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Is it possible to fuse DNA from two sperms and can a baby be born from that?
If this is possible, then isn't there going to be a chance to have a YY child?

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

The question was clear to me. Assuming this person is not a professionally trained molecular biologist, it's impressive enough they even realize that sex chromosomes are a known feature of human genetics. They sound genuinely curious about the implications of making babies using artificial genetic editing technology on cells which if ordinarily otherwise left naturally unaltered clearly it would not be possible. It's a very important consideration we must face this century.

@JohnCollins — Clarity is good, but not sufficient. In addition, to not demonstrating the expected prior research and containing two distinct questions, this is off-topic because it is a homework question. On the homework page the question "What is a homework question?" is answered with "A question that addresses a basic biology concept that may seem trivial to biology professionals". Knowing that at least one X chromosome is required for viability is something I would expect anyone with even high-school level biology to be aware of.

@tyersome So did you have at look at the OP's profile? They say they are only fourteen years old. I.e., only having just begun high school. This to me seemed like a genuine answer arisen from pure curiosity and from what I recall of my own HS education the level of biology getting into actual chromosomal details would only have "homework" in AP Bio, which was primarily a seniors course with some exceptional juniors. We should be promoting such curiosity as much as possible, in the youth especially, but even in any age demographic -- so unfortunately ignorant of modern molec bio are most.

genuine question*

Well, it would be difficult from specifically sperm, but if you mean from two members of the same sex -- two men, then the answer is yes. Yes it is (or, rather, will be) possible. Already, it has been done in mice (new baby mice were born from both only mothers and also only fathers):
https://www.cell.com/cell-stem-cell/pdf/S1934-5909(18)30441-7.pdf
In theory it would never be possible for two women to truly fully independently create a son (a male offspring) from their own cells, because neither of them would have the material for a Y chromosome. So that would need to be donated (just the Y chromosome). Two males could make either sex offspring (XX or XY). This would be possible through what is called induced pluripotent stem cell technology, likely CRISPR genome editing for performing the required epigenetic modifications (described in paper), and a whole variety of other quite new extremely complex advances in biotechnology which have recently been made (such as next generation sequencing for assaying the most viable possible artificially-induced sperm and egg [which could simply be made from skin cells] and variations thereof like ATAC-seq, which measures genome-wide chromatin and epigenetic information, microfluidics and nano-droplet technologies and the rise of single-cell assay capabilities of many kinds, and truly, an overwhelming further number of huge advances which would take too long to list here and which most people probably remain totally unaware of [or could even comprehend, unfortunately]). We are living in a "Golden Age" of what will without a doubt be forever historic massive, rapid leaps forward in our ability to become the designers of life, rather than the passive victims of its "natural selection".
It is not possible today, all of the mice made in the 2018 study, though they did survive through to birth and then some, were quite unhealthy and all died prematurely from genetic abnormalities (does this not happen naturally, all the time, too? Not just in mice but men as well!). But there's no doubt the understanding and refinement of the ability to do such a thing will only rapidly improve - in every field of science this has been proven to be true in modern times, literally exponentially so. And probably no more amazing than in the scientific understanding and bioengineering of living things -- once the structure of DNA was chemically precisely determined and understood (in 1953; when it was revealed not only how DNA is chemically bonded and of precisely what atoms in what 3D orientations but also why such a structure, that specific double helix anti-parallel complementary form, would make sense functionally as a source of information-containing incredible power -- the relation of its structure to the function of evolution, and of literally the birth and aging process of every animal) is when things really started to proceed at a rocket-launch speed clip. Now, at this point, your average person really does not fathom just how much our world is about to change.
It's likely in this century this will be a safe, totally feasible, possible technological power at our disposal. Now will it be legal? That's much more uncertain. But that's irrelevant to the question of is it physically possible, to which the answer is an absolute yes.

I don't think it is possible. There is a lot happening to the DNA of the sperm and the egg after fertilization, and just mixing the DNA of two sperm or two eggs would not achieve that. Also, a YY embryo would not be viable because the X chromosome contain vital genes that Y does not. That's why there are people with 1X but no one with 1Y.

Sperms contain X and Y chromosomes, but only as haploid sets.

No it is not possible,
sperm are missing most of the biochemical machinery need to produce a embryo, sperm have most most of their functional components to make them lower investment and faster. Sperm are lacking several important organelles, including the most important ribosomes. They are not fully functional cells.
https://www.ncbi.nlm.nih.gov/books/NBK26914/

Who's to say it wouldn't be possible to supply such organelles, say by inducing the sperm genome into a pluripotent state via introduction of transcription factors (and probably some yet to be known method for unpacking the extremely densely packed genome, yes -- totally feasible, as, that must happen during the formation of the zygote post sperm-egg fusion, no?). The genome -- the full DNA molecular sequence, with all its unique variants (BTW - a tiny percentage: ~0.1%), is all that is really required. It has been undeniably established that life is but heritable information, stored as DNA

In other words though sperm may lack said required machinery, what they do not lack is the instructions for building them. I'd be very wary of claiming almost anything we can imagine as far as biological artificial manipulation to be "never possible". 1) We simply cannot know that with definite certainty 2) All signs are increasingly suggesting that the possibilities for bioengineering will not only encompass all that we could currently imagine but far more, beyond what we can yet even have realized

Also - did you read your link? I just did. Absolutely fascinating. I didn't even know this at all. But sperm are up until the very final parts of their lives (i.e. very near prior to being expelled as semen) exist cytoplasmically connected to apparently thousands or perhaps more of other essentially clonal daughters cells, and thus, share one continuous open giant elongated cytoplasm called a synctium - and thus as they complete their differentiation, are not only diploid-sufficient, but tremendously polyploid -- they are well supplied with all the normal machinery required for transcription..

.. and translation. You are citing the 2002 edition of The Cell textbook. Much more is probably known now on the details. But presumably the residual bodies of the synctium may be retrievable in the semen, so, it's very plausible that from a mere single sample of one male's ejaculate, a bioengineering could be applied to create new viable zygotes. In theory possibly millions even.

@JohnCollins you seem to be interested ins something very different than the stated question. I suggest doing some research and then coming back with a specific question.


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Why do bacteriophages look like tiny little robots?
I get it, evolution is funny and works in mysterious ways. But come on. You can't tell me this thing doesn't look like a nanobot.
Why do bacteriophages look this way? With their cylindrical heads and multiple "feet"?

Welcome to the site! Personally I think the question is reversed; the discovery bacteriophages pre-dated the design of nanobots; hence the question ought to be "why do nanobots look like bacteriophages?" and as such it's not really a biology question.  For it to be a good fit for the site, you'll have to show clear biological links rather than visual links with modern technology.

Why do they look like that? Because they do - there's not some deeper reason why they might look similar other than because people might have designed nanobots to look like bacteriophages (or maybe they didn't), especially given 'nanobot' doesn't have a strictly defined shape.

Honestly, that only looks like a functional bacteriophage to me, so, yes, I can tell you that doesn't look like a nanobot to me. Then again, I studied bacteriophages, but never nanobots. I wouldn't recognize a nanobot if I was shown a photograph of one.

The reason they look like that is because they have very small genomes so they have to build themselves out of multiple copies of a few building blocks. This leads to a high degree of symmetry in the component pieces; in particular icosahedral symmetry in the genome storage capsid (made of 235 copies in the smallest phage, 3115 copies in G-phage, as described by Caspar Klug theory) and helical symmetry in the tail. (made of an arbitrary number of copies, depending on the length.)
Industrial manufacturing also relies on efficient use of standardized mass-produced parts, so it's not surprising that you'd see similarities.
Also due to various differences between bacterial and eukaryotic cells, bacteriophage rely on their own complex protein machinery to physically breach their hosts, rather than tricking the host into using its own membrane machinery to import the virus.

Many things on nanoscale look like small crystals or several small crystals put together - i.e., they adopt a limited number of symmetric shapes allowed for packing identical objects in three dimensions (see, e.g., the shapes given here). Viral capsids, composed of many identical proteins (capsomers) is an example of such crystal structures.

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How many drinks were consumed by each test subject in this study?
I was reading this study and came across the following line:

...subjects consumed either 500 mL of whey protein (25 g; PRO), alcohol (1.5 g·kg body mass⁻¹), 12±2 standard drinks) co-ingested with protein (ALC-PRO)...

Does the 12±2 translate to 10-14 drinks? This seems like a lot, so I went to the equation, 1.5 g·kg body mass⁻¹, but I'm not sure how to go about calculating that. Is "body mass" just bodyweight in kg here?
This is probably very wrong, but, if I take a bodyweight of 87kg and plug it in:
87kg⁻¹ (191lbs) = 0.01149425287
0.01149425287 * 1.5 = 0.0172413793

What am I doing wrong here?

"1.5 g·kg body mass⁻¹" can be equivalently written "(1.5 g)/(1 kg body mass)" or read "1.5 grams per kilogram body mass".
So, a 87 kg person would be given 130.5 g of alcohol. The units work out as:
(1.5 g EtOH)/(kg body mass)  * 87 (kg body mass) = 130.5 g EtOH
That is, you have (kg body mass) in the numerator and denominator, these cancel and you end up with just the g EtOH. When working with units, it's always a good check to write out the units you have and see that the units you end up with make sense for the answer you're trying to get.
Written out another way, you have the dose per weight; you want to multiply that dose per weight by the actual weight to get the dose.

Does the 12±2 translate to 10-14 drinks?

A standard drink in the US is about 14 grams, but these authors aren't in the US. A UK standard drink is 8 grams. Australia is 10 grams. However, they write in the paper:

The alcohol ingestion protocol (1.5 g·kg−1 BM; 12±2 standard drinks) began 1 h post-exercise and was consumed in 6 equal volumes of 1 part vodka (∼60 mL) to four parts orange juice

So if they are taking a standard drink to be 30 mL vodka (approximately 1 fluid oz) and giving 12 of those. 30 ml vodka is going to be just under 10 g ethanol, so by the Australian measure that all works out.
And, yeah, that's a lot of alcohol to drink, especially over just 3 hours. The paper begins "The culture in many team sports involves consumption of large amounts of alcohol after training/competition" - they're targeting the binge level of drinking observed around team sports.

The term "standard drink" seems to be particularly used in Australia.  Here in the UK we'd use "unit" in the same contexts

@ChrisH My understanding is that "standard drink" is used everywhere except the UK, though you'll also find "standard drink" and "unit" used interchangeably for the UK measure. https://en.wikipedia.org/wiki/Unit_of_alcohol reads "Standard drinks were referred to in the first UK guidelines (1984) that published "safe limits" for drinking, but these were replaced by references to "alcohol units" in the 1987 guidelines and the latter term has been used in all subsequent UK guidance."

Maybe so - "standard drink" is certainly never used here in public-facing material.  Perhaps my reading is biased in such a way I've mostly seen the term in an Australian context, or perhaps it's discussed more there even if it's the  correct term in more countries

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How many recombinations occur in an average human chromosome?
And is it a different number depending on which chromosome we choose (disregarding the change of this probability due to the differential size of the chromosomes)?

Welcome to the site!  Unfortunately, this is really too broad... It will definitely depend which chromosome you chooose, and in any case, recombination can occur during mitosis or meiosis... You'll really need to narrow down your question.  Thanks!

I was asking about recombination during meiosis, the recombination that homologous chromosomes undergo to produce gametes. I had no idea recombination took place during mitosis, unless you mean something totally different to meiotic recombination that happens to have the same name. So the question would remain like this: how many sites of recombination are there in, say, chromosome 1? (Although I would also like to know how much that number varies along every chromosome).


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What is the native structure of amyloid-beta protein under physiological conditions?
The amyloid-beta protein forms cross-beta structured fibrils. But under normal physiological conditions what is their predominant secondary structure. Is it alpha-helix, random coil or beta-sheet?

What research have you done yourself to answer this question?  There are many sources of information on this topic if you search the Internet. Tell us what you have found and why it doesn’t answer your question. See the Help on asking questions.


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Protecting an internal clevage site from restriction enzyme while cloning
2 restriction enzymes used to generate cohesive ends in a vector and foreign DNA(gene of interest you want to clone) also cuts the foreign DNA at an internal site. What are ways to overcome this?

What have you tried? Or is this a homework question?

I have tried protecting using DAM nethylases, but thaf gave a ladder of bands on gel electrophoresis analysis. So I am wondering how to solve this

Does your protocol use PCR and does your vector have a MCS?


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Can someone identify this insect species
I found a dozen of these insects on my wooden floorboards in the city of Athens, Greece (Mediterranean climate) (altitude 200m, 10 km from nearest shore). Currently it's Autumn. Size is about 0.5cm (see photo below).
Can someone please identify the species?

(I've also noticed numerous shed wings)

Check if they are ants (queen or drone forms).


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Do animals exist that grow body parts back into themselves?
goats sometimes grow their horns in a way that it "grows back" into its skull (e.g., https://en.goodtimes.my/2017/11/27/argali-sheeps-majestic-spiral-horns-can-protect-kill/).
However, this is a rare defect and not the "intended" way for the goat to grow, since it seriously hurts the animal.
I wonder, are there any organisms in which body parts merge with another part (as opposed to growing out of another part, as is standard) in this way, where it is not a mistake and instead a feature of the organism?
Thanks!

Would [babirusa[(https://en.wikipedia.org/wiki/Babirusa) count?

Does a narwhal count?

Human infants have 270~300 pcs of bones, that merge into 206 pcs in adults.


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Why does mitochondrial DNA have a high mutation rate, even though the mitochondrial function is highly conserved?
My understanding is that genes that are functionally important are more highly conserved. The DNA coding for ribosomal RNA is one example of that. I was surprised to find out that mitochondrial DNA had a high mutation rate. I'm mostly concerned with metazoan mitochondrial DNA, and more specifically, animal or mammalian mitochondrial DNA.
I've tried searching why exactly that is, and so far, from what I understand, it could be:

the lack of DNA repair enzymes in the mitochondria
the production of free radicals in the oxidative phosphorylation process leading to more point mutations

But how would the cell with these somatic mutations (or embryo with inherited germ line mutations) survive then? Are these mutations only passed down in the non-coding regions on the mtDNA, and the coding regions are indeed highly conserved?
I've also read that:

the high mutation rate refers more to the shifts in gene order on the chromosome
critical genes in the mitochondria migrate to nuclear DNA

I think I could be missing some understanding of wobble base pairing in the  mitochondrial translation system, or some quirks of the bacterial DNA, etc. I've hoping for a relatively complex and in-depth explanation of this. Thank you.

Could you please give a source for your statement about the rate of mutation in mitochondrial DNA. Also your assumption about importance and conservation — cytochrome c comes to mind as a counter example.

This is one example: Sen Xu, Sarah Schaack, Amanda Seyfert, Eunjin Choi, Michael Lynch, Melania E. Cristescu, High Mutation Rates in the Mitochondrial Genomes of Daphnia pulex, Molecular Biology and Evolution, Volume 29, Issue 2, February 2012, Pages 763–769, https://doi.org/10.1093/molbev/msr243
I would be happy to learn about why that assumption is wrong for cytochrome c as well. I'm looking in general to understand why mutation rates can be high for a highly conserved structure.

I'd put the reference in your question. Be careful. Your question referred to highly conserved function, not structure. Cytochrome c is a protein whose function is conserved through many species, but large sequence variation has occured, outwith the residues crucial for function.


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What are marine fungi like?
Particularly, what is their mycelium like and where exactly do they grow it?
I imagine that their spores travel though water same as terrestrial fungi travel through air until they stumble upon solid food (a carcass, a living host, sea floor rich with organic remains etc), at which point they begin growing mycelium network though that object. While I understand that there are many species of marine fungi, is my understanding generally correct?
Also, are there any fungi plankton: that constantly float in the water column and extract nutrients right from it, without ever having to "settle down"? If yes, do such fungi grow some special, "floating" version of mycelium?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, this site works well for focused questions rather than broad overviews of a subject. Have you read the most relevant wikipedia page? Note that also has an extensive references section that you can get into. Also, how about one of these freely available review articles?

@tyersome, I thought that the specificity of my question details should be evidence enough that I've looked and given quite some thought to the question myself. I even provided my understanding of what the the answer could be and asked for confirmation. I've read some articles and the wiki page: while they give a lot of specific detail (like habitats, distribution etc), I didn't quite get the impression of what they are like. Especially in terms of mycelium: because it's the key feature of terrestrial fungi, but at the same time doesn't quite make sense to have in open water.

As currently written your question seems to be asking for a review of an entire kingdom in multiple habitats across ~70% of this planet. I hope you can see that that isn't a reasonable question for this site, which is why your post has two close votes for "Needs more focus". If your primary question is about the growth form of planktonic fungi, then please [edit] your title and body to focus on that. It is important to clearly ask a single question (per post) as this ensures that you get a clear answer and that others can find this by searching. It will also helps you search more effectively.


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Do astrocytes connect and chemically communicate with other astrocytes?
I am building a novel model of neural tissue for the purposes of Machine Learning and am currently trying to unpick the functions of the astroglia.
The literature suggests that astrocytes ensheath synapses, providing them with structural support, given that the synapse is an oily droplet between two neuron 'tentacles' this makes sense, performs caretaker functions at synapses it ensheaths with regard to neurotransmitters and, via its perivascular feet, provides resources from nearby blood vessels.
The literature goes on to suggest that the astrocyte may play a role in some neurological disorders if the ionic 'effects' from one set of perivascular feet, namely one set of synapses, 'leaks' across an internal chemical barrier within said astrocyte, to spread the 'effect' to another set of perhaps unrelated synapses. I can see how this could influence and cause unrelated learning, which may be a hallmark of some neurological disorders, one of which the paper suggests is schizophrenia and its patterns of unearned and irregular learning.
I can appreciate how some form of localized learning or whole- or partial-pathway learning, as opposed to pure individual neuron-level learning, would certainly be beneficial to a learning network in speeding up learning.
Do astrocytes connect to astrocytes and if so how and what chemical messaging is present there?
I apologize that I am not a neurochemist only a software developer with a background in electronics and while I can follow some of the chemistry, I am interested in the functional purpose of these biological components. Nature only had chemistry to work with when these mechanisms evolved but, as an aside, if it had had access to electronics and software, one supposes the neural tissue would have been far easier for us to comprehend.

Astrocyte‐to‐astrocyte contact and a positive feedback loop of growth factor signaling regulate astrocyte maturation
(29 April 2019)
by Jiwen Li, Rana R. Khankan, Christine Caneda, Marlesa I. Godoy, Michael S. Haney, Mitchell C. Krawczyk, Michael C. Bassik, Steven A. Sloan, Ye Zhang
Published 'Glia'
This appears to give me the details I required.
Astrocyte maturation appears to be accelerated due to chemical signalling from astrocytes in their vicinity, but astrocytes do not 'signal', as understood as a network learning characteristic, to each other.
Thank you for your assistance.


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Gene Sequencing
The human genome project took an effort of around 15 years, billions of dollars and thousands of scientists working together.
So how is that the genetic sequencing of covid variants could be done at such a faster rate?

Welcome Tarique. We are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on and see our homework-question policy. Enjoy the Stackexchange network. (The human genome is over 130,000 times bigger and then there's Moore's law too).

Practice, practice, practice. The technology required is now in place.

The sequencing techniques have evolved, notably with spread of the next generation sequencing (NGS) and more recently nanopore. Sanger sequencing used in the first human genome project is a rather slow technique, although still widely used (especially in clinical setting).


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Effects of high extracellular fluid calcium ion concentration - what's the reason behind it?
The Guyton and Hall Textbook of Medical Physiology, p. 76, says:

For example, a high extracellular fluid calcium ion concentration decreases membrane permeability to sodium ions and simultaneously reduces excitability.

Why does this hold?
Naively, a high extracellular concentration of calcium ions should facilitate their flow through the calcium channels. Since the flow contributes to the action potential, the neurons should actually become hyperexcitable in the such a situation.
This post suggests that a high extracellular concentration of calcium increases the extracellular potential, thus causing hyperpolarization of the cell. However, this doesn't make too much sense either because, then, a high extracellular concentration of Na+ would also decrease the excitability in a similar way.
Note: this question is related to this one but I'm rather expanding it.

Can you provide some more context on the quote? The part you've included starts "for example" so presumably there is more content there of what this is an example of...


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A question about how the brain determines the source of a sound
If a person's eardrum vibrates, let's say, 440 times per second for 1 second, how does the brain know its because 1 sound source vibrated 440 times, as opposed to 440 sources vibrating once, one after the other, or 2 objects vibrating 220 times per second, but out of sync with each other, or any other combination? Thanks.


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centiMorgan distribution among human chromosomes
Using the rough estimate of 7,000 centiMorgans in a human... Is there an estimate that breaks down this total by chromosome (including the sex chromosomes)?  E.g., in the human karyotype, do chromosome pair 1a and 1b have n1 cM, 2a and 2b have n2 cM, etc. so that n1 + n2 +...+ n22 + sex chromosomes = 7,000?
If you understand what I'm getting at and can re-phrase my question to clarify it, please do so.

The short answer is "yes". Here is an early example: https://science.sciencemag.org/content/265/5181/2049.abstract
I am sure that with some searching around you can find the most recent version. I was able to find somewhat more recent maps here. The data has to be in the UCSC genome browser somewhere. Most likely you should find your 7000 cM estimate source and figure out which map that estimate comes from if you like that source.
These data structures are called "genetic maps" or "linkage maps". Each chromosome has positions that are defined by cM, and you could use that for your purpose I believe by just taking the largest cM value marker for each chromosome.
(Note that the two copies of a chromosome do not have independent genetic maps- after all, the map is defined by recombination between the two homologs. e.g. for chromosome 1 there is usually just one map, and therefore one maximum cM value- the map is an average across the human chromosomes sampled.)
Edit
The question seems to be related to a genealogical heuristic for identifying relatedness in cM values. I'm still not 100% sure how they measure this exactly.
The source shares expected values for relatedness here: https://secureservercdn.net/184.168.47.225/35b.ded.myftpupload.com/wp-content/uploads/2018/12/Relationship_Chart_FINAL_August_2017.jpg

The short answer suits my purposes well, as I am trying to get a rudimentary grasp on the mathematical and biological factors that apply to genetic genealogy.  I understand that parent/child relationships are a special situation, and with all other familial relationships "damned statistics," recombination, etc. are strong factors.  For some reason, self-reported sibling relationships in a 25,000+ person study by Blaine T. Bettinger are averaging significantly lower (about 2600 cM shared ) than the expected 3500 cM for a 50% DNA match.  Can you direct me to a source with a layman's answer?

@JosephFilip it would help to see the actual source to evaluate this. I am not sure what it means to share cM between sibs as it's a measure of physical linkage on chromosomes rather than genetic relatedness.

Edit: it appears to be related to this: https://thegeneticgenealogist.com/2018/12/17/examining-outliers-shared-cm-amounts/. I'm not a genealogist per se, I guess this measure kind of makes sense in that context, though it's unfamiliar to me. The layman's answer might be that blog post.

@JosephFilip Note: sibs aren't 50% matches, but rather a bit less than. Parent-child are 50% because of Mendelian inheritance (one chr copy from each parent), but sibs are comparing the outcomes of two such random draws (one for each sib). In other words the values you note 2600 cM are expected for sibs (see the chart linked in answer/blog post). see here for more details: http://hoylab.cornell.edu/relatedness.html

To a hammer, everything looks like a nail. To a 1970s math major, everything looks like an equation.  I did my own analysis of the grandparent/grandhild inheritance probabilities, but I can't figure out how to post it.  I used the assumption, known to be wrong, that chromosomes behave as identical immutable coins being tossed.  My calculations for averages and "normal ranges" match with "summary info" on genealogy and DNA test websites. They give a figure but don't say how it was derived.  The hoylab site says that sibs SHOULD BE 50% matches.  btw I do know that cMs are a rate not a distance.

ah- you know what, you're right, I faked myself out. siblings do share 50%, for some reason I just went crazy for a second there because the genealogy site said it was true. but if you do the simulation (which i did as sanity check) or check any reasonable source it is absolutely 50%, e.g. https://en.wikipedia.org/wiki/Sibling. i have no idea what's going on with the genealogist. possibly it is lower due to non-informative haplotypes (i assume you need good haplotypes to infer cM)?

Thank you for your patience!  The genealogy and DNA-test sites use very loose or incorrect terminology.  E.g. Ancestry returns a group of matches for, say, "6th-8th cousins", but there are a couple of dozen other familial relationships with the same degree of separation.  Gedmatch goes by "generations removed" so you get a list of people 2.1,2.3,4.2,...5.7 gens removed, whatever that means.  And they treat cMs as a distance.  If 1 cM=1% observed rate of occurrence, and there are 7000 cM, does that imply an avg of about total 70 "recombination" events in a specific sperm or egg cell?


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Why spider's web don't burn when electricity touches it?
I saw and spider on it's web at an electrical cable and thinked: If the web is made of proteins, why dont burn.
Sorry, the photo is dark because is night in Ecuador

Spider silk can conduct electricity. Some spiders use this material property of conductivity to capture prey. https://www.ncbi.nlm.nih.gov/pubmed/24323174
So I'm going on the assumption that both electrical lines spanning the web are bare and that they are live, i.e. carrying current. I will also assume that these lines are carrying the same current.
With electricity, it might help to think of the analogy of a waterfall. Water at the top of a waterfall has potential energy, which is converted to kinetic energy when it goes over the waterfall. The water accelerates towards the earth as it falls. There is a height or "gradient" between the top of the waterfall and its bottom, which allows water to accelerate from the top towards the bottom of the fall.
Electrons in electricity work in much the same way. Between two points along a conductor, you need a voltage gradient to establish an electric field, which moves electrons in a particular direction — just as the waterfall creates a gradient of high ground to low ground that enables water to flow.
If you have two wires (both conductors) running at the same voltage, and if you connect them with another conductor, like a spider's web, electrons will not run through the web because there is no voltage differential that creates an electric field that drives the flow of electrons between that connection. https://en.wikipedia.org/wiki/Electric_potential
Here, the web and spider are likely unhurt, because the two lines do not provide a voltage difference needed to have electrons move across the silk, like water would flow over a waterfall.
If the spider web was grounded — if its web were instead connected from one of the electrical wires to the earth — electricity would likely run through the web and, potentially, burn the web (and the spider). But from your photograph, it looks like the web is connected to both wires that ℗r assumption) are at the same voltage.
This is the same principle that allows electricians to work on maintaining electrical pylons without shutting down the power grid. https://en.wikipedia.org/wiki/Live-line_working
They work in such a way as to maintain the same voltage as the lines they are working on. If they were grounded — if they held a copper wire, say, that was plugged into the earth — or if there was anything conductive that the electrician was connected to that established a dangerous voltage gradient, and if they started working on live electrical lines, they would get fried. Same with the spider, if the web was grounded in a similar way.
Further, if the two wires were running at different voltages, then electricity could conduct through the spider web and cause some damage.
This answer relies on a lot of assumptions from the photograph. Feel free to clarify if those assumptions would change the parameters of the question and my answer.

I really doubt that this answer is correct.  If that's a single-phase line (typical of residential supply), there IS a voltage difference between the phase and neutral wires.  (Likewise if it's 2 wires of a 3 phase system.)  If the lines are live, and spider silk conducted electricity, there would be a sufficent current flow for the resistance to heat the silk, or any conductor, to its melting/vaporizing point.  All you'd get is a brief arc.   But in fact normal (dry) spider silk is a pretty good insulator.

These lines could perhaps be fence wiring to keep in animals, but I can't really tell and it isn't mentioned in the question. I would definitely suggest adding your answer, if you feel it is appropriate or my answer is incorrect.

Thanks Alex. Yes, your assumptions were correct, and the Live-line working assumption is very logic to me.


text:
Why does Meiosis produce 4 daughter cells instead of 2? Won't splitting the initial diploid cell into two haploid cells be easier?
At first, I thought it was because of crossing-over, but when I thought more about it, that didn't seem reasonable. Why don't cells just do meiosis like this? (I know that we don't understand all the why's and how's in biology yet, but if anybody has an explanation for this I would appreciate it)

Diploid cell has 46 unique chromosomes - 23 homologous pairs
Cell crosses over the homologous pairs WITHOUT duplicating them first
Metaphase and Anaphase produce two haploid daughter cells, each with a unique combination of genes within a chromosome - 23 total

Instead, this is what they do (or at least, how I understand them to do)

Diploid cell has 46 unique chromosomes - 23 homologous pairs
Cell duplicates all chromosomes - 92 in total - 46 unique chromosomes - 23 homologous pairs
Cell crosses over the homologous pairs
Metaphase and Anaphase produce two haploid daughter cells, each with 46 chromosomes - but only 23 are unique - the others are duplicates of that 23 (with the exception of the variance caused by the crossing over - what I mean is, all 46 were all initially from the same parent instead of the 23/23 found in a diploid cell)
The two daughter cells undergo Meiosis II in order to produce four total daughter cells -  Each has 23 chromosomes - All 23 are unique

So why does the cell take this more difficult path in order to achieve the same thing? Am I missing something out here? I would really appreciate some help. Thanks!

here is what I think why cells evolved to do meiosis like as it is now and not like you mentioned.
First I will try to tell you briefly (not in detail) how crossovers are made and how they ensure the segregation of chromosomes.
During meiosis the  cells are programmed to make DNA double strand breaks (DSBs). These DSBs are repaired by a pathway called Homologous Recombination (HR), where the breaks can be repaired into cross overs (CO) or non cross overs (NCO) using a template DNA (which could be DNA from sister chromosome or from homologous chromosome). For the homologous chromosomes to properly segregate during Meiosis I, at-least there should be 1 CO per homolog pair.
But in most studied organisms (including humans, mice), the number of DSBs largely outnumbers the CO number. For instance in mice there are 20 homolog chromosome pairs, so they need 20 COs for proper homologous chromosome segregation; but to produce 20 COs the cells are making 200-300 DSBs. And the remaining are repaired as NCO with homologous chromosome or as both CO and NCO with sister chromosomes.
So coming back to your possibility, if the cell was trying to do CO without DNA replication (without sister chromosome), it is risking its genome for less options for repair. More molecularly, sister chromosome is the ideal template to properly repair a DSB than homologous chromosome!

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text:
How to download omic data from ncbi? (SRA data or any suggestion?)
I proposed myself to replicate the results in this paper with an accession number PRJNA325650. So, I'm trying to download the data. Which will be the best way to do this?. I tried with the sratoolkit, and the SRAdb package in R but doesn't work.
My code:
In sratoolkit
Input:
prefetch PRJNA325650

Output:
prefetch.2.10.5 err: error unexpected while resolving query within virtual file system module - failed to resolve accession 'PRJNA325650' - The object is not available from your location. ( 406 )

In R (SRAdb)
Input:
rs = listSRAfile(c("PRJNA325650"), sra_con, fileType = 'sra')

Output:
Error in sraConvert(in_acc, out_type = c("study", "sample", "experiment",  :
  Input type shuld be in 'SRA' 'ERA' 'DRA' 'SRP' 'ERP' 'DRP' 'SRS' 'ERS' 'DRS' 'SRX' 'ERX' 'DRX' 'SRR' 'ERR' 'DRR'

Any suggestions or methods?

I’m voting to close this question because it is off-topic. In particular, this question has no biological component, but it might be suitable for migration to [bioinformatics.SE]. Please revisit the [tour] and read the [help] for details.

Sorry, but the tags "bioinformatics" and  "ncbi" are here and not in StackOverflow.

The fact that there is a tag is irrelevant to whether a question is or is not on topic. That is set out in the Tour. People here are happy with bioinformatics questions where the biological problem is to the fore, but less so with questions on particular software or coding. In any case you are more likely to get an answer on SE Bioinformatics, so I would advise you to move your question there.

Ok, I'm going to move it

I had a look, I can see the data in FASTA format.
The accession number is for a project with 50 samples, each of them a sequencing run.
First I went to genbank at
https://www.ncbi.nlm.nih.gov/
search that accession nunber selecting "all databases" to get the project page here
https://www.ncbi.nlm.nih.gov/bioproject/325650
Under "resources" there is "sequence data" "SRA experiments"
to the right I clicked on the number 50, taking me to:
https://www.ncbi.nlm.nih.gov/sra?linkname=bioproject_sra_all&from_uid=325650
I see the list of 50 samples, Clicking on the first I get to:
https://trace.ncbi.nlm.nih.gov/Traces/sra/?run=SRR3667045
Clicking "Runs" takes me to a page with the data viewable in many forms.
hope this helps.


text:
Looking for a good and complete Enzimology exercises book
I mean, I want to practice with challenging exercises and I want to know the theory behind them. So, I started reading:

Organic Chemistry: Yurkanis, P.
Enzyme kinetics: Bisswanger, H.
Biotechnology procedures and experiments Handbook: Harisha, S.
But just the first one has problems and not about enzymes at all.

So, I looking for a good (theoretic) and complete (challenging with exercises) book about enzymes.

I generally regard book recommendations off-topic. I cannot recommend a book but suggest you see if you can "look inside" Cornish-Bowden's Fundamentals of Enzyme Kinetics. He is well regarded, and there are some calculations in his book judging by the three pages of solutions to problems. Only three pages though.

So, why are off-topic?? The book you recommend me is very fine. It cover many of the topics in my syllabus. Just $55. Thanks man.

The reason it could be considered off-topic as an answer is that any recommendation is subjective opinion, and this is a question and answer site about biological problems. But glad my comment is of use.


text:
What is the name of this plant with a compound leaf of 8 leaflets?
this plant is present in my lawn and I don't know it's name. It is actually diseased and I'm trying to figure out what it is.

Can you please add some geographic location of your garden? Also information if this plant is native there or just planted would be helpful.

Is this related? https://gardening.stackexchange.com/questions/30373/what-disease-is-causing-raised-blisters-on-the-leaves-of-my-plant

I think it's [ https://en.m.wikipedia.org/wiki/Rauvolfia_caffra ] Still not sure, but it's worth giving a try... :)


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Why is Fst/1-Fst used when calculating isolation by distance?
In population genetics a common analysis when considering the genetic structure of a population is to examine isolation by distance - the relationship between the genetic difference and the geographic distance between populations. Commonly Fst (the P of variation attributable to differences between rather than within populations) is used as a measure of genetic distance and the analysis is usually some form of regression, however actual variable used for genetic distance is often Fst/1-Fst rather than the raw Fst estimate.
This practice I can generally trace back to Rousset 1997 (doi: 10.1093/genetics/145.4.1219) who appears to have set this standard, however I can find no satisfactory explanation as to why this is - the explanation provided in Rousset's paper uses a far higher level of math than I can interpret.
I assume that somewhere it has to do with a non-linear, more logarithmic relationship between Fst and geographic distance but I am hoping someone can provide a bit more detail on this (or correct me entirely!)

Hi, rainbird. Did you happen to see this and does it help? I'd try to help, but I really stink at math.

Hi, @anongoodnurse, yes I have had a look at the wiki but this entry really only discusses the calculation of Fst itself, not the relationship with distance. There is actually a separate wiki on isolation by distance but all of the Fst examples there use raw Fst. Actually so do quite a few of the recent papers it references, so perhaps this use of a modified Fst isn't quite ubiquitous, but it's still common enough to make me curious.

I do wish I could help. It's a valid question.


text:
Is there an adhesive that could used for larval fish?
I am currently working on an experimental design that requires a larval fish (~ 4mm long) to be affixed on a metal wire tip on its dorsal side. Now, I was thinking of a glue or adhesive to do the job, but it doesn't have to be strictly these, anything that sufficiently attaches the fish to the metal wire tip would do. The glue/adhesive would have to work well on wet surface and, ideally, something that is not toxic. Any advice or ideas are welcome.

You could try methyl cellulose, which my lab and others use. It's not exactly an adhesive, but it is quite viscous. It's common enough that it's in the Zebrafish Book: https://wiki.zfin.org/display/prot/Methyl+Cellulose+Mounting . Obviously, be sure whatever you do is approved by your animal care and use committee.


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Can epigenetics have positive impact on the genes are development?
I know that epigenetics have capacity to affect and degrade the genes thereby inducing problems/illness/degradation in body functions.
Can they also make better genes or have positive impact on genes or body? If yes, can someone give some examples?

First, let me qualify the idea of "problematic" epigenetic modifications by saying that the impact of a modification on an organism is often dependent on the environment.  That is to say that outcome is dependent on the interaction of genetics (or epigenetics) and the environment in which the associated genes are expressed; e.g. a mutation or modification that confers an advantage in a nutrient-limiting environment may be detrimental when nutrients are plentiful.
Second, it is helpful to think of epigenetic modifications as reversible switches rather than entities that "degrade the genes".  In fact, the etymology of "epigenetic" implies that such changes work at a level above that of the gene sequence, i.e. gene expression.  Canonically, DNA methylation and histone modifications (acetylation and methylation) modify the expression of a gene by regulating the ability of RNA polymerase to access that gene, either by directly influencing transcription factor binding or modulating the associations of nucleosomes and DNA. Read up on facultative heterochromatin.
As for examples, I point you to a set of papers that show associations between human starvation, epigenetics, and disease / mortality outcomes across generations.
DNA methylation as a mediator of the association between prenatal adversity and risk factors for metabolic disease in adulthood

[DNA methylation] at six CpGs, including at previously [serum triglyceride]-associated CpGs at TXNIP and ABCG1, mediated the association between famine exposure and [serum triglyceride]. [DNA methylation] at these CpGs was likewise associated with the expression of genes implicated in cell growth and energy metabolism.

Note that the authors present caveats to their analyses in the discussion. The New York Times also covered this publication.
Paternal grandfather’s access to food predicts all-cause and cancer mortality in grandsons
This publication is essentially a replication of the published works concerning transgenerational epigenetics in the Överkalix cohort.  They give a concise summary of how epigenetic changes caused by environmental stress may be heritable:

An intriguing aspect of these studies is the conjecture that an epigenetic pathway, carrying information across generations, may open up just before puberty, during the so-called slow growth period (SGP). Pre-puberty may be one of several “windows” for germline reprogramming in response to nutritional signals. A number of mechanisms for transmission across generations have been suggested, usually involving DNA methylation, chromatin formation or small noncoding RNAs. After fertilization, in the preimplantation embryo, epigenetic modifications acquired early in life are then usually erased, but not fully. Imprinting on specific loci may resist the post fertilization wave of reprogramming, eventually causing changes in offspring phenotype that are not driven by changes of the DNA sequence.

If you're looking for more examples, research genomic imprinting.


text:
What is this small black insect with an orange stripe?

Sorry for the poor quality of the second image, but a slightly different perspective may be useful.
This was taken in South Africa, Western Cape during the day.
They're fairly small, maybe around 5mm in length.
They were huddled together on an ivy leaf. I found another group of about five also huddled close together on another plant.

Some kind of Hemiptera nymph.

I guess they were grouped together because they had just hatched, and the eggs are laid in clusters.

Yes that does seem pretty similar thanks.

I checked again, and there are only three now of the other five I saw, but they're still huddled together in roughly the same spot.


text:
How do we know how long hermit crabs live in the wild?
This article states that hermit crabs in the wild are extremely difficult to track because they constantly change shells and even gender.  Later in the article, they say that hermit crabs can live 4 decades in the wild.  How can they know this if they can't follow a single crab for an extended period of time?

Hermit crabs increase in size over time and this is used to provide a minimum estimate for their age1.
You may also find this article interesting.

Reference:
SantAnna, Bruno Sampaio, Christofoletti, Ronaldo Adriano, Zangrande, Cilene Mariane, & Reigada, Alvaro Luis Diogo. (2008). Growth of the hermit crab Clibanarius vittatus (Bosc, 1802) (Crustacea, Anomura, Diogenidae) at São Vicente, São Paulo, Brazil. Brazilian Archives of Biology and Technology, 51(3), 547-550. https://dx.doi.org/10.1590/S1516-89132008000300014


text:
How can a disease be transmissible animal-to-human but not human-to-human?
I have heard some debate about whether or not the Wuhan virus can be transmitted human-to-human, but this doesn't make sense to me.  Why wouldn't it be able to?  Are there diseases that can only be transmitted from animals, not humans?

Does this answer your question? Viruses: Adaptation to a new host through repeated host jumps

I have heard some debate about whether or not the Wuhan virus can be transmitted human-to-human, but this doesn't make sense to me. Why wouldn't it be able to?

A virus has to be able to physically get out of one person and then into another in order to infect them.  If it can't do that, it can't spread between people.  Just because you can get a virus by (for example) eating an infected animal doesn't mean you'll be able to spread it to other people, at least without them eating you.

Are there diseases that can only be transmitted from animals, not humans?

Yes, and this is very common.  Rabies for instance can be transmitted from hundreds or maybe even thousands of animals to humans, but is virtually incapable of moving between people because it infects the nervous system which severely limits the ability of the virus to get into another host.

I would think (though I'm far from an expert) that rabies is a bad example.  A person with rabies might well be able to infect another person if, like other animal vectors, they bit that person.  Better examples might be insect-borne diseases.

@jamesqf There are no documented cases of human transmission of rabies, so while it could in theory happen, it doesn't appear to in practice. It is possible viral shedding is too low in human saliva, or that paralysis sets in too quickly in people vs other animals.

Sorry, I mean human transmission through bites. People have gotten it from organ transplants if the donar was infected.

Though I would wonder if it's a matter of humans being unable to transmit rabies via bites, or of infected people being kept from biting others, or perhaps not having the instinct to bite.


text:
Why do biologists judge intellect based on brain size?
I have seen many times, that scientists will say Species A is smarter than Species B due to a higher brain-to-body ratio.  I've even seen similar arguments made by comparing the sizes of specific regions of the brain.  For example, "Species A must have a more developed linguistic ability than Species B because it has a larger language center in its brain."
This doesn't make sense to me.  I don't think we can make these judgements because we don't know what "software" is being run in each brain.  I can run a merge sort algorithm on a weaker computer just as fast as a brute force sort on a stronger computer.  The raw computation ability of a computer doesn't necessarily correlate to how quickly it can solve problems.
What am I missing here?

What am I missing here? Brain mass is an easy to measure proxy for how much energy is being spent on computation. If that computation is not doing something of value, natural selection will tend to shrink the expenditure of energy, and thus the size of the brain.

In addition to the answers given here, I'd say there is a bit of a misconception here about the direction of inference. After adjusting for body size, it is an empirical observation that species with larger brains are more intelligent (and the same might be said for particular brain regions in different species). For species for which we cannot make observations (say, extinct species) or haven't yet, we can use this prior data to make informed guesses. The same is not generalized for brain sizes within species like humans so the same claim is not made there.

Your are confusing yourself with your analogy, brains are not like computers. The complexity of the "software" a brain can have is determined by how many cells and therefore connections it can have. In particular flexible (learned) thinking as opposed to instinctual "programs." Brains that are flexible need more cells to allow for more possible connections. Computers are not great analogies for brains they are just the best we have. but to use them a brain is like a solid block of ram, yes a large mass is not necessarily fast but it Can do a a far larger variety of tasks, intelligence is not a measure of speed (flies react way way faster than humans) but generally a measure of how many things you can be computing at the same time. the human brain is basically built to model the entire worlds around us including the brains of other humans, which is many many tasks happening simultaneously. Which is one reason brain size can also be used to predict how social an organism is, (at least in non-kin selected social behavior) social interaction requires modeling many complex things. You also run into the problem with defining intelligence, which is problematic to say the least.
And as another poster has pointed out natural selection will quickly eliminate unused brain mass, (neurons are super expensive to maintain, our brain eats about a third of the calories we consume) so they are strongly optimized for weight, so portions of the brain that are larger should, in general, be doing more to offset the cost, otherwise they will be quickly shrunk. So a portion of the brain that is large must be being used, and must be offsetting the caloric cost, also note many the parts of the brain are fairly basal to the groups being compared like mammals so the so the chances of drastically different fundamental ways of operating are fairly slim.  so if the same portion of the brain is very different in size between two related organisms chances are it is becasue that portion is doing more or less. It is even easier to see with sensory processing portions of the brain, if the olfactory bulb of the brain is huge it has to be due to an increased function in the the sense of smell because it really doesn't do anything else and how the sense functions has not changed. this is backed up by observation the brains of animals with poor senses of smell (like cetaceans) have tiny olfactory bulbs while animals with excellent senses of smell (blood hounds)have huge ones. Intelligence is associated with enlargement and complexity only in specific portions of the brain, not the brain as a whole.
That said brain mass is only a rough estimation.  It more done to control for body mass (which effects brain mass directly) as things like how folded the brain is can drastically alter the complexity without changing the mass much. No one assumes brain size is a prefect predictor for intelligence.

Correct me if I'm wrong, but aren't neural networks susceptible to getting stuck in local maximums?  So a species that found a good neural network will be stuck with it, while another may have found a different, much better neural network?

@Ryan_L Brains are networks of biological neurons, not neural networks.

@BryanKrause what about brains precludes them from getting stuck in local maximums?

@Ryan_L The answer to that question would both take a textbook to explain different ways biological networks can avoid local maximums, and also leave many examples where local maximums exist in brains (there are models of both depression and addiction, for example, that are probably best described as problems of being stuck in local maximums). But, note that I did not say that brains do not get stuck in local maximums, I simply said that brains are not neural networks. Your questions seem to be coming from over applying an analogy to the brain that does not fit.


text:
Is the nervous message sent by an eyelash being flexed sent all the way to the brain?
Since the reflex to close the eyelid once an eyelash is touched seems very fast, does the signal from the neuron detecting the touching travel all the way to the brain, get processed then back to the eyelid muscle?
Or does it have some kind of bypass that activates the eyelid muscle right away as some sort of reflex mechanism?

I don't think any reflex is controlled by the brain. Then again, I guess it might not be the case for something near the eyes since other reflexes tend to go through the spine's grey matter and the eyelashes obviously don't.

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text:
What do the colors mean in representations of amino acids?
I've seen sequences of amino acids depicted using colors, which I imagine correspond to whether the side chain is charged, etc. I can't figure this out, though, and I'm not a biologist or biochemist. I've seen what appear to be some different color schemes online. Is there a standard format / scheme such as for the following example?

I don't think there is a general standard for the color code of the amino acid – there are different conventions and software or paper authors may decide to use their own. You can see some examples of color codes here. As for your particular example, I would say it is more or less a custom color code, made for this particular case.

There is no ‘standard’ colour scheme for amino acids in the sense of one recommended by a standards or professional organization for biochemists. There are several schemes used in practice — either by software applications or individuals — based on two main criteria:

The properties of the amino acid the colours are intended to indicate
The colour choice of the individual author in expressing the intended similarity

The graphic below is taken from a page I found on the web by a random search and relates to a particular software package. It illustrates some possible colour schemes, none of which correspond to that in the question.

The ‘Chemistry‘ scheme focuses on one view of chemistry — acidity, basicity, aliphaticity, aromaticity, polarity (amides etc.) although it has had to make a choice in classifying tyrosine with tryptophan rather than threonine. The ‘shapely‘ scheme focuses solely on size and shape, whereas the hydrophobicity scheme does as its name implies. The ‘Zappo‘ and ‘Taylor‘ schemes (never heard of them previously) seem to be individual slight variants on the first two. The letter scheme appears to be just a way of distinguishing each amino acid for identification purposes, and molecular graphics software (e.g. Jmol) generally lets one colour amino acids along a protein in a graduated manner from (e.g.) red to blue to indicate the pathway of the chain (e.g. in this previous question on the list).
Oh, and I adopted another compromise scheme (probably using colours easily available in Excel) for a paper I published in 2021:

Coda
There is a tendency in schemes that reflect the chemistry of the amino acids to use blues for basic amino acids and reds for acidic ones. This possibly reflects the widely used chemical CPK colour code of blue for nitrogen (as in amino groups) and red for oxygen (as in carboxyl groups), and might have been regarded as an aid to recognition. (A simpler explanation might be a relationship to litmus paper.)


text:
Western blot trouble shooting - low voltage and yellow sponges during/after transfer
I have a western blot troubleshooting question that I haven't been able to find the answer to in manufacturer troubleshooting guides.
As a bit of background, I was transferring 2 western blots together in the same tank (we use a BioRad tank that fits 2 transfer modules side-by-side). Normally when transferring two blots in the same tank we run for 2hrs at 20v, as the tank takes about 30 minutes to get up to 20v. However in this case after 1hr the blot was still only running at 4v. I checked the tank and the power pack temperature, and both were not noticeably hot, so I don't think the pack was struggling with high resistance. After 2h the blot was still only at 4v, and had barely transferred at all.
Upon dis-assembling the transfer module I noticed that the sponged inside all had turned yellow, however only the sponge touching the positive electrode, and only the side of the sponge facing the positive electrode.
I'm not really sure what went wrong here to be honest. The only thing that I notably did differently was that I made the transfer buffer up the day before and left it in the ice machine overnight. The transfer buffer was glycine and tris with 20% methanol, in distilled water.
Any thoughts would be appreciated.

What concentration of glycine in the buffer? Sound very much like your transfer buffer wasn't correctly made or you had a non-conductive layer in the western that wouldn't normally be there. It is very unusual for Voltage to not reach the set point almost immediately.

Did you check the wiring in the transfer tank? Something could be corroded or otherwise damaged to the point of breaking, allowing only weak current to pass through. Also, make sure the leads are clean (use a brass brush to remove any corrosion) and of course check that your power supply is working properly...

Thank you for the comments. When I got back into the lab I double-checked the chemical shelf and it turns out I had put NaCl into the buffer instead of glycine! Currently soaking the sponges over the weekend to see if the yellow colour comes out...


text:
Brain evolution in the age of the caesarian
I have just been reading an account of the evolution of human intelligence in Matthew Syed’s recent book on diversity, called “Rebel Minds”.
He is not the originator of this idea, but he suggests that the limiting factor in the growth of the human brain beyond it’s already prodigious size is the size of the female birth canal, so that, above a certain size it had killed the mother and itself at birth.
I am not a biologist.  But I wondered whether there is any evidence of increase in brain size in the past (say) 50 years as more gravidae give birth by C-section?  Is such a change possible or probable as this procedure becomes more common?  Or are there other limiting factors, such as the weight that can be carried by the spine?

50 years - maybe two human generations - is hardly long enough for evolution to have a measurable effect.  Also, head size is not high among the reasons why C-sections are done.  Nor AFAIK is there any fundamental reason why human brains(or other species) could not continue growing after birth.  (E.g. marsupials.)

@jamesqf Thank you.  Yes it is obvious, now you mention it, that 50 years was a ridiculously short suggestion.


text:
Are there any papers that give examples of what is a "high" and "low" TPM expression value for given gene types?
My question relates to how to interpret TPM gene expression values, and what might be considered as "high" and "low" expression values, based on the gene type. For example, a receptor tyrosine kinase or an enzyme can catalyse many reactions and so only needs a relatively low gene expression to have a high effect, whereas something like a ligand may need a higher expression value.
Does anyone know of any rule of thumb TPM expression values that have been defined in the literature e.g. 50-100 TPM is considered standard for a receptor, etc?
Thanks in advance

This is very difficult to answer in absolute terms. Many factors influence expression. It is not just "how many proteins are needed" but also depends on e.g protein stability and translation efficiency, etc. I think terms such as high vs. low only make sense for a single gene when comparing expression across conditions.

No.
High and low gene expression are not absolute concepts, as the poster himself would seem to recognize in his speculations about different types of protein. In science you can only talk about “high” and low in relation to some reference normal situation, and this means making a measurement on some appropriate control.
What control is appropriate will depend on your biological system, and that requires careful consideration, followed by the necessary work. Is it appropriate to compare different tissues, ages, stimuli, organisms? What is not appropriate is to make a declaration in a vacuum.


text:
Thymus & T-Cell Generation and Maturity
I am a beginner in immune system. I am trying to understand the connection between T-Cell and Thymus as person ages.
It is clear from Guyton & Hall that till teenage the T-cell from bone marrow comes to Thymus which further gets filtered so that T-Cell does not attack self antigen (normal antigen of body). In this process of filtering out T-cells about 90% of the T-cells produced in bone marrow is destroyed in Thymus.
And then its said that, after teenage Thymus gets partially inactive OR it can be removed. Now what I am unable to understand is if Thymus gets removed/inactivated, in say a 45 year old person, who is going to filter the T-cells produced in bone marrow; by filtering I mean kill off the T-cells which can attack self-antigen of body.
If anyone can throw some light, it would be great.


text:
How long does it take for a new muscle fiber to be connected to motor neuron?
When new muscle fibers are formed through hypertrophy, how long does it take for motor neurons to connect  to the new muscle cells in order to be able to control them?
After taking a break from working out, I noticed that my strength has actually increased and I wondered that maybe although the new muscle cells were already built back when I was working out, they weren't yet connected to the nervous system and so I couldn't "access" this strength.

The question is quite interesting. what is the time required to newly establish a neural connection to newly formed muscles? Unfortunately the answer is NO.
No new muscles are formed by hypertrophy.
This is because you are referring to hypertrophy, not hyperplasia, which are essentially different. Hypertrophy is increase in the muscular fibers due to increase in mitochondria, myofibrils and other cell organelles. The size and volume of cell increases but the number of muscular cells remains same, hence there is no change in the nerve connections. The nerve connections essentially remain same. When you do strength training, the proteins i.e. actin and myosin undergo wear and tear. This damaged is repaired by synthesis of these proteins which is results in muscular hypertrophy.
Hyperplasia is increase in number of cells. Which brings us to next question, do muscle cells divide? The answer is YES, but it is largely restricted. These cells are termed as satellite cells.
So new neural connections are established probably only if new muscle fibers are formed.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

Thanks! So do I understand correctly that generally the total number of muscular cells remains constant, but the size of the cells increases due to strength training? And when does muscular hyperplasia occur and how long does it take for neural connections to be established when it occurs?

@timtam, yes! it is the strength and weight training that causes the muscular hypertrophy.  Muscular hyperplasia occurs during the muscle damage or when satellite cells are stimulated under the influence of growth factors. Although I am unsure of time required for formation of new neural connections for a new muscle fiber, but I think that a new neural connection is established as the muscle fiber is formed.

@TOXIN_SCIENCE thanks. what exactly causes this muscular damage in hyperplasia? Aren't sore muscles from workouts not also damaged muscles? Do you have any literature suggestions to read more about how neurons connect to muscles?


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Understanding the voltage of a living cell

Voltage, electric potential difference, electric pressure or electric tension is the difference in electric potential between two points, which (in a static electric field) is defined as the work needed per unit of charge to move a test charge between the two points. (from Wikipedia)

What exactly is a point in this definition? The voltage of a neuronal cell can be measured for example and a living cell is not exactly what I intuitively understand to be a point. Let's say I have such a cell with an electrical potential $V_m$ of $-80mV$ (is this the same as saying the cell has a voltage of $-80mV$?).
Am I right then that the voltage is a relative measure between the cell and the extracellular fluid? And is the voltage of this fluid then just the symmetric inverse, i.e. $V_{extra}=80mV$? How then can the voltage be measured between two bodies (neuron and extracellular fluid), because the concentration of charged ions might not be uniform across the fluid (or across the cell)? Could the voltage also be measured between two organelles within the cell or between the entire human body and the air surrounding it?

Voltage is always a potential difference, so you need two "points" to define one.
Technically speaking, a neuron doesn't have a voltage and the extracellular space doesn't have a voltage; there's only a voltage between the inside and outside of the cell. However, because technically speaking a neuron doesn't have a voltage, it can be reasonable shorthand to say "voltage of a cell" when you mean "potential difference between inside and outside of a cell". I wouldn't let that imprecision in terminology get you tripped up. In neuroscience we use the convention that the potential difference is with respect to the inside of the cell.
Yes, you can measure different voltages among intracellular compartments, as well. Yes, you can also have voltage gradients within cells and outside cells, though because these are aqueous solutions with dissolved ions, voltage tends to equalize in these compartments quite quickly (until confronted with the capacitance of a membrane). That is, if the concentration of charged ions is not uniform across the inside of a cell, there's going to be a net movement of charged ions inside the cell until things are effectively isopotential.
Measuring voltage with the air is going to be difficult, because air is an excellent insulator. But yes, you could define a potential difference between some place in the human body and something outside. If you've ever gotten a static "shock" you've abruptly discovered that there was a sizable voltage between the surface of your skin and whatever you just touched.
Undergraduate neuroscience textbooks typically have an extensive section on measurement and interpretation of biological voltages; two I would recommend are Purves' "Neuroscience" and Kandel's "Principles of Neural Science". The Wikipedia page "membrane potential" also seems like a good introduction.

Brilliant answer, thanks.


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Heat-treatment for protein expression
I want to express thermophilic protein in E. coli and the first step purification is to heat the crude protein. Since I don't know the optimum temperature to denature the contaminants, I plan to heat the protein in three different temperatures. I currently have 120 ml crude protein and I wonder, is it okay for me to divide the crude protein for each temperature? So, I will heat 40 ml crude protein for each temperature.

Yes.
In fact this is exactly what you would do if you wanted to perform the experiment to determine which condition is best. For these sorts of experiments you use one batch and split it amongst the experimental variables, so that you don't have to deal with inter-batch effects (e.g. different concentrations of protein).


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temperture on rate of mitosis in plants
does an increase in temperature cause an increase/decrease in the rate of mitosis (ie) the rate of cell division increases, more cells are undergoing mitosis at a  higher temperature? mitotic division increase?)

Welcome to SE Biology. Please finish reading the [Tour] to learn about this site. We try to use standard English on this site as it is for serious students and professionals in Biology. Sentence in English start with a capital letter — please edit your question and title, and while you are about it do a spelling check. It doesn't look good when the key word of your question is spelled incorrectly in your title.

Mitosis does not occur at very low or very high temperatures. Within the ideal temperature range, the rate of mitosis seems to increase linearly with temperature. That is, higher temperature supports a faster rate of mitosis, and a lower temperature results in a slower mitotic rate.
As a side note, I was able to find many sources surprisingly quickly, and it is recommended that you provide your previous research when creating a question on Stack Exchange. Since you are new here, I have decided to assist you by answering, but be warned that plain questions without any prior effort from your side will get no answers and could even be voted to close.
Sources
One:

They [work by Engelberg in 1965] showed that temperature controls the rate and speed at which a cell divides ... mitosis was very sensitive to temperature, and that cell cuture subjected to temperature between 24-31°C exhibited an accumulation of cells in mitosis ... the speed at which cells exit mitosis is temperature dependent (Rieder and Maiato, 2002). M-phase length is dependent on temperature and is longer at low temperature, likely due to a decrease in enzymatic activity. However, at high (42-44°C) temperatures, spindle assembly is also impaired and cells do not meet the requirements to proceed through spindle assembly checkpoint.

Two:

The rate of cell progress, or mitotic rate, throughout the mitotic cycle increases linearly with increase in temperature between the range 3 °C to 25 °C.

Three:

Observation shows that at 0° and at 40° the cells do not go through the cycle at all and that from 10° to 30° the speed increases in almost linear proportion.

Worth noting: This range may be true for many terrestrial plants, aquatic and marine plants have an optimal temperature that's somewhat lower.

@ARogueAnt. that's a great point. Feel free to edit my answer!


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Is there a term for fixation OR loss of an allele?
I remember reading a paper which used a term to describe either fixation OR loss of an allele via drift. Its definition is basically "the removal/fixation of a polymorphism in a population due to the action of genetic drift". An example of how it could be used in a sentence is:

The expected time to term is dependent on the effective population size of the population, $N_e$.

I can't for the life of me remember the term, or the paper, and it doesn't appear to be common in the literature as I haven't encountered it again. It's driving me insane! Does anyone know what this term might be?

It seems like “equilibrium” may work, though that is likely more general than the term you are looking for.

Also, I've heard "extinction or fixation" used in this context, re: The expected time to extinction or fixation is dependent on the effective population size of the population...


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Inexpensive and quick hematology tests
I was interested in measuring hemoglobin, hematocrit, erythrocyte sedimentation rate, and dna damage, but most methods require expensive equipment or take to long to perform.
I though about using 4ml EDTA tubes, draw the sample, then put it on a stable surface at a constant temperature after shaking it, wait for a period of time, maybe 40 minutes, and check the separation of plasma and RBC with a caliper to estimate ESR roughly. After that put it in a electric centrifuge, and after separation see the volume of RBC to plasma again with a caliper to estimate the hematocrit. Lastly shine a light from the bottom of the tube in a regular lighting environment and measure the color (which i suppose would mean higher red) through a digital camera, of the RBC aggregate to estimate the hemoglobin content.
For estimating dna damage I only know about the comet assay, but i feel is too expensive and very time consuming to perform, so any ideas would be appreciated.
I know these measures aren't standard or precise, but what Im interested in is if they are actually measuring what they are supposed to be measuring and are sensible enough to some level of variability.
I also want suggestions regarding the DNA damage measures, a very rough estimate is fine.

Is the intent here to satisfy your curiosity, or are you a health care provider in a location lacking proper equipment? If you want to test yourself for fun, go for it. Afterwards, compare to lab results to see how well you did. You might be surprised at how different your results are. (There's a reason labs do these tests.) "I also want suggestions regarding the DNA damage measures, a very rough estimate is fine." That's not possible (by any stretch of the imagination.)


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When comparing oral infection v IV infection in mice, why would the CFU given be different volumes?
In the paper, orally infected mice are given 1x10^9 CFU of C. Rodentium and IV infected mice are given 5x10^7 CFU of the pathogen. Does anyone know if there is a generic reason for this? Thanks in advance.,

Intravenous delivery of pathogen produces infection more efficiently than transmucosal delivery.
10^7 is 2 orders of magnitude less than 10^9.  It is not the volume that is different (although it may be), it is CFUs or "colony forming units" which is a proxy for viable pathogens in the inoculum.  The oral dose is 100x that of the IV.
Getting germs directly into the bloodstream bypasses the built in protections that our mucosal surfaces have.  The GI and GU tract have a lot of defenses.   For example an experimental SIV infection produced intravenously in monkeys requires an order of magnitude less virus than an infection established rectally or vaginally.
I would suspect that the CFUs of a given pathogen via a given route is something established empirically as producing the desired outcome.  If you used the same CFUs for an IV route as were required for the oral route, you might have a fair number of mice that just died from septic shock from the huge number of bacteria suddenly in the blood.  Given the 2 order of magnitude difference of inoculum (IV vs PO) to produce infection you might conclude that the stomach kills 99% of any inoculum.

Thanks that's really helpful and makes sense!


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Is a lion a bony fish?
If you ask Wikidata "Does the species lion (Q140) have a parent taxon line up to the Osteichthyes (Q27207, bony fishes)?", it answers yes:
SELECT ?item1
 WHERE {
  wd:Q140 wdt:P171* ?item1.
  ?item1 wdt:P171 wd:Q27207.
 }

Here's a direct link.
Now, I assume that this must be wrong at some level (I'm no biologist, so please correct me if I'm wrong), so I tried to find the error.
This query displays that path more explicitly, starting with mammals:

Mammals (Q7377) have Tetrapoda (Q19159) as a parent taxon.
Tetrapoda (Q19159) have Tetrapodomorph (Q1209254) as a parent taxon.
Tetrapodomorph (Q1209254) have Rhipidistia (Q150598) as a parent taxon.
Rhipidistia (Q150598) have Sarcopterygii (Q160830) as a parent taxon.
Sarcopterygii (Q160830) have Osteichthyes (Q27207) as a parent taxon.

The third point seems strange, because Rhipidistia are described as a taxon of fish, which would mean that all mammals are fish.
Maybe this comes from the fact that tetrapods (and therefore mammals) evolved from Sarcopterygii 390 million years ago, as described here.
Is "having evolved from" considered a parent taxon in biology? If not, which of the five statements above is wrong?

Hi Cheeesus and welcome to Bio.SE! As you guessed, lions are unsurprisingly categorically not bony fish. I think you should be clear about what exactly the parent taxons are. To me it looks like they are ancestors. So we may have evolved from species that were bony fish, but that does not make us bony fish.

@James, thank you. Yes, to me too it appears like the data in Wikidata confuses "parent taxon" in the evolutionary sense ("mammals evolved from bony fish") with "parent taxon" in a classification sense ("lions are a subtaxon of mammals").

If you take cladistics literally (instead of as a useful tool), then yes, lions - and humans - are just bony fishes, by the same logic that says birds are dinosaurs.  (But both are just bony fishes, so there :-))

Possible duplicate of Am I a lobe-finned fish?

related questions https://biology.stackexchange.com/questions/87725/how-does-taxonomy-work-the-case-of-the-avian-dinosaurs/87728#87728 and https://biology.stackexchange.com/questions/70874/are-humans-gnathostomates/70954#70954 you should really be searching for similar questions before oyu ask.

The path is correct. The safest reading is to say that the lion shares a set of characteristics with the lungfish. You can also say that lion and carps are bony vertebrates (Euteleostomes).
In evolutionary taxonomy, each taxon does not need to consist of a single ancestral node and all its descendants: it allows for groups to be excluded from their parent taxa (in other words, not "being part of" but, as you said, "having evolved from"). Thus, lungfishes are closer to the lions than they are from, e.g., sharks or trout. In other words (even if this is too simplistic to say so), their "common ancestor" is more "recent".
In the Linnaean taxonomic system, all fishes were in the same class. This corresponds to our "everyday life" classification of fishes but not to the most recents findings about the "common ancestors".
To make things clearer, you need to understand the concept of paraphyly. The bony fishes group is paraphyletic with respect to the tetrapoda. In other words, it consists of the group's last common ancestor and all descendants of that ancestor excluding the tetrapoda. "Bony fish" is therefore not a clade, but "Osteichthyes/Euteleostomes" is a clade (= a monophyletic group of the bony vertebrate with a common ancestor that looked like our "modern" fishes).

Thanks, but this should somehow be indicated when using the property "parent taxon". Lions and extant bony fish like clown fish both have Osteichthyes as an ancestral taxon, but you cannot really say "A lion is a bony fish", can you?

Oh, maybe I'm confusing Osteichthyes with Teleostei?

Yes, I think that this is where the confusion takes place. Teleostei is distinct from mammals, but they share a common parent taxon (Osteichthyes) from which they evolved.

Are there any extant Osteichthyes which are not Teleostei? I don't mean "extant species which have evolved from Osteichthyes", I mean species which are now considered a subtaxon of Osteichthyes.

you mean "modern" bony fishes that are not teleostei ? Yes, the lungfish, this is why I took it as an example.

Thank you so much. Paraphyly made things much clearer.

for me they are all at the same distance if you look at the length of the lines.


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Contrast Media for Plant cells
I currently have a waterweed (elodea) preparation for my optical microscope but i can only see some of the structures (membrane, wall, chloroplasts and the nucleus).
Now I want to see more (Like the Vacuole, Peroxisome, Mitochondria, Amyloplast, Ribosome, Golgi Apparatus, and endoplasmatic reticulum if possible with an optical microscope)
I know there are contrast media like the lugol's iodine solution (iodine-potassium iodide solution) but what will it show? And are there more?
Thanks in advance


text:
Are these algae responsible for concrete staining the same organism?
I am interested in studying the effects of algae that cause concrete staining on the walls in my city, particularly because this green growth is widespread in my country, Quito, Ecuador.

Since I am considering establishing an in silico Genome-scale Metabolic Model (GEM), I need to determine whether this type of algae is a distinct organism or a composite of fungi, archaea, cyanobacteria, and other microorganisms.
I have some doubts, as I have successfully cultured a sample of this green algae using wastewater, NPK fertilizer, and exposure to sunlight. Moreover, these algae exhibit remarkable resilience to fluctuations in temperature and oxygen availability.

“ determine whether this type of algae is a distinct organism or a composite of fungi, archaea, cyanobacteria, and other microorganisms” have you tried using a microscope?

since its naturally occurring the answer will almost certainly be no, monoculture is a human invention.


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Does the Lomax model describes enzyme kinetics?
I´m here looking for empirical experience over this revelation, which surely is not so amazing but better call biology experts.
I recently founded the Lomax Probability Distribution and noted that the cumulative distribution function $L(x)$ has a very similar form related to the Michaelis-Menten Kinetics rate equation $v(S)$. This since:
$$L(x) = P(X \leq x) = 1 - \Big[1+\dfrac{x}{\lambda}\Big] ^{-\alpha}$$
and
$$v(S)=\dfrac{V_{max}S}{K_m+S}$$
Are, in fact, the same equation with $\alpha = 1$ and $\lambda = K_m$ since $L(x=S) = \dfrac{v(S)}{V_{max}}$.
Can this equation be used to model enzyme kinetic rates?
Does you have applied it?
P.D. I´ve never heard of an application of Pareto-related distributions in enzyme kinetics, so maybe it is a good start for modeling biochemical processes. Specifically, since $\lambda = K_m$, we could use experimental data to model this interaction with more precision (maybe) since a model that allows uncertainty is unlike lambert/regression solutions that are only deterministic.

The kinetics of enzyme reactions are determined by their mechanism of action, which vary considerably. The general approach taken is to elucidate the mechanism experimentally and then apply mathematics to it, making various assumptions. It is not, as far as I am aware, to attempt to fit it to some abstract mathematical model.


text:
Can a baby have a combination of traits transferred by the parents?
like: B=black color.
b=white color.
e.g.: one parent has genotype for skin color as (BB) and the other parent has genotype for the same trait as (bb).
can the child have the skin color which not too dark and not too white like brown?

Yes (I'm tempted to say "of course", as I would be surprised if you had not personally met families where the children had phenotypes intermediate between their parents' phenotypes ...)
This phenomenon is called incomplete dominance.  Now that you know the correct terminology you can easily do a web search and get lots more information ...

thank you, i have been stuck on this question for a while and your answer really helped

any particular reason for the downvote?

i didn't down vote you...

I know, I was addressing that to whoever downvoted ...

Can't speak for the down voter, but this does seem to the sort of question that we shouldn't be encouraging with answers — specifically from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. This is "homework" since it addresses a basic biology concept that may seem trivial to biology professionals. I personally prefer to direct users who appear to have little or no background knowledge to Khan Academy.


text:
What are these mushrooms growing in my garden?
I live in Southern California. Over the last couple weeks, these two different kinds of mushroom have manifested in my garden. They seem to grow rapidly overnight, only to wither and show up somewhere else a couple days later. For reference, in these images they are about 2-3 inches tall. I'm concerned my neighbor's cat may try to eat them.

The second image is a type of coprinoid https://www.mushroomexpert.com/coprinoid.html There are specialiized mushroom ID groups on FB and Reddit.


text:
What keeps pyridoxamine phosphate inside the aminotransferase enzyme active site?
In the function of an aminotransferase enzyme after the first substrate (amino acid) has been deaminated there seem to be nothing binding the resulting pyridoxamine phosfate to the rest of the enzyme (thus defying the definition of prosthetic group).
So what keeps it inside the active site of the enzyme so that it is ready to donate the amino group when the second subtrate binds?
Bonus question: what keeps the lysine bound to the pyridoxal phosphate (internal aldimine) from losing a proton and becoming a quinonoid intermediate itself?

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Reading everything my course's book (Lehninger's Priciples of Biochemistry) has to say about aminotransferase enzymes in my opinion counts as an attempt to get an answer. And it seemed to me that the question was specific enough to show that I've done a bit more than little or no prior research. If this is not enough thanks for the info, I didn't know that.


text:
Changes in dna from dioxin poisoning
A person sprayed with a dioxin, how long would it take for a dna change? Instant or over time? Would that person having children afterwards pass on any(if any) dna changes?

Studies on model organisms suggest effects begin quickly, within 6-8 hours of exposure. Rat studies suggest liver absorption of dioxin reaches a maximum from 8-24 hours, with Cytochrome P450 protein expression levels peaking afterwards. Another study uses a comet assay that measures DNA damage after six hours of dosing, and damage is tied to dose level.
Epigenetic changes to sperm and eggs are heritable, passed along to offspring. These result from histone deacetylation and methylation, which in turn change how DNA are packed and unpackaged for protein expression, and change expression itself.
A summary article on epigenetic dioxin (TCDD) toxicity suggests that there are specific effects on protein expression involved in embryonic development in model organisms, which result in birth defects and immune system damage.
In addition to controlled lab experiments on rats and mice, the United States of America and Monsanto conducted a massive, uncontrolled science experiment on humans, dropping dioxin in great quantities on millions of Vietnamese civilians during the Vietnam War.
Children of exposed victims suffered spinal bifida and other birth defects. US military exposed to dioxin in the course of deploying this chemical weapon also had their children suffer greater rates of similar birth defects.

Awsome,  thank you for the information... also does anyone know what immune changes with dixon poisoning?  Thank you in advance...


text:
Minimum amount of RNA for cDNA conversion and qPCR
I searched several protocols for reverse transcription of RNA and all suggest using RNA concentrations of 1ug. Could a lower amount result in inferior transcript representation and therefore decreased quality of the qPCR results?
We use the SensiFAST SYBR Lo-ROX kit from BIOLINE. I was thinking of using 500ng instead of the suggested 1000ng. In order to accommodate the protocol, I would use 0.5ul of RTase to maintain the 1:1 (m/v) ratio. Buffer, DNase, water, and RTmix concentrations for the reaction I would keep the same. For the final dilution of the cDNA, I would dilute 5x instead of 10x to maintain equal concentrations.
Does anyone have experience with this? Does transcript representation suffer?
Do the suggested protocol adaptations seem reasonable?
Thanks for the help in advance.

Two answers follow:

Technical experience of many: it should be no problem to have the same protocol with a twice-lower starting concentration, without making any adjustments whatsoever. The suggested 1ug is very much on the safer side of things, 2-fold fewer transcripts makes almost no difference. Maybe at 1 or 2 orders of magnitude (10 to 100s) less will you run into problems or a need to correct your reactions.
Scientific orthodoxy: the most scientific piece of advice anyone can offer you would be to try it both ways and compare your results using qRT-PCR. I'm guessing both approaches will show very similar results.


text:
Is the transition epithelium a monolayer epithelium? Or is it a stratified epithelium?
I had learned that transitional epithelium is a type of pseudostratified epithelium, so I understood that transitional epithelium is a type of monolayer epithelium.
Wikipedia has the following description(but with source tag);
” These structural elements cause the epithelium to allow distension; however, these also cause the tissue to be relatively fragile and, therefore, difficult to study. All cells touch the basement membrane.[citation needed]”
https://en.wikipedia.org/wiki/Epithelium
From the above description, all　epithelial cell appears to be in directly adhered with the basement membrane.
However, the illustration in the Wikipedia entry for Epithelium is clearly multi-layered. Thus, it appears to be a stratified epithelium.
https://upload.wikimedia.org/wikipedia/commons/thumb/6/64/423_Table_04_02_Summary_of_Epithelial_Tissue_CellsN.jpg/900px-423_Table_04_02_Summary_of_Epithelial_Tissue_CellsN.jpg
So, I would like to identify which is correct;

Is the transition epithelium a monolayer epithelium? Or is it a stratified epithelium?

Urothelium, which is another way to refer to transitional epithelium is indeed a stratified epithelium.