment?


text:
Beneficial effects of the fungi of a termite mound on the diseases suffered by the termites
My motivation to join this Biology Stack Exchange is the article by David Pride that I've read from the Spanish edition of Scientific American, that's Investigación y Ciencia. The article is [1], and I think that is a very good work from the author and editors of this popular science magazine.
Question. I would like to know if the fungi of a termite mound have beneficial effects on health (related to diseases caused by viruses or bacteria) for the termites that live in the termite mound.
I add that Wikipedia has the article Fungus, and what's I evoke with my Question, is about if some species of fungi could live with the termites inside the termite mound and have beneficial effects on the diseases suffered by the termites. I don't know if this question is in the literature, feel free to answer my question as a reference request if you know references answering my question.
References:
[1] David Pride, Los virus de nuestro cuerpo, Investigación y Ciencia, Febrero 2021, Nº 533, pages. 76-83.

I'm mathematician. If you think that you can to improve the post (tags, grammar...) please do it. If you think that the post isn't suitable for the site add a comment that I can to delete it in next few hours. Feel free to add your feedback about the question in comments. Many thanks.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions are best received when they are clear and demonstrate significant prior research (tell us where you've looked for answers, what you do know about the topic). Also, the Investigación y Ciencia article is about human viruses not fungi or termites, so can you please clarify what in that article is relevant to your question? Finally, your last paragraph seems to mostly repeat the "Question" ...

Welcome! To find articles on this try the keywords “termite fungus symbiosis.”

..and mathematicians can develop into truly useful bioinformaticians.

Many thanks for your feedback (the keywords) and the comments of previous users about general information of the site. Next time I improve my posts. Many thanks all for the welcoming @PolypipeWrangler  (I am no longer young to continue studying).

I would like to add a thanking message for you @PolypipeWrangler and your colleagues of the site for this friendly welcoming, I add some subjects that I'm interested (don't related to this post but I share these for the friendly attitude of the users) because are curious, for example the hygroscopic property of honey; the Wikipedia article dedicated to Sepiolite in relation to processes for bacterial transformation, as refers the last phrase of this article dedicated to sepiolite; and I'm interested at the origin of life and diseases,... Isn't required a response, good afternoon to all users

In at least one case termite cultivated fungus produce antibiotics that benefit the termites and protect them from dangerous fungus. Of course just the fungus acting as food is also a huge benefit to the termites.
https://www.nature.com/articles/srep03250

As soon as I can (with score of 15 or more of reputation), I'm going to upvote your answer. I'm going to visit the page of Nature, and I'm accepting your answer.


text:
What's this stuff that looks like white chainmail armor growing on giant kelp?
I found some giant kelp coated with a material that is white, smooth, and forms a chain-mail pattern with small black oblong lumps in between the links. It feels pretty hard but not stiff (the kelp still flexes), and can't be easily removed from the kelp skin. The leaves under the coating appear to be stunted and malformed.
This was found in the Pacific in Southern California in the late summer.

I took a photo with a low-quality microscope.

Is it a parasite?

That looks like it could be the lacy crust bryozoan (Membranipora membranacea). That bryozoan is an epiphytic animal whose native range includes the Pacific coast; it does not feed on the kelp, but can weaken and damage it when abundant 1. Whether you should call this a parasite seems somewhat definitional and is something I'll leave to an ecologist to answer.
For comparison see the following public domain image from the USGS:
 Apparently photographed by: Eugene van der Pijll
In addition to the wikipedia article, you may also find this page from the Texas Invasive Species Institute to be of interest.
References:

North, W. J. (1976). Underwater California (No. 39). University of California Press.


text:
Does inactivated COVID vaccine also contain mRNA that is active in human body?
Inactivated vaccine primarily relies on proteins to elicit immune responses. My question is, does inactivated COVID vaccine also contain mRNA that could be actively transcribed into new proteins in human body, similar to those mRNA vaccine?
To my knowledge, the mRNA in mRNA vaccine is slightly modified such that it can be transcribed. Without those modifications, can mRNA in inactivated vaccines still be transcribed? If the answer is yes, then, is the concentration of active mRNA high enough that the transcription activities can be detected?

Short answer: no. Basically all the inactivated vaccines use cross-linking agents that will cross-link or damage the RNA (e.g. aldehydes, Beta-propriolactone or ethylene imine) through a chemical reaction. Many of these sorts of vaccines are then formed into subunit vaccines which undergo extensive purification to get the antigenic protein of interest.
A reasonable reference for this is (also the second link above):
Iris Delrue, Dieter Verzele, Annemieke Madder & Hans J Nauwynck (2012) Inactivated virus vaccines from chemistry to prophylaxis: merits, risks and challenges, Expert Review of Vaccines, 11:6, 695-719, DOI: https://doi.org/10.1586/erv.12.38


text:
Nei's gene diversity - calculation
I am completely new to biodiversity.
I have a question: how do I calculate Nei's gene diversity?
The formula I was given is H = 1 – Σpi2
I have an excel file with 3 different loci (Pgi-2, Pgd-2, Pgm-1). I will attach a screenshot of the table as I have no idea what I have to do. How do I calculate H for the loci?
Thank you!

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details and then delete or [edit] your post accordingly. In particular, this doesn't seem to be a question about biology as defined in the help — instead you appear to be asking about how to apply a formula. Who gave you the formula and is there some reason why you haven't asked them? Note that prior research is expected for all questions on this site, so this seems to be doubly off-topic.

It seems like you need to determine the value of $\pi^2$ for each locus, sum them, and subtract from 1. For ideas of how to estimate nucleotide diversity ($\pi$) see here. Also: your question would be significantly easier to understand if you used the built-in LaTeX math tools, or really any unambiguous math notation.

I’m voting to close this question because it is: 1) not about biology as defined in the help; 2) shows insufficient  evidence of prior research; and 3) lacks clarity.

The formula you were given is not Nei's genetic diversity.

Rather $$1 - \sum_{i=1}^R p_i^2$$ is the Gini-Simpson index. $R$ is the richness, or equivalently the number of genotypes in the data. Each $p_i$ is the frequency probability of the $i$th genotype.

You can find a description of Nei's genetic score here.

What are the integers in row 3 of the spreadsheet? Different alleles of the same gene?

Please use markdown instead of images to show us tables. It takes up less server space, and makes it easier for us to show you the calculation on your data. You can copy-paste your data into a table generator, such as here and just copy paste into your question.

Do you want to calculate Nei's score, or Gini-Simpson's score? They are not the same.


text:
When do retinal cells stop differentiating?
I am having a hard time recalling where I had heard this, but I do recall someone saying (perhaps in a video) that cells in the retina divide very rapidly during infancy due to ongoing development of the eye - they were saying this as a justification for the incurrence of mutations in the retinal cells of infants. I searched this up recently and can't find any source that supports this claim. I did learn that there are stem cells in the retina that remain after birth, so I was wondering if the person meant to say there are lots of undifferentiated cells in the retina of infants. I think the more holistic question that I should be asking is: why do eye conditions like retinoblastoma develop primarily in infants?
If it is because of a large number of undifferentiated cells in the retina of infants, can I also be let known when (i.e. at what stage in life) these undifferentiated cells exist in highest number and when they all (or at least mostly all) become fully differentiated?

I see three different questions in one post; adding some of your own research background is a great way to focus the question and specify a single question, which is better answerable in the Q&A format of the SE network. You can post multiple different questions if need be, but please add your own research efforts in regardless.

why do eye conditions like retinoblastoma develop primarily in infants?
One explanation is that infants grow fast. In general, each cell division is a risk of breaking/losing chromosomes. Breaks need to be repaired, but that can be faulty and lead to cancer. This explains why infants get cancer in general.
Retinal cells may be especially prone to DNA damage since there is no pigment to reduce damage by UV-light.
When do they all become fully differentiated?
They never become all differentiated. Many tissues contain adult stem cells that keep their stem-cell state until death. Their purpose is to regenerate tissue, especially when tissued need to be constantly renewing themselves (e.g. skin, intestines, and maybe retinal stem cells, too ).  (Reh et al.)
when (i.e. at what stage in life) these undifferentiated cells exist in highest number?
The highest ratio of undifferentiated/differentiated is probably found during embryonic development.

In some vertebrates, the development of the retina continues throughout life (Bhatia et al 2010)


text:
Is this a wasp nest?
Under a tree in an area often sunny, but not sunny enough for grass to grow, and also often humid, but not sufficiently so for moss to propagate, the two plants have left just enough of an ecological niche for a member of the animal kingdom.

Do you recognize this nest? Are these ants? Are they wasps? Should I be wary (of carpenter ants, of a particularly angry type of wasps)?

Where was this picture taken, and when? What type of soil is it? Have you seen anything unusual around? There are many, many different kinds of ants, ground wasps, and other species that dig holes in the ground. Some are aggressive, others not. Until you see something going into the hole or coming out of it, I wouldn't worry about it.

In addition to MattDMo's comment, holes are often re-used, so the critter that made a hole may not be the current resident. If you're looking at a substantial nest of any social hymenoptera you're going to see the occupants coming and going regularly. Less so among solitary species (which are also not typically aggressive).

A neat trick I've seen is to push a little dirt over the hole and wait to see what pushes it clear again, that'd give you an answer. If you can set-up a camera to take time-lapse snaps of the hole, that would be even better than sitting staring at it for hours.

@JiminyCricket. I might not suggest that for a yellowjacket nest, but in that case you're likely to see guards as well as foragers coming and going.

@BryanKrause - It's fine to test, just be ready to run far away and fast. How aggressive a wasp is (towards a disturbance of a nest) is proportional to the size of the nest. If it's a small nest, a wasp might only repair the hole. If it were a large nest, there would very likely be visible activity all day long. So the risk is low.


text:
Why does a non-functional retinoblastoma protein cause tumours in the cells of the retina specifically?
I know that the name of the protein itself is the retinoblastoma protein - but that's only because the result of a pathogenic variant is retinoblastoma. I'm trying to kind of reverse engineer the name and figure out: why would a non-functional Rb protein (since the Rb protein is crucial to the cell cycle of all dividing cells in our body) primarily manifest itself in the form of an eye tumour? Is there anything special about the cells in the retina that make it more prone to developing such a tumour in relation to the function of the Rb protein?
Would anyone have any insight to offer?
Thanks.

From Wikipedia:

The retinoblastoma protein ... is a tumor suppressor protein that is dysfunctional in several major cancers

So, although it's commonly associated with retinoblastoma, it's not limited to a particular type of cancer.

Retinal cells are not sloughed off or replaced, and are subjected to high levels of mutagenic UV radiation, and thus most pRb knock-outs occur in retinal tissue (but it has also been documented in certain skin cancers in patients from New Zealand where the amount of UV radiation is significantly higher)

Since the gene is commonly damaged from UV radiation, the retina is particularly vulnerable. UV radiation does not penetrate very deeply, but the retina is exposed to light per its function.

Two forms of retinoblastoma were noticed: a bilateral, familial form and a unilateral, sporadic form. Sufferers of the former were over six times more likely to develop other types of cancer later in life, compared to individuals with sporadic retinoblastoma.[10] This highlighted the fact that mutated pRb could be inherited and lent support for the two-hit hypothesis

The two-hit hypothesis is the idea that often one functional copy of a tumor suppressor gene is sufficient. For people with familiar cancers involving tumor suppressor genes, including the BRCA genes associated with breast cancer, usually what you have are people who are heterozygous for some non-functional version of the gene. That means that they only need one "hit" to the functional gene to facilitate development of cancer.

pRb restricts the cell's ability to replicate DNA by preventing its progression from the G1 (first gap phase) to S (synthesis phase) phase of the cell division cycle

Because pRb is associated with G1 to S phase transitions, you wouldn't expect it to be as important of a gate in differentiated cells in G0; that's why you're finding it in a childhood cancer: the affected cells need to be immature and dividing to be affected.
In summary, Rb loss-of-function mutations occur via UV damage. To be vulnerable to this damage, a cell needs to be actively dividing and exposed to UV. The developing retina fits these characteristics. People who inherit one non-functional Rb copy are much more likely to develop cancer, because they only require additional damage to one copy of the gene, not two.


text:
What are the differences between dual vector CRISPR/Cas9 lentiviral plasmids Lenti‐Cas9‐2A‐Blast and lentiCas9-Blast?
There are multiple  widely-used plasmids for using CRISPR/Cas9 with a dual lentiviral vector strategy (Cas9 & sgRNA on different vectors) in mammalian hosts with a Blasticidin selection selection marker.
In particular:
Lenti‐Cas9‐2A‐Blast(#73310) and lentiCas9-Blast (#52962)
What are differences between the two? Which vector is recommended (for use in mouse small intestinal organoids) and why?

You will have to include a lot more details about your protocol in order for anyone to give you pros and cons abot those two vectors. What kind of mammalian host? Please edit your question accordingly.
If there's a protocol in your lab, just use that one and see if it works. But I recommend that you do your own research and learn about the purpose of each and every entry of both plasmid-charts, so you know what you're doing.

I tried to to ask the question in way that the answer is useful for many people, but I included the host now.

It might also help if you add the type of host cells that produce your lentivirus.

I see these differences in lenti-Cas9-2A (compared to lenti-Cas9):

Absence of a bleomycin resistance. That just affects cloning
Changing from a CMV- to a RSV promoter for lentiviral mRNA production: That promoter is used for the host cells that produce your lentiviruses. They might react differently to different promotoers. So in the end, your viral titers might differ, when switching these plasmids.
Changing from a bGH- to a SV40 polyA signal  polyA signal. That might affect (production and) half-life of lentiviral mRNA both in your lentivirus producing-host cell culture and your mouse small intestinal organoids after transfection. You might want to start your research here: Humes et al. 2020

Together, I think both plasmids should work just fine. I'd say that the observed differences affect mostly how well your host cell culture performs in producing lentivirus. And these difference might differ a lot between cell types. But like I said, it's just the lentivirus production. If you got enough virus to apply to your mouse organoids for gene editing, it doesn't matter.


text:
help with mushrooms identification
I know that mushrooms identification is a difficult process. but I would like to ask for help in the identification of this one.
It growth over the grass in a backyard on Toronto, Canada.

If you still have access to the mushrooms, it would be helpful to know the spore color. In case you're unfamiliar with how to find this out, you can take a 'spore print.' Remove the cap from the stem, place it on a piece of paper (or preferably aluminum foil), cover it with an upside-down glass, and wait at least 8 hours. The cap will deposit spores on the paper, and you will be able to see the color.

Amazing picture, by the way. These are very photogenic.

Added the spore print. Thank you for the instructions.

Brilliant. I would call that black from the picture, but do you see any tones in it?

This is most likely a member of the genus Panaeolus, based on the black spore print (distinguishing from Psilocybe and Conocybe), growth in grass (distinguishing from Psathyrella and Naematoloma), small stature and thin stem, bell-shaped cap, brown cap and gills, and lack of a ring on the stalk (David Arora, Mushrooms Demystified). The gills in the photo appear mottled to me, which is a diagnostic feature.
Unfortunately, species in this genus are especially difficult to identify. Michael Kuo writes on Mushroomexpert.com:

Beyond a few "easy" species, identification in Panaeolus requires microscopic examination, a good interlibrary loan desk, and the ability to read French and German.

Panaeolus foenisecii is a common member of this genus with macroscopic characteristics that match your specimens (see Mushroomexpert.com and MykoWeb for detailed descriptions). The cap in this species changes color when waterlogged, which would be worth noting if you see it again. However, I am unsure of this ID without microscopic observation.

Panaeolus foenisecii. Image: Michael Kuo, Mushroomexpert.Com.


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Is there a risk that genetically modified organisms displace genes of other species via horizontal gene transfer?
It is known that species can rely on certain genes to survive. See for example this publication.
An argument often made by environmental groups is that genes introduced by genetically modified organisms can spread via horizontal gene transfer and could potentially displace native genes and thus lead to extinction of organisms. Are there any publications which support that assertion?

[converted from a comment that got unwieldy]
Why necessarily HGT and not simple breeding? There is a term genetic pollution for this, looks like it's somewhat controversial as an environmental issue but it seems a more readily available means (and undoubtedly happens at some rate).
HGT of e.g. microbial antibiotic resistance is well-founded, but there's not much evidence that lab antibiotic resistance genes are anywhere near as good as "natural" resistance genes. We tend to just use stuff that's already in nature.
One might look at glyphosate resistance in weeds, given the very high rate of glyphosate usage and glyphosate-resistant agricultural varieties. However that linked 2005 USDA report doesn't even bother to mention introgression from ag varieties, instead focusing on the much more numerous weeds that are naturally resistant, or have evolved resistance in response to glyphosate pressure in the field. Here is a more recent pop science article arguing that weed evolution is by far the most acute problem in this case.
So it's formally possible that genes escape from GMOs to the wild, but I'm not sure that there are any reports of genetic pollution actually being a "problem" from an environmental point of view (at least relative to the much more prevalent naturally occurring resistance).
There are of course still plenty of good reasons not to use glyphosate resistant varieties or antibiotics more broadly! There is some evidence of a glyphosate-cancer association, and more generally relying on these tools to support industrial monocultures has tons of environmental problems. Glyphosate application is almost certainly contributing to extinctions. It's more that this particular objection to biotechnology (GMOs escaping and outcompeting non-GMOs) isn't too convincing.

Horizontal gene transfer is a poor argument against green gene-technology. Like most arguments, it boils down to "The method in general is totally fine, it's just Monsanto that's evil, since as a monopoly, they do/did whatever the f*** they want".
The problem of horizontal gene transfer would be solved by transforming not the nuclear genome, but chloroplasts (Ruf et al.2021). By doing so, plants that reproduce in the wild "dilute" the transgene with each subsequent generation. However, this technique isn't seen in the industry.
I know that my botanics professor mentioned chloroplast transformation in a one-hour rant about the unfairness/stupidity towards green gene-tech. He also stated that restrictive laws allowed Monsanto to become a monopoly, which freezed any progress in this kind of industry. RoundUp everywhere.
Chloroplast transformation seems really promising though (Siddiqui et al 2020).


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What is the latest estimated probability for the self assembly of a primitive cell?
Peusner (Concepts in Bioenergetics, 1974) estimated the probability of the self-assembly of a primitive cell as $10^{-254}$. Given how much more we now know about cell biology, what is the latest consensus figure? I've found lots of papers and discussions about the mechanics but I haven't seen anyone else put a figure on it.

Is a primitive cell a protocell or protobiont in this context, or more like a modern cell as we find them today? Or something else?

I hate to say it, but if you can’t find such a figure, nobody here is likely to — probably because such calculations are not testable and have no relevance to experimental biologists. And why give a link to the Wikipedia entry for “cell biology”?

@Galen The best description I've found is "partitioned units resembling modern cells."

@David Surely it can be modeled?

I imagine so. But the devil is in the assumptions. It's all so much medieval theology — angels on dancing on the head of a pin. Biology is a practical subject.

@David I can't believe no-one's even ball-parked it though, there must be someone who has run the numbers.

It is easily the case that no one has 'run the numbers'. As David points out, there are different combinations of assumptions one can make. I rate them somewhere above "medieval theology" since we can impose physical laws and established statistical trends, but  even so they are quite varied and speculative. Even if some calculations have been done, it isn't clear how a 'best' figure could be chosen.

@Galen I can't quite dismiss it as theology either. Surely it's a significant factor in the estimation of the extent of extraterrestrial life?

There might be a marginal probability of life forming in a uniformly sampled region of space, but I doubt we are close to having such a number that we can have confidence in. Assembly theory seems like a more promising approach to identifying biosignatures, but that approach is still in its infancy.

I think an explanation of why this would be almost impossible, as a 'frame challenge', would be useful. .

See What is a frame challenge? and Does Stack Exchange allow for answers which question the validity or stance of the original question?.

@user438383 It's possible to estimate badly but it's not impossible to collate all of the developments of the last 50 years and update Peusner's estimate. If he was even half right then we are alone in the universe so it's not an inconsequential question.

@Jack - Does it really matter if we are alone in the universe? Does life elsewhere out there give meaning to our existence? If a million lifeforms exist that we will never encounter (a strong possibility, that latter phrase), does it mean our lives are less meaningful? It's interesting to speculate, but that's all it is, speculation.

@anongoodnurse It matters in the sense that it ceases to be an area of worthwhile research.

@Jack - I'm not sure of its worth right now. We have war, poverty, disease, starvation, lack of potable water, etc. Many things to take care of at home on our little watery rock.

It's not a useful question, as a majority of the discussion above has been trying to point out to you.

@MattDMo Of course it’s a useful question, because it’s a proxy for how much we actually know about the associated processes.

It's not a useful question for this site. It has 3 downvotes and 5 closure votes (some may be by the same people). I'd say that's a pretty clear consensus by the established users. And, as Maximilian points out in their answer, it's not the only way life could have evolved, so I'm not sure it's that useful in general. At any rate, I'm not going to debate this any more. You asked a question in a comment, I answered it. You can agree with it or not.

@MattDMo But how would you even compare two different accounts without calculating either probability? This makes no sense.

I think that it's worth directly examining the citations of the book in question.
In doing so, I found the following quote:

The abundance of the first 31 elements in the Periodic Table on Earth and in the known universe is highly correlated: Peusner [11] estimated the self-assembly of a primitive cell occurring as a spontaneous act, where the molecules and elements were present at a specific location on the Earth in a suitable sequence, as 10−254. Conversely, even a highly improbable event can occur. This only adds to the paucity of information and the confusion we struggle with when researching the origin of life. According to Peusner [11] this suggests the origin of life and evolution occurred in an ordered manner from the simple to the more complex.

In other words, there is a counterfactual to "self-assembly of a primitive cell" for the origin of life. Peusner himself seems to have considered this a somewhat ridiculous straw man according to this reading, not that I've directly read his book- in other words, abiogenesis via spontaneous generation of cells isn't constantly happening all around us, which hopefully isn't news to anyone.
Instead, the argument goes, you could gradually add components until you ended up with a primitive cell. This would presumably involve a sequence of still-improbable-but-much-more-probable events. This would presumably involve the RNA world or other such cases as intermediate steps to a cell. I am not sure what the probability of such things is, but there does seem to be some amount of speculative literature on this out there.
NB: I infer from the comments that you are mostly interested in xenobiology and the probability of other life existing, and are only interested in the cell assembly probability as the presumed path to the existence of life elsewhere in the universe.

'gradually add components until you ended up with a primitive cell' sounds ridiculously panglossian without any math derived from established biological and physical processes. With 50 years' of additional research, we must be able to make a more educated guess, but it seems like the answer to my specific question is that there is no more current estimate.

@Jack I think the point is that it's less panglossian than "cell from nothing", which seems to be what you're asking about. The lack of additional research on "cell from nothing" might be taken as a clue of how viable a path it's considered to be, whereas origin-of-life research is alive and well on other possibilities.


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Receptors and their distribution over the human population
For humans it has been reported that there are three vasopressin receptors (AVPR1a) and four dopamine receptors (DRD2). (Source: UNIPROT)
Question: Does every human contain all three variants of AVPR1a? Or is it the case that some individuals contain fewer than the three variants found in the total population?

do you mean variation in one gene or presence and absence of multiple paralogs/copies of these genes? I don't see where you are getting this info in uniprot, directly linking/screenshotting would be helpful.

Short answer: my database search yielded different results: Three receptors were identified with different names: AVPR1A, AVPR1B, AVPR2.
I have actually never heard of a distinct human population completely lacking one gene (I might be mistaken). Usually, only single nucleotide polymorphisms vary between populations. I also do not think that this matters, unless your project addresses specifically that question.
I find three paralogues of the vasopressin receptor (homologous copies of a "similar" receptor found on different chromosomes): AVPR1A, AVPR1B, AVPR2 (might have missed one though)
If these receptors pop up in a search in a human database, their mRNA (cDNA) was sequenced at some point from human tissue and annotated to the genome.
Protein Atlas shows two splice variants ("number of transcripts") of AVPR1A.
NCBI shows one splice variant of AVPR1a from three different databases (MANE, NCBI, Ensembl). (please see this tutorial to use the NCBI-genome viewer)


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Can DNA replicate without polymerase?
Would it be possible for short DNA molecules to replicate, for example, if it's heated to the point where the strands separate (as far as I know, that's what happens in PCR?) and freely floating bases could "connect" to their correspondent bases (A/T, C/G)?
I'm assuming that A/T and C/G bases strongly 'attract' each other naturally, perhaps that's where I'm wrong?

Not what you asked, but note that RNA can do this. (See also Wikipedia.)

@IlmariKaronen — RNA Can do what? RNA only replicates in certain viruses, where it requires  a replicase and NTPs. Speculation about replicative capability of primaeval RNA should be described as “might have been able to” rather than “can”.

@David Incorrect, RNA can self-replicate without any other molecule except the nucleic acids it builds itself from. Self replication of RNA was demonstrated over a decade ago. You are confusing Industrial use of RNA replication with what we know the molecule can do. Not only does it replicate it evolves into different linages as well. https://www.labroots.com/trending/cell-and-molecular-biology/22442/self-replicating-rna-molecules-life-arose and https://www.sciencedaily.com/releases/2009/01/090109173205.htm

@John - you make it sound like every RNA species is capable of self-replication. What you actually mean is  "self-replicating machines can be built from only RNA". These are two very different messages.

@markur I make it sound like no such thing.  I'll be crystal clear there are single strands of RNA that fully capable of self-replication, no other machinery needed. No replicase, not even multiple strands of RNA.  just water, ONE strand of RNA and some free floating nucleotides. Literally what the OP is asking for but RNA instead of DNA. no speculation. You are just wrong, RNA "can" self replicate without other machinery. I did provide links read them before claiming I "meant" something.

No, replication cannot happen in the absence of polymerase (on the timescales relevant to humans).
You are correct that in PCR, the first step is to separate DNA strands at 98 C. This heating dissociates the strands semi-permanently. So when you cool down the reaction, the strands do not re-associate very quickly.
When you cool down the reaction to 72 C, A/T and C/G can make temporary connections with their opposite bases. However, the free nucleotides cannot quickly form phosphodiester bonds with the growing chain of DNA in the absence of a polymerase. The nucleotide will most likely dissociate from the DNA strand before the correct bond forms. In other words, it is a kinetic problem.
However, at high temperatures, specialized conditions, and on long timescales, such as those present in earth's pre-biotic period, the answer may be different.

Is it fair to say that the polymerase is mostly helping the DNA to be put together somewhat "in order" (one nucleotide next to the other) so they can form stronger bonds with each other, becoming stable?

Nope. Not happening.
The high temperature (90 °C) needed to separate a DNA strand also makes an association of free floating bases to a template strand much too unstable.
Even if the bases associated with the template strand, they wouldn't spontaneously connect (phosphodiester bond formation) with each other. It needs a catalyst.
Also, it requires not bases, but dNTPs. dNTPs have phosphates (anhydride bonded) that deliver energy to the phosphodiester bond formation connecting each dNTP.

Only one phosphodiester bond is broken during dNTP utilization for DNA synthesis, so talk of three phosphates delivering energy is misleading, to say the least. The point is thermodynamics — provision of energy for phosphodiester bond formation — which bases cannot provide.

The bonds between the three phosphates are of anhydride type, not diester.  I removed "three", since it seems to be confusing.


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PCR: From transgene/microgram to cell concentration
I am doing research on CAR T-cell kinetics. The measurement of CAR T-cell concentrations across time is normally carried out with qPCR (see here, Fig. 1). These concentrations are generally reported as transgene per microgram of DNA. My question is how to go from this number to a cell count estimate, for example cell per microliter of blood, which is sometimes reported (see here, Fig. 3).
I understand this should be done with three conversion factors:
transgene/microgram * microgram/cell * cell/microliter * CAR cell/transgene = CAR cell/ microliter
I don't think the first two factors are hard to obtain, but I don't know about the third. I don't even know if this is right at all. Is there a straightforward or standard way to make this conversion?
From the first paper:

A TaqMan-based qPCR assay was used for the detection of
tisagenlecleucel transgene DNA (transgene copies/μg of DNA) in
peripheral blood and bone marrow samples, with a lower limit of
quantitation of 50 copies/μg of genomic DNA requiring 200 ng
DNA/reaction. The assay tolerates ±10% variation in DNA input.

Please clarify your question by elaborating that qPCR-method directly in your question. Readers aren't motivated to look up that method from a complicated research paper. For example, I ask myself if "transgene" means how much 'CAR-DNA' was found within a sample tissue?

I hope that can be of help.


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Why were there relatively fewer papers about cell fusion before the 1950s?
While working on my cell fusion technology report, I saw PubMed's cell fusion graph of results by year. There have been studies or research since the early 1900s, but until the 1950s, there were no more than ten papers. But, after the 50s, scientists studied a lot of cell fusion. I wanted to know why this happened, but I could not find any reasons on the internet. So, I ended up coming here.
I searched in Nature, PubMed, and google, but there was no detailed explanation of it.

Since you need to be able to grow cells for studying their interactions, I think the main reason for this is the development of cell culture techniques in the late 1940s and early 1950s. As an example of one of the earliest (cancer) cells in culture we can name the HeLa cell line, which was established from a cervical cancer in 1951.
There have been earlier attempts to grow pieces of tissues which at least have been partially successful, but for immortal cell lines attempts failed. See the references for an overview.
With the rise of cell culture in the 1950s, it was possible to reliably grow the cells needed for vaccine development, monoclonal antibodies and also cell-cell interactions.
The figure with the timeline comes from reference 2:

References

A History of Cell Culture
History of Cell Culture

I wouldn't underestimate the effect of public interest sparked by Watson & Crick's characterisation of the structure of DNA in '53 too.

@JiminyCricket. Interest in Biology was high at that time - even famous theoretical physicists as Max Delbrück changed over to molecular biology and genetics.


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Arizona spider that I cannot identify - help?
I cannot seem to find a "duplicate" photo of this spider anywhere and am curious what it is. It came by to say hello on my back patio in Vail, Arizona so I snapped this shot.
Any input would be amazing so I have more info if I should encounter another.
Thanks!

Could well be Latrodectus sp. Known as "widow spiders" including  the famous "black widow" Compare with this photo, but I'll let someone more knowledgeable ID this one.

It's a subadult female Western Black Widow, Latrodectus hesperus.  The pattern on the back will fade to black when she molts into her final adult growth stage, but the red "hourglass" marking on the underside will be quite visible from an early stage.  Good photo!  You can nicely see the big "mecha" legs that make adult Widows stand out so much from related Theridiid (comb-footed) spiders.  Even young female Widows can deliver a serious (but usually not dangerous) bite, but not all bites deliver a full load of (or even any) venom.  Still, and even considering that these spiders are extremely inoffensive, I wouldn't care to handle one myself.  Accidents happen!
Here's a link and photo:
https://bugguide.net/node/view/1854758


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What is the function of PCR in the whole genome sequencing?
Whole genome sequencing (WGS) method is using PCR in one of their steps. In the following page from the CDC, we find this diagram:
It says that the PCR is needed to "make copies of each DNA" but it does not explain specifically why this is needed. Indeed it seems to be clear it is done in order to enlarge the DNA we are after in the sample thus apparently providing easier analyses (at least that was my first thought).
As fat as I understand, PCR in WGS has some disadvantages in this that it is considered "biased" in the sense the target for amplification should be given in advanced, and also this uneven  amplification might result in false positive.
But then there are some "PCR-free" WGS. I tried to understand how having "PCR-free" WGS is even possible? isn't the PCR/step mandatory? if it is not mandatory and better results can be obtained without it, why to include it in the first place?

PCR is used to replicate each isolated genome fragment, yielding several copies of each fragment in your DNA solution (that‘s called a library = a collection of fragments + adapters).
This amplifies the signal of each isolated fragment, since each fragment will be sequenced multiple times. So you get multiple sequence results (called reads) per isolated fragment.
Years ago, the sequencing quality was far worse. You had to amplify the library, so that you can later confidently re-assemble all the sequences of every fragment into one big genome  (fragmentation is necessary, since the sequencing reaction can abort mid-sequence; Shorter sequences are far easier to handle). Also, starts and ends of each read are hard to sequence correctly. Having multiple reads per isolated fragment greatly helps with compensating for sequencing errors.
Also, WGS aims to identify single nucleotide polymorphisms, which can be sequenced more confidently using PCR.
HOWEVER, PCR-free methods seem to have circumvented these problems and have improved so much that they even yield better sequence quality when compared to PCR-dependent protocols Zhou et al. 2022.
I presume that PCR  can be problematic with WGS, because PCR might have trouble with reliably amplifying repetitive sequences, yielding erroneous results.
I also presume that the "PCR-bias" weighs more heavily on RNAseq than on WGS (which is why people talk about PCR-bias in the first place). RNA-seq often aims to quantify the copy number of each transcript, so the sequence itself is less important with RNAseq. However, PCR amplifies different transcripts more efficiently than others, leading to non-linear relations across the read-counts of all transcripts. Still, PCR is essential to RNAseq so that low-copy number transcripts aren't missed. Modern RNAseq technologies use UMIs (unique molecular identifiers) to correct for non-linearities.

Thanks. unfortunately I am not versed in this world, so not sure I fully understand answer. Do you say there is a trade-off between PCR-free and PCR WGS? As each would be a better fit for another use case?

If I understood correctly, there was a trade-off once upon a time.
Now there isn‘t anymore. Still, I might miss some usecases, where PCR is still needed. Please let me know which terms give you trouble and I‘ll gladly explain and further edit my answer


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How do atherinidae survive the drought?
I found isolated pools in which there are Atherinidae, through the pebbly shores of Piave River (North-East Italy, Europe - in attachment there is a picture of the remainder of shores, after the drought of this year, to let you see it context. Isolated ponds were found about 20m close to the shores, where you can see the vegetation - picture not mine ).

The pools are isolated (, there is no inflowing or outflowing water.
Water seems also stagnant. The distance of some pools is also very large (dozens of meters, in some occasion a hundred).
The drought here was extreme.
When I observed these ponds, it only had rained for a few days (about 3 in a week) after months without no rain: there were not conditions to have inflow of water, because around the ponds is completely dry, and my hypothesis was the ponds may not necessarily be remainders of evaporation of larger volume of waters that resisted months of drought, but originated after rain fall.
There are small fishes in the pools I thought were previously dry.
I think they may be Atherinidae, because they are small and resistent to salinisation of water.
I wonder how they made it to get here.
Could the eggs be preserved?
--
I'd like to learn more about these fishes, I love to explore their habitat.

Thank you David. Awesome that I see you are biochemist! If you would like to explain how to these fishes' metabolism  cope with saline water and extreme variability of their habitats, I'd love to hear!
I can think of at high variability of salinity, and high variability of available oxygen in water also for formation of algae, probably for eutrophysation due to type of agriculture in these area.

The question seems more biology (which I never studied) than biochemistry (although there will surely be a biochemical basis). There is presumably a literature on this sort of thing. Not sure what the technical terms are to use. You might experiment with Google.


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How would you measure the diameter/radius of a non-circular bacterial zone of inhibition?
Typically when we're testing the antimicrobial effects of some substance on bacteria growing on an agar plate, we get the area or diameter/radius of the zone of inhibition. But what do we do in cases where the zone of inhibition is not uniformly circular around the antimicrobial agent? How would diameter and radius measurements be of use in these cases and/or how would one adapt these measurements to more accurately reflect the area of the zone of inhibition?

I think a picture or two would be worth a thousand words here

We actually did something like this in one of my periods in biology class, all you need to do is take your measurement in millimeters. This measures the radius of the zone of inhibition. Multiply that by two in order to get the diameter.
If it's not uniformly circular, try getting the diameter of the circle you do know, and find the diameter/length/width of the unusual part. Just like in maths when you calculate total volume of a combination of shapes.
By unusual part, I mean the part that makes the circle around the microbial agent non-uniform.

If your inhibition zones are not uniformly circular (or at least close too it) you may want to revisit your methods and ask why this might be the case.
Are you applying your inoculum in a consistent and standardized manner? Is the inoculum too light or too heavy in any place? Are your disks too close together, or too close to the edge of the plate? Could your disk have moved after application (possibly due to excess moisture or condensation on plates)? Is the uneven zone close enough to another disk for the two agents to interact, either synergistically or antagonistically?  (see image)

Have you looked to see if any special cases apply, like Fosfomycin, in the EUCAST breakpoints table.
If all of those potential causes are ruled out, I'd say you should measure to the nearest (inner most) circular or semi-circular edge of the zone. Since diffusion tests are often used for antibiotic susceptibility testing of clinical isolates, users (and clinicians) are often more interested in the qualitative classification (susceptible, resistant, or intermediate) than the quantitative result. For example, in cases where a double zone in present, the EUCAST method recommends measuring to the inner-most zone, unless otherwise specified, to avoid falsely categorizing a resistant isolate as susceptible.
If it's irregular because it's overlapping with the edge of the plate, with another inhibition zone, or if synergism/antagonism(aka induction) are suspected, you could just measure to the circular part and ignore the overlap/interaction zone, but retesting with more space around the disk would be preferred.
References:

EUCAST clinical breakpoints table, version 12.0
Antibiotics in laboratory medicine, 6th edition. (image credit)
Development of the EUCAST disk diffusion antimicrobial susceptibility testing method and its implementation in routine microbiology laboratories


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What are these tiny, bouncy balls I found in my Calathea substrate?
I found two of these small eggs/seeds (?) in the substrate of the Calathea plant I just bought from a botany store. I cut one of them open to make sure it's not just plastics or similar.

About 4 mm across
Quite bouncy
It looks like they have something a little darker on the one side of the sphere, and the other side seems a little bit transparent
When cutting it open it was a little "crusty"

I looked up what Calathea seeds look like, definitely not like this. Any idea what this could be?

Since these are the non-organic fertiliser beads used when filling the pot (a few are sprinkled in before selling to slow-release nutrients) and not something biological such as snail-eggs, this question would be off-topic here. If you're interested in knowing more about them, check-out the [gardening.se] site which specialises in related stuff.


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Are there hobbyist microscopes which can take digital pictures of cells?
I'm reading a biology textbook and it's suggesting things like taking onion skin etc. and looking at it under a microscope to see its cells.  I'm tempted to do this for fun, and maybe share photos of what I find on Facebook.  (I remember using a microscope in school, but all I ended up seeing was air bubbles.)  I'm wondering if there is some way of doing this as a hobbyist (on a budget of, say, $100).
I saw this on Amazon:

but I'm not sure if it can see individual cells.  It doesn't look like it can do that.
Question: Are there hobbyist microscopes which can take digital pictures of cells?

Yes, but I'm not sure about the price. Look for something with 400x magnification or more, and to see cells get a slide microscope with lower illumination. Some come with pre-prepared slides that are stained to give contrast. Many without built-in cameras are compatible with separately-sold cameras.

“Hobbyist” seems poorly defined here. Is that just the cost of under 100$, or are there other requirements?

It implies I'm not particularly knowledgeable about what features I should search for.  I'm probably only going to use it a handful of times (for fun), so it shouldn't be expensive.  I don't have additional equipment.  And I'll probably ask random people on the Internet for suggestions of cool things to take photos of.

Search for "usb digital microscope". These are quite cheap (generally under 100$) with up to 1000x magnification, they are eay to use, and they connect to your computer for taking images. Obviously, the image quality is way worse than using a professional tabletop microscope, but I consider them useful enough for a hobbyist.

@Domen this is a cool suggestion that could readily be an answer, IMO.