text:
Can a gene-expression or epigenetic 'user-history' be found in the body?
(EDITED - a lot of what I am saying is implicit and simplified. I'm not looking to recreate the numerous textbooks and scientific papers on how DNA works).
As far as I can understand it, an organisms basic building blocks (proteins) are made up of DNA, Genes, and Chromosomes. The most basic form of this is DNA, made up of molecules in double helix strands. DNA carries all the instructions for the body in a simple 'database' or 'blueprint' form. Genes are chunks, or sequences, of the DNA telling the body 'what to do'(1) by reading the 'DNA database' in a myriad of unique coding sequences. Genes naturally(2) switch on and off throughout an organisms lifespan allowing amongst other things for an organism to grow from young to old. DNA is essentially(3) stored in Chromosomes.
External and environmental factors can influence the expression of genes, and the information stored in the DNA (4) - the study of which is Epigenetics. These Epigenetic factors can change over time, switching genes on and off. (5)
Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?
Apologies, I do not have a background in Biology. (6)

EDIT NOTES
(1) what to do, how to do it, when to do it. not necessarily all life supporting instructions but also the minute-to-minute, day-to-day processes etc.
(2) naturally. there is no black and white in nature, only shades of grey.
(3) essentially. not exactly and not in all cases but mostly.
(4) As in, factors influence the expression of genes (which in turn are made up of DNA information). I am not suggesting that external factors can influence the 'DNA database' itself but rather just how they are 'read', sequenced and expressed as genes.
(5) again, naturally. no sharp on/offs but variations of concentrations.
(6) I may not have used the correct terminology.

Please avoid editing your post so drastically after an answer has been posted. Also, you do not have to hide your misunderstanding via loads of tiny inaccurate notes that only acknowledge that you realize you might be inaccurate. What you do not understand is of interest as it is what help people to understand what you are after and what is unclear to you. Finally, all these tiny notes look very messy and I would recommend keeping the old version.

@Remi.b I agree major changes may affect previous answers - I wanted to clarify the poor phrasing so future answers could focus on the question more. That's why I purposely left most of the original content intact (I pretty much only expanded the sentence about the DNA building blocks into 3 or4 sentences). I tried to leave my edits to the messy notes :) so that viewers wouldn't have to go view the previous version of the question. Unfortunately I couldn't figure out how to get subscripts for the edit notes to make it less messy. do you think listing the notes all at the end would be better?

Main question

Does the body store a history of these expressions? Do the chromosomes
  (or some other part) of an older organism store a 'user-history' of
  which genes where previously activated when the organism was younger?

Cells can sometimes have a "memory" of the gene expression state which allows the cell to perpetuate its gene expression programme. This is facilitated by epigenetic mechanisms. Cells can also maintain a short term memory via feedbacks and switches (Casadesús and D'Ari, 2002). Immune cells store the memory of previous exposures to a certain pathogen (in this case each clonal population stores one piece of history which is unlike one cell storing the entire history). However, I don't think there is an explicit "user history" kind of mechanism. Most responses are dynamic (and memoryless); there are only a very few situations (such as immune response) that really need a history log. Usually the cellular memory is just one level deep. Storing deeper than that would cost the cell a lot.

Other corrections not directly related to the question

As far as I can understand it, an organisms basic building blocks
  (proteins) are made up of DNA, Genes, and Chromosomes.

This statement is extreme oversimplification. As a matter of fact, water is the most abundant molecule in the bodies of most (if not all) organisms. RNAs and proteins are essential molecules required for cellular functions. Lipids are also important as they constitute the cell membrane. Moreover, proteins are not made up of "DNA, genes and chromosomes". Your subsequent explanation of how the genes work is correct but this statement is quite wrong.

The most basic form of this is DNA, made up of molecules in double
  helix strands.

Misleading again. It is not correct to call DNA as "most basic form". In what way? This statement is also opinion-based.

DNA is essentially(3) stored in Chromosomes.

Chromosome is an assembly consisting of the DNA and some proteins. In a way, DNA is contained in the chromosomes. As also pointed out by Remi, your statement can have misleading interpretations.

External and environmental factors can influence the expression of
  genes, and the information stored in the DNA (4) - the study of which
  is Epigenetics. These Epigenetic factors can change over time,
  switching genes on and off.

This process is simply called "gene regulation" or "regulation of gene expression". Epigenetic mechanisms (such as DNA methylation and histone modifications) are one of the mechanisms of gene regulation but they are not the only one. You can simply google "gene regulation" and you'll get plenty of resources on this topic.

Thanks for the answer. Using my popular science biology background. Could the junk dna (whose purpose is not fully understood) potentially store some sort of extra information?

@EveryBitHelps It potentially can (and would no more be junk) but storing such an extensive amount of information would require a lot of "space".

First Paragraph - let's debunk what was poorly phrased
Many sentences you wrote are quite misleading. You should have a look at an introduction to molecular genetic to have a better understanding such as what you can find on Khan Academy. In short:

the double helix DNA strands are the building blocks of an organism

This sentence is very opinion based. as a matter of proof, one could for example replace the term double helix DNA by "cells" (or other terms) and many would still be satisfied with the sentence.

Genes are chunks of DNA telling the body what to do.

A gene is a part of DNA which contains regions coding for proteins. There are many sequences which are not coding for any proteins that are essential for the individual survival (such as regulatory sequences or sequence coding for rRNA for examples).

Genes naturally switch on and off.

The regulation of gene expression is actually much more continuous than just on/off. Also, regulation of protein concentration can occur at different levels and not only by regulating gene expression.

DNA is essentially stored in Chromosomes.

This sounds like chromosomes are boxes in which one can find DNA. In reality, DNA is a type of molecule which can be found under different forms. In humans (and other eukaryotes) most of the DNA (but not all) is present in the form of chromosomes.
Second Paragraph - What is epigenetics?

External and environmental factors can influence the expression of genes,

This is correct

and the information stored in the DNA

This is wrong. Environmental factors do not affect the sequence of base pairs of the DNA. It only regulate its expression. Such regulation of expression can last for a long time and even be transmitted to the offspring. The term epigenetics is loosely defined. In short epigenetics refers to the set of mechanisms that affect gene expression at short and long term. The classic mechanism of interet in epigenetics in the methylation of histone tails (quickly speaking, histones are proteic structures around which DNA is wrapped).
Your question

Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?

As explained above, some of the molecular mechanisms yielding to changes in gene expression can have long term consequences on gene expression (which can even be inherited). But there is not data bank (or other centralized or not source of information) that specifically record the expression of each gene at any one time in the history of the cell life.

Thanks for the answer in the last paragraph & half. I was trying not to get bogged down in the details of the basics (whole textbooks are devoted to) so that I could get to the question. I also appreciate I may not have used the correct terminology and a lot of what I was meaning was implied. But how can the first line you quoted about the DNA helix be referred to as 'cells'. eg "the cells are the basic building blocks of an organism"...no problem in itself. but now a follow up sentence "an organisms cells are found in cells"?? I'll fix the sentence idea to be clearer but not to cells.

I was only referring to the part of the sentence I quoted. My point was that calling "DNA strands" the building blocks of an organism makes little sense (or at best is very opinion based) and as a matter of proof, I wanted to show you that other concepts (like 'cells') could equally be called building blocks of an organism.

In between your post edit and your comment you seem to both much the clarification I tried to do on your sentences. You might be well aware of some of the things I tried to clarify and this is ok. The most important is to know whether your question was answered and if not, why. (In any case, I would recommend you waiting for answer or peer-review from other users before accepting an answer).

Ah! the cell comment makes sense then :) I was wondering about that! yeah, sorry. I must have missed your edit. I try accept answers once there is more than one answer as I find the ticked answer prevents users from attempting an answer.


text:
Is Plasmablast a precursor of Plasma cell?
I read it in Roitt's Essential Immunology.

Plasmablasts are precursor cells of short- and long-lived plasma cells and
  are generally described as a proliferating fraction of
  antibody-secreting cells, often found in the bloodstream
  emigrating to organs such as the bone marrow.

I coudn't find any authentic source repeating the same.
Is it true? Is this book authentic enough to follow?

I follow Kuby's for Immunology. I don't know about Riott's but Nature reviews would be the best for immunology.

@Polisetty Why do you think it is the best?

They have the latest stuff and amazing diagrams. Like the one below, even the subtle difference that the plasmablast has membrane bound Ig and plasma cells have secretory Ig has been made.

Antigen activated B-cells enter the germinal centre dark zone to form centroblasts which undergo somatic hypermutation. These then form centrocytes in the light zone. The various possibilities/routes the centrocyte can take are shown in the following figure. If the centrocyte undergoes a class switch recombination, it becomes a plasmablast.
A plasmablast is  defined as

Plasmablast
The B-cell lineage precursor of non-dividing plasma cells, which has the capacity to divide and that has migratory potential.

Once it matures as a plasma cell, it is out in the blood secreting soluble immunoglobulins or antibodies.
Another important definition to mentioned here would be of antibody secreting cells.

Antibody-secreting cells
A term that denotes both proliferating plasmablasts and non-proliferating plasma cells. The term is used when both cell types might be present

So, yes, they indeed are a precursor of plasma cells.
Also, it is necessary to clarify here that although both plasma cells and plasmablasts are antibody secreting cells, plasma cells lack membrane bound antibodies while plasmablasts retain them.

Finally, this is just the germinal centre response that is shown over here. Plasma cells and plasmablasts can also form in an extrafollicular response in extrafollicular sites in the spleen or in the medullary cords of the liver. That's another story altogether!
For a more detailed explanation, have a look at my other answer.
Image and reference: http://www.nature.com/nri/journal/v8/n1/full/nri2217.html

In your other answer you mentioned that they produce secreted IgM. This is also mentioned in Kuby. Is it an exception to what you said, they still producing membrane bound antibodies? Could you elaborate?

Thanks for pointing out. There's a small error. I'll update in a while :)

Both the answers have been updated @SanjuktaGhosh . Please have a look! Those plasmablasts are different extrafollicular ones

I appreciate that. However I regret not having access to the paid website, nature.com. :(

@SanjuktaGhosh Shouldn't you have access via your university?

@Ebbinghaus No I can't for my country is not enlisted there.

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text:
The Mystery of The Cretaceous' Songbirds
Before Passeriformes perched on the branches of our trees and sang their sweet, inspirational tunes, there was Enantiornithes, the "Opposite Birds".  So far, we have discovered at least 80 species from five different families.  (However, some of those names come from just one bone, so the nomenclature may not be valid.)
The really odd thing is that despite their diversity, they had become extinct during the Mesozoic-Cenozoic extinction event 66 million years ago, even though their rivals, the forefliers of today's waterfowl, shorebirds, tube-noses, rails and ratites, did not.
The question is:  How come?  Was there any paleobiology saying that this particular order of birds was too specialized to withstand an impact winter?

This is a fine question, but I don't think you are going to find answers. Simply, we don't know enough about the physiology or life history of these birds to know. All we have are skeletons (and some feather impressions). Even if we did know all about their biology, we still wouldn't be able to say why they went extinct. The same question could be asked of any speciose, seemingly successful group that went extinct.

The short answer is that we will never know.
Luck can sometimes be a factor of who lives and who dies. But such an answer doesn't feel satisfactory given such a diverse group such as dinosaurs and other groups like Enantiornithes.

Together with hatchling specimens of the Mongolian Gobipteryx[35] and
Gobipipus,[36] these finds demonstrate that enantiornithean hatchlings
had the skeletal ossification, well-developed wing feathers, and large
brain which correlate with precocial or superprecocial patterns of
development in birds of today. In other words, enantiornitheans
probably hatched from the egg already well developed and ready to run,
forage, and possibly even fly at just a few days old.[34]
A 2006 study of Concornis bones showed a growth pattern different from
modern birds; although growth was rapid for a few weeks after
hatching, probably until fledging, this small species did not reach
adult size for a long time, probably several years.[37] Other studies
have all supported the view that growth to adult size was slow, as it
is in living precocial birds (as opposed to altricial birds, which are
known to reach adult size quickly).[26] Studies of the rate of bone
growth in a variety of enantiornitheans has shown that smaller species
tended to grow faster than larger ones, the opposite of the pattern
seen in more primitive species like Jeholornis and in non-avialan
dinosaurs.[38] Some analyses have interpreted the bone histology to
indicate that enantiornitheans may not have had fully avian
endothermy, instead having an intermediate metabolic rate.[39]
https://en.wikipedia.org/wiki/Enantiornithes

So we have this. Enantiornithes weren't completely bird like. They may have invested less energy in parental care. Perhaps taken longer to reach adulthood, longer to reach reproductive age. May not be as warm blooded as birds but not as cold blooded as a crocodile.  Maybe that is why they went extinct.
The Enantiornithes did not care much for their young, since they were born pretty much hardwired to be independent. This hard wiring probably worked find in a stable environment, allowing adult to spend more time and energy making more independent chicks. But in a hostile, changing world of post-impact, that was simply too much for a hard wired, semi-warm blooded chick. Especially one that took longer to reach reproductive age than most birds did. And birds by and large do invest in parental care of their offspring.
The answer is perhaps obvious if we could go back in time and observe the entire genera of Enantiornithes. But in the absence of a time machine and only fossils and estimated growth rates... we can only speculate.

All kinds of things effect survival of an impact, you don't just have a winter, the impact sets off every fault and volcano causing earthquakes, eruptions, tsunami, acid rain, and widespread forest fires. It's not really about who is killed by these events but which groups are best at recovering from it. And too much of that can be determined by things that don't leave evidence in fossils. Slowly reproducing and specialized organisms tend to go extinct but they are by no means the only things that go.

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text:
Fst Differences Between Mature Trees and Seeds
For a single co-dominant locus in two populations of blue oak, I am given genotype frequency data (genotypes are AA, AB, BB) for adult trees (at least 150 years old) in both populations (pop 1 and pop 2) and from sampling of seedlings taken in fragmented woodland from the same populations (pop 1 and pop2) very recently. I am asked to detect any difference in Fst among adults and seedlings, and propose a hypothesis explaining how any difference observed could have come about.

To tackle this question, I calculated the Fst value between Pop1 and Pop2 using the adult's genotypic frequencies and then Fst between Pop1 and Pop2 for seedlings using the respective genotypic frequencies given for the seedlings.
The Fst values for the adult's was 0.004 and the seedling' was 0.113.
Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees.
I'm mostly stuck on the explanation for why this would happen. My gut response was that there is some selection against certain adult genotypes in population 2 in that they are unable to produce seeds? Or maybe that adults in population 2 are mating non randomly and therefore produce seeds that do not match the genotypes of the adult population?

I will assume the claim Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees. is correct and that you have done your stats correctly.
A complete analysis of the situation depends of how you calculated Fst. Did you use Weir-Cockerham Fst or standard Nei's formulation? How did you average (with or without weights) over population and loci? But without going to these details, here is an extreme scenario that explain why you could observe such patterns.
Imagine, the migration rate from any population and to any population is 0.5. In such case, in absence of selection you would not expect any divergence between populations. However, if genotypes AA and AB both have seed survival probability of 0 in pop2 (but not in pop1), then pop2 will be fixed for A2A2 at the adult stage even though when looking at the seeds you cannot see any evidence of divergence.

I'm not quite understanding your answer. In the context of the question and genotypic frequencies given, I just don't understand how the genotypic frequencies of pop1 and pop2 could be very in the adult stage, yet have moderate differentiation in genotypic frequency in the seedling stage. I apologize if I'm being unclear..


text:
Are all 23 chromosomes connected as one long strand of DNA?
This has perpetually confused me. Is our genome made up of two long strands, each strand made up of 23 continuous chromosomes that bind together, or are they 23 free floating separate pair of chromosomes? I think it's the latter because I just learn that genes on different chromosomes assort independently, which would be hard if the genome was a long string, but I'm still not sure.

Each chromosomes are separate clusters.

According to what I've learnt, we have 23 independent pairs of chromosomes. Each of them contains 2 chromosomes and different kinds of genes. The genes are connected in one strand. So it is the latter one. And the 23rd pair of chromosome is used to determine our gender actually. Females got XX and males got XY

Not quite. Humans have 23 pair of chromosomes. That means 46 independent entities. Except for guys, we're one short.

@bpedit Actually, males have 46 chromosomes as well. The 23rd pair is X and Y. While the Y chromosome is much smaller than the X, it is still a full chromosome. Not sure where you got the "we're one short" idea...

@MattDMo Ouch! You're correct. Am deleting comment. Suspect this is age related.

DNA does not run from one chromosome into another.

I think it's the latter because I just learn that genes on different
  chromosomes assort independently, which would be hard if the genome
  was a long string, but I'm still not sure.

Though chromosomes are NOT connected by DNA, your gene access argument is, furthermore, not a great argument. It would just be one tiny strand of DNA between two very-much larger chromosomes. The nucleus is able to operate with much tighter/difficult problems with respect to accessing DNA.
I'm glad you're thinking of it physically though ! Chromosomes are indeed kept track of and connected by nuclear-cytoskeletal stuff.

Since both of these answers are downvoted, and the downvoter provided no feedback on what is incorrect--can someone comment to teach me and the community what's correct/incorrect?


text:
Does protein kinase A accelerate glycolysis or slow it down?
In liver cells, the activity of PFK-1 is regulated by the PFK-2/FBP-2 complex, whose activity is in turn controlled by glucagon and insulin.
Glucagon activates protein kinase A.  Then protein kinase A phosphorylates the PFK-2/FBP-2 complex, so that the PFK-2/FBP-2 complex will make fructose-6P from fructose-2,6-bisP.  Since fructose-2,6-bisP activates PFK-1 (in liver cells), without it the process of glycolysis will slow down.
However I read from my notes that protein kinase A is dependent on cAMP (so that when the energy level is low, the increase in cAMP will cause protein kinase A to increase in activity).  It seems that protein kinase A should help increase glycolysis, so why does activating it by glucagon cause glycolysis to slow down instead?

There is a fallacy in your argument, which is the parenthetical statement:

so that when energy level is low, the increase in cAMP will cause protein kinase A to increase in activity

The activity of adenyl cyclase (the enzyme catalysing the production oc cAMP) is not controlled by energy charge, but by hormones such as glucagon. That is how glucagon has its effect on protein kinase A (better thought of as cyclic AMP-dependent protein kinase to remind you of this fact). That is why cAMP is known as a ‘second messenger’ — the hormone being ‘first messenger’ (and the enzyme that becomes phosphorylated being the recipient of the message). See, for example, Figure 21.14 from Berg et al.
Therefore the explanation in the Wikipedia article on PFK2 is quite self-consistent:

When glucose level is low, glucagon is released into the bloodstream, triggering a cAMP signal cascade. In the liver Protein kinase A inactivates the PFK-2 domain of the bifunctional enzyme via phosphorylation, however this does not occur in skeletal muscle. The F-2,6-BPase domain is then activated which lowers fructose 2,6-bisphosphate (F-2,6-BP) levels. Because F-2,6-BP normally stimulates phosphofructokinase-1(PFK1), the decrease in its concentration leads to the inhibition of glycolysis and the stimulation of gluconeogenesis.[8]

So the answer to the question posed in your title is: in liver cAMP causes the inhibition of glycolysis.


text:
Do all tumors form the same way?
Do all tumors - both benign and malignant - form when proto-oncogenes and/or tumor suppressor genes experience mutations? Were all malignant tumors once benign?

You might be interested in this.


text:
How's maturation different from differentiation/activation of B lymphocyte?
I was reading Wikipedia that said $-$

In mammals, B cells mature in the bone marrow, which is at the core of most bones. In birds, B cells mature in the Bursa of Fabricius, a lymphoid organ.

So it's got the name B-lymphocyte.
My questions:
Is the transformation of Haemotopoetic stem cell to Immature B-cell called maturation of B-lymphocyte and the transformation of Immature B-cell to Mature B-cell through a Naive B-cell called differentiation/activation of B-lymphocyte?
The maturation occurs in Bone-marrow and Activation/differentiation in Spleen or lymph nodes. The whole process maturatiion + activation is called development. Am I correct?
Note: My understanding of Immature B-cell is that it is a cell in the series of B-cell development that expresses BCR (an IgM) for the first time. While Mature B cell is a B lymphocyte which after interaction with antigen has turned into either Plasma cell or Memory cell.

yup. activation is when a naive b-cell binds an antigen generally in the secondaries. maturation is in the primaries..

Initially I thought it should be the opposite. You see Immature transforming into Mature B-cell, common sense says it should be maturation but it just the opposite. Well what is differentiation and development then? @Polisetty

@Polisetty Do you mind sparing your time explaining some very confusing immunological concepts to me.? They are Isotype, Allotype and Idiotype.

Why not ask a question? Ill try answering it


text:
I'm trying to identify a tree i saw in Taormina, Sicily, Italy. Can anyone help?
What is the identity of this tree? These pictures were taken in Taormina, Sicily.

Was an obviously planted tree or did it look like a native species of the region?

It was on farmland..so I would have guessed a native species, but it seems not; Thanks to RHA for explaining that its native only to eastern Australia. Greatly appreciated!

It looks like the Silky oak, Grevillea robusta, which is btw not related to our indigenous oaks (quercus).
It's native only to eastern Australia, so planted in Sicily.
https://pommepal.wordpress.com/tag/silky-oak/

This looks spot on.


text:
Identification of South Indian plant
I'm from South India and I'm having quite a fuss identifying this plant. It has totally transparent stems, and when I break them, water squeezes out. My local friend tells me that this was used in the olden days to clean slates. It has a bit fat stem. And another thing about this plant is that when you soak it in Ink, you can see the ink travelling up it. That's why it is so transparent.
I heard that it is locally called Mashithandu and I searched all  over the net for it, but can't find a name except that. I'm really sorry I can't add a photo. I'll see what I can do.

I presume you are talking about Peperomia pellucida. It is called  Mashithandu in Malayalam.

Reference: Wikipedia
You might like to go through this.

Description
Delicate, glabrous annual herbs; stems erect, 5-30 cm tall, pellucid,
  branched when well developed.
Global Distribution
Native of Tropical America; now Pantropical
Indian distribution
State - Kerala in all Districts

Common names
It is known as pepper elder, silverbush, rat-ear, man-to-man, clearweed (North America); prenetaria (Puerto Rico); konsaka wiwiri (Suriname); coraçãozinho or "little heart" (Brazil); lingua de sapo, herva-de-vidro, herva-de-jaboti or herva-de-jabuti (South America), ewe rinrin (Yoruba Nigeria), corazón de hombre (Cuba).[11] In Oceania, it is called rtertiil (Belauan); podpod-lahe or potpopot (Chamorro). In the different dialects of the Philippines, it is called pansit-pansitan or ulasimang-bato (Tagalog), olasiman ihalas (Bisaya), sinaw-sinaw or tangon-tangon (Bikol), lin-linnaaw (Ilocano) and "clavo-clavo" (Chavacano). In other parts of Asia, it is known as càng cua (Vietnam);sagar bataing သဂါဗတာင် (Mon); pak krasang ผักกระสัง (Thailand); "krasang teap" ក្រសាំងទាប (Cambodia); suna kosho (Japan); rangu-rangu, ketumpangan or tumpang angin (Bahasa/Malay); sasaladahan (Sundanese); rinrin (Nigeria), "shining bush" (Trinidad and Tobago), and mashithanduമഷിത്തണ്ട്, വെള്ളത്തണ്ട് and വെള്ളപ്പച്ചില (Malayalam); diya thippili දිය තිප්පිලි (Sinhalese). In west Bengal, India the plant is locally known as "Luchi pata". In Guyana the plant is also known as "Soldier Parsley."

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. In addition, scientific names (i.e. latin binomials) are much more useful than a list of common names. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

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text:
What would be the membrane's form if phospholipid tail lengths vary?
I was trying to visualize and draw the situation if the membrane lipid chain length varies.
I assume so many possible conditions if in a membrane some taller or shorter components mixed:
Such as:

etc.
But which one of this is correct? or all / some from them could be applicable?

It's difficult to judge cartoons when the molecules they represent are much more complex, however I'd say that as a general principle you never want the polar head group to enter the hydrophobic region, which happens in your pictures wherever the heads are misaligned.

Cartoon (better 'visual abbreviation') would occupy similar volumes as real molecules. As well as lipid tails would be able to bend because of conformational rotations (as seen in eclipsed and staggered forms of Ethane etc hydrocarbons)

Check out lipid rafts.

lipid rafts are complex structure with cholesterol and proteins. But I'm asking about phospholipid bilayer

As a starting point, check out the Wiki article on hydrophobic mismatch: https://en.wikipedia.org/wiki/Hydrophobic_mismatch - they discuss this for proteins, but many of the same things happen for lipids. Also check out the membrane microdomain literature - people do lots of studies on simple lipid/lipid coexistence, say: http://www.sciencedirect.com/science/article/pii/S0006349505731817 and citations within discuss this quite a bit, though it's a very physics-heavy approach. (A review that covers some of this is: http://www.annualreviews.org/doi/abs/10.1146/annurev.biophys.36.040306.132643 )

Some the scenarios depicted are not energetically favorable and will lead to very unstable membranes if at all.
In the presence of many short-chain lipids, where the difference in chain lengths is very drastic, it will become more favorable for the membrane to reorientate some of the short-chain lipids such that the hydrophobic gaps/pores in your cartoons convert into hydrophilic ones with the head groups forming the pore walls (see fig. below).

If the difference in chain length between the two lipids is not much, the bilayer will adjust its thickness to minimize the hydrophobic mismatch. In such cases, the bilayer will be thinner in some regions. The possibility of interdigitated bilayers is also very much there and will depend on the choice of lipids in question. Interdigitated lipid membranes have been reported before and you can look it up.

Great answer overall. I would recommend adding some references though.


text:
Genotypes in diploid/haploid cells under mitotic/meotic cell divisions
I am new to genetics , and am stuck with the following question at hand:

If $2$ cells with genotypes $(A/a)$ and $(A/a,B/b)$ undergo mitotic and meotic cell divisions respectively, what will be the  genotypes/gene compositions in the resultant diploid and haploid cells with respect to the above mentioned alleles?

Can someone help me how to proceed?

can you give a little more information - like what you think the answer might be? Is this a homework question?

@VanceLAlbaugh Not homework in the true sense. It is actually a question in one of the previous year's question paper (so I doubted to give the self study tag ) that I couldn't solve and sadly neither is my professor available , nor are my friends getting anywhere.

Related: http://biology.stackexchange.com/questions/53110/doesnt-meiosis-form-two-pairs-of-similar-cells-and-two-pairs-of-opposite-cells

Though broad, here I provide a summary in graphical way.
Mitosis:
 .

MEIOSIS: 2 successive steps : Meiosis-1 and meiosis-2
Meiosis-1

Meiosis-2

So lets see what happens with cells given at question.
1. Cell with genotype Aa
(monohybrid or one-point cross-experiments; that means we are looking to gene-pair at 1 loci; not looking to any other genes):
1. A.  Mitosis:
Possible genotypes of their offsprings: All Aa.
1. B. Meiosis:
gametes will show 2-possibilities ; A, a.

2. Cell with genotype AaBb
(dihybrid or 2-point cross-experiments; that means we are looking on genes of 2 loci; not to any other cells):
2.A. Mitosis:
all offsprings AaBb.
2.B. Meiosis:
If given condition says the loci for A (or a) and B (or b) are on same chromosome (linked genes) and no crossing-over is there;
then We will get only 2 types of gamete AB and ab.
If crossing over(s) take place between the 2 loci; then we'll get 4 types of gamete AB, Ab, aB, ab; but their ocurring frequency will deviate from Mendel's independent assortment.
If the 2 loci are not-linked; i.e. they are located in distinct chromosome; then also we'll get 4 types of gametes AB, Ab, aB, ab; but they will follow Mendel's independent assortment pattern.

Reference:

Concepts of Genetics, 8th Edition (EBook) By William Klug, Michael Cummings, Charlotte Spencer / Pearson; chapter 2 (mitosis and meiosis)
The science of Genetics, 6th edition, by George Burns and Paul Bottino, Macmillan.
Genetics/ P.K. Gupta/ Rastogi Publication Meerut

That was a wonderful explaination. Can you please (if possible) give me the source where genetics is so wonderfully expalined in detail?

@Qwerty I did it completely from memory and it is based on many days of classes and many books. Ok I'll look back to my books and will add some relevant reference.

@Qwerty I've added them

For your purpose you could also visit a book by Robert Tamarin, and for chromosome aberrations, there is an excellent genetics book by Monroe Strickberger (but I can't access it right now)

@Qwerty Thanks for your appreciation. glad to write something helpful


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Can genetic material actually provide a physical description of appearance?
A bodies genetic material provides the blueprint for your appearance. Your predisposition to be tall, freckled, blue eyed and blonde are encoded from birth.
However, external and environmental factors can influence the manner these instructions are carried out. For example malnutrition during childhood will affect bone and tooth growth. A lack of oxygen can lead to cerebral palsy with dramatic affects on the bodies muscle development (amongst other things).
Does your current genetic material indicate how you physically appear in real life and not just the genetic markers or 'potential'?
eg : If a scientist had a bloodsample taken today, I know they could say that the subject has obesity markers but could they actually say how fat the person was. Could they determine the difference between what the markers say and what the subject actually appears like?
Is current research limited but indicating that this might be possible in the future?

Is the wealth of information about how many cells, and what each of those cells are doing encoded within every other cell, or more generously--a blood sample? Probably not. On average you'd probably be able to determine a lot of characteristics somewhat accurately. In 2016, I'm neutral on the likelihood. In 2 or 3 decades, maybe we'll figure out some more bio that unlocks what you're asking.

A blood sample can tell you a lot about a person's level of obesity, but not necessarily from reading the DNA sequence, although that may help in some limited circumstances. Blood levels of HDL and LDL cholesterol can be measured, as can concentrations of glucose, insulin, and other indicators of diabetes, which is often related to weight and body mass index (BMI). However, I could not take a sample (or several samples over a timecourse) of blood from you and determine that you're 175 cm tall and weigh 95 kg.

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


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What is the energy produced by the mitochondria?
I know that the mitochondria is basically the power house of the body,
it consumes amino acids, fatty acids, glucose, etc and oxygen.
When these molecules meet up in a enzyme, a series of reactions happen (Krebs
cicle) which end up in CO2, H20 and energy.
Then the enzyme and later mitochondria will release its energy which will be stored in ATP molecules.
My question is what is this energy?

If your question is "what is energy"; then it is a purely physics question. Whom we call energy in physics, the same thing we call as energy in biology. Energy is a concept. It means 'ability to do work'. or in simple words, restlessness. Or unstability. A running bulette contains some energy so it can break an wall. As well if you keep a book on a table; it 'stores' some energy hidden in it. If instead a table you put the book on a  thin glass sheet with support only at edge;  it would broken. The energy came out.

Experimental result shown when an object do an work on another; the energy levels change, but that no energy get 'annihilated' or 'born'. It just 'dissipated to' / 'come from' the other object. Same for chemical reactions  (molecular works).

Quite in a manner of macroscopic objects, chemical molecules can give/ take/ store energy. When a chemical/physico-chemical 'change' occurres on a molecule; that means at the same time release or intake of some energy.  To make/ break a chemical bond, or to do change in a bond-length or  a bond angle or to rotate a group around a bond to change a dihedral angle, or to transport a molecule/ ion  from one-side of membrane to another side... each process give or take some energy.

The very wrong thing I see in your question is, "Then the enzyme and later mitochondria will release its energy which will be stored in ATP molecules.". From where you came to know that? At each step of each and every chemical reaction there is some energy-change in the molecular structures; and when one system release some energy, at the same time some other system take the energy.You raising a bottle that means you are adding some energy at the same time... not 5 minutes latter. Usually energy doesn't exist without matter. (except radiation or EMW).Heat-energy is too molecular vibrations

And EMWs (electromagnetic waves) would NOT persist more than moment. They'll enter some or some interaction with matter (molecules). The function of ATP is; when at some steps of respiration-reactions release burst-amount of energy; an energy-taking reaction (ADP+Pi --- > ATP) take place with help of special molecular machinery. ATP is a molecule, so it can be transported. Later-on where in cell the energy is required for any molecular work, the reverse reaction (ATP --- > ADP+Pi) take place, the energy come out.

The use of the energy in ATP is quite complex. Since my college days our knowledge of how ATP is used has broadened considerably.
Let's look first at the role of ATP in the sodium-potassium pump. This pump uses roughly 20% of the ATP your body produces, even more if you are a couch potato. ATP powers this process by attaching its terminal phosphate group to the pump. The phosphate group is highly charged. Its attachment pulls and tugs on some regions of the pump and repels other regions due to the fact that many of the amino acids comprising the pump are polar or charged. These electrical, magnetic-like, interactions change the shape of the pump. This causes sodium ions to be pumped outside the cell even though they are more plentiful there. When the phosphate is released, the pump returns to its original shape bringing in potassium ions and reloading sodium. It is this pumping action that, among other things, provides the energy for messages in nerve and muscle cells (action potentials).
Probably the important energy use of ATP is this. Many of the reactions your body needs are uphill battles. That is, there is more energy in the substances we wish to produce (products) than in the substances which we must use for raw materials (reactants). So, the ATP attaches its phosphate to the reactant. This raises the energy in the reactant making it now have more energy (more unstable) than the product we wish to produce. The reaction now becomes "downhill" and can proceed naturally ("spontaneously") without holding a bunsen burner under your bottom. This concept is termed "coupled reactions" where we take the "downhill" breaking down of ATP and use it to power the "uphill" production of a requires substance.
There are two principal reasons a molecule becomes more energetic when a phosphate is attached. It is now more complex. Complexity increases instability, a consequence of the laws of thermodynamics. Another reason is that the highly charged phosphate creates stress in the molecule due to electrical interactions with other parts of the molecule.
Here's an image (mine) to show the concept of coupled reactions:

Thanks for discussing the role of coupled reaction, i.e. performing a slight unfavorable reaction at 'cost' of highly favorable reaction... that exactly fits to the concept of 'currency', profit and economics. However here the ultimate 'gainer' is nature (entropy working same way as profit of seller) and 'loser' is organism.

@AlwaysConfused Thanks! We've come a long way since textbooks likened the energy in ATP as beling like a loaded spring that could somehow do work.

But still I think a spring analogy is correct; but the 'molecule' ATP is not that spring. rather the 'reaction' ATP <==>ADP +Pi (in appropriate eqlb.) is the spring. A spring too, take energy due to coupling with some other action (hand move), and when it release some energy (do an work); it is too a coupling.

ATP is a form of chemical energy. Hydrolysis of the third phosphate group produces quite a bit of energy:
ΔG° = −30.5 kJ/mol (−7.3 kcal/mol)

ATP is used in a variety of cellular processes, from signal transduction to biosynthetic reactions, motility, and cell division.
An interesting bonus fact: an adult human body only contains about 250 grams of ATP at any one time, but turns over its entire body weight in ATP during the course of a single day.

nice fact, we basically run on 250 gram "battery"
but my question is "what is energy?"

@aurelius I don't understand your question, then. The energy is stored in the phosphate bonds of ATP - it's chemical energy. It can then be converted to mechanical energy, heat, electrical energy (neuron impulses), etc.

my question was this  but I couldn't express it right so I tried it again here if you are curious: http://skeptics.stackexchange.com/questions/35461/what-is-energy

You seem to have misunderstood energy as some sort of substance which is produced as a product of cellular respiration like CO2 or H2O then released into the bonds of ATP molecules. Remembering that it is not a substance and that it is transferred(and not made) by the breaking and formation of bonds in the process of respiration should help clear that out.

Do correct me if I'm wrong.

it is not that I thought of energy as a substance, I know what energy is not, but I don't know what it is, except that it is the driving force of the universe and that it can take many forms. It is just that I cannot picture it in my mind. Even I consume, store, produce, waste, transform energy and still I can't get it right.

@aurelius Have a look at this Physics SE question: http://physics.stackexchange.com/questions/3014/what-is-energy-where-did-it-come-from .


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Would the human body react faster to touch or sight
I am currently working on an assignment for my physics class, but I believe my question is biology related.
For a two person lab, I am trying to time how long it takes a tennis ball to fall two meters, Using basic physics equations I was able to determine that the ball should take around 0.66 seconds to hit the ground but my results are generally very off.
Would I be able to react faster if I were to stop the timer when I felt the ball hit my other hand, or would I have a worse reaction time than if I were to use my current method of stopping the timer when I see/hear the ball hit the ground.

Try them both and see what works better. Why bother asking here?

Averaging them both would work, but technically speaking I want to know what would work. I am at home and I have no access to the materials .

Pretty certain it is touch. As far as I know the sensations of haptic feedback can create a motor reaction without requiring any higher-order cognitive processing, meaning that they'll take the monosynaptic route. On the other hand, the visual processing takes longer, because in this case, higher order cognitive processing is required.

Are far as experimental design goes, you'd have to take into account that the person stopping the timer is probably predicting when it will hit the ground. They'd be looking at the movement of the ball in the few centimetres before it  actually hits the two-metre mark. Similarly, you'd have to determine how to start the timer. Do they start after they notice the ball being dropped, or do you do a similarly-predictive countdown (e.g. "1, 2, 3, drop").

I can't say what I would do, but I would try very hard to find a non-biological "trick" to measure the time lapse. This may be the purpose of the exercise (or it may just be to try to physically see that the equation works). Just to give you some idea of what is humanly possible, scientists have a "trick" (used at the LIGO observatories) that allows measurement of a change in length (of a 4 mile laser beam) of less than the diameter of the nucleus of an atom). By the way, I agree .. TOUCH.

A "touch" or "haptic" sensation will be much faster due to several reasons:

Haptic feedback can be processed without the presence of any higher-order cognitive processing, therefore meaning that the signals are being processed via a monosynaptic route.
There are short reflex arcs between the spinal cord and the limb (meaning that you can react before you are consciously aware of it)

A visual sensation will be much slower:

The processing of the signal will require higher-order cognitive processing, and this takes time. I read that it takes between 50ms-200ms. (polysynaptic route)

Interesting article about this topic

but does it practically make any difference for an experiment like this?


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microscopic slide cleaning and maintenance
we do lot of gram staining and some spore staining. we normally wash our slides with detergent then rinse in D/w, dry it and store it. But on reusing this slide we have to flame it and also clean it with alcohol number of times to make it grease free. also these reused slides have some sort of deposit which does not go with cleaning and evend oes not hamper our staining too.  can anyone please suggest the best simple way to clean microscopic slide and to make it grease free and how to store it.

Whoa! Dint know we could reuse gram stained slides. I remember reusing slides last for plant sections. But recycling always seems to be a good thing :)

We were often suggested to simmer the slides in detergent water... whatever new or re-used. We often did it on Lab. (Because the slides we bought from market, contained something greasy so that watery film divided into beads). (We used Blue Star (TM) slides ) However, sometimes removal of greasy layer opens some minute scratch-marks so the slide looks slightly turbid.

For permanent slides (in the slides library), if we use oil, we are required to dip the slides in xylene once were done.

@Polisetty I never cleaned slide with xylene but I doubt how-much evaporable it is. It was quite sticky and made the hand oily for long. Also, though some practical-instructions tell to clean the lens-oil with xylene; the xylene really did very bad to the oil-immersion lens (maybe it damaged the lens coatings or maybe it not removed properly). We usually  cleaned the lens first with moist cotton cloth and then a dry one.

oh no that is for permanent slides that will be again put under oil

@always confused. we too use blue star or himedia slides. i also have same issue after washing and drying the slides, on preparing smear it does not give smooth smear but beads like. will try simmering slides in detergent water and check. thanks

I meant not only re-used slide... brand new slides from the packet also shown breaking the smear into bead-bead. However after simmering with soap/ detergent water don't forget remove the detergent. Sometimes a trace of remaining soap/ organic solvents/ surfactants may help facilitate beautiful smear but that is not the procedure.

An old technique to clean used slides is to just toss them in a jar containing equal volumes of distilled water, ethyl alcohol 95% and xylene. Shake from time to time. When needed wipe them dry using a clean, lint free cloth and use.
The techique was at the time (1930's?) in use in the lab of prof. Baudet (Veterinary parasitologist, Utrecht University) and is mentioned in several editions of the "Précis de Microscopie" by Maurice Langeron.
Langeron mentioned that the slides treated that way were "perfectly grease-free".
Another method is to wash the slides, rinse in distilled water and store for some time in a mixture of ethyl alcohol and acetic acid.
When on a tight budget, used Carnoy fixative was (is?) used.
This is a trick that was (is?) in use at some botanical labs in Eastern Europe.
It's mentioned in some of the German literature on microtechnique, if memory serves me right in Braune, Leman and Taubert's "Pflanzenanatomisches Praktikum".


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By just looking at an unlabeled picture, how do you know it is a protein?
I'm learning about proteins and need to understand this concept. What makes this colourful ball of squiggles identifiable? Why is it a protein, and not any other biomolecule (like DNA for example)? What are the colours showing? What are the variations in the shape of the image?
Basically, the question is: What is this image trying to tell me about this protein?

This question is unclear. Are you asking "What is this protein?" or "What about this structure makes it a protein?"

DNA is a double helix. This, obviously, is not.

I'm tempted also to say "experience" - for example, to me this is clearly a TIM barrel fold...

@MattDMo DNA was my added example. I think OP wanted to know something along the lines of: "How do people recognise this instantly as a protein rather than any other biomolecule?"

Shapes
This is a common way of illustrating a protein and is often called a "protein cartoon". There are other common ways of illustrating proteins.
This cartoon shows you where α helices are (spirals) and where β sheets are (arrows) which are important structural elements. The strings connecting those structural elements are flexible "loop" regions.
If you want to query this against other structures and see which protein it is, check out PhyreStorm. You'll need the PDB file, not just an image.
Colour
The colouring is also common. The N-terminus (the first amino acid) is coloured blue, and the colours go through the rainbow to red, the C-terminus (the last amino acid in the polypeptide chain).

Even though this question has been answered (and the answer accepted), I want to add something regarding scientific language and convention.
Language in general is a means of communication which allows people to share ideas they have inside their minds. Scientific language is used for sharing scientific knowledge between people, and apart from verbal and written communication, it also uses drawings of all kinds to better illustrate complex ideas that are usually invisible to the naked eye (whether we are talking about molecules in chemistry, biological microsystems in biology, forces in physics, etc.).
The image in question represents the conventional way of portraying a protein structure, and this widely-accepted convention is characterized by certain colors and shapes, as stated in the above answer. I imagine that anyone seeing this kind of representation for the first time would not know immediately that this is a computer rendition of a protein, because no one knows what a single protein looks like before actually studying about it. But once you are told it is a representation of a protein, you accept it and "tag" it in your mind, so that next time you see it, you already know this is what a protein "should" look like.
And the more you study it, the more natural this language becomes for you.

you're pointing something very important to understand to students of science - most of what we learn in classes is not actually the study of the subject, but rather the conventionally accepted languages and modes of representation used by the scientific community to talk about the subjects and convey information.


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Can coding DNA be used for DNA fingerprinting?
I am confused if coding DNA can be used for DNA fingerprinting because I have read that non-coding segments of DNA are used to identify and analyze DNA. I want to know if coding DNA segments are of equal length in all individuals?

It's not non-coding regions in general, it's specific repeat sequences - microsatellites - that are highly variable. In principle you could use a full genome sequence to identify individuals.

When selecting sequences to use for DNA fingerprinting, you have to use sequences that are highly variable within the population.  Coding sequences mostly aren't, and they aren't going to vary much in size, the way tandem repeat sections do.

You are correct, but even so you need to provide a reference to document your answer and to allow the reader to find out more details.


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Why do plants create enough energy for the entire ecosystem?
In my environmental class, we were recently learning about the $10\%$ law that basically says only $10\%$ of the energy goes from one trophic level to the next.
This got me thinking about why energy flows from one level to the next.  Specifically, why do plants create enough energy for the entire ecosystem?  Wouldn't they do fine without us, and wouldn't that save them the work of creating all that excess energy?

First of all, plant do not 'create' energy; they collect it (from available sunlight). Secondly, they do-not collect it for their predators. They collect it for themselves.

They don't create energy! They use the energy from high-energy photons from the sun and convert that into molecules with high energy chemical bonds. Many plant species have evolved to need animals to reproduce, but yes, as a whole, a plant-only biosphere would probably be stable.

As @AlwaysConfused points out, the assumption in the question is problematic, and this has resulted in vague answers that can't directly answer the question. I'm voting to close the question because it is unclear to me what the question is bearing in mind the assumption is false.

Plants collect it perhaps because just it is available to them. Every fact in nature have 'cause'; but some fact doesn't have 'purpose' to serve. Rather,  probably there was no purpose or benefit for the plant for stopping collect  energy.

I agree that the question is problematic and a bit unclear. Generally, it invites confusion to phrase why questions in terms of taxonomic groups ("why do plants create...") - why-questions on evolutionary outcomes usually don't make much sense.

building upon @fileunderwater's comment, I've been taught and found it true that in the life sciences, "why" questions generally need to be rephrased as "how" questions to be answerable, leaving the remaining "why" essence of the question to philosophy. When we rephrase as "how" and learn lots from that, it can shed much light on potential answers to "why".

Plants collect energy for themselves via photosynthesis, not for others.
It is used for it's own growth and survival.
It's energy is then redistributed to other organisms when either the plant dies and decomposes or when it is consumed. Many organism cannot collect their energy like plants do, and thus must feed on organisms (like plants) that are able to collect and store energy. This is in many cases detrimental to the plant (it should be intuitive why being eaten might be bad), and many, many plants do have traits to discourage other organisms from eating them (plants with toxins, thorns, etc.).

Let's look at a very simple "ecosystem", cows and grass. Imagine there is 1000 kilograms of grass available. This can support about 100 kg of cow. There's your 10% figure, but mass here instead of energy.
When the cow eats the grass it must break down the food to get both matter and energy. Everytime energy is transfered, some of it is "lost" as heat. So as the energy in the bonds of the molecules of the grass are transferred into energy in the bonds of molecules making up the cow, much of that energy is wasted, radiated away from the cow as heat. The cow also has many tasks to perform that also use the energy in the grass. It has to walk around grazing, chew, make more cows, etc. By the time all this is accounted for, the cow has used 90% of the energy in the food to provide for its own energy needs as well as the waste.
In the process of breaking the grass down for energy, the cow transformed the food, from which it extracted the energy, into carbon dioxide and water. The carbon dioxide was breathed out into the atmosphere. Only 10% of the matter in the food remains to add mass to the cow. This is why the cow only put on 1 kg of weight for each 10 kg of grass.
So that cow, having only retained 10% of the matter that was in the food, only has 10% of the energy since energy is stored in the chemical bonds of the matter.
The 10% rule is an approximation. A number of my students were in FFA (Future Farmers of America) and raised animals. One of the tasks they were required to do is keep track of the weight of feed and compare it to the weight gain of the animal. Many that I spoke to did better than the 10% but much of that was probably due to the higher quality of the feed they used.

What is FFA? is it an institute or such?

@AlwaysConfused FFA = Future Farmers of America. You must be a city boy! :) I edited that in above, should have done first time around. [this comment to be deleted]

I live in India so normally I don't heard about future farmers of America.

I agree I live in city for study-purpose and also true I'm much couch-potato because I'm autism-spectrum so could not develop habit to play with others even on tremendous peer-pressures, but it is also true I do-not fit in a city, rather a village or perhaps a forest suits better to me. However I assume here more villagers would be unaware about FFA than city-peoples.

" The cow also has many tasks [...], make more cows. "
The way this is said made me smile :)


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Why do anaerobic bacteria require a low redox potential for their culture media?
I'm reading Clostridium ,which is an anaerobic bacteria in my microbiology text and it says,

of more importance than the absence of oxygen is the provision of a sufficiently low redox potential in the medium. Third can be achieved by adding unsaturated fatty acids, ascorbic acid, glutathione, cysteine, etc.

Why? Do they reduce oxygen free radicals or something? Well, are these present in Clostridium's natural habitat?

The higher the redox potential is, the higher the oxygen dissolved in the media will be. Lowering this potential insure that the oxygen concentration is lower and that the anaerobe will be able to grow easily.
Several steps can be done while preparing the media such as boiling to remove oxygen and adding chemical which reduces this redox potential to dissolve oxygen back into the medium.
As for the natural habitat, they naturally have no or really really low amounts of oxygen. If the habitats containing little oxygen have other molecules able to reduce redox potential is a good question.
Lowering the redox potential is mainly important for the medium since there is oxygen involved (hard to remove 100% while preparing media).
I hope my answer helps.

Thanks! Also on further reading I found out that the pathophysiology of gas gangrene cause by anaerobes is also related to the reduction of redox potential and hypoxia.


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oversecretion of the thyroid gland
What are the reasons for the oversecretion  of thyroxin in the thyroid glands?
Its name was mentioned in my book but there was no explanation.
What are its symptoms,can it be fatal?

what book? where else have you looked? this is a relatively straightforward question/answer if you search the internet...

Elevated levels of thyroid hormone in the blood is called thyrotoxicosis. If this is due to a hyperfunction of the thyroid gland, it is known as hyperthyroidism. In common parlance, these terms are often interchanged.
Although a simple google search would tell you more, I add some detail here.
Hyperthyroid can have various causes. There can be a functional cancerous/ non-cancerous mass in the thyroid gland producing the hormone. Or as in graves disease which is an autoimmune condition where antibodies mimic to stimulate the thyroid gland to hyperfunction.
Non hyperthyroid causes of thyrotoxicosis include inflammation of thyroid or thyroiditis, where preformed hormone is released. It can also occur sometimes in a condition called struma ovarii where the tumor in the ovary turns into a thyroid like mass producing the hormone. Another possible case is an iatrogenic one where the the problem is due to the patient taking exogenous thyroid hormone.
Thyrotoxicosis is not fatal and can be controlled by drugs. Symptoms include cardiac problems, high BMR, ocular changes (bulging eyes), diarrhea and many more.
A special case of Graves disease called thyroid storm is a medical emergency and can be fatal.
Heres the medscape link for further reference. http://emedicine.medscape.com/article/121865-overview

what is a thyroid thaw?

There can be a functional cancerous/ non-cancerous mass in the thyroid thaws producing the hormone.

Typo there! Corrected :)

Your answers are usually of much better quality than this one, which has a lot of errors. It makes me wonder if you actually read the medscape article. -1 (Sorry)

@anongoodnurse I actually wrote this up from Robbins pathology. I gave the Medscape one as an online reference. Frankly speaking I dint read i dint read it. Anyway, could you please point out the errors?


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Mechanics of Chromosomal Crossover
When chromosomal crossover occurs, two matched chromosomes swap matched sections of their chromosomes. My question is: how does the cell select where to to make the break on both chromosomes? Is it based on some attempt to match sequences on the two chromosomes, or purely on distance from the centromere? The mechanics of the former could be achieved by breaking the two strands of each chromosome at different places. The mechanics of the second is a simple walk from the centromere with a random(?) selection of where to cut.
The purpose of this question: if the process is based on distance from the centromere then it would provide an explanation the presence of junk DNA. Successful crossover requires that the number of functioning genes on the two chromosomes not be radically altered in quantity. A failed crossover would result in at least one of the gametes being non-viable, reducing fertility. If crossover is based on centromere distance then the location of genes becomes a factor in the success of a crossover, erecting a fitness barrier between populations with radically different gene placement, even if gene content is identical.
If this is a question without an answer, currently, one way to address it would be to try to cross breed knockout mice that don't have junk DNA with ordinary mice that do. If the fertility of the cross breeding is significantly lower than than knockout with knockout and normal with normal, or if the cross breeds are less fecund, then that would provide evidence for position based crossovers, and a function for junk DNA in the crossover process.

How does the cell select where to to make the break on both chromosomes?

There are proteins that direct the selection of a site where a double strand break will be made on one chromatid.

Crossovers are not randomly distributed: The histone methyltransferase PRDM9 recruits the recombination machinery to genetically determined hotspots in the genome and each incipient crossover somehow inhibits formation of crossovers nearby, a phenomenon called crossover interference. Each chromosome bivalent, including the X-Y body in males, has at least one crossover and this is required for meiosis to proceed correctly.
  Credit; Reactome

.

Is it based on some attempt to match sequences on the two chromosomes, or purely on distance from the centromere?

The sequences are matched but not as you have assumed. Following the introduction of a double-strand break in one chromosome the regions around the break are processed (by proteins) and these processed ends invade the opposite chromatid. The formation of a Holliday junction follows, these are the "X" structures between strands in the image below, and they requires base-pairing;

Image credit; EMW2012

Interesting. How does the protein "know" where to look on the blue DNA for the matching sequence (the strand invasion part before the process split)? Or does the protein that opens the blue pair along it until a match is found? Those genetically determined hotspots are particularly interesting. Is each crossover hot-spot's (CHS) sequence unique? In other words, can the crossover mechanism accommodate radically different chromosome lengths if the relationship among CHS's and genes is right?

Yep, it's top-shelf interesting. The chromatids are aligned with one another as a tetrad during Prophase I of meiosis. This animation shows how the steps progress by showing only the DNA but note that many proteins regulate the steps; including locating the matching sequence (see Reactome link in answer for key proteins). The linked paper above shows the differing binding sites for alleles of human PRDM9.

I guess you could put it, succinctly, this way: the search for the matching sequence in the blue DNA has to start somewhere, and it has to complete in a limited amount of time for the process to succeed. How do the relative lengths and positions of matching sequences affect the success rate of the operation of the mechanism? Does it succeed at the same rate for radically different lengths with the same relative configuration of functional regions as for more matched ones?

Just my take here. I have difficulty envisioning a mechanism that would insure the "walking" distance from the centromere was the same on both chromatids. How would that be coordinated? Since the chromatids are not in continual contact their entire length, this would entail two "walkers" that somehow coordinated their steps.
Furthermore, there is a lot of truly "junk DNA" between genes. By truly junk, I exclude the non-gene DNA portions we haven't fully documented the function of but which have uses that require their conservation. But there is a significant portion of DNA that is not conserved (which provides the basis for RFLP analysis in DNA fingerprinting). This means that, while the nucleotide lengths within genes and other important regions may be identical between homologous chromatids, the length of segments in between is not guarenteed to be so. An error of "walking" just one extra base within a gene would result in a frame-shift mutation likely rendering that allele useless.
I think there must some local exposure of the base pairs in some areas of contact between chromatids for chiasmata to form. This would also seem necessary simply for the chromatids to recognize their homologues.


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Can mitochondria with "depleted" mtDNA reproduce?
Background
There's a popular group of antibiotics known as fluoroquinolones, abbreviated FQs. They're quinolone abx with a fluorine atom added at position 6 to increase cell permeability. Popular varieties of these drugs include ciprofloxacin, levofloxacin, norfloxacin, and many others. They also go by brand names Cipro, Levaquin, etc. They have a well known side effect of wreaking havoc on the body's mitochondria through numerous pathways.

This stunning image shows the in-vitro result of administering a clinically relevant dose of ciprofloxacin to human tissue for 24 hours (1). The study notes "short, swollen, fragmented mitochondria (smaller aspect ratio) with highly reduced branching (smaller form factor)"
Because the fluorine atom allows for deep tissue penetration, FQs can cross the double membrane of mitochondria, and because FQs are designed to target "double helix" DNA of some bacteria, they also appear capable of targeting the same double helix DNA structure in mitochondria. In bacteria, the FQs bind to the DNA-gyrase, causing breaks in the DNA that are fatal (2) to the bacteria.
Question
A study published in Molecular Pharmacology (3) shows that mtDNA is "depleted" by Cipro:

Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks. These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase II-like activity, resulting in a loss of mtDNA.

The full text of this study is not available as far as I can tell. I can find scientific literature on depletion of mtDNA (4) but what does this mean for the long term health of the mitochondria / cell?

Can mitochondria with "depleted" mtDNA reproduce, passing on the damage from breaks in the DNA? Or is the mitochondria and cell doomed?
More open ended: Is there any literature suggesting mitochondria damaged by oxidative stress can recover (first image), or are they also doomed?

References

Bactericidal Antibiotics Induce Mitochondrial Dysfunction and
Oxidative Damage in Mammalian
Cells
Fluoroquinolones: Mechanisms of Action and
Resistance
Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells
Mitochondrial DNA metabolism targeting drugs

Can mitochondria with "depleted" mtDNA reproduce ?

If by depleted, you means reduced number of mtDNA copies, then yes, as long some copies still remain, these can be replicated.
Mitochondrial genome is replicated asynchroneously from nuclear genome [Bogenhagen, 1977], through a particular process (review [Holt, 2012]), and is present in multiple copies. These copies can be different, due to mutation.
Mitochondria do not "reproduce" in the common sense, as they do not undergo mitosis, but have a fission and fusion mechanism (review [van der Bliek, 2013]). The fission products get their half of the mtDNA copies at random when the two mitochondria separate.
Mitochondria with depleted mtDNA can (and do, according to your image) undergo fission.

passing on the damage from breaks in the DNA?

There are DNA repair mechanisms for the mitochondrial genome. In this case, the mechanism of choice to repair double strand break is  microhomology-mediated end joining (MMEJ) [Tadi, 2016], that try to align the ends of the DSB through use of 5-25 bp homologuous sequence. This ususally results in the deletion of some material near the break.
The resulting mutation is conserved, and passed on through replication of this particular mtDNA instance. The mitochondria will contain a mix of mutated and non-mutated mtDNA from now on.

Or is the mitochondria and cell doomed?

One could say a particular mitochondria is "doomed" if there is no [viable] copy of mtDNA; if it is not able to maintain adequate internal membrane potential, it will try to fuse with other working mitochondria, or be eliminated through autophagy/mitophagy.
The cell itself could be "doomed" if there are not enough mitochondria left to meet energetic demands. (or, through mitochondria-induced aptotosis). Some particular human cell type have hypersensibility to fluroquinolones (tenocyte, chondrocyte, osteocyte), with increased cell death, but other types have not manifested this behaviour. [Barnhill, 2012] The reason for this sensibility/resistance is not elucidated.

Thanks! Lots to digest. Do you mind if I edit in some relevant studies? Also, the image doesn't show fission I believe, the first scan just happened to include one mitochondria and the second happened to include two.

Hmm, there is one cell on the first picture, and two on the second. The mitochondria are the green fluorescent-marked structure inside these cells. (using Mitotracker green marker, this is explained in the Mitochondrial morphometry paragraph of your first paper). OK for the edits.

Ah ok I think I initially misinterpreted the image then. So the mitochondria are only the blurry green areas inside the black circles? Does the non-triangular look of the surrounding tissue imply anything? I believe these are two separate samples as I understand it, not a before and after picture.


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Derivation of Michaelis-Menten kinetics for discrete stochastic simulations
According to this article,

[...] the propensity function for the conversion reaction S → P in the
  well-mixed discrete stochastic case can be written $a(S) = \frac{V_{max}\cdot S}{K_m + S/\Omega}$ where $\Omega$ is the system volume.

I don't quite understand how this formula is derived from the non-discrete Michaelis-Menten kinetics $v = \frac{V_{max} \cdot [S]}{K_M + [S]}$ (see Wikipedia). According to my understanding, $[S] = S/\Omega$. If we apply this to the formula from Wikipedia we get
$$
\frac{V_{max} \cdot[S]}{K_M + [S]} = \frac{V_{max} \cdot S/\Omega}{K_M + S/\Omega} = \frac{V_{max} \cdot S}{\Omega \cdot K_M + S}
$$
which is not the same as $\frac{V_{max}\cdot S}{K_m + S/\Omega}$. So, how can one derive the formula from the quoted article (if it is correct)? If not, how can we correctly get to a discrete propensity function from the Michaelis-Menten kinetics?

I guess the article is incorrect. I checked different possibilities but none of them seem to give this relation. The papers cited by this article also do not have this formula. Their supplementary data also does not explain anything. If $K_M$ is defined differently then this formula may possibly be right but since the article does not mention anything like that, we should not assume so.

I think I figured it out myself. Since $a(S)$ is in $\frac{mol}{s}$ and $v$ is in $\frac{\frac{mol}{l}}{s}$, we have that $a(S)= v * \Omega$.
Therefore
$$
a(S) = \frac{V_{max}\cdot [S]}{K_M + [S]} \cdot \Omega = \frac{V_{max}\cdot S / \Omega \cdot \Omega}{K_M + S / \Omega} = \frac{V_{max}\cdot S}{K_M + S/\Omega}.
$$


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How many mutated genes from a complementation test?

With 1, 3, and 5 being defective together, that means they are on the same gene. 3 and 5 are defective together too, meaning they are on the same gene as 1. Why does this slide say that there are 3 mutated genes? I must be missing something, I don't think I understand something.

There are 5 mutations being tested in these complementation test.
The first gene, carries mutation number 2.  In other words, mutation number 2 complements mutations, 1, 3, 4, and 5, and fails to complement itself.
The second gene, carries mutation number 4. In other words, mutation number 4 complements mutations 1, 2, 3, and 5, and fails to complement itself.
The third of the three genes, carries mutation 1, in one strain, mutation 3, in a second strain, and mutation 5, in a third strain.  In other words, mutations 1, 3, and 5 all fail to complement each other, yet all three complement mutations 2 and 4.
There are 5 different strains in this experiment, and there are five different mutations (one in each strain), but the five mutations only affect three different genes.


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How do red blood cells obtain energy without mitochondria?
RBCs don't have mitochondria so there is no Respiratory chain in them. But how does they get energy from Lactate. Because Lactate produce NADH which gives energy only in respiratory chain.

They do not get energy from lactate. We are pleased to welcome you to SE-Biology but expect you to do a little research before posting. Google for red cell metabolism, check Wikipedia and see what previous questions on erythrocytes have been posted here.

What process(es) do you think RBC's would need energy for, compared to the "average" cell? Does a keratinocyte need energy? Does the function of hemoglobin require energy? (These are serious questions, the answer to which I hope will help you make your question better.)


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What for a Kinase Assay?
I am wondering why to use a kinase assay, since we can extract the proteins from cells and then do a Western with the specific antibodies we want to use.

Welcome to SE Biology. However you need to provide much more background to your question before anyone can help you. What is the context of your question? What experiment are you doing? What are you trying to discover? Is this a teaching experiment or real research?

There's a very simple answer: scale. If a drug company wants to screen a million-compound library to find which ones inhibit the kinase activity of a certain target, they're not about to do a million IPs and a million Western blots. Instead, they'll use recombinant kinase and substrate peptides, with a variety of readout systems to choose from.
Other reasons include not having a good phospho-specific antibody to the substrate, very low expression of the kinase and/or substrate, complicated protocols necessary to activate the kinase in vitro, lack of a good model system, and more.


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Probability of number of boys and girls being born on a single day
I am new to genetics, I have the following question at hand :

If four babies are born on a single day, what are the chances that
$A>$ Number of boys and girls will be equal.
$B>$ All $4$ will be girls.
$C>$ At least one baby will be  a girl.
$D>$ Which combination of boys and girls is most likely?

My solution:
Let $X$ be the number of boys .
$X$ follows $Binomial (4,{1\over 2})$ , since the probability of a child being a boy is half.
So the answers are
$A>{3\over 8}$
$B>{1\over 16}$
$C>{15\over 16}$
$D> $ Equal number of boys and girls.
Is everything right ?

I'm voting to close this question as off-topic because  it's about probability, not biology.http://meta.biology.stackexchange.com/questions/3111/not-all-questions-featuring-something-biological-are-biology-questions

@rg255 I agree. You can do so. But that doesn't mean you will downvote the question !

Voting allows content that is useful and useless to the community to be identified - your question is not biology so not useful to our community, therefore I downvoted.

@Qwerty mouse over the downvote button and read the message: "This question does not show any research effort; it is unclear or not useful." Additionally, please read "Why is voting important?".

I know this is kind of tedious and only practical when you are considering no more than 10 children  (which I think is a lot to parent), but anyway, I like to solve these problems with a binomial expansion.
So we have binomial probability so 2 options - either a boy (n) or a girl (g) at equal probability or 50% or 1/2.
(b + g)^n = a binomial expansion according to the coefficients of Pascal's triangle.
Where n = 4 children, then the row of Pascal's triangle is 4 in which the first row of pascal's triangle is technically row 0.
Equation: (b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
Problem A)
So the probability that the number of boys and girls will be equal is
Probability((6(b^2)(g^2)), where (b^2)(g^2) means two boys and two girls, an equal number.
When b = 1/2, and g = 1/2, or well ... b + g = 1
6(b^2)(g^2) = 6[(1/2)^2 * (1 / 2)^2] = 6 * (1/2)^4 = 6 / 16 = 3/8
B) All four will be girls: Prob((1(g^4))
= 1(1/2)^4 = 1/16
C) At least one baby will be a girl:
That corresponds to 4(b^3)(g), 6(b^2)(g^2), 4(b)(g^3), and 1(g^4)
The probability that at least one will be a girl is
= (4 + 6 + 4 + 1) * (1/2)^4 = 15 / 16
D) Which combination of boys and girls is most likely?
That would be 6(b^2)(g^2), so when b = g = 1/2
Prob(most likely combination) = 6/16 = 3/8 or two boys and two girls.
Note that if you add up all the combinations, the result is 100% of all probabilities:
(b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
When b = g = 1/2, then basically:
(1 / 16) + (4 / 16)+ (6 / 16) + (4 / 16) + (1 / 16) = 16 / 16 = 1 = 100%
You did it right. But I suppose this is another way to evaluate a binomial like this.

A BIG typo- $2$ boys and $2$ girls, not $3$.

Good work, but basiacllly what you did is like - instead of directly evaluatng $3\times 4=12 $ you wrote $3+3+3+3=6+6=12$....

Yeah, I was typing this so quickly!


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DNA extraction from plants and algae don't use phenol. Why?
I don't know if here is the correct place to make this question, but I've been noticing that protocols for the extraction of photosynthetic organisms DNA don't use phenol. Only CTAB / Chloroform.
Why?
Because bacterial or animal extraction are phenol:chloroform based.
Thank you

CTAB is for removing polyphenols and polysaccharides which are found in plant tissues. Animal cells/bacteria don't have these. You can do an additional phenol-chloroform extraction if you want.
See this protocol by Monsanto.

Weigh out 6g of processed tissue into a 50ml conical tube appropriate for centrifugation. Note: For unprocessed tissue, weighing
  m ay occur prior to processing as long as entire processed sample is
  transferred to the conical tube.
For each 6g sample add 25ml of a solution consisting of 24.25ml, pre-warmed (55°C) CTAB extraction buffer, 0.5ml 2-mercaptoethanol
  (2-ME), and 0.25 ml of 10mg/ml proteinase K for a final concentration
  of 2% (2-ME) and 100µg/ml (proteinase K).
Incubate the tube for 60 minutes at 55°C. Cool the tube briefly on bench (10 minutes)
Add 20ml of phenol:chloroform:isoamyl alcohol (PCI, 25:24:1).  Cap the tube and mix vigorously by vortex or inversion.
Centrifuge for 10 minutes at 13,000×g and 20-25°C to separate the aqueous and organic phases. Transfer the upper aqueous phase to a
  clean 50ml conical tube.
Repeat extraction two times for a total of three extractions (steps 4-5).
Transfer upper aqueous phase to a new tube and add approximately 2/3 volume of -20°C isopropanol and gently invert the tube several
  times to mix.
To precipitate the DNA place the tubes at -20°C for at least 30 minutes and up to three days.
To pellet the DNA centrifuge the tubes at approximately 13,000×g for 20 minutes at 4°C.
Redissolve the pellet in 4 ml of TE pH 8.0. Transfer to a 13ml Sarstedt tube and add approximately 40µl of 10mg/ml RNase, then
  incubate at 37°C for 30 minutes.
To extract the DNA add 4ml of chloroform:isoamyl alcohol (CIA, 24:1).  Centrifuge for 10 minutes at approximately 13,000×g at room
  temperature.  Transfer the upper aqueous phase to a clean Sarstedt
  tube.
Repeat step 11 then add half volume of 7.5M ammonium acetate, gently mix by inversion/pipette and add 2 volumes of 100% ethanol. Mix
  by inversion/pipette and place at -20°C for 30 minutes to overnight.
Centrifuge at 13,000×g for 20 minutes at 4°C to pellet the DNA.

I have used phenol:chloroform many times for algal DNA and RNA extractions. These protocols needed only minor tweaks to adapt it to a particular species (some cell walls can be extremely though). The general principle behind phenol chloroform works on almost any sample once you have lysed/pulverised the cells. The only major issues occur when tissues are extremely fatty or full of carbohydrates.
I have also used CTAB but it seems to be less universally applicable to algal samples.


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What kind of viruses can be found in sperm?
It is well known that the HIV virus can contaminate other people via sperm. But is this the only virus that sperm successfully could contain, or could for example rhinoviruses also be part of sperm?
What causes the difference if there is one?

Those are some viruses that can exist in sperm :

Zika : Zika and Sexual Transmission
Ebola : How Long Does the Ebola Virus Survive in Semen?
Hepatitis C : Hepatitis C virus detection in the semen of infected patients
Human papillomavirus infection (HPV) : Correlation between HPV sperm infection and male infertility
Herpes simplex : Detection of herpes simplex virus DNA in semen of men with genital HSV-2 infection
Hepatitis B : Effects of hepatitis B virus on human semen parameters and sperm DNA integrity

Do you know if there is a special cause for there present in sperm or is it just a matter of getting dropped by the bloodstream in the region of the organs involved by producing sperm no matter what kind of virus?

@Marijn, I think they will be within the DNA that sperm contains.

It almost looks like your children going to be a kind of virus than ?

Of course the virus normally will be inside their cells.

When I think of a virus I think it as a whole structure including membrane etc. But when it is in the DNA it is only a part of the virus. Because isn't a cell after multiple copies making of the virus exploding whereby all the viruses including membrane etc are loosed in the blood and other plasma's?

In most of the cases the explosion doesn't happen in sperm, honestly I don't know why.


text:
Is there a difference between "cell line" and "cell strain"?
I'm translating one Russian text where a cell line is transfected to produce a drug. I wonder if I can sometimes use "cell strain" or simply "strain" instead of "cell line" or instead of "producer" (продуцент, meaning "the producer of the drug", i.e. the cells that produce the drug).
I googled and found this answer on Yahoo answers:

Cells in culture can be passaged a finite number of times before reaching a crisis which can be compared with aging. The number of passages, before reaching crisis, has been termed the Hayflick limit and is related to the longevity of the species from which the tissue was originally derived.
Within the Hayflick limit, the cells are referred to as a cell strain.
Cells that survive the crisis and continue to grow are referred to as a cell line. Cell lines can also be derived directly from cancer cells. There are many properties that distinguish cell lines from cell strains, including altered chromosome number, changes at the cell membrane, and reduced requirement for certain growth factors.
Therefore:
A cell strain is defined as an euploid population of cells subcultivated once or twice in vitro, lacking the property of indefinite serial passage. Cell strains ultimately undergo degeration or death (senescence).
A cell line is an aneuploid population of cells that can be grown in cultures indefinitely.

Is this true? Is a cell line always aneuploid and capable of indefinite growth, as opposed to being euploid and incapable of indefinite growth?

"Strain", in general, is usually used for whole organisms (whether they are unicellular or multicellular). For example, there are mouse strains.
"Cell line", on the other hand, is a very specific term that is used to refer cultured cells obtained from a multicellular organism. They need not be necessarily aneuploid.

Is a cell line always aneuploid and capable of indefinite growth, as
  opposed to being euploid and incapable of indefinite growth?

Aneuploidy does not have any causative relationship with indefinite growth. Most cancerous cells evade the cell cycle checkpoints, which allows them to grow out of control. Some of these checkpoints also ensure proper segregation of chromosomes. Bypassing them leads to aneuploidy.

Are cell lines essentially immortal?

Usually primary cell cultures are not referred to as "cell lines" these days. However, originally, any cultured cell that grows in vitro is called cell line. From Freshney (Basic Principles of Cell Culture):

When cells are isolated from donor tissue, they may be maintained in
  a number of different ways. A simple small fragment of tissue that
  adheres to the growth surface, either spontaneously or aided by
  mechanical means, a plasma clot, or an extracellular matrix
  constituent, such as collagen, will usually give rise to an outgrowth
  of cells. This type of culture is known as a primary explant, and the
  cells migrating out are known as the outgrowth (Figs. 1.1, 1.2, See
  Color Plate 1). Cells in the outgrowth are selected, in the first
  instance, by their ability to migrate from the explant and
  subsequently, if subcultured, by their ability to proliferate. When a tissue sample is disaggregated, either mechanically or enzymatically
  (See Fig. 1.1), the suspension of cells and small aggregates that is
  generated will contain a proportion of cells capable of attachment
  to a solid substrate, forming a monolayer. Those cells within the monolayer that are capable of proliferation will then be selected at
  the first subculture and, as with the outgrowth from a primary
  explant, may give rise to a cell line.

Elsewhere, a cell strain is defined as positively selected subpopulation of cells:

A cell strain is a subpopulation of a cell line that has been positively selected from the culture, by cloning or some other method.  A cell strain will often have undergone additional genetic changes since the initiation of the parent line. Individual cell strains may, for example, have become more or less tumorigenic than the established line, or they may be designated as a separate strain following transfection procedures.

This definition does not say anything about what kind of selection was used. You can select for cell that express GFP, for instance. So that strain would be simply designated as GFP+.


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Can a non-disjunction event occur in meiosis II (in the paternal gametes) to result in an XXY male?
My professor stated that non-disjunction in meiosis II of the father cannot produce an XXY male. However, a disjunction event in meiosis II of the mother can. I'm not understanding why this is (?)

The reason maternal non-disjunction during meiosis II can produce XXY offspring.

In this case, meiosis I occurs as normal so that after the first division the replicated homologous chromosomes, each consisting of two chromatids connected at a centromere, have separated. If a non-disjunction occurs at this point, haploid cells will not be formed. Instead, the sister chromatids of a replicated chromosome will not be separated and a gamete containing two X chromosomes will be formed. When this gamete combines with a sperm containing a Y chromosome, the offspring has the XXY genotype.

The reason paternal non-disjunction during meisosis II cannot produce XXY offspring.

This is similar to the maternal case except that after meiosis I, in one cell will be two YY chromosomes while the other cell will be two XX chromosomes. When non-disjunction occurs (assuming it occurs in both divisions), these chromosome arrangements remain the same and two cells are formed. One with two XX chromosomes and one with two YY chromosomes. If either of these gametes combines with a female X gamete, either XYY or XXX will be formed but never XXY.

Wikipedia discusses nondisjunction occurring in males or females, and both can result in the karyotypic condition (XXY) called Klinefelter Syndrome that often results in a male phenotype.