text:
Fairy little bug
Can someone please enlighten me what kind of a creature is this sweet little friend?

Welcome to Biology.SE. Please [edit] your post to include the size, approximate geographic location, and anything else you observed about this insect — e.g.s: behavior, what kind of plants are in the area. Where you saw this is essential to and the size may be very helpful for getting an accurate identification. You may also find it helpful to take the [tour] and then go through the [help] starting with [ask] questions effectively on this site. Thanks.

related: https://biology.stackexchange.com/a/93176/16866

This is a planthopper nymph. These are a quite diverse group of insects found worldwide. Which one you have is open to further answers, and will be based on your locality and the species of plants and insects in that location.
The furry "tail" and the fish-like mouth-parts/head give it away.


text:
What was the largest flying insectoid pollinator?
Megachile pluto is a large resin bee whose body length may reach 38 mm and a wingspan of 63.5 mm. But that's nothing compared to the prehistoric and extinct Meganisoptera including the Meganeura, which had 'dragonflies' whose wingspan exceeded 70 centimeters!
There are "recent studies" linking animal gigantism in the Paleolithic to the increased atmospheric oxygen content.
Considering the size of some prehistoric insects I can't help but wonder: how big was the world's biggest insect(oid?) flying pollinator?

Define what criteria you're using for big: wingspan, body length, mass, or ?  Also, if the Meganeura were like modern dragonflies, they were probably predators, not pollinators.

Good question. Wingspan might be a fairly good measure, or body length. With no answers so far I'll gladly settle for ANY measure of size at this point.
-- As for the huge dragonflies being predatory? I'll be in my bunker.

keep in mind flowering plants did not evolve until the Jurassic.

Meganeura is from the carboniferous 360Mya, currently the biggest non insectoid is an 8 inch hummingbird. https://en.wikipedia.org/wiki/Giant_hummingbird?wprov=sfla1

Currently the best fit is probably a 28cm butterfly, lepidoptera fossils say its the biggest known insectoid pollinator, although it seems resonable that a 50+ cm lepidoptera can have been around recently.

@aliential: I'd say the largest non-insect pollinator is probably H. sapiens.  It's a learned behavior, though.  For mass rather than wingspan, I'll offer the hawk moths, some of which are indistinguishable from hummingbirds without close examination.

source: Stack Exchange

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

sort: votes


text:
Is the quiescent centre only found in monocot roots?
I read that the quiescent centre is present between the dermatogen and calyptrogen. As calyptrogen is only present in monocot root, does that mean quiescent centre is only found in monocot roots?

I don't know the answer specifically but unlike the dicot roots the monocots donot show secondary growth in case their roots suffer injuries. So even if the quiescent centre be present in the dicots it makes more relevance in the monocots...

that's a very valid point, thanks for the answer!

Note that quiescent centers are typically defined by cell division activity not anatomical placement and are not confined to monocots.
For example, this paper discusses the quiescent center in Arabidopsis roots1.

Reference:
1: Doerner, P. (1998). Root development: quiescent center not so mute after all. Current Biology, 8(2), R42-R44.

Thanks for the article! I found it very informative.

You're very welcome!

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text:
What is the percentage of food that goes to a lamb fetus?
Does any one know the percentage of food eaten by a pregnant ewe that goes to the lamb fetus?
Specifically how much does the mother take for her body from every one kilo of food
and how much does the fetus take?

Welcome to Biology.SE! It is expected that you will do research on your own before asking questions here — for example you could start with this: https://extension.oregonstate.edu/animals-livestock/sheep-goats/nutrition-lambing. –––––––– For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

In addition, since the answer to this question will vary considerably by gestational stage please edit your question to clarify what you want — e.g. an average over the entire pregnancy.


text:
Is there any non-human animal social group that punishes members with "imprisonment" or a similar method?
I was reading this blog on Scientific American, which discusses whether wild animals are happier than domesticated ones. I've also read about strong territorial instincts in some species. This reading led me to ask whether there is any non-human animal social group that punishes members with something similar to "imprisonment".
When I say "imprisonment" I mean restricting the mobility and survival freedom of members, for some social or cultural reason.
By "imprison", obviously I don't mean the use of cages or prisons or any of the manmade ways of imprisoning. I wish to know about whether, in any species, a member acting alone (or acting together with others of their own), build a virtual territorial wall/ring around another member(s) of their own species, acting almost like an imprisonment? This may not be physical exertion of muscle force, but may by making (say, for example) continuous noises as a group to restrict the territory of their own member.
Maybe, one can exclude adult members forcefully protecting their young ones, because that would be in their instinctive interest, even if the young ones' instinct is to violate a restriction. Also please avoid answers on behaviour of one species defending their territory. That's not the same as restricting by "constructing" a limiting threshold in an enclosure-like fashion.

does slavery count, as e.g. ants? https://en.wikipedia.org/wiki/Slave-making_ant

Interesting, thanks. I knew about bees for class-divide. I meant imprisoning for bad behaviour or for some kind of misfit in the community.

whoof... that is a really big topic that seems to be more about animal social/cultural structure than a particular sort of social tool (imprisonment). Editing the question to reflect this new information. i'm not the person to answer this, other than to suggest to read more. maybe there is something here that can help you: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936173/

Welcome to Biology.SE! Your recent edit has made your question quite a bit clearer, but I have no idea what you mean by "survival freedom". In addition, you seem to be excluding the large group of animals that modestly refer to themselves as Homo sapiens. I've edited your post to make that clear and also removed your last paragraph, which seems both disingenuous and irrelevant to your central question. I also made some small corrections of typos etc. Please make sure that I have not altered your intended meaning.

consider that very few human societies use imprisonment, only ones with a large food surpluses and large populations, most human societies use shunning instead which is quite common in social animals, but that does not work with groups much larger than dunbar's number, where most people are strangers. Imprisonment is an invention created due to limits in our evolved social controls not something instinctual. Also consider whether shunning would count as imprisonment by your definition.


text:
What are the reasons for using oligo-dT instead of oligo-U to isolate mRNAs?
dTTP oligonucleotides are used to isolate mRNAs because mRNAs (in eukaryotes) have a poly A tail which binds to the complementary oligo-dT. However, why do we not use oligo-U instead (uracil)? I would guess it is because ribonucleotides have the additional 2' OH which is reactive, so less desirable, but is there any other reason?

Note - This answer only covers the comparison of rA-dT (RNA:DNA) and rA-rU (RNA:RNA) duplexes, and not more exotic options involving deoxyuridine (dU) and ribothymidine (m5U).
I can think of three possible reasons why oligo-dT may be preferred over oligo-rU for poly(A) hybridization and mRNA capture:

The rA-dT duplex is more stable than the rA-rU duplex, thus affording a more efficient pulldown.
dT oligonucleotides are easier to synthesize or more stable than rU oligonucleotides (and therefore cheaper to manufacture).
There are methodological considerations beyond the hybridization step that make oligo-dT a better choice.

Let's address each of these...

Hypothesis #1 $\rightarrow$ The rA-dT duplex more stable than the rA-rU duplex.
Conclusion #1 $\rightarrow$ probably not
Using NMR to observe the exchange rates of imino protons, Huang and Russu compared the stabilities of homologous duplexes containing tracts of  rA-dT, dA-rU, rA-rU, and dA-dT base pairs.1 Overall, they found the rA-dT and rA-rU duplexes to be similar in terms of base-to-base stability:

(i) Among the four nucleic acid structures investigated, the highest base-pair stabilities are observed for the dA-dT tract of the DNA duplex; the lowest base-pair stabilities are observed for the dA-rU tract of the dA-rU RNA-DNA hybrid.
(ii) The stabilities of individual base pairs in the rA-dT tract of the rA-dT hybrid are the same as those of rA-rU base pairs in the RNA duplex and are intermediate between the stabilities of DNA dA-dT and hybrid dA-rU base pairs.
(iii) The stabilities of base pairs in the rA-dT tract of the rAdT hybrid and in the rA-rU tract of the RNA duplex do not vary very much with the location of the base pair in the tract. In contrast, in the DNA duplex and the dA-rU hybrid, the highest and lowest stabilities are observed for the central base pairs in the tract.

This opposes an argument that oligo-dT is preferred due to enhanced stability of the resulting RNA:DNA duplex. An important note here is that the study cited above only tested tracts between 4 and 10 base pairs long, whereas most mRNA capture protocols utilize dT oligos in the 12-25 nt range.2

Hypothesis #2 $\rightarrow$ dT oligonucleotides are easier to synthesize or more stable than rU oligonucleotides.
Conclusion #2 $\rightarrow$ yes
As stated in the question, RNA is generally considered less stable than DNA due to the reactivity of the 2′-hydroxyl group. During solid-phase RNA synthesis, iterative protection and deprotection of the 2′-OH is required for addition of each new nucleoside, meaning that there are many more steps in RNA synthesis than solid-phase DNA sythesis when comparing equal-length oligos.3 Practically, this means rU oligonucleotides are much more expensive to order that dT oligonucleotides. As of 12 July 2021, IDT quotes me \$8.55 for 100 nmol oligo(dT)19, whereas the same amount of oligo(rU)19 costs \$142.50.
Beyond the cost, the reactivity of RNA and the ubiquity of RNases means one must take special precautions when handling and storing of RNA oligos, as explained by IDT:

The inherent chemical structure of RNA makes it less stable than DNA because the additional hydroxyl group attached to the 2’ position of the pentose ring in RNA nucleotides makes RNA more liable to alkaline hydrolysis. In addition, RNases are pervasive, making RNA more susceptible than DNA to degradation. Thus, RNA oligonucleotides should be stored as an ethanol precipitate at –80°C for greater stability. For short-term storage, we recommend resuspending RNA oligos in a nuclease-free neutral to slightly acidic buffer containing a chelating agent, such as IDTE. However, it is always important to avoid RNases and alkaline hydrolysis when RNA oligos are stored.

Hypothesis #3 $\rightarrow$ There are methodological considerations beyond the hybridization step that make oligo-dT a better choice.
Conclusion #3 $\rightarrow$ yes
In state-of-the-art mRNA library preparation kits such as those available from New England Biolabs and ThermoFisher Scientific, the bead-bound dT oligos serve both as the baits for poly(A) hybridization and as the primers for first-strand cDNA synthesis. These kits use RNA-directed DNA polymerase (e.g. MMLV Reverse Transcriptase) for cDNA synthesis, which requires a DNA primer from which to polymerize new DNA. Thus, any protocol utilizing an RNA:RNA hybridization at the pulldown step would have to dissociate the strands and introduce DNA primers before reverse transcription.

References

Huang Y, Russu IM. Dynamic and Energetic Signatures of Adenine Tracts in a rA-dT RNA-DNA Hybrid and in Homologous RNA-DNA, RNA-RNA, and DNA-DNA Double Helices. Biochemistry. 2017 May 16;56(19):2446-2454.
Anderson AJ , Culver HR , Prieto TR , Martinez PJ , Sinha J , Bryant SJ , Bowman CN . Messenger RNA enrichment using synthetic oligo(T) click nucleic acids. Chem Commun (Camb). 2020 Nov 21;56(90):13987-13990.
RNA Oligonucleotide Synthesis. ATDBio.


text:
Can crows see in ultraviolet? If so, does their plumage look different in UV?
Apparently birds which appear identical to the human eye can look quite distinct under UV light. Additionally, drab looking birds might have more "spectacular" looking plumage when considering wavelengths outside of the visual spectrum.
Question: In the specific case of crows, (1) can crows see in the ultraviolet range? (2) is the plumage of crows still monochrome when considered in the UV spectrum? Is it dichromatic?
Google seems to return very little about this, although this random person claims that crows can see in UV and their plumage does not look monochromatic under UV, while this article says they can not see in ultraviolet. Neither provides citations for their claims, and I am not familiar with the academic literature on this subject. Any help would be appreciated.
This question seems related inasmuch as crows seem black to the human eye. However, I know that some animals can see in UV, and am curious about whether this extends to crows.

Corvids (and raptors) are reported to not see UV Håstad et. al. 2005.
However, American crows are reported to recognize sex-specific differences in plumage that are invisible to humans Eaton 2006.
Unfortunately, I don't have access the latter paper so I don't know what the basis for that discrimination is or how to reconcile that result with those of Håstad et. al.
You might also find this well referenced blog post that summarizes these results to be of interest.


text:
Leaf formation on unknown tree: cocoon or something else?
A small tree in my yard has leaves which appears to double over themselves. The first two pictures show this phenomena, and the third is the same tree to maybe aid identification.

I can't absolutely guarantee when this first appeared, but I believe it was this growing season, and I know it's been there at least a month (unless it's reoccurring, I am not tracking the individual leaves).
My first thought is cocoons or some other insect behavior. Can anyone tell me what it is?
(What kind of tree it is will also be valuable, in case we can't find the answer to the leaf question here)
EDIT: Location is outside Boston, MA (USA).

Looks like a filbert (hazelnut) but I'm not certain of species...your location might help a bit and should always be included for species-identification questions. A picture of the full tree might help, too, I believe the "bushiness" of a filbert might help identification. Your "cocoons" are full of immature nuts at the moment.

@BryanKrause: Added location, outside Boston.

What a blast from the past! I used to pick wild hazelnuts when I was a child. The wild ones were covered with sharp spiny projections, but the nuts were worth it. Lucky you!

Based on the location and assuming this isn't a domesticated hazelnut there are two likely hazelnut species.  The lack of the distinctive "beak" seen on the Beaked hazelnut means this is most likely an American hazelnut (Corylus americana):

The hairs along the young branch are also consistent with this (see for example the Plant Guide from the USDA).
Note, however, there are hybrids between American and European hazelnuts so it is beyond my ability to be completely sure by visual inspection alone.


text:
Is lignification within plants a reversible process? If so which factors can reverse lignification?
Lignification is an important process in plants such as trees to allow for structural rigidity. Is this process reversible by the plant and if so which factors influence this reversibility?

A quick search found Ursache, 2021 that says in the abstract lignification is "thought to be irreversible", but I haven't chased it down.

Do you mean specifically delignification that occurs in vivo by means of metabolic processes in the same plant that performed lignification? Delignification is a well-known process of microbial decomposers e.g. white rot (https://bnrc.springeropen.com/articles/10.1186/s42269-019-0094-x), and which could presumably occur in living tissues infected by some pathogen, but I don't think that's what you mean.

I edited your post to make it more concise — please re-edit if you think I've altered your meaning, but try keep your posts as clean and clear as possible. To thank someone for a helpful/useful comment just upvote it (as I did). It would also be helpful if you added in more background — i.e. tell us where you've looked for answers, more about what you do know about the topic, and where exactly you still have questions. Also, can we assume that by "factors" you mean enzymes or are you more interested in things like environmental conditions?

I'm interested in any factors that's why I let it unspecified. A quick google scholar search did not return any results if plants are capable of reversing lignification. As I'm pretty limited time-wise I offered a bounty..


text:
This looks like it was somebody’s home - but who?
Found this near the edge of a forest in upstate New York. It looks like the remnant of a cocoon of some kind. I would appreciate any help in identifying its original maker / occupant.
I hope my fingers give a reasonable indication of scale - estimating about 30 mm across.

looks like a tiny loofah!

That looks similar to the dried fruit of Echinocystis lobata (wild cucumber), which grows throughout New York. The fruit is about the right size (~3 cm) and shape, whereas the best alternative I can come up with is smaller and differently shaped (Sicyos angulatus (burr cucumber)).
I'm confident that this is something in the cucumber family, but there could be other related plants. If you had images of dried vines/leaves associated with your specimens it might help confirm this or suggest alternatives.

Source: iNaturalist (© Robert D Stevenson).

Source: Dylewski, Ł., Maćkowiak, Ł., & Myczko, Ł. (2018). Physical defence of the wild cucumber Echinocystis lobata in an invasive range changing seed removal by rodents. Plant Ecology, 219(7), 863-873.

We do have some vines growing in the area where I found this. Thanks for the quick and thorough reply!

@Floris: You're welcome — if you can get pictures of the whole plants later this year (especially with details of the flowers, fresh  fruits, leaves, and stems) it would be helpful to edit them into your question.

good recommendation- if I see these things growing (rather than the skeleton on the ground) I will surely do that.


text:
Change Genbank entry date with Biopython
I can create a new Genbank record in Biopython with the following code:
from Bio import SeqIO, SeqFeature
from Bio.SeqRecord import SeqRecord
from Bio.Seq import Seq
from Bio.Alphabet import generic_dna
from Bio.Alphabet.IUPAC import IUPACAmbiguousDNA

my_sequence = "ATAGGGACUCATAGATA"
my_record = SeqRecord(Seq(my_sequence, IUPACAmbiguousDNA()))
my_feature_location = SeqFeature.FeatureLocation(2,5, strand=1)
my_feature = SeqFeature.SeqFeature(my_feature_location, type="CDS", id="Cre")
my_feature.qualifiers["foo"] = "bar"
my_record.features.append(my_feature)

print my_record.format("gb")

The corresponding genbank file then looks like:
LOCUS       .                         17 bp    DNA              UNK 01-JAN-1980
DEFINITION  .
ACCESSION   <unknown id>
VERSION     <unknown id>
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
     CDS             3..5
                     /foo="bar"
ORIGIN
        1 atagggacuc atagata
//

How can I change this bit UNK 01-JAN-1980?

So, the problem is that you are probably using wrong class for your record. Compare Bio.SeqRecord class with Bio.GenBank.Record class. Reason why in your GenBank format you have this reference date (01-JAN-1980) is because your record has intrinsically no date attribute, so SeqRecord.format set undefined fields to default (look through the source code to see where this happens).
What you want to do for creating GenBank record is following:
$ python
Python 2.7.10 |Anaconda 2.3.0 (x86_64)| (default, May 28 2015, 17:04:42)
[GCC 4.2.1 (Apple Inc. build 5577)] on darwin
Type "help", "copyright", "credits" or "license" for more information.
Anaconda is brought to you by Continuum Analytics.
>>> from Bio import GenBank
>>> from Bio.GenBank import Record
>>> my_rec = Record.Record()
>>> my_rec
<Bio.GenBank.Record.Record object at 0x1030b1890>
>>> my_rec.sequence = Seq(my_sequence)
>>> my_rec.sequence
Seq('ATAGGGACUCATAGATA', Alphabet())
>>> print(my_rec)
LOCUS                         bp
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
ORIGIN
        1 atagggacuc atagata
//
>>> my_rec.date = '13-JUL-2015'
>>> my_rec.features.append(my_feature)
>>> my_rec.data_file_division = "ROD"
>>> print(my_rec)
LOCUS                         bp                    ROD       13-JUL-2015
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
type: CDS
location: [2:5](+)
id: Cre
qualifiers:
    Key: foo, Value: bar
ORIGIN
        1 atagggacuc atagata
//

Notice, how print(my_seq) outputs data in GenBank format by default (since that is a GenBank record after all). I am sorry I cannot really talk on differences between GenBank.Record and Bio.SeqRecord and why/when use one object or another.
Anyways, looking up reference documentation is always a good habit: http://biopython.org/DIST/docs/api/Bio.GenBank.Record.Record-class.html

have you tried the code you suggest? appending my_record.date = "13-JUL-2015" or my_record.data_file_division = "ROD" does not modify my resulting record.

Many thanks! As a follow-up question, do you know how I could actually save a Bio.GenBank.Record object? The SeqIO.write(main_record, destination+".gb", "genbank") I used before gives me TypeError: 'Record' object is not iterable. The obvious solution, SeqIO.write([main_record], destination+".gb", "genbank") gives me TypeError: object of type 'Record' has no len()...

Actually, I turned that into a question in its own right.

For Bio.SeqIO.write(...)``` you have to give it SeqRecordobject(s), it does not understandBio.GenBank.Record`` objects.

Using the SeqRecord object approach with Bio.SeqIO, you would do something like this:
my_record.annotations["data_file_division"] = "PLN"
my_record.annotations["date"] = "24-DEC-2015"

Note that only valid NCBI GenBank divisions, or their EMBL equivalent, will be accepted.

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


text:
View ABI chromatogram plots with python
I would like to view the chromatogram traces from a few ABI (.ab1) files. I would prefer to use python for this, or a function with python bindings, or at least some open source package such as EMBOSS.
If after viewing a plot I could also extract the plotted data in the form of an array, that would be a huge plus.
I have tried the relevant Biopython parser, but it only returns a list of nucleotides (not th actual chromatogram). I have also tried abiview, but I get plots such as this, which makes absolutely no sense:

Could you help me out?

Is there anything that you want to do with the file that you can't already do with a free package such as Finch TV?

I think this might explain the .AB1 file format, which would be the first step toward writing your own file parser. If you can get the X and Y data out for each channel, you could plot it however you wanted. Good luck.

Have you looked at abiview from the package EMBOSS? See this Biostars post: https://www.biostars.org/p/4097/

The Biopython 1.65 ABI parser should expose the chromatogram data, as of Biopython 1.66 it should expose everything.
UPDATE: Example using this for plotting here: http://biopython.org/wiki/ABI_traces

I would strongly recommend using Matlab, it does not read ab1 files directly, but it can if Staden tools are installed. The reason being is that the data is presented a lot better and there is documentation. I recently wrote a QQC calculation script in Matlab as proof of principle and I will rewrite it in python (due to server building) using it as a benchmark.
In Biopython the manual says:
from Bio import SeqIO
handle = open("myfile.ab1", "rb")
record=SeqIO.read(handle, "abi")

And that is where it stops. It does have the data. The trace data is stored as annotations:
import json
print(json.dumps(record.annotations, sort_keys=True, indent=4))

Specifically, the actual raw data is:
print(record.annotations['abif_raw']['DATA9'])
print(record.annotations['abif_raw']['DATA10'])
print(record.annotations['abif_raw']['DATA11'])
print(record.annotations['abif_raw']['DATA12'])

but wait! The bases are not ATGC. but GATC as found here:
print(record.annotations['abif_raw']['FWO_1'])

Having played with ab1 files in Matlab using the command:
[Sample, Probability] = scfread('temp_via_matlab.scf');

I know that there is not only raw data (Sample), but also probability data. The latter tells me where the peaks are (e.g. Probability.peak_index(100)) and how good they are. This will be very helpful. That data is saved here:
print('PLOC1 is peak_index in Matlab', record.annotations['abif_raw']['PLOC1']) # tuple of int
print('PBAS1 is what base it is', record.annotations['abif_raw']['PBAS1']) # str

Note that it is a wee bit different from MatLab and there are keys called PLOC2 and PBAS2 which have the same data as their 1 counterparts from what I can tell.
For a more detailed explanation of the many keys present see the vignette for the R package sangerseqR, which does the same and is annotated slightly better than biopython —although scfread in Matlab is a lot more neater (hence my recommendation).

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


text:
Damselflies: which exact species of Coenagrion
I recently took the following pictures of Coenagrion spp.(6th of June, in Versoix forest (small pond), Geneva area, Switzerland, Alt: ~450m).
Picture detailed & cropped:

For the identification, I hesitate between two species:

Coenagrion pulchellum
Coenagrion puella

The male one seem to be Coenagrion puella while the female one has black patterning like a Coenagrion pulchellum.
I read in a book (Les Libellules de France, Belgique, Luxembourg & Suisse from Jean-Pierre Boudot, Daniel Grand, Hansruedi Wildermuth et Christian Monnerat) that the male Coenagrion pulchellum can have very similar field marks to male Coenagrion puella (for example the typical black U-shaped marking).
Which species are these — is it possible that the two species can crossbreed (male = Coenagrion puella and female = Coenagrion pulchellum) or are the female field marks a more reliable indicator of the species for both (male and female = Coenagrion pulchellum in this case)?

I corrected the formatting for the scientific names — if you are interested, this is an introduction to scientific naming conventions and these are the complete "rules". I also edited your post for concision and clarity.

Yes, thanks for your edit, in fact I never know how to format latin names in SE sites (I often make a draft in an external text editor before), but for sure my question looks better now. Also, I am not a native English speaker, then thanks for the corrections/rephrasing :).


text:
Please identify this syrphid (hoverfly)
Last summer I took these pictures of a member of the Syrphidae on my balcony (Switzerland, Geneva area, Alt. ~380m, June 2020 @19:14)
Pictures:

I hesitate between three species but it could also be another one:

Scaeva dignota
Scaeva selenitica
Scaeva pyrastri

Because the pale marks on tergites 3 and 4 seems parallel to the anterior margins of the tergites, I would eliminate the third one, especially because the marks are also more yellowish than white.
For the two other species, I am not sure because I checked many pictures on the internet, but some are wrongly tagged (google images results).
Any entomologist can confirm the exact species of this hoverfly?

Awsome pictures, we have them in Austria too ;) Personally I tend to the 'Scaeva selenitica', but that's just my uneducated guess..


text:
How does injecting low doses of allergens cure allergies?
Allergy shots (aka. allergen immunotherapy) help people adapt to allergens by injecting a gradually increasing doses of one or more allergens.
Does this procedure tell the body that this allergen is safe and there is no need to mount a response to it? In other words, does this mean that there will be no reaction at all rather than just a reduction in the allergic reaction.

These question is obviously off-topic as it is asking for theoretical suggestions for curing a medical condition. Answers to this must, of their nature, be off-topic. This is a question and answer site, not a discussion site.

@David — I tried to fix the question since it has a decent answer, do you think that helped?

@tyersome — OK but what are “allergy shots”. Are they low doses of the allergen? If so I would make that clear in the question. I would also change the title to something simpler like “How does treatment with low doses of allergen cure allergies?”

@David — Thanks for the suggestions. Good enough now?

@tyresome — Fine. Thank you for your effort. I still think it is too medical, and I'm not sure the answer is really more than superficial. But it's rather water under the bridge.

But are there ways to tell the body that this allergy is safe and there is no need to amount a response to it?

Yes, that's what allergy shots (Exposure Therapy) does. Exposure Therapy is an effective, albeit sometimes imperfect, method of letting the body know that a substance is common and that it shouldn't mount a response to it. Over time the body re-calibrates itself to accept the allergen, although in some cases it's never fully accepted.
A complete "cure" can be attained via allergy shots, but the extent of the therapy's success will rely almost exclusively on the individual's immune system. Some people can be cured completely, others will never be cured.

If not, why not?

There will probably not be a general "allergy" cure anytime soon because we're still not 100% sure why the body responds in such an overprotective matter sometimes and not others. Even if we fully understood at some point, there are many ways which the immune system can go awry that result in allergies.
There isn't a single, double, or triple point of failure along the line - just about any immune cell, whether Mast, Eisonophile, T-Cell, T-Reg, B-Cell, etc. can misidentify a substance and contribute to an allergic reaction (although some are more likely candidates than others). More than that, just about any substance can become an allergen for people. There's a well-studied case of a woman who became allergic to Copper because of repeated exposure via an early version of IUD that she had implanted.
So with nearly every immune cell capable of mounting a response, and nearly anything in the world capable of provoking a response, the best route - at least thus far - has been repeated, increasing exposures to teach the body what is "OK" and what isn't. The absolute best way to avoid allergies later in life is to simply promote outdoor playtime and a widely variable diet to children while the immune system is operating at peak efficiency and learning capability.

I have been thinking about this topic as well. A theoretical way (as you asked for) would be to kill all the immune cells which hold the (mistaken) memory of the specific allergen being dangerous. I haven't looked into it yet, but it would be interesting to see if post-chemotherapy patients had any changes with their allergies.
A future way of going at it might be to design specific killer cells to find and destroy only those immune cells with matching receptors (bait and kill).

This is a question and answer site about biological problems that allow objective answers. Only answer questions that conform to this type. This question invites speculation and is clearly off-topic. Your answer is such speculation and is only suitable for a discussion site which this is not.

Immune Amnesia
I have a speculative idea of how someone might start to turn off allergic reactions in the immune system.
I've read that the measles virus can cause "immune amnesia".
If biologists had a deep understanding of why this happened, then maybe they could use that understanding to wipe of immune memories that cause allergic reactions.  Maybe they could use a genetically modified measles virus, maybe something else inspired by this.
I'm sure someone else must have thought of this before, but I haven't seen anything when I searched.
I think it would be an interesting beginning for a research project.  But I'm not a biologist, so I wouldn't really know.

This is a question and answer site about biological problems that allow objective answers. Only answer questions that conform to this type. This question invites speculation and is clearly off-topic. Ideas — especially not crazy ones — are not suitable answers to any question.


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Number of serotonergic neurons in mouse/rat DRN
What is the (approximate) number of serotonergic neurons in the dorsal raphe nucleus (DRN) of mice and rats?

The mouse and rat dorsal raphe nuclei contain about 9000 and about 11.500 serotonergic neurons, respectively. It turns out the corresponding 1988 and 1982 references are widely cited - directly as well as indirectly. I could not find any newer data/evaluations.


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Why does cold weather feel more uncomforatable than very cold weather?
Just off the bat, I know (and used to believe) the theory that it's about humidity and wind speed (as e.g. discussed here) but I have started to have some serious doubts after considering a few more scenarios I've found myself in.
To describe the issue — if you're not already familiar with it yourself — I generally find cold weather (roughly -5 to 10°C) extremely uncomfortable, but very cold weather (roughly -20 to -5°C) feels great and exhilarating — to the point that I dislike going outside in late autumn, regardless of how I dress, but in mid winter I can go out in just a shirt and overcoat and feel great. Even below -20 it still feels great, just that at those temperatures you can't stay outside for long without your ears and nose going numb.
There are a few possible explanations I have considered:
1. Winter could be dryer and less windy than autumn, so the perceived temperature is actually higher.
This is the only answer I could find referenced, but I doubt this now, for a number of reasons:

It doesn't feel warmer at all. -20°C winter air hits you like a truck when you go out the door, but it's a nice truck :D.
I used to live in Saint Petersburg, which has cold winters and is right by the Finnish gulf (high humidity and strong winds), and that didn't seem to modulate the perception much. Winter there still felt a lot more fun than late autumn in southern Germany.
In any case the notion that very cold air is as a general rule warmer than cold air is ludicrous. If anything it would be a matter of how different weather conditions affect perception at roughly the same temperature.
If anything, at roughly the same temperature I think wind makes the cold air feel better.

2. It could just be humidity
It's possible that due to the vapor pressure of water at different temperatures -20 by the sea could still be less humid that 0°C far away from it. Sadly, though I notice this phenomenon every year, while I have often consulted the temperature I have never consulted the humidity, so it's hard to say whether 0°C would feel better at different humidities. However, if it's just a matter of how well the air drains heat from your body, I don't see why humidity but not wind speed would affect the perception.
3. It's about acclimation
I thought since winter follows autumn, maybe it's a question of finally getting used to the cold. This would make a lot of sense if it weren't that I still feel the same about different ranges when traveling to different places with no acclimation.
4. It's about emotional associations
Winter, and very cold air, are associated with fun activities, like skiing, skating, nice snowy scenery, christmas markets, new year's fireworks, etc. Autumn and slightly cold temperatures are associated with... nothing interesting really. So it could be that it's a matter of feeling better about the temperature than the temperature feeling better. Honestly this seems like a cop-out explanation, but I couldn't find a lot of better ones.
5. Fight-or-flight response
It could be that very low temperatures trigger a stress response in the body which can be enjoyable or at least overshadow the feeling of discomfort from the cold. I personally feel very energized in winter, so that might be why (though 4 could also explain this). I guess this is something that could easily be tested, but I haven't found any studies looking into this.
6. Perception range of cold receptors
It could be that TRPM8 receptors stop signalling at colder temperatures, and/or only get triggered at very low temperatures. From what I could gather TRPM8 starts signalling at 26°C in the interstitial space, not air temperature outside the body. I am not sure at what ambient temperature the interstitial space of lower skin layers drops to 26°C, but this answer would in any case mean that wind speed and humidity still play a role. Given that you can feel cold air and very cold air almost immediately (and tell the difference), it's possible that there exists at least one other receptor. I couldn't find out what such receptors might be, but it is possible that the sensation generated by TRPM8 could be considered enjoyable while sensations generated by other receptors less so (or the other way around).

In any case, I'm curious whether any of you know any good literature on cold perception, specifically focusing on why very cold temperatures might feel less aversive than slightly cold ones. Explanations 1 and 2 just seem to wave the issue away with a bit of half-assed thermodynamic wisdom, whereas things like 4 might be a bit too soft of a theory to be properly tested. I think 5 and 6 sound like the most promising ideas.


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Transfecting cocoon or chrysalis
Do you know whether anybody tried to transfect insects during their cocoon/chrysalis stage, and if so do you have a link to such studies?
I was thinking it would be easier to do given that it's a more macroscopic manipulation than during initial development, and that — given that the organism dissolves itself — one could obtain (almost?) organism-wide coverage via a simple injection.

I'm not sure I understand. How much material are you thinking? I'll confess right off the bat that I know very little about transfection, but what method would you use (viral? Chemical, e.g. cationic lipids/ other?)? What do you want to introduce into the cell(s)? A small amount might infect (sorry, transfer genetic material) into a few cells, but how do you know how much might harm/kill the organism, or does that not matter? Sorry for all the questions, but it might be better if you clarify re. intent. You may very well know far more about this than I do.

What do you want to introduce into the cell(s)?
Either DNA or RNA. As for the rest of the questions regarding methodology, I think that's what an answer would contain.


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Defining Resistance and Sensitivity Thresholds for IC50
I have a dataset containing IC50 data for each of my cell lines and up to 80 drugs. Basically for each drug I want to be able to define an IC50 threshold where if a cell line has an IC50 above that threshold it is resistant, and if it is below that threshold it is sensitive.
I'm trying to think of the best way of doing this: I was thinking of taking the median for each drug as the threshold but I realize that's quite crude. Are there any more robust statistical techniques I could use to define such a threshold for each drug?
Thanks!

You might want to see the distribution of IC50s. If the majority do not obtain resistance, the histogram may show a normal distribution. Then you would know where less than 5% or 1% of population distribute.
If you have a few cell lines know as resistant against the chemical, you could use them to decide threshold.
PS
Each drug has different effective dosage. You can not draw the same threshold for different drugs. If you have lots of cell lines, you could apply the strategy I mentioned above for a single drug.

IC50 has an exact definition, that is half-maximal inhibitory concentration. To get this you need to make a series of dilutions of each of your drugs and test your cell lines in each concentration and assess how they grow (eg measure Optical density, colony size, cell count or whatever applies to your cells and setup). Then you can set up a inhibition curve that is a function of the concentration. This most likely looks like a sigmoid curve and the inflection point gives you the IC50 value.
An example image form the wikipedia page of IC50 (recommended to read):

So in your case, you already have IC50 values (for wild types I assume), and you need to assess your (probably mutant ?) cell lines to see if they are sensitive or resistant. Standard lab practice recommends using wild-type controls and at least 3 parallel controls. You can compare the average growth of WTs to your cell line at the IC50 concentration you already got in your dataset, and calculate standard deviation, and 95% confidence interval. With some simplification if the 95%CI of your cell line is greater than the wt 95%CI it is most likely that your cell line is resistant to that drug, on the other hand if its lower then that cell line is sensitive to the drug in question.


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IC50 and area under the curve
I was hoping to get some clarification on how drug response data (i.e. IC50) are presented. On publicly available datasets like Genomics of Drug Sensitivity in Cancer, area under the curve (AUC) values are also presented alongside IC50 values. How are these AUC values for a particular drug/cell line calculated and are they correlated with the IC50 values?  If I want to compare the potency and efficacy of many drugs for a cell line (i.e. rank the drugs from highest potentcy/efficacy to lowest) should I use the AUC or IC50 values?
Any help would be greatly appreciated!

Have you read this: wikipedia: area under the curve (pharmacokinetics)?

Area under the curve is the integral of the curve where plasma concentration is plotted against time. A xenobiotic can be potent but still have a large area under the curve, and vice versa. Toxicokinetic factors that affect the area under the curve is absorbance, distribution, elimination etc. Even a less potent xenobiotic can become a lot more potent if its half-life is increased (has a high AUC). If the xenobiotic is really potent (exerts its toxic effects at lower concentrations) it can become less damaging if its elimination rate from the blood plasma is high. Compare IC50 values.

Are you referring to area under dose-response curves? This is very different from pharmacokinetics. A comparison of AUC and IC50 in this context is given in http://www.sciencedirect.com/science/article/pii/S0092867413009604 . Basically, AUC takes effect size (% cells killed) into account, while IC50 does not reflect this.


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shRNA knockdown not showing with Western
I've recently been performing shRNA transfections and was hoping to get some advice on why I'm not seeing any knockdown via western blot
I transfected by MDAMB468 breast cancer cell lines with shRNA against PTEN from the pLKO.1 lentiviral vector. I selected for the transfected cells using 1ug/ml  puromycin for approximately 6 days. During this time there was very few cell death amongst the cells compared to my control plate (untransfected cells with 1ug/ml puromycin), suggesting that the transfection was successful.
After the 6 days I harvested my cells for protein and RNA extraction. I performed a western yesterday to assess knockdown, but noticed that there was hardly any differences (if any!) compared to my shGFP control. I haven't done a qpcr yet but I plan to this week.
I was wondering if anyone has experienced something similar, especially when working with PTEN? could it be that the cells need to be selected for a longer period (i.e. more than a week) before assessing protein knockdown?
Thanks!

I don't know much about this protocol, but is it possible that you transfect enough for antibiotic resistance expression, but not enough for shRNA to actually work?

I assume that you transfected the plasmid directly not producing viruses. If you want stable transformants, you might want to subculture them and maintain a bit longer. It is because efficiency of integration of plasmids into genome could not be that high--less than 0.1% of population obtain stable resistance by integration into genome. After 6 days, cells were still healthy in your case. This means you might get good transfection efficiency and after several times of cell division, your plasmids were diluted and the effects might be low even if cells maintain resistance against puromycin.
If transient expression (KD) works in your experiment, you might want to check expression level of your target at day 2 or 3. If you prefer stable cell lines, you can increase puromycin concentration, and if you agree, you pick up single colonies after cells not having plasmids in genome are dead. Among these colonies, some have more plasmid copies other have less. You can choose cells least expressing your targets as well as moderately expressing cells if you want. Because you might want to see expression level dependency.
For some cells, 5ug/ml puromycine is used according to this link.

thanks for the suggestions. I don't have much experience with shRNA transfections, but do you think it's possible that the protein (PTEN) is quite stable and the cells would need to be cultured for longer (what would you recommend, 2 weeks?) to see the knockdown? I'm interested in doing the qPCR to see how the mRNA knockdown looks...

@tolo9397 Try that qPCR. It is possible that your shRNA sequence is not binding like you wanted it to. Have you verified that this shRNA actually knocks down your gene of interest?

@tolo9397 As you mention, in general, KD effects could be delayed from a shRNA expression peak because of protein life time. So, cells may be cultured one or two more days compared with protein expression vector transfection. If the delay is more than that, you might want to transfect shRNA expression plasmid again several days after the first transfection to keep shRNA effects high. If you need stable transformants, this is not the case, though.

@tolo9397 PTEN is a popular protein, so you could find KD experiments published like http://www.nature.com/nm/journal/v17/n4/full/nm.2309.html#supplementary-information


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Weight of fresh vs frozen tumours
I have some mouse tumours that have been snap frozen in liquid nitrogen following an in vivo study, and I thought it might be interesting to also determine the weight of the tumours. I was wondering if weighing frozen tumours would still be accurate, or if I should have measured them before they were frozen? Would one expect the weight to be significantly altered just by snap freezing samples?

If the tumours were sealed before being frozen, then of course the weight is the same. The temperature of something does not change its mass. However, the frozen ones might be heavier if, during the process, more water (or other substances) got trapped into the tumour. At the end this is a problem of enginneering and about your freezing method and not a question of biology.

I'm voting to close this question as off-topic because it is a question of engineering of the freezing technique and not a question of biology.

I think this is specific enough to a biological technique that it's on topic.

I agree with Bryan; closing this question would be failing to see the forest for the trees.


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Does the anatomy of our hand result in (computer) mouse-accuracy that varies by direction of movement?
First off, I apologize if this isn't the right stackexchange sub-site for asking thsi question.  I was torn as to where I should post this question: it could plausibly belong in Biology, User Experience or even Arqade.  However, given the root of my question has to do with the "wiring" of the human hand, I elected to post it here.
My hypothesis/question:
Let's assume that wrist adduction/abduction is responsible for horizontal movement of the mouse cursor and that finger extension/flexion is responsible for vertical movement of the mouse cursor.  (I am, of course, willing to revisit this assumption, if necessary.)  Would it be accurate to say that we are "hard-wired" to be capable of higher precision in vertical movement of the mouse cursor than in horizontal movement?
Description of mouse grip:
In making the above assumptions, I assume a fingertip-grip style of the mouse (as opposed to the claw and palm grips). The (corner of the) wrist rests on the table and acts as a pivot for allowing side-to-side motion (i.e., horizontal motion of the mouse cursor).  Meanwhile, flexing/extending the fingers allows for pulling/pushing the mouse away from us, (i.e., vertical motion of the cursor).  The main (admittedly unscientific) reason behind my hypothesis is that vertical movement of the mouse cursor uses similar finger motions as those used for hand-writing (which is, after all, a highly precise activity).
(I understand that my question makes the assumption that we are capable of more precise movement with certain muscles of our body than we are with others - please let me know if that's a flawed assumption.)
Why do I care about this?:
If my hypothesis is correct, there would be implications on mouse settings (namely, horizontal and vertical DPI*) that are conducive to both high accuracy and speed.  The key issue is that if we keep our wrist in place (i.e., no sliding/lifting of our pivot point) - then we're able to move the mouse a greater distance side-to-side (i.e., horizontal motion of cursor) than we're able to move it toward/away from us (i.e., vertical motion of cursor).  However, if there is evidence to support my hypothesis, than an appropriate adjustment (which wouldn't result in a loss of accuracy) would be to have a slightly higher vertical DPI than horizontal DPI.
*DPI = dots (i.e., pixels per inch).  For example, I have a resolution of 1366x768 (which is in units of dots or pixels) and a 600 dpi mouse, which means that my (physical) mouse needs to be moved ~2.3 inches (1366 divided by 600) in order for the mouse cursor to move the full horizontal distance of my monitor.  To put it simply, lower DPI results in higher accuracy but it is preferable for our wrist to remain in-place in the interest of speed.

Finger movement is more precise than wrist movement. Further, because of RSI, it is better to move the arm than the wrist :) BTW: your question seems to mix up maximum distance and accuracy. Accuracy is better in fingers because of their function, not because their maximum covered distance is smaller..

Thank you!  That is exactly what I'm looking for.  Feel free to copy paste into an answer.  I'm probably unclear in how I described the issue.  I simply meant to say that because the maximum covered distance (by finger movement) is smaller, it would be convenient to be able to use a higher sensitivity in this direction - but that making this change would only make sense if your fingers were capable of more precise movement to begin with (which, thanks to your answer, I now know to be true!)

Assuming the case where you move a mouse left and right with the wrist and up and down with the fingers, then yes, finger movements are more precise. The fingers and facial musculature are body parts with the most exquisite fine motor-control. The wrist, on the other hand, probably less so. The wrist is definitely involved in fine motor skills such as writing, but the fingers even more so.
I wasn't able to find a good reference about the level of precision for different body parts at the behavioral level. I can, however, approach the question from a neurophysiological point of view. The amount of motor control available for different body parts can be visualized by means of a motor homunculus. The motor homunculus shows how many neurons are available in the cortex for a given body part. The larger the cortical surface dedicated to a body part, the larger the corresponding body part is presented in the homunculus (Fig. 1).

Fig. 1. Homunculus drawn on the motor cortex (left) and the homunculus presented as a figurine (right). Sources: Conference on Human factors (1997) and Autism Index, respectively.
The fingers have a huge amount of motor cortex dedicated to them compared to the wrist. There are a lot of 'buts' to add, most notably the larger number of muscles in the fingers versus the wrist, which explains part of the difference. Nonetheless, the homunculus does show the relative functional importance of the fingers in motor processing power of the brain, while the wrist is virtually invisible on the homunculus (Fig. 1, left panel).
Lastly, you seem to be mixing up 'distance' and 'precision' in your question. While the wrist may cover a greater distance, it is not because of this that the precision is smaller. The fingers have more neuronal processing power behind them and can be exquisitely fine tuned. In other words, the precision is not determined by the dynamic range (distance), but by the processing power dedicated to the motor function.
As a side note, because of RSI, it is recommendable to use gross arm movements instead of fine wrist and finger movements.


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COVID-19: size, real image
I'm an electronics engineer. I was thinking about how to detect the presence of COVID-19:

Obtain the sample.
Increment image/sample, (I need the real size to determine increment/magnification)
Digital image processing — detect presence using artificial intelligence or Recognition.

What is the approximate size of COVID-19? Is there a real image of COVID-19?

Reading good please, I'm asking for size and images proper of Biology field.

@tyersome The question asks simply the size of Coronavirus. It does not ask about image recognition.

SE Biology is concerned with the mechanisms of biological processes. General information about the coronavirus is available from a variety of reputable sources, some of which are listed here. As your concern is for detection of the virus you would be well advised to consult such sources for information about how this is currently performed and the problems actually faced. Others have hammers too, and don’t necessary think that everything is a nail.

2019-nCoV also has enveloped virions that measure approximately 50–200 nm in diameter
  with a single positive-sense RNA genome.

Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study, The Lancet (2020)


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Can anyone identify this spider? (greater Poland region)
This is in Poland, in the Greater Poland area, found a few days ago by a garage in the city.
I didn't have any coins on me to give a sense of scale, but the body is roughly 1.5cm long. It was dead when I found it.
I'm curious because I haven't seen any spider like this one during my stay here, they're all tiny specimens normally and this one really stuck out.

That looks like a Funnelweb Weaver (family Agelenidae), specifically Tegenaria atrica,  based on the patterning of the abdomen and thorax.

Female Tegenaria atrica, picture by Jørgen Lissner

Their range includes Poland:

Range: Andorra, Austria, Belgium, Bulgaria, Croatia, Czech Republic, Denmark, Faroe Islands (introduced), Finland, France (Corsica), France (Mainland), Germany, Great Britain (Channel Islands), Great Britain (Mainland), Great Britain (Northern Ireland), Greece (Crete), Greece (Dodecanese Islands), Greece (Mainland), Ireland, Italy (Mainland), Latvia, Liechtenstein, Lithuania, Macedonia, Netherlands, Norway (Mainland), Poland, Portugal (Mainland), Romania, Slovakia, Spain (Mainland), Sweden, Switzerland, Ukraine, Yugoslavia (van Helsdingen 2009.1).

Source: http://www.jorgenlissner.dk/families.aspx

These giant house spiders (atrica/duellica etc) were moved into the Eratigena genus 7 years ago, along with the Hobo spider (E.agrestis). Tegenaria includes the barn funnel weaver and similar.


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identification request - tiny flies invasion
Since they are tiny, this is the best photo I can do:

We are in Berlin, Germany. It has become very hot outside and the flies have invaded us for the last couple days.
The insect is about 1mm long, 0.2mm wide, they are absolutely tiny. They fly but seems to like camping on the ceiling.
The have come in massive numbers, probably over a thousand, but they're so small we barely see them. They don't seem to be interested by our food, nor water, etc but rather just stay in cool and darker areas.
Since we have a newborn, I don't want to use insecticide to get rid of them, so I'm trying to figure out what they are and then.. what to do next :) Right now I am welcoming spiders!

Probably some Thrips species (aptly named "Gewittertierchen" in German). At worst, they are a nuisance.


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identification request - medium size fly invasion
I have two invasions going on!
the one here: identification request - tiny flies invasion
and this one:

We are in Berlin, Germany. This fly is 2.5mm long vs 1mm wide, and seems to like the dark and colder area of the apartment. They arrived at the same time as the tiny ones in the other link, but they don't look similar, so I don't think this is the adult form of the other kind but maybe I'm wrong.
They came with the heat, looking for shelter.

Without a clear view of the wing venation any answer would be sheer speculation; if the critters are still around and you can get a photo showing all the wing venation clearly (all we can see for certain at present are the ends of two of the longitudinal -- as opposed to cross -- veins) adding such would help immensely.

@ArthurJFrost, we're currently in another country; but when we're back I will check if they are still around


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Do findings on promoter methylation of the serotonin transporter gene and amygdala activity contradict the established view of serotonergic function?
In this article http://www.nature.com/neuro/journal/v17/n9/full/nn.3778.html it states that

Increased promoter methylation of the serotonin transporter gene predicted increased threat related amygdala activity.

I'm finding this somewhat difficult to understand. Increased promoter methylation would imply that the serotonin transporter gene is less expressed, so less serotonin is taken up by the presynaptic neuron, leading to increased serotonin levels in the synaptic cleft. Surely the increased serotonin levels would lead to decreased amygdala response to threat? After all, selective serotonin reputable inhibitors (SSRIs) are used to treat anxiety disorders and depression by reducing uptake of serotonin and increasing serotonin levels as well. It seems like these two are suggesting two contrasting effects for the same cause?
I would be grateful if someone could point out where I have misunderstood. Thank you in advance :)

I don't think there is an obvious contradiction here.
(1) Mapping neuronal function to the perception of threat (or emotions in general) is often advertised as well-understood, but in fact it is not. Serotonin-concentration-based models (such as the monoaminergic theory of depression) are unavoidably imprecise because ”the brain is not soup”. Additionally, it is also impossible with current technology to measure actual serotonergic signalling in vivo with whole-brain comparability (though progress is being made, e.g. via: fMRI contrast-agents and stimulus-evoked opto-fMRI for monoaminergic systems).
(2) Numerous pharmacological interventions which increase signalling at the serotonergic synapse have been documented to cause widely varying effects (compare e.g. monoamine reuptake inhibitors, monoamine release agents, and monoamine receptor agonists). While selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, are commonly reported to decrease anxiety, serotonin receptor agonists, such as LSD, are reported to induce acute anxiety (though interestingly small numbers of LSD administrations, in conjunction with psychotherapy, have also been reported to reduce anxiety in the long term).
The conclusions thus far would be: (1) we can't be entirely sure about how serotonin mediates or counterbalances anxiety (2) but the specific kinetics of activity at the serotonergic synapse seem to be just as relevant as the actual amount of signalling. You may think, however, that the effects of SSRIs are kinetically similar to reduced expression of the serotonin transporter, SERT. This is however not the case, as under SSRI treatment it is generally believed that chronic downregulation of 5-HT1A inhibitory autoreceptors is responsible for the therapeutic effect, rather than the acute increase of serotonin concentration in the synaptic cleft (this being in line with the fact that therapeutic SSRI effects are observed chronically rather than acutely). Further evidence corroborating the notion that constitutively reduced expression of the serotonin transporter increases anxiety can be found from studies on the 5-HTTLPR polymorphism. In these studies the short version of the allele, which leads to reduced expression of SERT, has also been reported (though afaik this effect is not very robust) to correlate with increased activity in the amygdala.

Excellent answer. To emphasize an important point that the OP may have missed, improvement of anxious/depressed symptoms don't occur until weeks after starting an SSRI (corresponding to the chronic effect of SSRIs). Serotonin levels in the synaptic cleft only increase in the short term (the acute effect). By the time you see symptom improvement, serotonin levels are no longer elevated. This is fairly complicated, and often glossed over, suggesting SSRIs work because of a simpler, but incorrect 'depression = not enough serotonin' mechanism.


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What happens to plants if they are exposed to "sunlight" 24h a day?
I just wondered if one could grow plants faster, if they were exposed to sunlight-like light all the time.
In a similar question which is not the same, I could confirm that plants have different processes going on at day and at night. However, it didn't answer the question about the consequences of permanent exposure to sunlight.
However, I don't understand what would happen if there was light all the time. What would happen to different plants if they are exposed to "sunlight" 24/7?
(Similarly: What is the "optimal" amount of sunlight time for different plants? Is it basically what is common in the environments they typically grow in?)

Possible duplicate of Do plants need sleep?

Look into crop growing in Alaska, Scandinavia, and other places where there is nearly continuous sunlight in summer.

This review (from 2011)1 states that it depends on the plant species and cultivar.

Some continuous light (CL)-grown photosynthetic organisms show
  increased productivity. However, CL also induces negative effects in
  several plant species. The most visible CL-induced negative effects
  are leaf chlorosis and necrosis. CL also lowers photosynthetic
  parameters ... The CL-sensitive species include eggplant, geranium,
  some onion species (Allium fistulosum), peanut, some cultivars of
  potato, tomato, and even lichens (Xanthoria parietina) and mosses
  (Pleurozium schreberi and Ceratodon purpureous).

Among the plants that have better yields under continuous light are lettuce, roses, some potato cultivars, some algae.
The reasons why some plants can be damaged under continuous light aren't completely clear (at least they weren't in 2011). One of the problems is carbon imbalance. Leaves produce too much sucrose and other organs such as roots are not able to process it fast enough. This leads to high sugar concentrations and can cause leaf senescence. Continuous photosynthesis also results in more photo-oxidative damage and plants that better detoxify reactive oxygen species have less negative effects from continuous light.
So look for research on the particular species you want to grow or just experiment with different light conditions.

 1. Velez-Ramirez, A.I., van Ieperen, W., Vreugdenhil, D. and Millenaar, F.F. 2011. Plants under continuous light. Trends in plant science, 16(6):310-318.

Plants - like essentially eukaroytic &/ phototrophic organisms - have circadian clocks, regulating a bunch of cellular processes including the 'light' and 'dark' cycles of photosynthesis. Circadian systems can control a lot different things so disrupting them  can have all sorts of effects - which is probably also why some plant species are affected in different ways than others.


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Can any animals photosynthesize?
Plants and animals have the following distinct properties:

Plants live from solar energy by photosynthesis, they use solar energy to make sugar and oxygen out of carbon dioxide, which gives them energy. Animals live from the sugar and oxygen plants created and produce carbon dioxide for their energy.
Animals can move across the planet while plants are tied to the ground.

Clearly, animals have a harder time to survive with no plants within their reach than plants have without animals coming close. This is logical because solar energy is always there while plants are not.
So my question is: Are there animals that can do photosynthesis? It's obvious that an animal with plant-like stateliness would be non-beneficial since it relies on eating other plants for it's energy and there may not always be plants within reach from it's spot.
But animals using the sun and carbon dioxide for energy production does not sound so stupid.

Night animals could also gather energy in their sleep.
Much easier than plants, animals could make sure nothing blocks their sunlight.
Many animals go through periods of hunger because food is scarce, for some of them this period is paired with high sunlight levels. (the dry season f.e.) (EDIT: This is just an idea, of course photosynthesis requires water, which is absent in the dry season. But still, in warm period with enough water, there's sometimes too much animals to feed from the available vegeation.)

Some things I already took into consideration:

I know that plants, because they are small in mass (compared to the area with which they can collect sunlight) and static, don't need nearly as much energy as animals do. Is this the main reason?
I know that f.e. reptiles, but in fact all cold-blooded animals, already use the sun's energy. But they only use the heat from the sun to warm their bodies, they don't photosynthesize.

Does symbiotic photosynthesis count?

@DVK What's that? I can't seem to find a good information source on that.

That's when an animal hosts some photosynthetic symbiote, like algae.

You might want to change your question title to : Are there animals that can do photosynthesis? The term "race"  doesn't have much meaning in biology.

More a comment rather than an answer, but there is some evidence of both natural and artificial transfer of genetic material between plants and animals - if you google "plant genes in humans" you will come up with some fascinating results. I don't have authority to make comments yet.

It's better if you give some examples of "fascinating results" I suppose.

@RobertJones I converted it for you :)

It actually has many example, there are already accepted answer. But I want to point out one thing. Solar energy per area on earth is not enough to be used as main source of energy for movement. Movement and thinking, in fact a whole animal lifestyle, consume too much energy to live with photosynthesis. It is far more easier to consume other organism for energy. That's why almost all autotrophes are stay still like plant or being a plankton like bacteria

first search for "list of photosynthetic animals" ...Sea Slug - Elysia chlorotica. ...
Spotted Salamander - Ambystoma maculatum....
Oriental Hornet - Vespa orientalis....
Pea Aphid - Acyrthosiphon pisum.... and corals also

There are 5 answers, all "yes" (though the first one is disputable).

First: there exists at least one animal which can produce its own chlorophyll:

A green sea slug appears to be part animal, part plant. It's the first critter discovered to produce the plant pigment chlorophyll.
The sea slugs live in salt marshes in New England and Canada. In addition to burglarizing the genes needed to make the green pigment chlorophyll, the slugs also steal tiny cell parts called chloroplasts, which they use to conduct photosynthesis. The chloroplasts use the chlorophyl to convert sunlight into energy, just as plants do, eliminating the need to eat food to gain energy.

The slug in the article appears to be Elysia chlorotica.

Elysia chlorotica is one of the "solar-powered sea slugs", utilizing solar energy via chloroplasts from its algal food. It lives in a subcellular endosymbiotic relationship with chloroplasts of the marine heterokont alga Vaucheria litorea.

UPDATE: As per @Teige's comment, this finding is somewhat disputable.

Second, animals need not produce their own Chlorophyll, and instead symbiotically host organisms that use Photosynthetis - e.g.  algae and cyanobacteria. This approach is called Photosynthetic symbioses.

Overall, 27 (49%) of the 55 eukaryotic groups identified by Baldauf (2003) have representatives which possess photosynthetic symbionts or their derivatives, the plastids. These include the three major groups of multicellular eukaryotes: the plants, which are derivatives of the most ancient symbiosis between eukaryotes and cyanobacteria; the fungi, many of which are lichenized with algae or cyanobacteria; and the animals. We, the authors, and probably many readers were taught that animals do not photosynthesize. This statement is true in the sense that the lineage giving rise to animals did not possess plastids, but false in the wider sense: many animals photosynthesize through symbiosis with algae or cyanobacteria.

Please note that while most organisms known for this are fungi, and some rare invertebrates (corals, clams, jellyfish, sponges, sea anemones), there is at least one example of vertebrate like this - spotted salamander (Ambystoma maculatum)

Non-chlorophyll synthesis

A 2010 study by researchers at Tel Aviv University discovered that the Oriental hornet (Vespa orientalis) converts sunlight into electric power using a pigment called xanthopterin. This is the first scientific evidence of a member of the animal kingdom engaging in photosynthesis, according to Wikipedia.

Another discovery from 2010 is possibly a second piece of evidence:

University of Arizona biologists researcher Nancy Moran and Tyler Jarvik discovered that pea aphids can make their own carotenoids, like a plant. “What happened is a fungal gene got into an aphid and was copied,” said Moran in a press release.

Their research article is http://www.sciencemag.org/content/328/5978/624, and they did not consider it conclusive:

The team warns that more research will be needed before we can be sure that aphids truly have photosynthesis-like abilities.

Third, depending on how you understand Photosynthesis, you can include other chemical reactions converting sunlight energy.
If the answer is "usual 6H2O + 6CO2 ----------> C6H12O6+ 6O2 reaction done via chlorophyll", then see answers #1,#2.
But if you simply literally translate the term (synthesizing new molecules using light), then you can ALSO include the process of generating Vitamin D from exposure to sunlight that
humans do thanks to cholesterol (link)

Non-biological answer.

As a side bonus, Ophiocordyceps sinensis is referred to as half-animal half-plant (not very scientifically IMHO). But it doesn't do photosynthesis.

I don't think it is really clear that sea slugs actually incorporate algal genes in to their own genome for the purpose of photosynthesis. Your link is based on this paper: http://mbe.oxfordjournals.org/content/29/6/1545.long
The possibility that the low number of reads is due to the presence of algae in the powdered sea slug is high and is the most parsimonious explanation of the results.
The paper is super interesting & provocative - how would this gene transfer occur? Also, it takes complete thylakoid membrane for photosynthesis, not a few components - possibly there's complx host intercton

I was all set to answer anothervquestion which has now been marked as a duplicate of this one. My answer adds new information relevant to the accepted answer here, so I have decided to post it here..
One longstanding candidate for something approaching this idea is the green sea slug Elysia chlorotica which uses chloroplasts derived from the alga Vaucheria litorea. Various pieces of evidence have indicated that the longevity of these chloroplasts in cells of the sea slug's digestive tract is explained by the presence of algal genes that have been transferred to the mollusc genome. However the most recent analysis of germline DNA  in the sea slug has revealed no evidence for such horizontal gene transfer. It seems that all of the evidence for algal genes and algal gene expression in the sea slug must now be explained in terms of somatically-acquired algal DNA.

Bhattacharya et al. (2013) Genome Analysis of Elysia chlorotica Egg DNA Provides No Evidence for Horizontal Gene Transfer into the Germ Line of This Kleptoplastic Mollusc.
  Mol. Biol. Evol. epub ahead of print


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Why is this bumblebee attracted to a methane leak?
In this video from Bloomburg Quicktake, the reporters discover at a methane well (Skip to 14:21) a GHG leak that has attracted bumblebees. Does natural gas smell sweet to bees? Why would the bees be attracted to the leak?

It's entirely possible they were there coincidentally (and got scared by the humans filming them, and decided to take shelter in the pipe), or they were just curious.

What did you find out when you googled this?

Please extract one or more frames from the linked video and add them to your post (this can also be done as GIF) — posts must not require leaving this site to be understood and links can change or break.

It is possible that the bees are attracted to the methane because it might replicate the emission of methane from appealing vegetation alive, dead or dying — specifically the kind of standing wood that might lead to a home for a carpenter bee (easily mistaken for a bumblebee).
"Methane emissions from trees: Tree trunks act as methane source in upland forests (from Science Daily)"

What we've found in this study is that some coarse woody debris acts kind of like the soil and consumes methane while other pieces of coarse woody debris emit small amounts of methane, which is also what we saw with living tree trunks," said Warner.

Welcome to Biology.SE! This is an interesting idea and could become a good answer with more reading and [edit]ing — in particular the linked Science Daily article doesn't say rotting wood is the source and I doubt that is what carpenter bees want. Answers are also more likely to receive a favorable response if they include supporting references to primary literature. This is a good example of how to format references.  ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.


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Do Termites and Silverfish metabolize cellulose the same way?
I am fascinated with silverfish and would like to understand more about their metabolism.
I learned that they can survive on a diet of cotton which is nearly pure cellulose. Do they metabolize cellulose in the same way as termites?  Or do some insects have different metabolic pathways for cellulose?

It has been known for 40 years or more that some insects such as termites digest cellulose by synthesizing their own cellulases, whereas others have a symbiotic relationship with gut micro-organisms that perform this digestion (see Martin, Comp. Biochem. Physiol. (1983) 75A 313-324  — requires subscription — or this short popular science article).
What is the situation for silverfish — Lepisma saccharina? Today the evidence that generally determines whether an insect can digest cellulose itself is the presence of the genes for the cellulase enzymes in its genome. There is a relatively recent review of this in Annu. Rev. Entomol. (2010) 55 609–32 — again requiring subscription for access — in which the species in which these genes have been detected are listed. I know nothing about organismal biology or taxonomy, and can only summarize the species represented there for others to comment on:

Orthoptera
Blattaria
Phthiraptera
Hemiptera
Coleoptera
Hymenoptera

This doesn’t seem to me to include Lepismatidae (which Wikipedia tells me is the family), but what do I know. (I only know the genes aren’t present in fruit flies.) However some earlier indirect experiments studying the effects of antibiotics on insect cellulase levels suggest that Lepismatidae may have their own cellulase.


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Intrinsically disordered proteins as potential drug targets
Intrinsically disordered proteins (IDPs) are a class of proteins that do not adopt a stable secondary or tertiary structure under physiological conditions in vitro, but still have biological functions. Many IDPs are implicated in cancer, neurodegenerative diseases, and diabetes, which makes them attractive drug targets. Are there any successful examples of that? Are there any drugs which disrupt protein-protein interactions (where one of the proteins is an IDP)?

IDPs are indeed attractive drug targets and there are ongoing efforts to develop drug molecules that block interactions between a disordered and a structured protein. According to this relatively recent paper, however, these efforts have not brought a drug on the market, yet.
A few promising studies have shown drug-like molecules that inhibit protein-protein interactions based on intrinsic disorder of one of the partners and target:

oncogenic fusion protein EWS-FLI1 and RNA helicase A. A small molecule has been found that targets the disordered region of EWS-FLI1, blocks the interaction with the helicase and inhibits growth of Ewing's sarcoma.
p53 tumor supressor and its interactor Mdm2. Mdm2, by binding to an intrinsically disordered region of p53, targets p53 for ubiquitination and also causes it to be transported out of the nucleus. Promising small molecules  have been found that associate with Mdm2 and thereby block its interaction with p53.
c-Myc oncoprotein and the interaction with its partner Max protein. This study demonstrates two small molecules that bind to c-Myc and stabilize its disordered conformation, which inhibits its interaction with the Max protein.

The challenge in targeting protein-protein interactions for therapies stems largely from the fact, that the protein-protein contact surfaces are much larger than those involved in protein–small-molecule interactions (1,500–3,000 Å2 and (300–1,000 Å2, respectively) [2]. They are often flat and have no defined binding pocket. Also, IDPs often don't bind natural small ligands, that could act as starting points in developing drugs.
You may find this paper helpful:
Metallo SJ, Intrinsically disordered proteins are potential drug targets, Curr Opin Chem Biol. 2010 14(4): 481–488.
BTW: for a comprehensive, manually curated list of disordered proteins and regions, please check the Database of Protein Disorder.

Thanks for your answer and the references. I will definitely look them up. I already read the Metallo, SJ paper, which is an excellent paper! What concerns me the most though, is that all IDPs can interact with multiple small molecules or other proteins, so they cannot be specifically targeted. That's why I am very interested whether specific interactions have been discovered.

I have been working on this problem for quite some time now and believe me getting specific binding is a real issue with IDRs. Also, since these regions don't contribute to the core structure of the protein, the residues are less conserved (more prone to mutations). So in the case of evolving drug-resistance contributing proteins this becomes a bottleneck.
I have done some work on IDPs as potential drug targets: Unraveling the potential of intrinsically disordered proteins as drug targets: application to Mycobacterium tuberculosis.
But the concept has been taken well by even the conventional structural biologists.
As the paper suggests, my work is focused on Mycobacterium tuberculosis. Multi-Drug Resistant (MDR) and Extensively Drug Resistant (XDR) forms of TB have added to the tuberculosis loads not only in the developing but also developed nations. Drug resistance has been associated with proteins (mostly those involved in transport and metabolism) that have helped this pathogen grow resistant to the first line drugs or more. I refer to such proteins as "Drug resistance associated proteins".

Thanks for your answer. I will definitely read your paper. I also saw a list of your papers on linked in. I am particularly interested in the protein-protein interactions. By the way, what do you mean by "drug-resistance contributing proteins"?


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Type of Tree With Somewhat Squarish Fruit
I live in the SF Bay Area and am trying to identify a tree on my street. It's the fruit that is confusing me -- does anyone know what this fruit is?
It's not a rare tree -- there are at least several more on the surrounding streets.
Mature leaves are about 6" long and greater.

Could you put something in to indicate scale?

Looks like the regional government maps every street tree: https://data.sfgov.org/City-Infrastructure/Street-Tree-Map/337t-q2b4 Maybe you can find it!

A photo of the bark/trunk would be useful too, and if you can break off a leaf and see if there is any latex that oozes out of the wound.  Unless of course you found it in the street tree inventory.

That looks like a persimmon — your first image is of immature fruit.
Compare with:

UC Davis — Fruit and Nut Education
Google Image link

Good job... I was thinking about persimmon too, but for whatever reason could not find a picture of those leathery sepals.  Now I know.  The bark would have been distinctive.


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Does anyone know what insect species this is?
The insect has an approximate length of 2.5 cm and It was found in Panama, Central America.
It was living hidden between the leaves of a papaya tree (Carica papaya).

it looks like some kind of grasshopper nymph, but I couldn't find anything particularly close to it.

A better view of the animal's topside would help in the identification; at present, we CAN say order Orthoptera, suborder Ensifera (long-horned grasshoppers AKA katydids and crickets); with four segments in each foot it isn't a member of Grylloidea (most of the "crickets").


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Bug Identification North Carolina Help
I found this bug up in North Carolina and it freaked me out because I found it inside. Would anyone be familiar with this type of bug?
I apologize for the bad angle, it is not a bee at all, but had a striped body, which made me curious!

Welcome to Biology.SE. Unfortunately I think it is unlikely that this can be identified based on the poor quality of the image and the specimen. It might help if you [edit] in why you are sure this wasn't a bee. Please take the [tour] and consult the [help] starting with [ask] for details including the expectations for questions on this site. See also the species-id tag info page for suggestions about how to ask this kind of question — for example including a size estimate is very important.

If you still have the specimen, please take a better picture, e.g. a “bird’s eye view” if the insect were still alive. It’s hard to make out any distinguishing features.


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The pollination of lupins
Do lupins produce nectar? According to this study it seems like there are conflicting conclusions regarding this. And in this study the supposed inability for Lupinus argenteus to produce nectar is utilized to study whether the addition of nectar changes pollinator behaviour.
If the answer to this question is no, then why do these bumblebees insert their tongue inside the base of the flower, because it certainly looks like that is what they are doing. Do they do so regardless of whether a flower contains nectar or not, just to verify whether there is any present in the flower? But if pollinators only visit lupins for pollen to eat then why do they stick their tongue inside the banner where it seems to me that there should be either trace amounts or no pollen at all.

Welcome to SE Biology. Please finish reading the Tour before posting. That way you will find out how this site works. I have edited out reference to two questions, as we only take one at a time. I am no botanist, but did you really mean “banner”?

Yes, banner as in the uppermost part of a papilionacepus flower (zygomorphic flower shared by almost all plants of the pea family). My phrasing is not specific enough: the banner in this lupin flower is folded slightly towards the bottom creating a "crevice". It is this crevice that the bees in the video seemingly stick their tongue in.

Ok. Banner it is. I should stick to animals.

Is there some reason to think that all lupines must be the same? If so, then please [edit] that into your post. If not, then is Lupinus argenteus the species of interest and is that species what is being shown in the linked video? Also, what species is the bumblebee? ——— While providing links and sources is good you should also summarize what is in the papers and video; all posts must be self contained (i.e. must not require users to follow links). In addition, it would be great if you extracted and posted relevant frames or short segments as gifs from the video.

The lupine from the video appears to be L. polyphyllus, and this paper suggests L. polyphyllus doesn't produce nectar.


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Why isn't hearing the same as tasting? How do we feel and differentiate external stimuli?
When I was at school, I learned that:

Skin, tongue, ears, and other sensory organs have sensors/convertors that turn external environment stimuli into "electric" signals.
Neurons send information as electric propagation of K+ / Na+ along their axon. Hence, the real nature of the stimuli is definitely lost in translation.
Each region of the brain is a cortex specialized for vision, sound, smell, and other sensations yet they all are made of the same neurons.

So:

Then how do we feel? How are "electric" signals turned into taste or smell?
Why does the brain not feel the same way about these different stimuli, rather than only differentiating amplitude and frequency of the signal?
Why do we even feel pleasure or pain at all? A machine would just transfer the information.

That part was never explained to me. Is it quantum (entanglement?) physics-related? Or even metaphysical? Does anyone really know?
Philosophically speaking, I am not even sure I taste things or feel music the same way other people do.

Ordinarily, it's not good to ask so many different questions in one question on Stack Exchange. However, in my view these questions all actually boil down to one central question, so I've provided an answer in that regard.

Why does your computer's keyboard do different things than the mouse or a attached camera?  (Or any of the multitude of other sensors you can buy?)  They're just electrons moving through identical gates etched in chunks of silicon, aren't they?

@jamesqf so you don't get it...drivers and hardware only process information, they don't feel it, the question is more complex than that

@fdsfdsfdsfds: No, YOU don't get it.  Just as those drivers all run on essentially identical hardware (after the actual sensor), so the different areas of the cortex are "drivers" made of neurons.  Then you consider that the types of information are fundamentally different: it would be fairly useless to display an audio file all at once, or play an image file as a stream of bits.

@jamesqf If you want to post another answer, great, but...I think there is a lot of uncertainty in something you seem to be certain about. Even as an extreme materialist I agree that there is a difficult understanding here that isn't the same as one applied to computers. OP has a pretty common question and I was kind of surprised to not find a canonical answer here yet - maybe I missed one.

@jamesqf  you're confusing processing (how data is pre-chewed by the brain) and the feeling produced by that perception; try "building a machine" that mimics brain, and tell me how you made it actually taste food and feel pain or pleasure, while it is built from good old hardware/software, and the only thing the it receives are electrical data.. I am talking about the taste/smell itself, and it's profound subjective nature... there must be something deeper and out of human reach, Bryan is right, read his answer, he, at least, gives different tracks to follow to learn about the subject

@Bryan Krause: I don't want to post an answer because I am trying to point out (politely!) that "answers" are pretty well meaningless, because the question is nonsense.

@jamesqf  just read me instead of deliberately ignoring something you refuse to understand...information will never be converted into a taste (a QUALIA)

The problem you are seeking an answer to is referred to as the hard problem of consciousness, the term originally coined by David Chalmers, or more generally the mind-body problem.
Just how "hard" this problem is seems a bit unclear; some people argue it isn't truly "hard" at all, but they make these claims in support of their own particular views of the nature of consciousness. Since not everyone agrees with them, it seems like to at least some extent the "hard problem" description is appropriate.
There certainly are quantum explanations, and you will find proponents like Stuart Hameroff, but most neuroscientists consider his theories to be crank science since he hasn't provided any evidence of his theories, only hand-waving explanations of how they could be plausible.
There are also metaphysical explanations, going back to the dualism of Rene Descartes. The problem with these metaphysical theories is that they aren't scientifically disprovable, and the more we learn about the brain the more of its functions can be explained physically. Dualism is ultimately a religious or philosophical stance rather than a scientific one.
There are several neuroscientific theories of consciousness, including integrated information theory(IIT) and global workspace theory(GWT). For IIT, consciousness occurs through the integration of information in a causal structure like the structure of a brain. GWT proposes that consciousness occurs through the transmission of information through particular central brain structures. In both, the qualia that are experienced occur through the neural substrates of either the processing or the information carried. Hearing and tasting are different because they involve different groups of neurons and synapses; you don't typically taste a sound because the parts of the brain that process taste are not getting direct auditory information.
However, that doesn't mean that senses are completely disconnected: it is possible to form relationships between senses by association, like how both written and spoken language evoke the same meanings, or how certain colors seem to be associated with "hot" versus "cold" temperature.
As far as what it means to experience things how others do, I'd recommend Nagel's What Is It Like To Be a Bat? which argues that subjective aspects of consciousness cannot be completely understood, but that there are objective features that can be understood. So, although you cannot know that others taste or feel music in subjectively the same way as you, you can objectively understand that other people can taste sweet and sour, can hear music in a similar frequency range, etc.

thanks I'll dig these for sure..I am glad I was going the right direction, and you gave me so much material to read...I have seen many Roger Penrose videos recently on youtube, I guess he must have been digging a lot around that subject (and others apparently)

"involve different groups of neurons" I guess you're right, I heard that some people had a brain issue making them ear food and smell sound or something, but even if the brain is wiring things in a deviated way, in the end smell is smell, sound is sound, taste is taste; I build robots and I always wondered "how would I make it feel pain or pleasure"; not sure it would be a good idea ethically speaking