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Help in identifying this dot-sized insect crawling on my bed
While laying in bed scrolling on my phone I found this crawling in it. It is extremely small, no bigger then the  period in this text, could barely see it with the naked eye, I had to zoom in like 10-14x with the phone and the image is not the best.

I live in Louisiana and have 2 pets, a cat and a dog. I am around livestock at times and live in a rural area and also hunt in the wild. Please help me identify this insect.

Please update if you end up finding more than 1

Good post.
It's a tick, possibly first instar, probably a nymph and definitely unengorged, for example Ixodes scapularis (post-edit there are numerous other candidates). This is the obvious answer, particularly with a dog, possibly cats in a rural area. They are definitely diurnal and will travel via pets. Ticks are present in Louisiana, but not endemic to my understanding - so its rarity would fit.
An ixodid tick would fit the bill. In the top picture it's very difficult to see its legs - I think that's the camera angle - unengorged ixodid ticks have long legs, longer than their body. Again post-edit, there are numerous alternative tick species in the US.
If you zoom in on the second picture - that's a tick, it has 8 legs (to my counting) and they are distinct and larger than its body .... The back legs are very characteristic but I can't get a good photo to demonstrate the identification.
The difficulty I'm having is deciding what instar it is. I don't think it's a larva, because its legs are too small in comparison to its body. I definitely recognise the back legs - but I can't place it. I'm wondering whether it's a nymph or adult male, at a guess I'd go for nymph. An adult male BTW will not feed (but I think they can attach - not sure), anyway they're really hanging around for a female. Basically it would fit this being a male better, but they are a bit bigger than nymphs.
Face to face the difference between larvae, nymph and adult male is obvious because of their size differences. Here it's difficult to see that. BTW it appears to have a marking on the back of its "shell" zoomed in on the second photo - that will be diagnostic to a tick expert; there will be Lyme's experts on the site and they'll be able to give a species identification.

At first (top photo) I thought it was first instar Cimex lectularius unengorged (bedbugs) - that's the photo below far left.
The evidence that its not Cimex

rural area, bedbugs are in cities
its broad daylight and Cimex are strictly nocturnal.
they only have 6 legs. The second photo zoomed shows 8 (to my sight anyway (* post edit note, I'm not really sure it has 8 legs on review, it might have 6*).

Image above is a Cimex first instar engorging (feeding on blood) to demonstrate the change in morphology as they feed. The image and associated info are from here.

I've been asked to respond to a "peer-review" process by @theforestecologist.
Male ticks and feeding
First up the comments stated that male ticks feed and I clearly stated they do not feed. The citation given in the comments was from CDC's website, I think it was here. An example of a statement supporting this idea is (I don't think it was the specific sentence cited),

After the eggs hatch, the ticks must have a blood meal at every stage to survive.

I studied Ixodes ricinus for my PhD, i.e. European ticks and the expert opinion was that the male ixodid tick didn't feed. This has been comprehensively addressed by Troughton and Levin (2007) "Life Cycles of Seven Ixodid Tick Species (Acari: Ixodidae) Under Standardized Laboratory Conditions" in J. Med. Entomol., the journal is an authority in arthropods. The authors' did not observe any engorging behaviour for Ixodes scapularis males,

Males were rarely seen attached to the rabbit, but they were observed copulating with females and crawling around the feeding bag between attached females. The majority of males died while on the rabbit by the seventh day.

"Attached" is the only way the male tick can feed, it's not clear whether they are feeding however and they are not engorging. Basically, the male tick can spend 1 to 2.5 hours copulating, whilst the female will feed for several days. Thus "briefly" and "rarely" will be "minutes" and for a tick even at larvae stage this is not sufficient to engorge and moult to the next stage of development. After the male tick has mated that its final stage of its lifecycle. The CDC statement applies to larvae, nymphs and female ticks.

Distribution of Ixodes scapularis
It's important to note Louisiana has been key to the ecology of Ixodes scapularis from when the first surveys were performed. This is a comprehensive study from Eisen and Eisen (2023), Ticks and Tick-borne Diseases

The time series clearly shows I. scapularis was present in Louisiana from 1912 onwards. Thus the OP is in the vicinity of what is commonly called the "deer" or "black-legged" tick.
The reason why I brought this up early is the OP states they go hunting, presumably with their dog, and presumably for deer, so the OP will be within ecoregions of  where the deer ticks distribution is described above.

Evidence for ticks
Its important to note there are numerous and morphologically diverse tick species in the USA, not just the "black-legged" or "deer" tick, but also the brown dog tick, American dog tick, winter tick, the lone star tick and so on... The photo could be any of those. The presence of both "hard" ticks, aka ixodid ticks, and "soft" ticks in the US, together with their complex instar lifecycle mean there is a huge morphological diversity of ticks in the US. It's not like Europe. In Europe there's only one predominant species of ixodid tick.  In addition, partial engorgement of a soft tick, such as a lone star tick could represent the top photo, but in my opinion not the second photo (zoomed in).
Could it be a tick larvae?
Yes,

if you believe the second picture zoomed in has 6 legs not 8 legs -- then its a larvae, e.g. CDC describes tick larvae as having 6 legs, also Dubie et al (2017) (below).
ixodid tick larvae can be just less than 1mm (below), depending how they are measured
there is a strong fit with the OP's hunting and deer tick ecology
there is no hair visible on any part of either photo by the OP and that is a critical anatomical feature of all mites along with 8 legs.

In addition, it could by any number of species not necessarily the deer tick (see below for winter tick and American dog tick [which are closely related]). On review does the tick have 8 legs or 6 legs?  It might only have 6 legs - in that case it's a clear identification of a tick larvae.

The above image shows from left to right, the larvae, nymph, male instar and female instar of I. scapularis (deer or black-legged tick). The point is that larvae are very small, but equally unfed nymphs are also small.
Could it be a nympth?
Quite possibly:

Nymphs have 8 legs (is there 8 legs in the zoomed second photo? There could just be 6 legs)
Nymphs can also be very small (picture of I. ricinus below)
The ecology and OP's hunting as well as the lack of hair fit in the photos fit with this being a tick.

Note the image of I. ricinus above is taken from van Duijvendijk et al 2016 Parasite and Vectors The ticks are visibly different from any American tick, but the size distribution are very similar. What I want to show is that nymphs (top right of the 4 ticks) are also small. The larvae is the bottom right of the 4

What species of tick is it?
The ecology fits the deer tick, but it could be any number of ticks. For example, an alternative is the brown dog tick could easily be a candidate:

An image of the brown dog tick
Second alternative example is Dermacentor albipictus (winter tick) is intriguing, whose habitat will include Louisiana, if you zoom into the second photo the OP took there is a "lighter patch" just below half down on the ticks shell. That must be diagnostic because thats rare in ticks (lone star females have a "white spot" but it's not the same location). That has distinct resonance to the image of a winter tick from Dubie et al (2017) Identification of Immature Stages of Common Ixodid Ticks Found in Pastures in Oklahoma 2017 Southwestern Entomologist 42(1):1-14. It important to note the picture is taken using strong light and this will shift the leg colouration. The image of interest is the top left and the publication makes it clear that there is variation in size of the "white spot" on the tick larvae (some tick larvae don't have it). A coloration spot is really unusual for a juvenile tick.

Third alternative examples is the American dog tick is the same genus Dermacentor variabilis and both are ixodid ticks.
Finally, it may be possible it's a soft tick such as the lone star tick (the image here is an adult female).
Note The brown dog tick and American dog tick are different genera of "hard" tick aka ixodid tick. Similar names but genetically quite different. The deer tick is also an ixodid tick.
Anyway you get the idea, there are lots of ticks in the USA and their diversity is not always well documented, i.e. Dubie et al is 2017 for a morphological identification paper (that would never happen in Europe :-) ).

Could the photos be mites?
In summary No. The counter hypothesis is that this a mite rather than a tick. Personally, I can't see this, but to demonstrate this: a comprehensive overview on the differences between ticks and mites is give at https//study.com entitled "Video: How Do Ticks & Mites Differ?". The video is a great resource and makes it clear mites can look like ticks but there are key differences:

mites are much smaller than ticks, the overwhelming majority being <1mm
for example, mites that live on the human face (which we all have) are not observable by eye
mites have hair and ticks have no hair (see below)
ALL mites have 8 legs (I'm not sure whether the OPs photo has 8 legs).

There are no visible hairs in any photo by the OP and if the photo by the OP has 6 legs - it sure ain't a mite.
The second issue is what mite species could it be? Common mites that that can be confused for ticks would be beetle mites, chiggers mites and chicken mites but none of these fit (below). There might also be also be associated signatures, for example chicken mite infestation.
Beetle mites
Beetle mites can be confused for an engorged tick larvae, but like all mites they have visible hair (below):

Chiggers mites
The issue here is like many mites they are very small <0.3mm and the question is whether cellphone could achieve that resolution? The other issue is they bite human legs causing a red spot, which I think (I could be wrong) itches. Ticks bites don't result in inflammation, chiggers bites do (maybe the OP has this?). Tick bite "inflammation" BTW is the onset of Lyme's infection.
Chicken mites
If the OP has chickens then the onset of a chicken mite infestation is possible. Chicken mites are large up to 1.5 mm which is huge for a mite. However, chicken mites don't look like the photos the OP has shown, particularly their legs are a different colour, in addition they are known as red chicken mites and these arthropods can be red,

Summary

It's a tick larvae if the second photo comprises 6 legs and not 8. The ecology fits very strongly with deer ticks and dogs do pick up ticks: deer ticks, brown dog ticks, American dog ticks, winter ticks, lone star ticks - huge morphological diversity in the US.
It's a nymph if the second photo comprises 8 legs. Again the ecology fits strongly, but again the morphological diversity of US ticks is large.
It's a mite if the resolution of a cellphone can identify a mite <0.3mm for many mites, or large mites <1mm, but fail to identify the hair of the arthropod. There would need to be a candidate species which better fits any species that I am aware of, nothing I know fits at all.

Final note  I can't see any other outcome except that its a tick

Definitely not a bed bug. Though, I also don't think this is a tick.  Looks like some other mite. Your answer includes appreciated depth when comparing to bed bugs, but you really lack any strong/cited evidence to support that this is a tick vs any other mite species (let alone any cited evidence for the specific species you suggest -- with presence of dog not being very convincing by itself). Look at leg orientation and apparent lack of scutum. OP's pic is small, so this isn't easy, but your post needs more cited evidence to support your answer

@theforestecologist thats a tick - I studied Ixodes ricinus for my PhD (European ixodid tick), but its good we agree its not an insect. Your information on the CDC is inaccurate and potentially misleading; it depends what you mean by "male ticks". The issue is that the male instar is not believed to feed, however all larvae, nymphs feed - they take a single blood-meal to moult to the next stage. Thats how it is written it; I would urge not to press the point, which at best is highly debatable. I am very sorry but I cannot agree with your posts; an expert in Lyme's disease is required.

I don't think it's impossible for the OP's image to be a larval tick, but I still personally doubt it. However, what's important is that you've not provided enough explicit evidence to support your answer. In other words, I don't want you to read any of this as "me vs you" -- it's a bad picture so it's not 100% clear either way. Instead, please read all of this as a form of peer review encouraging you to provide more explicit detail for why you're correct and for the need to provide reputable sources to back up your claims and address commentator concerns. Build the strongest argument you can.

Again I will put together a literature review as promised. Please note, it is weekend at the time of writing and tomorrow is Christmas Eve.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

Thanks for taking the time to edit. The inclusion of additional links/citations is good. However, your edits overall are meandering and unclear. Many issues exist throughout. Most importantly, you did not strongly address the issue at hand: why tick vs any other mite. The lone section that addresses this uses a lousy source (study.com, in fact not even a strongly written nor accurate study.com post written by a man with MA in Physics Education who teaches high school chem & physics). Odd choice by a tick expert. Though longer, the post is not improved and has many issues. Please [edit].

@theforestecologist I will respond with formal citations. I will contact study.com independently to ask them to comment on the validity of their study material and cite your criticism in the context of their IP.


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Long black cave insect in Thailand
I encountered this strange insect in a cave in Thailand (Kaew in Sam Roi Yot, to be specific) a couple of weeks ago. Google and iNaturalist are failing me. I think it's about 3 inches long not counting the antennae. It didn't have a strong reaction to the light but did sink further into the crevices.

No Idea. Thaibugs might be a place to start.

Current consensus on iNaturalist seems to be that it is some sort of whip scorpion. Cool!
What to me looked like the head and "eyes" in the above photo are the pedilaps being held tightly together in front of the actual head. If you look closely at the rear end, you can also see the "whip" folded forward reaching towards its head. I am unable to determine which species it is exactly (this one is more long and skinny than anything I can find examples of), but here is an example of a whip scorpion holding its pedilaps together in a similar fashion.

Welcome Jay. Link-only answers are considered to not be enough and may be deleted. If you're able to add details and then use the link in support of your answer then that would save your answer from that fate. See the [help] article how to write a good answer for guidance.

Could you at least mention some morphological feature seen in the photo that would indicate the plausibility? Do whip scorpions have "claws" in front? (example) I don't see any large appendages at either end of the specimen in the photo. Is the specimen facing up or down? Thanks!  (and Jimmy Cricket is correct; link-only answers where readers must go off-site to get any supporting information are strongly discouraged in Stack Exchange; an answer needs to retain value if and when the links break in the future)

Updated with more details, sorry guys!

Thanks for the edit, looks great! I saw it because I clicked "follow" under the question. In the future, if you want to reply to a specific user, see How do comment @replies work? found in FAQ.

Did you mean "pedipalps"?

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sort: votes


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Does the species number of microorganisms in the genital tract significantly increase through an indirect sexual tree?
Let's say:

The indirect sexual relationship tree (assuming condoms are not used) can be huge.

The A at the tree end had only one sex partner B for a period (e.g. a few months and thus joined the huge tree).

STI tests get negative results for A and B, so you can think their immune systems work fine.

Does indirect contact significantly increase the species number in A's genital tract? For example, compared to a typical species number N, from N to 100N or even more if the tree is large enough (there is an upbound of course). Or does the species number change slightly due to some inherent biological limit in the genital tract?
Considering there are many microorganism species (most of which could be viruses) in the human genital tract -- known and unknown, unique to individuals, and common in humans, this is more of a statistical issue.
I consulted someone who seems to be a scholar, she says:

I think the species number would be almost the same -- unless the original number in A is fairly small -- for example, several only.

Are there any known studies or discussions on this topic? I tried search engines but most research studies focus on specific microbial species.

As you have been told previously, one question per post. Please add your references too.

@JiminyCricket. Sorry. The question is edited. As this is a suspicion, I do not have a specific link. Is this allowed? (I tried search engines but found almost nothing on this problem.)

The question has numerous potential problems and I'd suggest it was badly worded.
The specific issue is the way the "non-pathogenic microbiome" is worded by isolating it from STDs in the face of re-emergent and endemic infections. The microbe more broadly could play a protective role in other infections, e.g. UTIs, or cervical cancer (waving my arms about a bit). So it certainly worthy.
If the OPs question was a clinical study it would encounter opposition from infectious disease specialists on an ethics panel, i.e. they would possibly reject the study as it is currently written:

Chlamydia and gonorrhea are endemic in the USA (CDC report) and the largest source of preventable infertility on earth, for example even in China (Liu et al 2022).
Both infections have complex incubation periods, therefore a patient can be infected without it showing on a diagnostic test; even with the best techniques (NHS, UK, e.g. Reyes-Lacalle 2022).
Diagnosis efficacy is variable depending on the underlying technique: MAb based, PCR and culture. Hence again a patient can be infected but the infection isn't detected (Hiller et al, 2021).
Undetected infections significantly risk female infertility (for example Tsevat et al. 2017)

To summarise: the problem with the OP's question is that this might be inferring that a diverse microbe offers STD protection (unlikely). If it was re-focused it could be a really good question.

The OP's question is so badly worded that a completely opposite interpretation is also possible: the worry that as-yet-unknown microbes (not including known STI-associated pathogens) may exist in such numbers in the "indirect sexual tree" as to threaten anyone entering this so-named tree with an increased chance of cancer from a multiplicity of unknown but pathogenic organisms. As such, the question is so poorly defined that the answer you provided may not be the answer the OP is looking for at all. That's why asking for clarification in comments before answering is so helpful.

(Although if your interpretation is the one the OP meant, it is a valuable answer, though it doesn't address the hypothetical: that in the reproductive tract there may exist untold numbers of pathogens capable of causing cancers.)

@anongoodnurse Your first interpretation of my question is what I meant to ask. The key info I want to find is "Is there any biological factor that limits the spice numbers -- especially for viruses". The problem is that I used “diversity,” which usually excludes viruses (I learned this today). So would a question like "Does the species number of microorganisms in the genital tract significantly increase through an indirect sexual tree?" be better? I was told such a question is "nothing of biological interest". Could you please give me some advice?

I had thought of "a diverse microbe offers STD protection" -- I know little about this except for an intuition that "this is unlikely" (especially for viruses).  The interpretation from the first comment here is what I tried to ask. But such a question seems to be "of no value",  Is this because "we have little overall understanding of unknown microorganisms"?

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bioinformatics /genomics
i am looking for likely truncation sites to prove recombination in sequences. i have 4 sequences. i believe one to be the "real sequence" and the other 3 to be recombinants caused by cleavage possibly due to Arg c proteinase. I know my sequences overlap due to multiple alignments i have performed using UniProt and i have chosen the enzyme due to carrying out cuts on Expasy cutter. If anyone could point me in the right direction this would be much appreciated.
many thanks in advance

-1 question not currently legible and not clear what you are struggling with. edit the question to make it readable and make the question itself clearer.

thank you i have rephrased the question, i am new to this site i am looking for truncation sites in sequences if you have any information on useful literature it would be greatly appreciated.many thanks

Can you please make this a redable post? Posting a ton of sequences seems not helpful to me at leat unless you re-phrase your question. These are protein sequences, so you will not find any stop codons.

i have specified i am not looking for stop codons but truncation sites the sequences are the ones i am comparing, i am sorry they are not readable as i cannot paste them "in frame".....if you could please direct me towards literature on identifying truncation sites as i believe these sequences to be recombinants of each other due to the alignments i have performed. many thanks

Truncation sites of what? Proteins? Protein translation? Transcription?

my professor said pro peptides.....i believe the 3 of these sequences are recombinations of 1 main sequence i retrieved from UniProt

Then I would recommend using a sequence alignment tool (clustalw should do it) and align the sequences to find out if there are similarities.

i have done this and i have the alignments which shows there are overlaps...i just don't know what to say to prove my observation beyond what i can see....so i was told to look for "likely truncation sites" to back up my observation, hence my post do you possibly have any recommendations of what direction i should be looking in? many thanks

using the "preformatted text" option on the alignment text would help to make it much more readable. And RE your comment on you other post - I am being helpful so there is no need for rude comments, properly written and clear questions get better answers, this is how things are done on the SE sites.

thank you with regards to the pre formatted text option, and it was not a rude comment i am new to the website and everyone has been extremely helpful however if you read the post you would see it is not a duplicate question and an unnecessary response since i am new and trying to navigate my way around the site. many thanks

http://chat.stackexchange.com/rooms/1997/biology this would be agood place to get that sort of help

thank you, do you know anything on sequence recombination due to cleavage and/or truncations?

The sequences you have posted seem to be (protein) amino acid sequences. The stop codon are present in DNA sequences and in mRNA sequences.
In DNA, the bases are A, G, C and T; stop codons are TAG, TGA and TAA.
In RNA, the bases are A, G, C and U; stop codons are UAG, UGA and UAA.
In DNA and RNA, other letters are used to specify degeneracy.
What you have here looks like protein sequences. So, there are no stop codons in sequences you have posted.

thank you this is correct i meant to say i was looking for truncation sites not stop codons.

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Artificial Propagation and it's relation to asexual reproduction
I know that asexual reproduction is also called vegetative reproduction. However I do not understand it's relation to artificial propagation. Is it a technique used for asexual reproduction (the method by which plants reproduce asexually) or is artificial propagation another name for asexual reproduction.
Am I right when I say artificial propagation techniques provide the means for plants to reproduce asexually?
Also, is my understanding of asexual reproduction and artificial propagation correct:
In asexual reproduction, a parent plant produces offspring that are genetically identical to it and to each other. Asexual reproduction produces clones as the offspring and the parent are clones of one another. Asexual reproduction can be an advantage when environmental conditions are stable and an organism is well-adapted to its environment. The genetically identical off spring will also be adapted to that environment. Asexual reproduction is carried out by the different artificial propagation techniques. Artificial propagation is the cloning of a plant from a portion of its roots, stems, or leaves. In asexual reproduction in plants, also called vegetative propagation, new individuals are grown from a portion of the roots, stems, or leaves of the existing plant. Artificial propagation involves using plants’ natural ability to reproduce vegetative. This process enables farmers and gardeners to select the parent plants for specific traits.

Artificial propagation is (generally) human-directed, while asexual/vegetative reproduction is a natural process. Take a look at the wikipedia article on vegetative reproduction for more information on how and why artificial propagation is sometimes preferred to vegetative reproduction.

You can also have a look on the artificial reproduction article in the Wikipedia.

Artificial propagation is the cloning of a plant from a portion of its roots, stems and leaves. It does nor use reproductive organs of a plant to propagate.

Welcome to Biology.SE. We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give a one-line answer; explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed especially when they are a poor duplicate of an already existing answer. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly.

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Sporophyte and gametophyte

My textbook says that in both groups of seedless plants (vascular plants, non-vascular plants) the gametophyte is a free-living plant, independent of the sporophyte.
I don't understand this statement and am now wondering if the sporophyte and gametophyte  are stages in a plant's lifecycle, or are they individual parts of the plant, or are the sporophyte and the gametophyte different plants altogether? Secondly, does this differ depending on the organism?

Different plants or different structures that make up the same organism?

The sporophtye is the diploid stage in the life cycle. In comparison, with humans, you and I would be sporophytes.
The Gametophyte is the haploid stage in the life cycle. In comparison, with humans, spermatozoids and ovules are gametophytes.

Independence
Note for what follows: "independent" can be understood in terms of "ability to survive". Being independent according to its ability to survive. One might use the word "independent" for other concerns though! For example: "Independent" in the sense "no nutrient exchange between the two"
Therefore, one could say that in humans, the gametophyte is not independent (in it's ability to survive) of the sporophyte. Similarly, in moss (bryophyta), the gametophyte is not independent of the sporophyte because the gametophyte grows on the sporophyte using its nutrients (one could say that the gametophyte parasitize the sporophyte but that would be a bit misleading!). If the sporophyte is independent of the gametophyte (or vice-versa), it means that there is alternation of generations. In other words, sporophyte and gametophyte live separately (like two different individuals).
Life-cycle
You can find tons of examples of weird life cycles, in particular in plants, fungi and parasites but not only. And you may find many examples for which the type of sexual reproduction or the type of life-cycle are hard to defined with these relatively simple concepts.
Identity
The question of identiy (how separate or genetically different should two individuals be so that we consider them to be two different individuals) is rather a question of philosophy. Such discussions about identity occur when we talk about clones (ramet and genet), about life cycle or about level of organisation/level of selection. The book Major Transition in Evolution (Revisited) provides many of the philosophical discussion on the subject of identity in population genetics.

Oops I missed your comments 2 months ago. I edited the link. Thanks you!


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Why do zygotes divide internally and not externally?
As far as I understand, two gametes fuse to create a zygote. Gametes are created via miosis, they are haploid and when they fuse they become a complete cell (diploid). And diploid cells divide via mitosis.
However, I wonder why a zygote does not become two zygotes? What is different about it that makes it divide internally?
In other words, why does a liver cell become two separate cells, yet the zygote becomes two cells inside the same shell?

Update:
Maybe this image can help:

The zygote is dividing. But what is that external package? Why do those divided cells remain in a circular sac (Sorry for this stupid terminology, I want to make myself clear)?
But in simple mitosis (the image below) divided cells are not inside a package anymore. They are 100% separate from each other.

As I have understood it, the divided cell remains in the parent tissue. A liver cell after division becomes two cells inside the liver. The container is the liver.
However, the zygote is not like that. It's internal mass divides and remains inside the same zygote. I don't know what's so hard about understanding this for your guys.
Maybe the zygote is not the outcome of the fertilization of the egg and sperm. Maybe an egg has a package and a cell inside it, and that package is not part of the cell. That's why I'm asking.

What do you mean "inside the same shell"? Zygotes divide just like liver cells...

look up monozygotic twins

It seems that I'm missing something here. Maybe a zygote is not a cell. Maybe it's a biological envelope, containing a cell, and then the inner cell divides. But the monozygotic twins images do not show that. Bot inner cells, and the envelope divide.

@BryanKrause, please look at this image for example. The inner cell (blue dot) divides, and the outer shell also divides.

What do you mean by "shell" a zygote divides into two sperate cells just like all cell divisions. Are you maybe thinking of the corona radiata, which breaks down after fertilization.

If the term zygote is a diploid cell, then when it divides there is nothing strange in the fact that it becomes two diploid cells. If the term zygote indicates its special origin, it is impossible logically for a daughter cell to have the same origin. Your expectation that the zygote would divide into two haploid gametes seems bizarre. The “magic” thing would seem to me to be meiosis and fusion. Once you have a zygote it’s not quite back to normal because the cell must differentiate, but mitosis is the default cellular behaviour.

If you don't understand the parts of an illustration you should probably ask about that before guessing and asking a confusing question based on your guess.

@John, then please clarify my misunderstanding instead of criticising me. Thank you.

@SaeedNeamati its not criticism its how questions work, the site is for answering specific questions

@John, is the image I have shown up not clear? What can not be understood from that image?

You have half  dozen questions here, I will answer one, that outer membrane is called the zona pellucida. it exists to control fertilization. https://study.com/learn/lesson/early-embryonic-development-human-stages-formation-mechanisms.html

@John, so I was right. The egg is not a cell. It's a cell inside a package. The Zona Pellucida is not part of the normal cell that divides. It acts as the container for the fetus and placenta.

No it breaks open long before either is formed, again research don't guess.

@John, please don't be harsh. Either help or leave this question for others to answer. I have watched dozens of videos regarding this. I have done my research to ask this question. And you just complicate things. So either help or please leave.

I'm complicating it by trying to lead you to asking a coherent question instead of just voting to close for asking several separate questions. Or at least figure out where your confusion is coming from.  there is no difference between liver cells and zygote cell division. a liver cell divides into 2 separate liver cells and a zygote divides into 2 separate zygote cells. A dividing liver cell does not become 2 livers why would a dividing zygote cell become 2 zygotes? if you want to know about the function of the Zona Pellucida ask that as a question. You could also look into cell adhesion.

this may help you https://www.twins.org.au/how-to-determine-zygosity/89-placenta and https://twinstudies.org/zygosity-and-chorionicity-of-twins/


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What is the name of this plant or shrub?
I just found a plant in India.

Here is its leaf.

I tried looking it up on flowers of India & wikipedia, but both databases are too
much to read manually.
Physical description:
Each Stem has 6 leaves on it, Leaves are opposite & Elliptic shape, Entire margin & Pinnate veins on it.
I am thinking it is shrub, not a tree.

I replaced night time images with day time. Hope this will help to ID this species easy.


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Solitary wasp larval behavior
Once placed in proximity to its future meal, how long does it take for the larva of a solitary parasitic wasp to begin feeding? I have several books on wasp behavior, but none address the time involved. An internet search also proved fruitless. I am asking out of curiosity and also to ensure accuracy in a story I am working on. I am sure it varies, I am just trying to get a general idea. For example, is it possible for larvae to begin feeding as soon as they are deposited?
(Edit: I added details to this question thanks to the first answer I received on this question)
(Edit: I've spent some more time looking into this and thought I'd share some information, should anyone be interested. Indeed, larvae can begin feeding within two days of being deposited. The larvae of Cicada-Killer Wasp (Sphecius speciosus), for example, begins feeding in 2 to 3 days, according to "The Strange Lives of Familiar Insects" by Edwin Way Teale. In "The Hunting Wasp" by John Crompton, the introduction sets a general range of 2 to 3 days, although I have read online of some wasp larvae taking longer.)

It depends on species and situation.
There are a lot of different solitary wasps, the kind you are referring to are parasitic wasps, that lay their eggs in or on a host for the larvae to feed on before they pupate to reach the final stage of their lifetime.
Some larvae that consume a host in groups take as little as twelve days to consume their host and eat their way out.
However, this wasp species can even have their larvae remain in the larval stage through winter and adapt through seasons. it's entirely dependent on what sort of wasp you're asking for what the time span would be for a larva to mature.

Thank you for your answer! I tried to upvote it but am too new.  What I'm wondering is when the larvae might begin eating. Could they start as soon as they are deposited by a wasp? I understand it will vary.

@AdamOrth They could indeed start eating fairly soon after the wasp has deposited them, the eggs do have to hatch first but that could be a matter of hours.

Thank you, I suspected this but was not sure.


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Overnight bacterial culture
I am working now to prepare an overnight bacterial culture. My question is should i pick only one colony of the bacterium streaked plate in order to make an overnight culture and what will happen if i picked two or three colonies?. I am working to make a deletion mutation in one bacterial starin using the phage transduction method. The technqiue said that i should make an overnight culture in 20 ml of the medium. So, i wondered if it would be two low if i pick only one colony in such amount.

Broadly the answer is 'yes, work from a single colony' but can you give a few more details of your experiment so that the potential pitfalls can be explained?

I am working to make a delation mutation in one bacterial starin using the phage transduction method. The technqiue said that i should make an overnight culture in 20 ml of the medium. So, i wondered if it would be two low if i pick only one colony in such amount.


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What is this flying bug in Denver, CO?
It seems to be a flying insect about 2-3mm in length. It also doesn't seem like it's very good at flying. They seem to crawl around my desk until I try to hit them, which is when they'll start flying.
Location: Denver, Colorado, USA
They seem to come out more at night.

Can you get a better image? Also, a description of the environment?

@arboviral that's about the best pic I can take with my iPhone, sorry :( the environment is my computer desk, it's pretty bright as I have a few monitors that are on all  the time

Could you get one with the wings in focus? Without some idea of wing patterns and venation there will be serious limitations on what we can do, I'm afraid.

@arboviral I added another picture with the wings spread. Hopefully that helps? :)

A little - but unfortunately probably not enough, I'm afraid! Based on the activity period, size and photos I had been wondering if it was a biting midge (Diptera: Ceratopogonidae) of some sort - take a look at some sample photos here: http://www.padil.gov.au/maf-border/pest/main/140521/49023 - but I'm now much less confident about that; the head looks too big and I can't see the distinctive antennae.

@arboviral they don't bite though. I think they are some sort of fly? I put apple cider vinegar into a cup and they all flew into it. does that give you a clue? I don't think they are fruit flies, they don't have red eyes.

These are Scuttle Flies (Order Diptera, Family Phoridae) (the wing venation, best seen on the lower left individual of the top photograph, is characteristic); the group has several hundred species in America north of Mexico.  So far as I am aware, the generic key in Manual of Nearctic Diptera, Volume 2 (available online here, pages 25 to 48) will still yield useful results, but cannot be used on these photographs.  The 30 pages in bugguide.net's gallery (starting here) eliminate a few of these, but not nearly enough to go further on the evidence we have.


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Why do flowers naturally reproduce with their own species?
I have always wondered why flowers reproduce with the same species naturally. Why can't the pollen grains get to a different species flower through via the wind, water, or insects?

Sometimes they do.  There are many naturally-occuring hybrids of (close) species where their ranges overlap, and many more produced by human intervention.  But in a sense the question is backwards: things become different species because they can't easily interbreed: either by geographic or temporal separation (that is, they bloom at different times), or perhaps some biochemical incompatibility.  If they could easily interbreed, they'd be the same species :-)

I know with cactus at least some self-fertile plants will ripen the male and female sex parts at different times. The female parts will mature and accept pollen from nearby neighbors, then the male parts mature and provide pollen to any plants with mature female parts (possibly even itself.

To complement what Charles (Darwin is it you? :)) said, and JM97 hinted at the comments, there is also another factor impeding the cross pollination between different species, that is the pollen-pistil interaction.
Basically whichever pollen can come in contact with the flower but only pollens carrying specific recognition signals (I'm not an expert but I suppose is specific compounds on the coating of the pollen that are recognized by the pistil) can actually start the fertilization process.
This has of course interesting consequences, namely self-pollination incompatibility: some plants are more than happy to self pollinate (e.g. barley or Arabidopsis) but some others use this same process to exclude the pollen coming from the same plant and only allow fertilization from pollen coming from other plants of the SAME species (basically what most European royal families were NOT doing...)


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Fibrosis vs stenosis vs sclerosis
I can't figure out the key distinguishing factors between these three and I keep seeing them being used almost interchangeably.
For example aortic valve fibrosis and aortic valve stenosis.
As much as I have understood:

Fibrosis is related to muscle tissue and myofibrils
Stenosis is the result of fibrosis, because muscle tissue loses the ability to expand
Sclerosis is the thickening of the tissue

What are the distinguishing notes between them?
update
One example is this YouTube video from Ninja Nerds.

As you may know, on this site, prior research is required by the OP. It would be more helpful if you actually cited sources for the definitions of fibrosis, stenosis and sclerosis, e.g. "this site defines fibrosis as...", etc. By those means, you're much more likely to get an answer. Thanks.

@anongoodnurse thank you so much. The question is updated.

To begin, look up the three terms in Wiktionary, which actually has a decent set of etymological connections for the words.  You'll see fibrosis is about [typically collagen] fibers, stenosis is about narrowing, and sclerosis is about hardening.  Of course, in any specific context these meanings don't get you that far by themselves - multiple sclerosis is about a lot more than hardening per se.

You already answered yourself the question: these three words are here to designate different phases of a general process. This general process is triggered by the appearance of fibrosis, which is an alteration of a "normal" cicatrization process.
What happened -simplified way- is:
When a part of the body is attacked, a repair process is triggered. Stem cells activated and duplicate to replace the destroyed part of the body. But the process is not entirely "one for one":

For genetic gene alteration reasons, some stem cells will not function
Because the signal that triggers reparation could use various paths, some paths will push stem cells into differenciation, thus the end organ will have less stem cells that at the beginning
For some reasons I don't understand to explain them, some tissues of the organ will expand faster than others. If parenchymal tissue is less expanded than connective tissue during the reparation phase, the overall new "material" (=a mix of the different types of tissues) in the destroyed part of the organ will be "dead tissue"

These three causes and their immediate consequence are called fibrosis.
Because of the third point, there is stenosis in the dead tissue: it cannot expand anymore.
Because the dead tissue is attacked again and again, it will be reduced and could not be replaced: this is sclerosis.


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Evolutionary history: did any organs start out as autonomous organisms?
I've read that the cell nucleus was once an autonomous organism that was "enslaved" by the larger cell at the time of the Eukaryotic Revolution. Are there any organs in the human body that we know of that started out as autonomous organisms (of course they would be unrecognizable in their current form)?

Very short answer
No!
Long answer
It is not the nucleus who was an independent organism but the mitochdonrion (organelle) (One might discuss this point and say that both are correct, it is just a philosophical issue of the identiy of the eukaryotic cell). The plastids (the chloroplasts for example) were also independent organism. In consequence, in every cell, we have DNA in the nucleus and DNA in the mitochondria. The mitochondria is contained in every cell of our body and is transmitted via the ovule (and not the spermatozoid) to the offsprings.
Now let's think about your hypothesis that one of our organ (let's say, our liver) might have been an independent organism in the past. Therefore, this organ would contain different DNA than the rest of the cells of our body. How would you transfer the DNA of your liver to your offspring? Well, it is hardly imaginable.
Moreover, it has been argued that because we now have a complex and efficient immune system, a endosymbiose would be very unlikely.
But no, none of the cell in our body come from a previously different organism. But every cell of our body is some kind of chimera of two previous cells. Note: the vast majority of our DNA are present in the nucleus and not in the mitochondrion.
For more information about endosymbiose, have to look to this and this (wiki articles)
It seems much more easy to have two organisms that stay together during reproduction when reproduction is mediated by striking.
You may find some funny examples (border cases) of two organisms that don't separate during reproduction in corals (zooxanthella), leafcutter ants (and their fungus), parasitoid bees (and the virus that females create in their ovary) and lichens

Remi.b is perfectly correct if the question were restricted to humans (and yes, nucleus is not thought to be a result of symbiogenesis; actually some bacteria have similar structures).
But in the animal kingdom there several cases when certain organs "start(ed) out" as more or less separate organisms:

Many parasites have dwarf males and giant females (which actually feed on the host). These females when reaching maturity recruit actively swimming males, which upon attachment to female genitalia functionally become testicles and get nourishment from the female. The resulting organism can be viewed as hermaphrodite (although "self-fertilization" results in crossing). This phenomenon was described for example for Rhizocephala (Crustacea).
Similar cases are known for free-living organism: for example, in some species of the deep-sea anglerfishes males are dwarf and after attachment to females become "parasitic".
Siphonophorans (colonial Cnidaria) have several distinct organs (swimming bubble, locomotive organs, hunting tentacles and so on), but this differentiation is achieved via specialization of individual members of the colony - zooids. One can argue, that these organism were never separate, but for example one can still tell, which organs are medusae and which are polyps, each one of them "is homologous to a free-living solitary animal". In other colonial hydroids one can find something reminiscent, but the degree of integrity of the whole colony never reaches that of Siphonophorans.
In some species of bryozoans (which are colonial as well), several zooids (they are called "heterozooids" in this case) devote their lives to defend or move the colony, becoming highly specialized organs of the colonial organism.
There are probably other systems fitting in the question, can't remember right now.

I'm leaning toward down voting this - I think, though it is good, it doesn't answer the question. It seems the OP is interested in cases where organisms have been "captured" and used as organs by animals, specifically humans, in an evolutionary transition context rather than phenomena within a single generation. The closest analogy I can think of is the mitochondria, formerly a free living cell, which was engulfed by cells to be used as an organelle millions/billions of years ago.

@GriffinEvo.. The case of zooids is acceptable.. though there is no evidence of enslavement... Perhaps this term can be excluded because even for mitochondria we dont have an evidence that they had been actively enslaved

good point about the zooids @WYSIWYG - downvote removed


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Chromosome 2 alternate explanation - apes gaining a set of chromosomes?
I'm preparing for a debate (just between friends) on evolution (I'm in support), and one of the points I plan to bring up is the Chromosome 2 evidence.  I'm now trying to predict their potential rebuttals.  The common statement I've seen is that since the apes have 48 chromosomes and humans have 46, then there are two possibilities: either we "lost" a chromosome, which would be fatal, or there was fusion.  This, I believe, was an actual prediction prior to the answer of Chromosome 2 being identified.  But couldn't there have been a third possibility - that the apes gained a pair of chromosomes, perhaps thru splitting of some kind?  This seems reasonable to me due to the other claim that we didn't evolve from apes but that we share a common ancestor, and so the ape lineage could have acquired the extra chromosome after the split.  (Note I'm a total biology noob, so if this doesn't even make sense, then please tell me.)  I understand that this isn't the way it turned out, that Chr 2 looks exactly as we would expect from fusion, but prior to this discovery, couldn't the apes gaining a chromosome have been a possible reason?  TIA.

does this help? http://biology.stackexchange.com/questions/5558/chromosome-2-fusion  What else might you need?

BTW splitting happens too.

shigeta, i saw that article and read it before I posted this question.  That page doesn't seem to answer my question directly - specifically, WAS IT PREDICTED or was it simply taken as evidence once it was discovered?  So ideally, someone could provide a reference to a paper or article that was published that says "we predict that...two chromosomes will appear fused", and which was subsequently confirmed by a later paper or article.  I've heard it was about 30 years, but I have no valid source.

I guess part of the question is...what exactly are you bring up Chromosome 2 as evidence of, exactly?  It's evidence of that chromosomal rearrangements are possible, but that isn't terribly helpful to you, so I'm not sure why you are bringing it up.
I think the fusion is a rebuttal to a claim that the disparate # of chromosome is a problem for the claims of common ancestry between humans and other apes, but if they don't mention it, I'm not sure why you would need to use that particular fact.
Have you consulted talkorigin's 29 evidences of macroevolution?  Lots of good stuff there.
http://www.talkorigins.org/faqs/comdesc/

It is useful, IF it was predicted.  This is one of the main differentiators between valuable theories and useless theories, and hence this is why I'm asking the question.  Creation, even if it allows fusion, doesn't predict it.  Given that apes have 48 and humans have 46, the "prediction" from creation would be "that's just the way god made it" and say nothing about fusion.  But evolution's prediction would be that we would see fusion (or other effects) and that's why it is useful.

Things don't have to be useful to happen in evolution. They have to (at the time they are happening) be no disadvantage for the organism. And no, you can not predict, what is going to happen in evolution as this doesn't follow a certain path. You can think about things that can happen (as is has with the chromosomal difference between human and ape) but it doesn't have to happen. It is a proof for a common ancestor to compare genome sequences and there where the differences are.


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blue/white screening - results are opposite as expected
We inserted GFP-gene into plasmid Bluescript SK+, transformed E. coli with this construct, and then plated on an agar plate with Ampicillin and X-gal to do a blue/white screening. We got blue colonies and white colonies, and normally the white colonies are considered positive for the insert and the blue ones are negative for the insert.
The problem is that the results we got are actually the opposite. If we look at the plate under UV-light, we see that ALL the blue colonies are fluorescent, which means they actually produce the GFP, and ALL the white ones are not!! How would you explain this??
Thank you
Edit: i thought that maybe the insert could be in frame with lacz', so we get fusion proteins. However this doesn't explain why we got white colonies which are not fluorescent

What enzymes did you use to perform the insertion? Also, what happens if you transform the original non-cut plasmid?

i forgot this information. We used kpnI for the insertion, which does blunt-end cuts. We also plated bacteria transformed woth the non-cut plasmids and we got some white colonies and only one blue colony.. but none of them is fluorescent

KpnI is not a blunt restriction enzyme. Are you sure you didn't confuse it with another enzyme? Also, if your negative control is giving white colonies, then your plasmids are likely to be defective.

Oh yes pardon, kpnI makes cohesive cuts

If the antibiotic was not working for whatever reason, you could get growth of un-transformed bacteria.

Given the fact that the negative control uncut plasmids are producing white colonies, it seems that there have been significant mutations within the lacZ gene in the plasmid, causing the uncut plasmids to become white due to inactivation of the gene.
I would suggest purchasing a new batch of pBluescript, or if that is not possible for whatever reason, perform a miniprep on one of the blue colonies and sequence its multiple cloning site to verify that the MCS is present and not mutated before continuing. If you are not going to buy a new batch of plasmids, it would also be prudent to verify the plasmid's length using gel electrophoresis.
The most likely explanation is that the plasmids are mutated, and therefore you are getting bad results in the blue/white screen.


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Do RuBisCo and Haemoglobin have any similarity?
In RuBisCo and haemoglobin both can bind to CO2 as well as O2. Do these proteins have any structural similarity?

Why is this tagged "human-biology"? 2. Did you just wiki these proteins up?

No I was reading photosynthesis in NCERT where I found that RuBisCo also accepts CO2 and O2 and so the question came in my mind..!

I deleted "In plants" at the start of your question as there is no haemoglobin in plants. (There is leghaemoglobin, but, although structurally related, it’s not the same.)

Try reading about these proteins. Apart from wikipedia, you can check out pfam which classifies proteins into families. Globins and RuBisCO are very different protein families. Perhaps the only similarity is that both these are made up of amino acids!

Isn't Pfam classification a bit too advanced for someone reading grade 10 textbooks? :P

@KoustavPal No, I don't think it is that difficult (the summary page at least). Plus, RuBisCO is probably not introduced in 10th grade. I remember it was 11th. The question is a closure candidate on the grounds of "homework" without an effort. I didn't VTC because the OP is probably a highschooler.


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Mathematical/statistical models for forecasting population distributions of age, sex, weight, and height
I come from a mathematical background but I have no experience with the topic of mathematical biology.
Are there well established mathematical/statistical models for forecasting the evolution of population distributions of biometric parameter such as age, sex, weight, and height? For instance, I have often heard that the proportion of elderly people in the population is projected to increase. What models are being used to generate forecasts such as these?

It's not possible to accurately predict the course of evolution in humans. I imagine the models you are thinking of are based on socioeconomics rather than biology.

You better let the national statistics offices of every country know then because they all make future projections of age and gender population distributions. Health bodies make projections of weight distribution. So I am wondering what models are being used to generate these type of projections. I am particularly interested in models that take a stochastic viewpoint, although I am also interesting hearing about deterministic models.

Those models aren't base on biological evolution which is what I interpret your question to be asking about.

I get where your coming from. The models I am looking for information on relate to population dynamics which is a field of mathematical biology.

It might be irrelevant to your question but search for "allometry".

The term you are looking for is demography - there are literally thousands of papers published on this topic.
Each of your topics mentioned has its own models and prevailing theories, so without an exact question it is very hard to answer as to which model you might find best.
Having said that there are well established models of things like geometric growth of populations (proposed by Thomas Malthus in 1798). The United Nations does a lot of modeling of populations and the like. You might be interested in their freely available publications and information here.


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During weight loss, do we inhale more oxygen?
During weight loss, triglycerides which are composed of carbon, hydrogen and oxygen, are broken down. During respiration, the inhaled $O_2$ is bonded to a carbon atom to form $CO_2$ which we exhale. However this process happens anyway, even one isn’t trying to lose weight. So that suggests to me that during weight loss people must inhale more oxygen, otherwise where are all those extra carbon atoms that we now have going?

Read about ketones.

First one needs to make it clear that oxidation of foodstuffs, either those in the diet or from deposited reserves, occurs in order to generate energy (ATP) for life’s processes — the most evident to the non-biochemist being to perform muscular work. So, as the poster correctly implies, this will occur in both fasting and non-fasting individuals, and the fairest comparison would be between the same individual performing the same amount of energy-requiring processes.
Let us consider this comparison in the simplest situation where the person “losing weight” is fasting, i.e. has no food intake (rather than being on some fancy diet). After his glycogen has been depleted, the fasting individual will be producing all the energy for his various needs by oxidizing triglycerides that had been deposited previously in his fat cells. The amount of oxygen he inhales (assuming this is strictly related to requirement — I’m not a physiologist, so I don't know) will be that required to oxidize the triglycerides to produce this required energy.
Now compare this to the same individual, not fasting. His energy needs have been assumed to be the same as in the fasting state, but he is generating this energy from his food intake. Making the unlikely assumption for comparison that this were all triglyceride, the amount of oxygen needed to oxidize this would be exactly the same as the fasting individual.
I think that deals with the fallacy in the question, perhaps caused by not reflecting on what the oxygen inhaled by the non-fasting individual is used for. Technically one should admit that if the simplistic assumptions do not hold, the strict equivalence would not either. Different foodstuffs (carbohydrates, fats, proteins) are in different oxidation states, so the amount of oxygen required to oxidize them in the fed individual would depend on diet. If the food intake of the fed individual were greater than his needs and he was depositing glycogen or fat, extra ATP would be required to do this, which would likely be generated by oxidative phosphorylation. No doubt one can think of other possibilities, but these were not the focus of the question.


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Do the left half and right halves of the diaphragm undergo the same displacement during breathing?
Do the left half and right halves of the diaphragm of a normal person move exactly the same distance between inhaling and exhaling?

Did you check diaphragm muscle images? They are fairly symmetrical.

A short answer is that the displacement of the right and left part of the diaphragm during breathing may not be the same.
ASYMMETRY
Thoracic diaphragm (Wikipedia):

In humans, the diaphragm is slightly asymmetric—its right half is
  higher up (superior) to the left half, since the large liver rests
  beneath the right half of the diaphragm. There is also a theory that
  the diaphragm is lower on the other side due to the presence of the
  heart.

Genetic specification of left–right asymmetry in the diaphragm muscles and their motor innervation (PubMed):

The diaphragm muscle is essential for breathing in mammals. Its
  asymmetric elevation during contraction correlates with morphological
  features suggestive of inherent left–right (L/R) asymmetry.

EXCURSION
Excursion (displacement during breathing) of the right and left part of  the diaphragm may or may not be the same, which may differ from case to case.
Manual evaluation of the diaphragm muscle (PubMed):

In most cases, the diaphragm shows a symmetrical respiratory excursion
  of ~2–10 cm...

Imaging of the Diaphragm: Anatomy and Function (RadioGraphics):

The excursion may be somewhat asymmetric and there may be a slight
  delay or lag on one side, typically the right.


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How can space travel affect women’s fertility?
From Time:

The reasoning behind the prerequisite, according to officials, is that
  spaceflight could potentially harm the women's fertility.

How can space travel affect a woman’s fertility?

The most obvious issue is exposure to radiation. Once you're beyond the earth's atmosphere and magnetic field you are exposed to much higher levels of radiation from cosmic rays and solar flares. It's also possible that microgravity (weightlessness) could have effects on the reproductive system, but this isn't well studied yet.
However, given the source you link to to (a nine year old article speculating on why China required female astronaut candidates to be wives and mothers), this may simply be a medical rationalization for a political decision. Radiation can damage male fertility too, and the effect of microgravity on the male reproductive system is also not well understood.

There's already too many men in China, compared to women (gotta love sex-selective abortion!), and I'd say cultural decision, not political.


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How much energy is used to construct a pound of fat tissue?
A widely cited figure is a pound of fat contains 3500 calories of energy in fatty acids.
However, a pound of fat also contains adipose cells, arranged in adipose tissue, connective tissue etc.
When a human breaks down fat to use as energy, from what I understand it doesn't break down the fat cells, just liberates the triglycerides stored inside those cells.
Those fat cells, and connective tissue took energy to assemble as well.
How much energy is used to create a pound of fat tissue?
Let's assume that all the cells and the triglyceride stored inside them are created from scratch.

A rough answer to a rough question
According to a study conducted in the 1960s, human adipose tissue, on average, contained (per 100g wet weight) 87g fat, 2g protein, 2g sodium and potassium and 10g water. (Nothing else was measured.) This suggests that approx. 3% of adipose tissue is solids other than triglyceride.
The figure quoted is presumably the energy yield for the complete oxidation of triglyceride. The energy yield for the complete oxidation of the non-triglyceride solids in adipose tissue  — the appropriate, if hypothetical, comparison would be less than that for triglyceride, which is much more chemically reduced, so the yield for the oxidation of non-triglyceride might be approx. 1–2% that of triglyceride.
The energy needed to bio-synthesize any organic compound (triglyceride, carboyhdrate or protein) is more than is obtained from it by oxidation because a negative free energy change is needed to drive reactions. Hence, as regards the relatively constant (slowly turning-over) portion of the adipose tissue, the cost would be higher — perhaps 2–3% of that quoted produced by oxidizing the triglyceride.
The problem with this question
Some people say that there is no such thing as a stupid question. Nevertheless, there are questions that are formulated as if their answer will establish solve some problem, when in fact it will not because the premise on which it is based is false.
In this case a comparison is made between the triglyceride and non-triglyceride content of adipose tissue with the implication being that the latter should be assessed in the creation of the former:

“Those fat cells, and connective tissue took energy to assemble as
  well. How much energy is used to create a pound of fat tissue?”

As already mentioned, it is invalid to make a numerical comparison between the energy required to synthesize one compound with that released by the oxidation of another compound, as it costs more to synthesize a compound than is released by its oxidation.
However, quantitatively more fundamentally wrong is the implication that the one-time synthesis of the structural components of the cell should be costed into the repeated oxidation of triglyceride in that cell. How many grams of triglyceride are synthesised per gram of cell structural material during the lifetime of a cell? Very many, I should imagine if the cells turn over much more slowly than the lipid they contain.
It would be more pertinent (assuming that you are interested in such things) to ask what the cost is in terms of the energy used by whatever muscles are used by the lungs to breath in the oxygen needed to oxidize the fat, and the energy used by the heart muscle to pump the blood containing the oxygen to the fat cells so that it can be oxidized.
Finally, it is naïve to think of the energy cost of maintaining a fat cell in terms of the synthesis of its structural components. Other metabolic processes are continually occurring that require energy even in fat cells.
No doubt it would be possible to perform a calculation that took all these things into account (although what would you start with “from scratch” — ingested carbohydrate or carbon dioxide and water?). Personally, I am happy to accept that the system makes a profit and interest myself with the details of how it operates and adjusts to different circumstances.

Maybe more to the point regarding the second half of this answer: all of the maintenance of fat cells themselves (as well as all the activity of the lungs, heart, etc) is wrapped up in the concept of "basal metabolism", so it's sufficient to consider the calories stored in a given mass of fat when approaching the issue from a 'calorie economy' perspective.

@BryanKrause — You’re right, the basic metabolic rate stuff would take all that into account. It’s the kind of thing physiologists do, and no doubt they have figures for different tissues. Perhaps one of them could enlighten the poster.

Great answer thank you!


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How is RNA content distributed in daughter cells during cell division?
During cell division, DNA becomes equally distributed between the daughter cells. But how is RNA content distributed in the daughter cells?

I think you will have to be more specific with your question. Are you referring to some specific organism or cell type? Symmetric or asymmetric cell division? Are you interested in specific examples of uneven RNA distribution, or how RNA is generally distributed? My guess is that most RNA is equally distributed between daughter cells, but there are definitely examples of the opposite. ASH1 mRNA in budding yeast, for example.

RNA is either swimming in the cytosol or be associated with the ER (endoplasmatic reticule) during co-translational protein import into the ER (see secretory pathway).
So in order to answer your question: Daughter cells inherit their RNA simply by chance as cytokinesis just cuts the mother in half and each RNA finds itself on either side, OR they are separated just like the ER.
Each cell 'should' have the same copy number of each RNA, but since daughter cells simply produce RNA all the time, there is no need to be as precise as with chromosomes.
However, there are some specialized motor protein complexes that transport specific RNAs to one (like myo4d transporting RNA along actin filaments). This is called 'asymmetric division'. Please start your research here.


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Technical term for a mutation that only occurs after a preceding one
Consider a hypothetical population of 1000 organisms.
(a) 300 of these 1000 have a T to G substitution at a specific position 1.
(b) 200 of these 1000 have an A to T substitution at a second position 2.
(c) All of the 200 with the substitution at position 2 (b) also have the substitution at position 1 (a).
As a non-geneticist, I would call the second mutation a refinement of the first mutation. Would that seem reasonable, or is there a specific technical term for this phenomenon?

Can you clarify why it would be a "refinement"? Why do you suppose that there is any connection between the two mutations? Why not just a second-site mutation that occurred later in the same clone as the first mutation? I'd recommend looking into previous work tracking mutations across time, e.g. https://www.genetics.org/content/200/2/619

Your question needed a little tidying up and someone had suggested some changes. I have tried to lay it out in a more concise and readable fashion. In particular I have removed the term "refinement" from the title as that really begs the question. Better, I think to describe the phenomenon and then give it your own description in the body of the question. But you are free to revert as you see fit. (But use SE's own tool console for emphasis. Whatever you did, didn't work for me.)

Yes, good point. Refinement is a bad word because it has a value to it. I don't suspect that there is any relation between the two mutations. As a mathematician I'd say that the set of organisms that have a mutation in position 2 is a strict subset of the set of organisms that have mutation in position 1, but this is also bad notation somehow. (Thanks @David for great edits).

I am not a geneticist either, although a molecular biologist, so cannot be sure whether there is a term for what you describe. For my part, I would describe the results in a factual manner before considering possible explanations of the type suggested by @Dirigible.

The description of the second mutation depends on the nature of its relationship to the first mutation.

If the first mutation reduces fitness of the organism, and the second mutation tempers the fitness reduction, then the second mutation would be compensatory.
Compensatory mutations are common in bacteria that acquire antibiotic resistance.  Consider a strain of E. coli that acquires resistance to streptomycin by mutating the rpsL gene, which encodes a 30S ribosomal protein targeted by streptomycin.  In the presence of streptomycin, the rpsL mutant is obviously more fit than wild type E. coli.  In the absence of streptomycin, however, ribosomal mutations lead to inefficient translation.  Compensatory mutations may then arise elsewhere in rpsL or within another gene involved in the ribosomal complex, partially alleviating the fitness defect caused by the initial mutation to rpsL.

If, instead, the mutations are synonymous and otherwise unrelated in their functional potential, I would simply call those mutations coincident in the genome, though this isn't really a "technical" term. If you wish to describe the relevance of these synonymous mutations in context of the three distinct genotypes given in the question, you could say that the first T to G transversion differentiates strain X from ancestral Wild Type, and the second A to T transversion differentiates strain Y from ancestral strain X.  This assumes that both of these mutations occurred once in the genetic history of this population.

Thanks - I am not thinking about the fitness though. What would you call it if all mutations were synonomous.

@FrederikRavnKlausen, I've updated my answer.  Do you have a specific organism or system in mind, or is this truly hypothetical?

Thanks, I have the Sars-Cov-2 in mind. Here there is a very specific strain the Wuhan reference and with respect to that one can track the mutations one after another so they actually quite accurately behave as the example above. @Dirigible

@FrederikRavnKlausen, That's helpful. I'd recommend editing your question to include that information.  At the moment, your question is very abstract, and reads a bit like an XY-problem.


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Does Thymoquinone give cedar its distinctive smell?
What chemical gives cedar wood its distinctive smell? Is it the same that gives Nigella sativa its cedar-like smell?

Schreiner, Linda et al., “What Does Wood Smell like? Characterization of Odorants in Wood,” accessed January 7, 2022, DOI: 10.3217/978-3-85125-593-5-82.

mentions Thymoquinone, "known to be the major compound in black cumin seed (Nigella sativa)", which is also in incense cedar, but is Thymoquinone the primary chemical giving cedar its distinctive smell?

@tyersome I've added my research, focused the question to be about Thymoquinone.

Unfortunately, no time to write up an answer or research further. But see Odor-active constituents of Cedrus atlantica wood essential oil which attributes THE ODOUR of cedar wood to vestitenone and 4-acetyl-1-methylcyclohexene but also contains the sentence "The composition of Cedrus atlantica essential oil is generally dominated by alpha- and beta-himachalenes" (emphasis mine) which seems to agree with what is written here.  To my mind, the Phyochemistry article looks good


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Is cancer a defect of the immune system?
Is cancer due to a defect in the immune system?

No, it isn't. Although cancers have to escape the immune system, they usually don't affect it, except for B cell lymphoma, but this doesn't make it an immune system disorder. Disorders of the immune system are diseases like SLE.

Please try and do some research before posting. At least explain why you think that cancer would be an immune disorder. As it stands, your question is like asking whether McDonald's makes cars. Unless you give some reason why you think it might be a car maker, the question makes very little sense.

This question appears to be off-topic because it is a wild stab in the dark with no research or any indication of why the OP might believe this to be the case.

@terdon: So, the question is too broad?

Yes, too broad and also too basic. We expect users to do research before asking, a cursory reading of the 1st paragraph of wikipedia's entry on cancer would show you that it is "a broad group of diseases involving unregulated cell growth" and not an immune disorder.

I think this is a fair enough question, a suppressed immune system can result in higher susceptibility to cancer. The immune system kills mutated cells as well as foreign pathogens. There is a lot of high level research into the development of cancer and its link to the immune system.

I agree with @Spinorial one role of the immune system to prevent cancer. If it cannot fulfill this task, then it is the main cause of cancer, and not the mutations of cancer cells. Afaik. there are immune cells which actively defend cancer cells, so I think cancer can be called as immune disorder.

It can be named an immune system limitation or imperfection though, not disorder. Disorder is something that is out of order, and there is no such normal immune system that can beat cancer. Not in humans at least. Still don't understand why the question is downvoted. Users are very rude here and tend to downvote every question they consider not interesting.

@ZAB Thanks. I've edited my question accordingly.

How the hell is this question off topic? How cancer relates to immunity is not on topic for Biology? What is this SE even for then?

@DanielGoldman If you can, please cast a vote to re-open. thanks

Cancer is uncontrolled division of abnormal cells. This is caused by mutations in a cell which causes a cell to divide more frequently and the lack of control by intracellular AND extracellular mechanisms. The extracellular mechanisms include growth inhibition by hormones, local factors, contact and also the immune system.
These cancerous cells could be immune system cells and then, in that respect, the cancer could be considered an immune system disorder. Or the cells could be of different origin, but due to the lack of a functioning immune system (particularly NK cells), the cells may divide uncontrollably whereas otherwise they would've been tagged for immune or self destruction. Or a cancer may be caused by a virus; in this situation an immunocompromised patient is more susceptible to a cancer caused by this oncogenic virus. In these cases the risk of cancer is increased due to a compromised immune system. So cancer risk may be increased in these circumstances but cancer still is not an immune disorder.


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Are the 8 principal sugars in glycoproteins "essential sugars"?
Are there "essential sugars"? Some have suggested that the 8 principal sugars found in glycoproteins are "essential sugars":

Galactose
Glucose
Mannose
N-Acetylneuraminic acid
Fucose
N-Acetylgalactosamine
N-Acetylglucosamine
Xylose

I realize the liver can convert glucose to many different sugars, so by "essential sugar" I mean a sugar that is difficult to obtain from diet or that the liver requires much energy to convert from glucose.
How difficult is it for the liver to convert glucose to the other sugars listed above?

Your main question can be answered by simply copy/pasting it into google. Did you try to research this before posting? I assume you did, so what is it that was unclear to you?

that wasn't so classy changing the question when we tried to answer your original one. oh well.

@shigeta: Well, the question was about to be deleted anyways…

There are no essential sugars.
In the context of nutrition "essential" usually means "must be obtained from the diet". So for example the amino acid methionine is an essential amino acid (for humans).
Within this definition there are zero essential sugars. A Google search for essential sugars reveals lots of sites like this one. The site lists glucose as the first "essential sugar". In fact we can make glucose from a range of other nutrients including amino acids, lactic acid and glycerol. The second sugar on the list is galactose - we can make that from glucose. And so on...

To put it in hard words: Its pseudoscientific bullsh*t.

By "essential" I mean "difficult to synthesize of not obtained from the diet."

I think you will have to define "difficult". But really, now that you have edited your question, you are asking for an entire chapter from a biochemistry textbook.

@AlanBoyd is right that the term 'essential sugar' is not a scientific or biologically defined term and is not true given the meaning of the word essential that is in use in biology.
In alternative health and diet circles, the term 'essential sugars' refers to a set of simple carbohydrates which are hypothesized to be important for good health and nutrition in people.
Even if this were a valid approach in humans its very unlikely to be the same specific sugars and proportions for other animals and living things.
So given all these caveats the reference I found for 'essential sugars' lists these 8: glucose, galactose, fucose, mannose, glucosamine, galactosamine, neuraminic acid, and xylose.
As far as whether this really helps us, I personally don't think this is the key to good health in and of itself.  It really oversimplifies all of the biomachinery we have to break down and utilize carbohydrates.
As the diet recommends the eating of vegetables which aren't too green, avoiding fructose, it doesn't seem to hurt.  Carbohydrates from food are often the product of breaking down complex carbohydrates.  I feel as if watching the glycemic index of your food and avoiding soft drinks and too much fruit juice will get you further in terms of health.  Avoiding simple carbohydrates entirely in your diet also has advocates and there is some medical research that backs it up.

I don't even see reason to avoid frucose, since the body can make frucose-6-phosphate from glucose-6-phosphate. Frucose, which the cells take up also get phosphorylated, so this doesn't make any difference.

thanks for mentioning.  I take it you mean fructose?  That part about not taking in high fructose has some pretty good science behind it.  In humans (and rats etc) fructose is only metabolized in the liver so when you have a large ingestion  of fructose the local concentration in the liver becomes very high and it manufactures fat as opposed to breaking down to other carbohydrates.  http://www.sciencedirect.com/science/article/pii/S0168827808001645

Yeah, I mean fructose, damn typos. But it doesn't make too much sense to worry only about one carbohydrate. Nutrition has to be balanced, so if we avoid fructose, but live otherwise unhealthy (meaning too much fat and so on) this will change nothing.

hey @Chris - that's biochemistry for ya  - the devil's in the details :)   in general engineered foods are suspect as far as i'm concerned and probably aren't healthy as they are not a product of the environment we evolved from - my soapbox...

I am a biochemist :-) And I don't worry too much about food - but I try to avoid a few things.


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How long does it take for cancer to be detectable if it grows from a single cell?
Assuming cancer has its origins at a single malfunctioning cell, how long would it take for that cell to grow from the point at which it is malfunctioning enough so that it can be detected by the immune system, to the point at which it be detected with:

Routine modern medical tests
Cancer specific blood test
Noticed by the host (symptoms)

This will probably be hard to tell - and depends strongly on the type of cell. Some cancers grow very slow, while other are rather fast.

I know some cancers grow fast, but I doubt there is any cancer type where the single cell becomes a symptomatic cancer overnight. Or within a month. I mean the single cell has some barriers to overcome, like the ability to grow blood vessels. I am not familiar with all the barriers however. If one is aware of them, it should be possible to get an average, and min, max estimates for the time.

The barriers you mention are outlined well in the classic Hallmarks of Cancer paper: http://www.cell.com/abstract/S0092-8674(11)00127-9
The main problem with finding a general answer to this question is the large diversity in cancers, and the resulting problem in defining what hallmarks are sufficient to call an individual cell cancerous. There are cancers that can't be detected by the immune system or blood tests and will hide for a very long time symptom-wise, and non-cancerous tumours that can be detected in various ways very early on.
Let's say for your timing reference you simply take the point of neoplasm diagnosis (for neoplasms that turn out to be cancers after testing). At this point, figuring out how much time this cancer has spent being cancerous is very difficult, and to my knowledge has never been done. It could be possible to determine:

The number of genetic or epigenetic malfunctions that made the difference between benign tumour and cancer for this particular neoplasm (once again, hard to define)
An approximate rate of acquiring those malfunctions. Conceptually, one could ex vivo culture the cancer and monitor the rate of aquisition of further mutations in cancer-related loci or epigenetic markers.

Depending on how that rate looks, it may be possible to reverse extrapolate the rate of acquisition before diagnosis, and thereby estimate an approximate timepoint of acquisition of the first proper cancerous malfunction.
Besides that, "it probably took more than a few days" is the only statement I can confidently make, although as far as biological theory goes, it's perfectly possible (though highly unlikely) for a cell to acquire a set of mutations sufficient to become cancerous in a single round of replication.


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How does the brain recall information?
In computers, finding a single word is realized through serial attempts across all available connections to find a specified target.
How does the brain solve this? How does the whole process, from the command to recall some memory to actually "play" its algorithm look like?
By "recall" I mean literally, attempting to bring back an image, a word, a melody or any remembrance from memory.

"In computer, for finding a single word there has to be a movable part that tries all the connections to get what you're finding." - there are literally no moving parts in modern computers with solid state drives and fanless processing units. Moving things (e.g. magnetic hard drives) have nothing to do with computer's ability to find information. It's all about file system abstraction and hierarchy.

@EliKorvigo aha...IT teacher told me...anyway, I still can't imagine the mechanism neither for the brain and computer

This is a great quesion! There is lot of work still being done on this. Unfortunately I don't think I know enough about CS or computer engineering to make analogies, so I'll give a quick crash course and some examples instead and hope you find it helpful. Long story short though is that we are just now making really exciting headway into how memory might actually be stored and recalled and its usually a very dynamic, active, and possibly even stochastic process, not really like a search algorithm in a computer at all.
The brain works differently than a computer in that it encodes all of its information in frequency of signal firing and the patterns of firing between circuits with varying stregnths of connections based on experiences. Frequency is dependent on the neuron itself and patterns of firing between circuits are dependent on where the neurons project to, and how strongly they interact with the next neuron. At this very basic level memory is stored and recalled by placing proteins in the membranes of neurons that are strongly activated to make them easier activated in the future. These are sort of the first steps toward memory. This is called long term potentiation and just means that this neuron is primed to fire more readily and stronger in response to similar input in the future.
To build on this,  there is a classic example of this occuring and causing sensitization ( an exaggerated response to the same stimulus) in conditioning experiments in the sea slug Aplysia. Aplysia has a reflex where it will withdraw its gills slightly if you touch its siphon. You can pair a shock to the tail (unconditioned stimulus) which elicits a large withdrawal of the gills, with a conditioned stimulus (touching its syphon to elicit the withdrawal reflex) to get the sea slug to associate the two. The end result is that the sea slug will learn/"remember" to withdraw its gills fully in the presence of the syphon touch. No learning cannot happen without recall of some sort, and in this example the slug was associating and learning from two "circuits" to produce a different behavior.
In something a little more complex than a slug, memory and recall still functions much the same way, its just the circuits that are interacting are entire brain regions. Most people view the hippocampus as acting sort of like a relay center and boot loader for different memories by taking external input and sorting them to the right parts of the brain. A good example of this would be the difference between dorsal and ventral streams of information in the brain. For a really basic breakdown of this phenomenon there are two areas of your brain that I will focus on - the parietal lobe and the temporal lobe. The parietal lobe is known to be involved in spatial processing, and the temporal lobes are known to be involved in semantic and auditory processing. When information enters the brain (eyes, ears, nose etc.) it will be processed by sensory structures, sent to the thalamus and hippocampus to be "relayed" to the right areas of the brain. Relayed in this case is going to be dictated by whatever connections and how strong they are in the brain. In this case from proteins expressed in the cellular membrane that make some neurons in the hippocampus more responsive than others, so they are more likely to fire. Then, it depends on where they are projecting to that determines where they information is sent.
It just so happens the brain is arranged in such a way that neurons projecting dorsally, or to the parietal lobe I mentioned, will tell you "where" the stimulus is, and those projecting ventral to the temporal lobes will tell you "what" it is. This is achieved because these lobes are highly interconnected to even more regions in the brain and send their processed "where" and "what" info as input to other regions. These regions will all fire a certain way in response to this information and that pattern of firing can be considered a recollection or memory. Sorry that this is dense and so crash course-y but I hope it is helpful in clarifying how the brain recalls some information. Of course this is  a developing field and we are learning more about how it functions every day. These are just some classic examples.

The ventral and dorsal streams in the visual system are the what and where streams in visual processing from the bottom up (optic-nerve - thalamus - V1 - etc). OP asks for recall of visual images, i.e. top-down. This is not an answer to the question.

@Christiaan, he answered the question. I think you are getting confused by his reference to the processing of sensory information. What he is saying is that the signals produced by sensory structures trigger a chain reaction (i.e. action potential) that is transmitted from one neuron to the next in a very specific network of neuronal connections to store an equally specific memory associated with whatever sensory signal was sent. Correct me if I misunderstood you drtran, and +1 for a well put and accurate answer.

@ CDB I did mean that sensory input will trigger memory recall by activating specific networks. I should have gone further and said that there can be other types of input into these networks to elicit memory recall other than external stimulus. For example, top down processing from the cortex can be considered an external stimulus to the hippocampus if the hippocampus is your reference frame. I just thought external stimuli would be easier to explain.

@Christiaan, splendid, thank you! I suspected that it was merely a misunderstanding. I'm glad that I could clear it up.


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A doubt in biotech question
Which type of gene does not occur naturally in living organisms?

Bt gene
Endogenous cytoplasmic defense gene

The answer is 2.
I can't find out what this gene is! Does it mean the gene for methylation and restriction enzyme synthesis or some such thing? Does it even exist?
P.s. I am just a student and do not have in-depth knowledge of biotech.

where does this question come from? "Bt gene" seems to have something to do with transgenic corn https://entomology.ca.uky.edu/ef130

Endogenous just means that it is naturally occurring in the organism:
http://www.dictionary.com/browse/endogenous
endogenous cytoplasmic defense gene is a general description of a gene that is cytoplasmic and whose function is defending the organism. There isn't THE Endogenous cytoplasmic defense gene. There are many endogenous cytoplasmic defense genes. Note that it is the protein coded in the gene that is cytoplasmic, not the gene itself. It should say 'gene for endogenous cytoplasmic defense protein'.

Cytoplasmic gene means plasmid and stuff?

Why is the answer that if it does occur in organisms?


text:
What are the exceptions to Mendel's laws?
What are the exceptions to the $-$

Law of dominance
Law of independent assortment
Law of segregation

My knowledge:
Exception of law of dominance:

Incomplete dominance
In incomplete dominance when a red snapdragon flowered plant is crossed with a white flowered plant an intermediate phenotype appears in the F1 hybrid instead of a parental phenotype.
Codominance
Unlike dominance in codominance when a A ($I^AI^A$) blood group individual mates with B ($I^BI^B$) blood group individual the offsprings have blood group AB ($I^AI^B$) instead of A or B.

Exception of law of segregation:

Nondysjunction
During meiosis homologous chromosomes/sister chromatids and hence genes may move to a common gamete violating law of segregation.

Exception of law of independent assortment:

Linkage
When genes are present on the same chromosome they tend to remain together and enter into the same gamete. This is the reason behind deviation of dihybrid test cross ratio from 1:1:1:1 and occurrence of parental combination in high frequencies.

Am I correct? Are there any more exceptions to these laws?

One of the biggest exceptions is that these laws are not applicable to haploid organisms.

Recombination and linkage are different things or same ???

You are right but the list is certainly not exhaustive. Here are a few more concepts you may want to consider.
Exception of law of dominance:

epistasis
Allelic effect at a given locus depend on the variants at other loci
environment dependence and specific case of frequency dependence
The concept of dominance can be used for any quantitative trait. Typically, when the quantitative trait of interest is fitness, then the trait often depend on the environment. A typical and interesting case is when the fitness depends on the frequency of alleles in the population. Depending of the frequency of the allele at a given locus, the relationship might be a relationship of dominance, additivity or dominance for the other allele.

Exception of law of segregation:

meiotic drive
from wiki: "Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time."

Exception of law of Independent assortment:

epistasis for fitness
Imagine a case where a given combination of allele is lethal at very young age, then you would never see these two alleles together in an individual. It is per se, not a case of exception to independent assortment but it gives the feeling of such exception. A case more extreme when a given combination of alleles prevents fecundation could however be considered as an exception to independent assortment.

Another e.g worth including Sex-linked genes, they do not follow mendelian law of Dominance.

Also Sex-limited traits [where a functional autosomal gene (allele) is completely slient in one sex] and sex-influenced traits [where a functional allele changes behaviour, dominant/recessive behaviour with sex of the bearer].