text:
How can a haploid plant be bisexual?
According to Wikipedia:

Meiosis is a specialized type of cell division that reduces the chromosome number by half. This process occurs in all sexually reproducing single-celled and multicellular eukaryotes, including animals, plants, and fungi Because the number of chromosomes is halved during meiosis, gametes can fuse (i.e. fertilization) to form a diploid zygote that contains two copies of each chromosome, one from each parent.

So it means that a haploid plant body will give rise to either a male sex organ or female sex organ that produces gametes to form zygote thus completing the alternation of generation.
We also know that chara a monoecious plant can be dioecious, which means that haploid plant body is producing both antheridia and archegonia which produce gametes by mitosis.
Coming to my question, "HOW CAN A PRODUCT OF MEIOSIS BEFORE FERTILISATION BE BISEXUAL?"
Does this implies that reduction division is not responsible of sex differentiation? If yes then what is responsible for sex differentiation in plants like chara where a haploid produces both gametes ?
Explanation will be appreciated

I am not sure I understand. You define male and female based on the size of the gametes. If the gametophyte is multicellular it can still produce gametes that are of different size. Isn't it?

@Remi.b          So ,there are no allosomes in plants unlike humans?

An allosome is a non-sexual chromosome. Yes plants have allosomes. Most species (of plants and animals) do not even have sex chromosomes but only have allosomes. I don't understand how it relates to the post though. Looks like something is unclear in your understanding of sex and sex determination system but I don't know what.

Meiosis does not determine sexual form. Eukaryotes use meiosis and fertilization to recombine genes to form new combinations.  Meiosis does produce haploid cells from diploid cells, but that has nothing much to do with the sexual forms involved.
In the case of the algal genus Chara, the organism's life cycle is entirely haploid except for the single-celled zygote formed during fertilization; this is called a haplontic life cycle.  Being haploid does not require an organism to be of one sex (or any sex), so there is no difficulty to being monoecious and having both male and female structures on a single organism.  The reason for having two kinds of gametes, sperm and ova, is simply practical: the specialized job of sperm is to move to another gamete, adn the job of the ova is to provide a maximum amount of nutrition for the future zygote (which means larger size and hence limited mobility).

Even Chlamydomonas.


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How different are these terms: Phylloclade, Phyllode, Cladophyll and Cladode?
We started with Plant Morphology in class (specifically, the morphology of angiosperms).
My teacher's provided us with the following terms and their definitions.

Phylloclade
A modified stem that is flattened or cylindrical and capable of unlimited growth. They are green and capable of photosynthesis. Examples include; Opuntia, Epiphyllum, Casuarina, Euphorbia.
Cladophyll (also called a Cladode)
A modified stem capable of limited growth. They are green and capable of photosynthesis. They bear an axillary bud at the their middle, from which flowers develop. Examples include; Ruscus, and some Asparagus species.

 No mention of the term "Phyllode"...yet.

Now I'm sure I understand the definitions provided, however, I'm beginning to seriously question the validity of those definitions.
Apparently, these terms aren't documented very well, and after two hours of constant Googling, I arrived at:

Phylloclade (From the Wikipedia page of the same name)
Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors. [Examples provided]: Ruscus, Phyllanthus and some Asparagus species.
Cladophyll (From the Wikipedia page for "Petiole")
In some plants, the petioles are flattened and widened, to become phyllodes or phyllodia, or cladophylls and the true leaves may be reduced or absent. Thus, the phyllode comes to serve the functions of the leaf. [Examples provided]: Some Acacia species.

This is annoying, seriously.
According to the definitions provided by my teacher, we're dealing with something called a "Phylloclade" and something else called a "Cladophyll" (= "Cladode"). They don't mention the term "Phyllode", though.
Based on the Wikipedia definitions, however, we're dealing with something called a "Phylloclade (= "Cladode", if you ignore minor d̶i̶s̶r̶e̶p̶a̶n̶c̶i̶e̶s̶  differences in their definitions, which are mentioned later on in the Wikipedia article), and something else called a "Cladophyll" (= "Phyllode")

My questions:
1) What are the correct definitions of the terms "Phylloclade", "Phyllode", "Cladophyll" and "Cladode"?
2) Are the examples (provided in my notes and the Wikipedia articles) actually relevant/correct? For example: Does Ruscus possess  Phylloclades (as suggested by the Wikipedia article) or does it possess Cladophylls (as suggested by my teacher)?
3) Building on question (1): Does "Phylloclade" = "Cladode", and "Cladophyll" = "Phyllode"?

there seems to be a discrepancy in the term cladophyll in thiswebsite it is a modified leaf but in thiswebsite it is a modified stem.

But my high school level textbook however claims cladophyll and cladode to be synonymous so it's a stem.. but the wiki page definitely says it's a leaf modification. This is ambiguous!

Apart from the discrepancy of the cladophyll term I can say that both your teacher and the wiki page are correct.
If you read the Wiki page carefully it states that

Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors.

(As you have also quoted)
This is simple because both phylloclades and cladodes are stem modification for photosynthesis and xerophytic adaptation as well. So in this context they are interchangeable
Also if you have further read the article it states why the terms are interchangeable and why not. The different levels of definition are given:

Definitions of the terms "phylloclade" and "cladode" vary. All agree that they are flattened structures that are photosynthetic and resemble leaf-like branches.

one definition, phylloclades are a subset of cladodes, namely those that greatly resemble or perform the function of leaves,[2] as in Butcher's broom (Ruscus aculeatus) as well as Phyllanthus and some Asparagus species.

The definition given by your teacher can be interpreted by these two definitions stated in the Wiki page:

By an alternative definition, cladodes are distinguished by their limited growth and that they involve only one or two internodes.[3] By this definition, some of the most leaf-like structures are cladodes, rather than phylloclades. By that definition, Phyllanthus has phylloclades, but Ruscus and Asparagus have cladodes.

Another definition uses "phylloclade" to refer a portion of a leaf-like stem or branch with multiple nodes and internodes, and "cladode" for a single internode of a phylloclade.

But phyllode is a leaf modification, specifically a modification of the petiole for photosynthesis and a xerophytic adaptation to some extent. (Source is the Wiki page itself)
So to conclude

phyllode is completely different from phylloclade and cladodes.
Taking the type of morphology of the plant into consideration and the definition used, phylloclade and cladodes may be used interchangeably or may not be.

I will write an update if I find an answer to the discrepancy part

Just Remember the two main ; Phylloclade is a STEM modification for desert like area in which the stem becomes broad and fattened (in opuntia) or cylindrical(in euphorbia) !!
Phyllode is a LEAF modification and found in Australian Acasia in which the PETIOLE becomes a little braod and start performing photosynthesis!!
More key differences can be found on here https://www.differencebtw.com/difference-between-phyllode-and-phylloclade/

source: Stack Exchange

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

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

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Does the Histogen Theory apply to plant roots as well as stems?
My school textbook briefly mentions a certain "Histogen Theory" (von Hanstein) of plant growth/development. However, I can't find any authoritative source on this matter online.
According to my book, as well as this site, the Histogen Theory is only used to model the development of the shoot (stem) apex.
But according to the definition on Merriam-Webster, the Histogen Theory is applicable to both the shoot and root systems.

Question:
Is the Histogen Theory applicable to only shoot apices (as some sources suggest), or does it instead, apply to both shoot and root apices?

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


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Why do birds flap/shake their wings?
Here is a video that will show the behaviour I'm interested (see between 12:30 and 12:32).
I want to know if this behaviour has a name and why birds are doing this. I observed this many times, with offsprings getting fed, females and males adults. I'm curious about studies that looked at that behaviour.

I'm not enough of an ornithologist to answer this, but I'm pretty sure this is a begging behaviour. Using that term should get you somewhere searching for studies. The 2 seconds in your video isn't the most clear example, but here is more: https://www.youtube.com/watch?v=dhNOLL6CZog


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Is narrow sense heritability heritable?
I was wondering if narrow sense heritability $(h^2 = \frac{V_A}{V_p})$ was heritable itself. $(h^{2'} = \frac{V_A}{V_{h^2}})$

Would you explain what gave you this idea?

I would recommend looking into phenotypic robustness, which is to some degree heritable: https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1003041

Yes, it is, but you'd have to define heritability as heritability for a certain phenotype.

Heritability of heritability
Heritability is a property of a population (see here for more info), not of an individual. One can only calculate heritability for a trait if this trait can take a value for every given individual because you need variance among those individuals (as it is made clear from your equations). In other words, the trait you want to calculate the heritability from has to vary from individual to individual.
As we are looking for the heritability of heritability, then heritability would need to be defined at the individual level in order to calculate its heritability. But heritability is not defined at the individual level.
It makes no sense to talk about the heritability of heritability. Just like it makes no sense to talk about the heritability of the fitness variance or heritability of the species geographic range.
Phylogenetic signal for heritability
You might be interested of whether related lineages tend to share similar heritability (for a specific chosen trait). I do not know of any study on the subject, but it seems likely that related species are more likely to experience similar population size and structure and similar selective pressure on a given trait than more distantly related lineages. Per consequence, I would expect that heritability shows a phylogenetic signal. It would be wrong to say that heritability is heritable though.


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Majority rule definition
In this book, they talk about the majority rule.

Majority rule, which retain s the edges present in more than 50% of the trees.

They used that rule also in this article (Grant, P. R., and B. R. Grant. 2010. Conspecific versus heterospecific gene exchange between populations of Darwin's finches. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 365:1065–1076.)

We applied the majority rule (p . 0.500) to assign individuals to
  groups.

This was when using the software STRUCTURE.
I haven't found a convincing definition of the "majority rule" except definition in politics.
So what is the "majority rule" and how is it applied?

Majority rule is a binary decision rule that attributes an individual a category or rank based on the majority. I think you would get a fairly comprehensive answer if you asked this on stats.stackexchange.com

There's also an interesting example of judges voting for skaters here, but again it doesn't provide a clear definition (pg 288)


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What are the 2 general systems to understand the whole natural world?
In Graham Bell's book Selection, it's written:

To some it may be a cause of regret that the natural world cannot be understood in terms of a single set of rules and laws, but at least, so far as we know, the whole of the natural world can be understood in terms of just two general systems, and no more. This book is an account of one of these, in the context of biological systems. It is an account of the Second Science

The first system or process is Selection. What is the second?

I wonder if it might be genetic drift?

The categorization of the entire of knowledge regarding the natural world is sexy but the categories aren't necessarily natural (wiki > natural category). 99.999% of scientists (me included even if I am an evolutionary biologist) would disagree to consider the the process of selection would hold half of the knowledge we have about the natural world. It does not even hold half of our knowledge in evolutionary biology!

In any case, whether his saying makes sense (or even whether the question of what he says) is a matter of opinion and is therefore off-topic.

If you are interested the philosophical discussion of how to divide our knowledge about the natural world, you can give it a try on Philosophy.SE (once you figured what the second general system is) Or you could try to chat about it with Graham Bell directly over a coffee as you both work in the same University!

@Remi.b thanks for your comments. While you are there, you could ask what Dolph thinks about it? :D I still think that this is a legit question and that it could be interesting to discuss. I guess that saying it's a general question about biology or philosophical question is an opinion too. Maybe if the question is: what are the 2 general systems to understand the natural world in biology might be more biology related? What's your advice on how to edit that question so that it fits, in your opinion, into this forum?

@M.Beausoleil As a rule, questions that evoke discussion aren't good SE questions. The point is to produce questions that have an answer that can be accepted as the best answer out of fact and presentation, not out of rhetoric.

On reading the rest of that passage via google books I think you and others are simply interpreting it wrong. He isn't saying Selection is one of the two ways to understand the world he is saying that one approach is to reduce to basic principles, like physics and chemistry, and the other is that this isn't possible. He is saying his book is one example of an attempt to understand something that cannot be reduced to basic principles alone.


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Under what category should myosin come?
Are myosin microfilaments or intermediate filaments? Or are they simply motor proteins? Under which category should I put them? I am highly confused.

Myosin are motor proteins. Microfilaments (AKA actin filaments) are the tracks for Myosin. Filaments of different sizes are the structural components of cells, giving them their shape, rigidity, etc., as well as providing an intracellular network for transport. Myosin walk along these filaments.
In myocytes (muscle cells), myosin pulls actin filaments towards one another.

Picture from here: https://www.ncbi.nlm.nih.gov/books/NBK9961/

but in muscle cells?

@JM97 Please see edit.


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What is A in IgA?
What is the significance of letter A in immunoglobulinA?
What are the significance of other letters D, M , G, E in diffeternt types of antibodies?

The letter suffix in the name or abbreviation of an immunoglobulin specifies which type of "heavy chain" the immunoglobin contains. The heavy chain is the large polypeptide (amino acid chain) found in the antibody.  In mammals there are five different classes or types of heavy chains, and these types are given Greek letters to differentiate them.
As Wikipedia says,

The different suffixes of the antibody isotypes denote the different
  types of heavy chains the antibody contains, with each heavy chain
  class named alphabetically: α, γ, δ, ε, and μ. This gives rise to IgA,
  IgG, IgD, IgE, and IgM, respectively.

Thus the Ig suffix letter is the Roman letter corresponding to the equivalent Greek letter of the heavy chain that Ig contains.

Does the heavy chain has name A or it's an abbreviation?

For igA, the heavy chain is of type α (Greek letter alpha, not Roman A).

@mgkrebbs whoever named these proteins named the chains with similar greek letters for compatibility. I don't think they were named based on the chains they have. See the linked post. I think the answer there explains the possible origin of these names.


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Interleukin 6 class cytokines
Wikipedia says:

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation.

So does this means that il6=LIF ? or does it implies that both il6 and LIF belong to some common class of cytokines?  If latter is true then what is the name of that class?

From the interleukin wikipedia page for IL6 :

number of other cytokines may be grouped with IL6 on the basis of sequence    similarity.[21][22][23] These include granulocyte colony-stimulating factor (GCSF) and myelomonocytic growth factor (MGF)

from the Leukemia inhibitory factor wikipedia page:

LIF derives its name from its ability to induce the terminal
  differentiation of myeloid leukemic cells, thus preventing their
  continued growth.

From this we can suggest that LIF is grouped with the IL6 because of its action on myeloid leukemic cells and specifically on their growth (MGF).


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Anti malarial drugs and g6pd deficiency
Why does antimalarial drugs causes hemolysis in g6pd deficiency patients?
I know that g6pd protects the cell from oxidative stress by maintaining glutathione in reduced state but how does the antimalarial drugs cause the deficiency of gsh? I came across this(https://malariaworld.org/blog/hemolytic-anemia-and-antimalarials) site and it says:

The antimalarial activity of quinine and compounds vicine and convicine present in broad beans eventually follow the same path. In the gastrointestinal tract they are hydrolyzed to form unstable pyrimidine aglycones. They reduce red blood cell GSH and generate hydrogen peroxides and free radical species.

I highly doubt the last line, how does gsh produced not prevent the cell from hemolysis?

Antimalarials, fever, age (of the RBC), other drugs, and a host of other things increase oxidative stress in RBCs (which results in the production of H2O2.)
The line you point out as a problem is a bit confusing, but it is entirely correct. It helps to keep in mind that 'glutathione' exists in two forms in the cell: glutathione disulfide (GSSG) and glutathione (GSH). GSH is the reduced form. So a reduction in GSH (the reduced form) does lead to an increase of H2O2.
Another way to say it is that in the absence of G6PD, the amount of reduced glutathione is decreased.
Glucose is used by RBC's as food, and G6PD is needed to metabolize it. G6PD reduces a molecule of NADP to NADPH + H+, which then reduces glutathione disulfide into GSH (reduced glutathione). That molecule is used in the reduction of H2O2 to H2O.

If there is a deficiency of G6PH, there will not be enough NADPH to reduce GSSG, leading to decreased levels of GSH; H2O2 levels rise, and oxidative damage to proteins in the RBC occurs.

Glutathione metabolism consists, in large part, of its oxidation to the disulfide and recycling to the reduced form by the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) by mediation of glutathione reductase (Figure 1⇓). Reduced glutathione is important in the detoxification of free radicals. In normal cells, NADPH is regenerated by G6PD during oxidative stress. Impairment of this step prevents reduced glutathione recycling, exposing the cell to oxidative damage. Alternative pathways to G6PD-dependent NADPH production exist in most human cells but not in erythrocytes, and the lack of protein synthetic machinery deprives the erythrocyte of the opportunity to replace enzyme that has been lost. For these reasons, these cells are uniquely vulnerable to oxidative stress in G6PD deficiency.

These damaged proteins bind to the red cell membrane, which is then processed in the spleen; the spleen removes the damaged part of the RBC membrane. A few passes of this, and the RBC can no longer maintain the integrity of its cell membrane, and it breaks up (hemolysis).
Glucose-6-Phosphate Dehydrogenase Deficiency and Antimalarial Drug Development

Oh! Reduce= decrease, I thought reduce means reduction ( as in redux reactions)


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RNAse activity review
I was searching for any review unravelling the structure-function motifs responsible for RNAse activity. Or at least a well-composed review of RNAse superfamilies that are described nowadays (with linkage to their functional activity). My PubMed search performed didn't give any valuable results for that.
Any specialists to comment?
Thanks in advance!

Not a specialist but was wondering whether your interest and expectation was motifs related to catalysis or to substrate specificity.

@David I'd rather say both. But mainly focusing on the catalytic sites.

I did a few searches, just for fun, but all I came up with was:

Yuhong Zuo and Murray P. Deutscher "Exoribonuclease superfamilies: structural analysis and phylogenetic distribution"
  (2001) Nucl. Acids Res. 29 (5): 1017-1026. doi: 10.1093/nar/29.5.1017

Not very recent, but it's open access. It might be possible to search for more recent papers that have cited this. Although I haven't tried it myself, I found suggestions for doing this at https://www.bc.edu/libraries/help/howdoi/howto/pubcitation.html.


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Regarding cancer cells and telomeres
If cancer cells have telomeres are they different than the telomeres in non-cancerous cells? Would cancer cell telomeres be somehow 'set-up' to function almost indefinitely; in other words are 'they' very 'robust' or 'durable'? If these cancer cell telomeres are 'durable could their functioning cause any apoptosis mechanisms to 'shut down'?

In cancer cells, the telomerase is not "formed" but activated, mainly due to an amplification and a gain of copy of the 5p chromosome arm, containing the gene coding for TERT. For example, a very common way to immortalize primary cells to establish a cell line is to stably express TERT.
Shortened telomeres initiates DNA damage response pathways, resulting in the activation of ATM and ATR, and downstream kinases CHK1 and CHK2, and phosphorylation of p53. Once activated, p53 upregulates genes that mediate cellular senescence and/or apoptosis.

Telomerase is activated in a cancer cell, it is not formed. In a 'regular' non-cancerous cell is telomerase 'formed' and if so is the 'activated' telomerase in a cancer cell different than the 'formed' telomerase in a non-cancerous cell. Different maybe in chemical make-up or 'amounts used' ?

If telomerase is not formed but activated is it 'within' a cancer cell but 'dormant'? Does telomerase promote the formation and/or repair of telomeres?

Are there any natural substances that can be injested that promote the formation or activation of telomerase?


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Regarding cellular self-destruction
I heard and read telomere 'health' or 'length' ( if that's right ) has alot to do with cell 'health'. If telomere 'abilities' are 'restored' to a 'healthier' status then the cell it is in functions as though it were 'younger'.  I was wondering since cancer cells grow without limit and 'older' cells or unstable cells grow with less ferver do cancer cells have functioning telomeres within them and would they somehow be alot more 'robust' then telomeres in normal cells? If this is true could telomeres from cancer cells somehow revitalize the telomeres in normal cells?

Do cancer cells have telomeres? Since cancer cells grow unceasingly would their telomeres be 'extra' robust?

You can edit your question when you want to change it. There is no need to do this in the comments.

Telomeres are at the end of the chromosomes and get shorter with every cell division, since the lagging strand is missing a start point for the DNA polymerase. This limits the number of cell divisions to 40 to 60 before the cells go into senescence and stop dividing (they are not dying at this point). This phenomenon is called the "Hayflick limit".
Cell populations which need to divide more often or cells which need to maintain a long telomer status (stem cells) because they give rise to other cell populations, have an enzyme called telomerase which has it's own (RNA) template and can enlarge the length of the telomere. See the figure how this works (from the Wikipedia article on Telomerase):

To answer your question: Younger cells have longer telomeres (compared to older cells). Usually cells stop dividing, when their telomeres get too short to avoid chromosomal damage, due to the progressive shortening of the chromosomes. In cancer cells the pathways controlling this (for example p53 and the retinoblastoma pathway) are often mutated, so that the cells divide forever. This leads to chromosomal instability, further mutations and chromosomal disarrangements, which can cause real havoc.
It also happens for some cancers that they manage to reactivate their telomerase, thus keeping their telomers at a healthy length and preventing chromosomal damage. By this activation they get around reaching the Hayflick limit for the maximum number of cell divisions and are truly capable of living forever. The famous HeLA cell line for example is telomerase positive.
The activity of the telomerase in one cell has no effect on the neighboring cells.

In some types of cancer cells, an enzyme called telomerase can actually rebuild the telomeres, making a cell appear "younger" than it actually is and preventing it from senescing (reaches a point where it stops dividing).

Telomerase, a eukaryotic ribonucleoprotein (RNP) complex, helps to stabilize telomere length in human stem cells, reproductive cells and cancer cellsby adding TTAGGG repeats onto the telomeres using its intrinsic RNA as a template for reverse transcription.

Shay et al. 2001
This Myerson review from 2000, Role of Telomerase in Normal and Cancer Cells,
 provides a good overview of telomeres in normal and cancerous cells.
It's not that telomeres (shown in image below) are more robust in cancer cells, they are actually rebuilt by the telomerase enzyme.

(Socratic)

Is senescence related to apoptosis in some way?

Do stem cells have a special type of telomere?


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Regarding benign tumors and what 'stops' them
Benign tumors can grow to dangerous size yet are they capable of metastisizing ; if not what stops this? Also with a benign tumor if you call its cells 'near' its edges its tumor 'cell wall' I was wondering if the cells in its Tumor Cell Wall still have apoptosis mechanisms in them that function?

If tumors metastasize, they are not benign.

Afaik they still have apoptosis, but they slowly develop a resistance to signals which can trigger it. That's why they need stronger signals to stop proliferating than normal cells .

How do benign tumors develop a resistance to signals that can trigger apoptosis? If a benign tumor has stopped growing would this mean it has some active apoptosis mechanisms?


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Cells with no apoptosis mechanism and their 'byproducts'
If a culture or sample of cells is such they all have no apoptosis mechanisms yet they have not been at present determined to be cancerous ; given such a cell culture is there a way to determine by their byproducts or how they signal themselves or other cells that they have no 'working' apoptosis mechanisms?

I am not sure, if I understand your question. You want to know if (or how) cells with non-functional apoptosis (however this happened) know themselves that their apoptosis is no working? And how they communicate this to other cells?

If cells with non-functioning apoptosis mechanisms can be detected by some type of test this would indicate a possible tumor as tumor cells don't have functioning apoptosis mechanisms. ( at least that's what somebody else said on this exchange)

Is there a way to test a cell or cell culture in some way simpler than analysing their genome to determine if they have actively working apoptosis mechanisms? Does a cell with a working apoptosis mechanism 'produce' or 'give off' certain signals or chemical signatures that can be detected by some 'test'?

I am not aware of any. Since apoptosis relies on signalling towards it, you can only try to trigger it and see what the outcome is. Probably nothing, that we want to try on a large scale.

Could a non-harmful virus or bacteria that normal cells could survive but would effect a cell with no apoptosis mechanism in a detectable way?

Given a specific type of cell are there certain situations like a biochemical event occuring near or adjacent to the cell that would 'normally' cause the cell to self-destruct if its apoptosis mechanisms were working. So if this biochemical event or process was artificially 'made' to occur near or at the cell's location and it didn't self-destruct it would indicate its apoptosis mechanisms were not functioning. Is this correct?

I think so, yes.

Could such an artificially induced process be used to test if certain cells or tissues are cancerous?

Can we stop discussing this in the comments and you make it a new question?


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About artificially induced processes that would normally cause a cell to self-destruct
Are there certain biochemical processes that would normally cause a cell to self-destruct but if the cell being tested has apoptosis mechanisms that have malfunctioned or been 'turned off' the cell will not 'malfunction' because of the induced process ? Are there such biochemical processes that could indirectly indicate which cells have no functioning apoptosis mechanisms? If so would this be a possible test for cancerous cells?

In some cases yes — when there is a mutation in apoptotic regulators such as Bcl2 family of proteins. In other cases it is difficult to identify and only identification is that those cells are growing rapidly; in other words failure to undergo apoptosis is not the cause but the effect of the cancerous transformation (as in case of p53, Ras, Myc mutations etc).


text:
Concerning Apoptosis
What if cellular growth and repair is 'forced' to occur repeatedly in a region where it wouldn't normally happen , if the biological area was 'healthier'. Could this more aggressive cellular growth and repair cause any apoptosis mechanisms to shut down permanently?

One long standing hypothesis of cancer formation is that it originates in a 'wound that never heals'.  I was about to add that there is little hard evidence for wounding as a significant cause of cancers but Google found this fascinating report on Marjolin's Ulcers
 which I had never heard of.   Whether it was the wound or a comorbid virus or something else.....
You may also want to search the current thinking of how a chemically inert 'irritant' - an asbestos fibre - can cause mesothelioma.

The definition of a tumor is a population of cells that:

Divides out-of-control

2.. Does not exhibit apoptosis
3.. Does not differentiate
Additionally the two-hit hypothesis states that at least two genes need to be involved.
There are many genes,  predominantly involved in the regulation of the cell cycle, that when their function is disrupted the cell exhibit uncontrolled replication. Attenuated expression or constitutive activation of the genes does not necessarily affect apoptosis. However, and to give you the quick answer – it depends on the gene involved. Some genes are involved both physiologies. Check out the protein AKT.


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problem with natural selection
I fail to see how natural selection can build any kind of new functionality.
New functionality in a design requires sacrificing a complex series of meanwhile useless steps before the new functionality works and becomes advantageous.
For example, if I want to upgrade a stationary chair to a wheelchair, there are many intermediate steps that must be done (which are not advantageous) before the added functionality becomes advantageous.
If a human being sits there and tries to intelligently assemble the wheelchair in such a way that it will be advantageous at each step, he will not be able to do it. it just doesn't work like this.
Can someone fill me in as to how this works and whether there have been experiments that demonstrate this, for example, having someone assemble a simple functional design with the limitation that every few step adds advantageous functionality.

This is a common misconception of natural selection: Not everything which appears needs to be new (there are szenarios in which other organs change) and not every step needs to be advantageous. It is enough if it causes no negative effects.

@Chris let's say for example sonar in bat navigation. how many changes are needed in coordination b4 the functionality becomes advantageous?

have you ever tried to build a chair like this? it just doesn't work.

Evolution by natural selection does not require that every intermediate step produces some kind of useful functionality - you are assuming some kind of cost to fitness imposed by intermediate steps which is great enough for selection to be effective. Evolution via natural selection leads to change because deleterious changes are selected against, and advantageous ones are selected for - however, selection is not the only force affecting evolution and not all changes to traits have fitness consequences (or strong ones at least).

There are homo sapiens who can guide themselves with echo location.  How can you argue that it's impossible to evolve when we humans already have it, without requiring specialized adaptations?

@Chris if the intermediate step is neutral (neither advantageous nor disadvantageous), then you no longer have the pseudo-intelligence of natural selection helping you and it becomes more or less random.

Mutations are random.

@Chris right. so you dont have the help of any pseudo-intelligence and cannot expect a complex intelligent design to emerge from this process.

Why do you expect that there is some help necessary? Evolution simply happens. And it takes time - a lot of time.

This is fundamentally a teleological argument.
The error is in assuming that the intermediate steps were a precursor to the present functionality. For example, interpreting an 'intermediate' bird wing as a fully functional wing, intended for flight. In fact, there is no prerequisite that present characteristics or functions have evolved from intermediates that were intended FOR that characteristic or function.

what you say is correct, but some things are totally useless without a combined and coordinated functionality and they are irreducibly complex. bat sonar for example requires sending out sound waves, a biological transducer, a signal processing etc. before there will be any useful functionality from this. what intermediate steps could possibly be useful here?

You CAN get useful functionality from systems before they are in their modern configurations.  The structure of the eye, the bombardier beetle; intermediates CAN have uses.  How can you hope to prove that every single element of every single complicated system didn't?

@swbarnes2 true, but don't you agree that for some systems there is a minimum complexity before they can be of any advantageous functionality. and that minimum is in fact enormously complex.

There are so many wrong-headed premises here, one hardly knows where to start.
First of all, natural selection is the process of changing the frequency of alleles in a population, mutation is what creates new ones.
Second, just because you can't think of every intermediate step doesn't mean it's impossible.
Third, you are assuming that natural selection is so uber powerful that every single stop must be beneficial, and there's no evidence that that's the case.  Evolution preserves lots of neutral and nearly neutral mutations.
Fourth, you are assuming that each step in some kind of path way can only possibly be used for the pathway it's in today.  That's not true either.
If you want somewhere to start in the literature, try some papers by Lenski:
http://www.ncbi.nlm.nih.gov/pubmed/22992527
http://www.ncbi.nlm.nih.gov/pubmed/23918358
If you really want to argue that it's impossible for, say, E.coli to evolve the ability to metabolize citrate, because it's too hard to get from here to there, you need to address the empirical fact that these bacteria did just that.

perhaps E.coli had this functionality built in to the dna. I have seen papers which claim the organism has the ability to modify the dna on its own.

If the functionality was pre-built, why don't all E.coli have it?  Did you read the paper, or even the abstracts?  Modify its DNA with intent?  I'm sorry, but there is no evidence of that.  I don't see what the point of asking questions is if you are going to make up facts to bolster your per-determined conclusions.

pre-determined conclusions? I follow the truth wherever it leads me. for E.coli the process of how it evolved this ability has not been proven that it was through random mutations, correct? We just know it has an ability the parent did not have. but it could well be that there is some kind of pre-built mechanism in the E.Coli for making various "intelligent" variations of daughter cells and these variations.

regaring the E-coli, I found this which plays it down "but it’s doubtful that Lenski’s E. coli have achieved any more than two mutations, so have not even reached Behe’s edge, let alone progressed on the path to elephants or crocodiles". from http://creation.com/bacteria-evolving-in-the-lab-lenski-citrate-digesting-e-coli  any thoughts? thanks for your patience

e-coli already had some ability to metabolize citrate


text:
Why high quality DNA should be between 10 and 20 kb?
On this website, they are saying that, when using a gel electrophoresis to assess DNA quality, :

High quality genomic DNA should give a major band of 10-20 kb on the
  gel.

Why is that so? I thought it could be because of the size of the chromosomes, but chromosome X in humans is 156,040,895 bp, which is far from 10-20kb. So why is that threshold of 10-20kb? Is DNA breaking usually in chunks with that size?

The website specifically talks about DNA samples intended for sequencing. The DNA in these samples was/is/will be extracted from cells and this extraction procedure leads to fragmentation (breaking into chunks). Since the expected average chunk length will greatly depend on the extraction process, I guess its reasonable to assume that 10-20kb can be expected from the most common protocols.
Much larger or much smaller fragments will also cause problems with the sequencing. (This is again method dependent, but generally true with varying fragments sizes that can be sequenced with the different available methods)


text:
How to get an adaptive landscape from a fitness function?
In Schluter (2000), it is mentioned that one can convert a fitness function (see image (a)) to an adaptive landscape (see (b) and (c)). The key is to calculate the mean phenotype of a population and calculate the mean fitness value for that population (based on the fitness of each individuals). The shaded area in (a) under the 2 peaks curve is a population distribution of phenotype z. But like the image shows, how can one draw the adaptive landscape if you have only one population?
I get that the fitness landscape can be calculated with splines and the results plotted as the predicted values of the spline analysis. But how can one generate an adaptive landscape? In the lab, it would be to generate new populations with the whole range of phenotypes and get the mean fitness of the population. But for organisms that sampled in the wild, it is not possible to get the full range of phenotypes and thus calculate different mean fitness across the whole range of phenotypes. How to get a adaptive landscape with phenotypes (and possibly from populations found in the wild?).

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


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Why darwins, a measure of evolutionary change, is calculated on the log scale?
In a famous paper, Haldane is describing the idea of rate of changes in "darwins". Here below is the excerpt where he introduces the math about the concept.
Haldane, J. B. S. 1949. Suggestions as to quantitative measurement of rates of evolution. Evolution 3:51–56.

Now suppose that in time $t$ the mean length of a structure has
  increased from $x_1$ cm to $x_2$ cm, the mean value of the
  proportional rate of change
$\frac{1}{x}\frac{dx}{dt}$ or $\frac{d}{dt} (\text{log}_ex)$ is
$\frac{\text{log}_ex_2-\text{log}_ex_1}{t}$

I don't understand why he is arguing that the difference should be logged. Why can't you just use:
$\frac{x_2-x_1}{t}$?
What justifies this line below?

$\frac{1}{x}\frac{dx}{dt}$ or $\frac{d}{dt} (\text{log}_ex)$

Why not just using:
$x\frac{d}{dt}$?

The reason why there is a logarithm in the mean value is because the original equation has the form (1/x)dx/dt. The author wanted to remove the (1/x) factor by taking the antiderivative which is log(e)x and absorbing it into the dx symbol so they could rewrite dy/dt as Δy/Δt. Unless your question is why is there a (1/x) there in the first place?

If you have an answer for "why is there a (1/x)?" I'll take it! Is it because it is how you write a geometric mean with a derivative?

I don't think so. This isn't my field of study, but if r = growth rate = (1/x)dx/dt and if you rearrange that formula as rx=dx/dt then it takes on the form of the population growth formula x=x0e^rt maybe that helps?

There are several purposes for log transformations, but one of the most common that occurs in biology is when changes are relative aka multiplicative. See for example this answer from CrossValidated.
If I told you that one lizard has a tail 5 cm longer than another lizard, that doesn't actually tell you much about how different it is. If the first lizard had a tail 1 cm long, that's a pretty massive difference! If the first lizard had a tail that was 100 cm long, the 5 cm difference is pretty minor.
Taking the log shows this:
Big (relative) change:
$log_e(6) - log_e(1) = 1.8$
$6 - 1 = 5$
Small (relative) change:
$log_e(105) - log_e(100) = 0.049$
$105 - 100 = 5$
The simple differences are both 5, but the log differences show you a big change versus a small one.
Logarithms are also more convenient than ratios for rates of change because they are easy to manipulate to predict change over any time interval assuming a constant relative change over time.
Taking the 6cm vs 1cm example above, lets say we want to guess the change when only half of the time is elapsed. If we take half of 1.8 = 0.9 and solve the following for X:
$log_e(X) - log_e(1) = 0.9$
$X \approx 2.5$
So we'd expect after only half the time, the length would have been about 2.5 cm.
$2.5/1 \approx 6/2.5$ meaning that the relative change for each subdivision of time is equal.
You could try this for any dt, too, and plot out X as a function of time with any dt when you use logarithms. You can't do this directly with a ratio like "6/1" because you can't directly subdivide that "6/1" into smaller time intervals (trying to do so would take you into the world of logarithms again :) ).
test <- function(time,x1,x2) {
  out = exp(log(x1)+(log(x2)-log(x1))*time)
  return(out) }
time = seq(0,2,0.01)
plot(time,test(time,1,6),
     xlab = "Time",
     ylab = "X",
     type = "l",
     main = "Change in morphology through time")
points(x = 1,
       y = 6,
       pch = 21,
       bg = "black",
       col = "black")

Ultimately, what matters most is what thing you are measuring and how you want to interpret a particular type of change. For things like lengths or average counts, often a relative multiplicative change makes the most sense.

I did tested your example. Here is the script below in R.
y = x*2

(y)-(x)
log(y)-log(x)
test <- function(time,x) {
  out = exp(0.6931472/time+log(x))
  return(out)
}
plot(test(1:10,25),xlab = "Time", ylab = "X")``` It shows a reduction in X as time goes by, in an exponential manner. Is that what you were trying to say?

@M.Beausoleil Maybe something more like `test <- function(time,x1,x2) {
out = exp(log(x1)+(log(x2)-log(x1))*time)
}
time = seq(0,2,0.01)
plot(time,test(time,25,50),xlab = "Time", ylab = "X")` Starts at 25 at t=0, increases to 50 by t=1 (that is, the original time difference between x1 and x2), continues to increase up to t=2 at the same growth rate (that is, doubling every 1 dt). Function is the same as yours but I think its easier to interpret this time axis.

Another related point: plotting in log scale shows reductions in a better way. Usually, if the reduction appears to be smaller than increases for the same absolute magnitude of fold change. With log transformed data, your reductions will just be negative but the magnitude will not appear smaller.

I would also want to add that although log transformed data is easier for representation of relative changes (or in cases where the data span several orders of magnitude), it is difficult to say if effects of traits on fitness would be dependent on absolute differences or relative differences. For e.g. if the trait is growth rate: a small linear increase can magnify into a high fold change after several rounds of division.

This might help also: Why is it that natural log changes are percentage changes? What is about logs that makes this so?: https://stats.stackexchange.com/questions/244199/why-is-it-that-natural-log-changes-are-percentage-changes-what-is-about-logs-th

I don't know why this doesn't make sense, but when you look at it on the "linear" scale test2 <- function(time,x1,x2) {    out = x1+(x2-x1)*time   return(out) }  you get  test2(0,1,6);test2(0.5,1,6);test2(1,1,6)
test2(0.5,1,6)/test2(0,1,6);test2(1,1,6)/test2(0.5,1,6) . For the first time interval the rate approximately doubled  3.5 compared to the rate for the second interval of time 1.714286. Why is it the case? Basically, why is the "relative change for each subdivision of time is equal" not the same in the linear scale?

@M.Beausoleil What's the confusion? For the log scale, we've said the proportional change for a unit time is constant: increasing 6 fold for every 1 unit time (so from 1 to 6 and then from 6 to 36). For a linear scale, the absolute change is constant: +5 for every unit time. So 1+2.5 at time 0.5, 1+5 at time 1, 1+10 at time 2. If we want the relative change to be constant, we need to use a log scale (that's the answer to your original question about why Haldane is using a log). As WYSIWYG mentioned in a comment and me in my last paragraph, that's not always what you want, but often it is.


text:
What does endochorous dispersers means?
In an article (Guerrero and Tye, 2009) it talks about endochorous dispersers.
Guerrero, A. M., and A. Tye. 2009. Darwin's Finches as Seed Predators and Dispersers. The Wilson Journal of Ornithology 121:752–764.

The highest proportions of feces containing viable seeds were of Small
  Ground Finch (G. fuliginosa) and the ‘‘insectivorous’’ species
  Woodpecker Finch (Camarhynchus pallidus) and Warbler Finch (Certhidea
  olivacea). These two may be more important endochorous dispersers than
  other species that eat more fruit but are better seed predators.
  Intact seeds were found in 23% of fecal samples; 50% of the samples
  with intact seeds had viable seeds.

I've looked on google and found nothing...
Do you know what that means?
It seems it relates to mast-fruiting plant species.

I found the definition here, which is a cool package in R:

animal - all vertebrate dispersed seeds, without distinction between
  attached(epichorous) and ingested (endochorous) dispersal of seeds


text:
Is there a GPS super tiny for passerine birds?
I wonder if there is a really tiny GPS device that can be mounted on passerine birds (or circa 10 grams birds) without affecting their flight. This web site shows information for bat’s GPS. But it also only last for 24 hours. I wonder if there is some lightweight and long battery life about 2–5 grams. I found this also, but haven’t found if it contains a long battery life.
Is there a study on GPS tracking small birds?

The technology is not there (yet) for deployments on 10 gram birds. The limits for GPS technology are around the 50 g range, for birds. Also bear in mind that the smallest loggers are generally not capable of transmitting, so you would need to recapture the animals to retrieve your data.
As your question implies, there is a strong trade-off between device weight and battery life. There are GPS devices weighing as little as 1 g, but their lifespan is very limited (10 fixes for the 1 g device; 50 for a 1.1 g device).
As a side note: your question implies that small passerines can carry 20 - 50 % of their body mass in tracker without their flight being affected. The ethics boards I am familiar with generally limit trackers to ~ 5 % of the mass of the animal.

A quick search on Adafruit came up with this 8.5g GPS chip, but it's just the GPS, no battery and no transmitter. This solar panel might be their smallest, and might power the GPS, but also weighs 8g and likely couldn't power a transmitter. So after you add a battery and transmitter, is it ok to track how the birds crawl with 50g of stuff on their backs?


text:
Chromosome naming convention: Why are there chromosomes named "1" and "1A"?
I've been stumbling on multiple genome of birds where there is a "1A" chromosome and a "1" chromosome. For example, the zebra finch has 1A and 4A. What does that mean?
Do you have any resource about naming conventions for chromosomes and if this naming convention is specific to birds?

I would suggest looking at some of the reference genome papers. My guess is that the chromosomes are named as such based on their synteny to the chicken genome; e.g. look at Accessory Figure 3 here for your zebra finch, and note that chromsomes 1 and 4 are split in the zebra finch relative to Gallus.
The direct comparison from that paper is to an Accessory Table 1 that I can't actually find.
I would guess that in most cases it's because of a synteny comparison to some reference, in this case chicken that splits a chromosome in the new genome. For example sequences homologous to the chicken chr1 are on two finch chromosomes 1 and 1A.

This is my suspicion as well, similar to the ape chromosomes 2A and 2B.


text:
Why is the variance of the Wright-Fisher model not equal p(1-p)/(2N)?
I was looking at the properties of the Binomial probability distribution and it says that the variance is np(1-p). In population genetics, n = 2N. So I would expect to see that the variance is 2Np(1-p).
But when looking at the Wright-Fisher model, I often see that the variance is $p(1-p)/(2N)$ (see this presentation page 6).
How to derive the variance of the Wright-Fisher model to get this variance from $Prob\{X=i\}=\frac{n!}{i!(n-i)!}p^i(1-p)^{n-i}$?

The binomial variance $2N p (1-p)$ is for the number of individuals $n'$ carrying the allele in the next generation. The frequency of the allele in the next generation is $p'=n'/(2N)$, so its variance is $$\text{Var}[p'] = \text{Var}[n'/(2N)] = \text{Var}[n']/(2N)^2 = p(1-p)/(2N).$$

This is because $Var[n'] = 2Npq$ which is the variance of the binomial model $(2Np(1-p))$ Right? Because $n'$ is also coming from a binomial sampling

@M.Beausoleil: yes, exactly.


text:
Does the order of amino acids matter in making up a protein?
For instance, if a protein is made of 2 amino acids, that is, AB, would the same protein form if the order of combination of amino acids become BA? If yes, would the behavior of interaction of that protein change? For instance, if AB interacted with another protein XY, would BA interact with XY in the same way?

See some discussion of this here: https://biology.stackexchange.com/questions/88137/why-does-protein-folding-not-depend-on-the-order-in-which-it-is-synthesized

Yes.
The 'order' of amino acids is the protein sequence, also known as the primary structure. A peptide (short protein) with sequence XYXYXYXYX is very different from XXXXXXXYYYYYYY.
Your example is a bit trickier, since it seems like AB should be roughly equal to BA. However, each amino acid has two ends - the amino and carboxyl - and so a dipeptide like this is more like NH2-A-CONH-B-COOH with a peptide bond in between.
The really tricky question is : are two sequences 'the same' if they are different by just one or two letters. In other words is AAAAAABAAAAAA different from AAAAAACAAAAAA - and this is the study of mutations of proteins.
There is a lot more to say on this topic, of course.


text:
How should I interpret for example AA result, when SNPedia only has CC/CT/TT listed?
I don't know how to properly formulate this question because I'm new to this, so please edit this if you can...
For example when I would check SNPedia for rs gene, it would have listed CC/CT/TT genes, but my result says AA, so how should I interpret this? I assume it has not been tested, but I want to know for sure, because I have encountered this numerous times already...

You'll need to learn about DNA strand orientation: https://www.snpedia.com/index.php/Orientation

Ah! Thank you! I'm just a beginner at these things. :)


text:
What are multiallelic genes?
Is there a clear detailed description for multiallelic genes? Are they simply genes that are more than two alleles?

are you talking about multiallelic traits?  if not, maybe add a citation for us to see the original usage of the term.

More than two alternative forms (alleles)of a gene in a population occupying the same locus on a chromosome or its homologue is known as multiple alleles.
Multiple alleles arise due to mutations of gene.A gene can mutate several times by producing a series of alternative expressions.Different alleles in a series show dominant-recessive relation or may show co-dominance or incomplete dominance among themselves.
In Drosophila,a large number of multiple alleles are known.One of them is the series of wing abnormality ranging in size from normal wings to no wings.The normal wing is wild type.The extreme expression with no wings I.e is just stumps is due to one allele 'vg',in homozygous condition .
For reference.
http://eagri.tnau.ac.in/eagri50/GBPR111/lec04.pdf


text:
Can a ribozyme be present on two different RNA molecules?
Suppose we have a ribozyme that consists of an 'enzyme' strand and a 'substrate' strand. (e.g. hammerhead ribozyme)
Is it possible to have the enzyme strand of the ribozyme on one RNA molecule and the substrate strand on another RNA molecule (such that it allows multiple-turnover reaction)?

Are you asking specifically for hammerhead-like ribozymes or would any ribozyme do? The spliceosome, for example, may match your description.


text:
Y-chromosome and phenotype
I have a male colleague which has a son that does not resemble its father in any degree (apart of being male). The "father" is thin, tan-skinned, brown-eyed and the "son" has blue eyes, blond and already slightly overweight boy. Their faces have no any signs of similarity.
Since, the son gets Y-chromosome from a father, it is interesting to know if the Y-chromosome possesses any phenotypical feature apart of testicular development?
I did not find any Y-gene that influences the phenotype.
So, the second part of the question: Can other 22 parental chromosomes be so "recessive" that a child will have no "any" external signs resembling its biologic father.

actually it's been noticed that when offsprings are born, they resemble the father more than the mother, it's suggested that it's sort of an assurance to the fathers that the offspring is actually theirs. But let's analyze the eye colour, since eye colour like skin colour is a multi-allelic trait, therefore black being the dominant ones and brown being the second after that, meaning it contains at least one recessive feature, the mother actually had to be recessive on the eyes to produce a blue eyed boy....P.S. I'm commenting because I cannot find references for all this atm.

The Y-chromosome only really contains genes relevant to sex determination[1], with estimates of protein-coding genes ranging from 50-450. For instance the SRY gene, also known as the testis-determining factor [2], is only found on the Y-chromosome.
Phenotypes such as eye colour are coded on the autosomes (i.e. not the sex chromosomes), and as such are determined by alleles inherited from both parents. As Koustav Pal mentions in his comment, many such traits are multi-allelic (i.e. determined by multiple regions of the genome), and are therefore more complex than first appear; eye-colour can change over time, and there are many more complexities that do not fit into the simple "blue", "brown", "green/hazel" categories [3]. This also applies to hair, so the child you mention could become more like their father as they grow older (or not!).
Because each individual posesses two alleles for each possible trait (one from their mother, one from their father - we each have two whole copies of the human genome in our cells*) a person can be a carrier for traits, such as blue eyes, whilst themselves having brown eyes. In fact the situation is so complex (>15 genes affect eye colour) that two blue-eyed parents could have a child with brown eyes [4] - the historical perspective was the brown eyes were dominant over blue eyes.
I have focussed on eye colour because it is a good case-in-point: there are clear genetic determinants and heritability, and it is more complex than the popular perception. Regarding hair (or skin) colour, single-gene mutations can cause pale skin and red hair [5], but beyond these cases the same rules seem to apply; that there are multiple genetic determinants (which means the Mendelian single-allele dominant/recessive model does not really apply) that affect the amount of eumelanin (which is dark brown) and pheomelanin (which is reddish) produced, with together combine to make the spectrum of colours we see in the population - it is not true to say that there are only blond OR brown haired people, as many people lie somewhere between [6].
This has not been an exhaustive review of these topics by any means, and there may be further evidence either way, but it seems quite clear that it is not unusual for offspring to not actually take the appearance of one or both parents. There are many traits you mention (such as build) that I don't go into detail, but there is emerging evidence that these are incredibly polygenic (caused by many small-effect genetic variants - e.g. height [7]) and as such could lead to the same phenomenon.

http://ghr.nlm.nih.gov/chromosome/Y
http://www.ncbi.nlm.nih.gov/gene/6736
http://udel.edu/~mcdonald/mytheyecolor.html
https://www.uq.edu.au/news/article/2007/02/eyes-have-it-multiple-gene-question
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3095693/
http://udel.edu/~mcdonald/mythredhair.html
http://www.nature.com/ng/journal/v46/n11/full/ng.3097.html

* well, most cells - red blood cells and gametes do not.


text:
Are there any (chemical) processes occuring inside a seed while it's in a dormant state?
If a seed were in a glass jar without a chance of germination, are there any (chemical) processes occurring inside the seed while it sits there?
My intuition tells me no since my understanding of seed dormancy tells me that dormancy serves as a delay mechanism to increase the chances of survival of the plant.
I deductively reason that dormancy prevents germination by pausing all reactions (processes) in a seed until a combination of conditions triggers the process that initiates germination.
I've done some research online but I can't find anything to support the "pausing all reactions” portion of my statement which would answer my question.

We can consider two processes that a seed might care about:
(1) Ordinary chemical reactions that just happen in the cytoplasm of the seed cells. It's very hard to stop chemistry! Even in the freezer, chemical reactions occur (slowly). This is why long-term storage of biological specimens is generally in an ultra-cold freezer (-80C). Chemical reactions could degrade DNA and proteins and prevent seed germination, so seeds take steps such as drying to reduce the chemistry going on. But, clearly this just slows down the reactions, as seeds of all types gradually lose their ability to germinate (some faster than others). Spore-forming bacteria are the most successful organisms in this regard: they drastically dehydrate the interior of the spore and surround it with a highly protective coat, and there is evidence that some can literally remain viable for millions of years.
(2) Seed metabolism: enzymatic reactions and the normal biochemistry of the cell. "Dormancy" means in part that seed cells shut down processes like transcription and translation and minimize their metabolism. But, research suggests that the metabolic activity of seeds is not zero - among other things, there are active enzymes that are involved in repairing damage to DNA and proteins.

This is a good answer, but your answer requires references. Please [edit] it and add support for your claims.


text:
Does size matter?
As I compare the morphologic differences between mouse models and the human disease for which they are analogous, I have become interested in what difference interspecies size has on molecular function.  For example, the mouse colon has a diameter of 1 mm, the human 75mm it seems to me there should be many genetic/transcription differences between species just as a pup-tent (analogous to a mouse) requires a much different support structure than a 10 story building (analogous to a human) yet I find little about this in the literature, can someone help or show me where this has been addressed?  Thanks!

It would be useful if the title question was more revealing of what is actually being asked

The renowned biologist JBS Haldane was concerned with the problem of size and wrote about it in his essay of "On being the right size". Two situations he discusses may be of interest.
The first is that large animals are not just scaled-up versions of smaller ones. He calculates the weight-bearing ability of bones to show that the increase in cross-section of bone in a scaled-up person could not accommodate the increase in "weight per square inch". The conclusion here, I think, is that a different type of structure is required to deal with the weight of a larger animal. In the sort of molecular genetic terms that did not then exist, one would need a different program of transcription.
A second situation relates to the size of eyes and the size and number of rods and cones they contain. Here he argues that there is little intrinsic difference between the cells that make up the eyes of mice and men (this is 1926), despite the difference in number (and hence eye size). In this case the gene transcription would be expected to be similar.
He also talks about the modification of lungs and gut to provide a required increase in surface area in larger animals. This would seem similar to the case you raise. Is this more of the same or a fundamental difference? I leave it to you to decide.
The original essay is out of copyright and can be found on the web. However you might also be interested in a printed collection that includes other of Haldane’s essays as well.

@MattDMo Point taken. I've rewritten my answer entirely.

looks good! Could you include a link to the online version of the essay as well?

@MattDMo I've done that now.


text:
Genetic notations
Genetic testing revealed these two mutations (hypothetically):
IVS11+6G>A and IVS11-4G＞A
Could you please explain every part of this notation, especially "+" and "-" signs.

have you tried googling first? if not, this query yields a useful page: Nomenclature for the description of sequence variations. Quote: 88+1G>T (alternatively IVS2+1G>T) denotes the G to T substitution at nucleotide +1of intron 2, relative to the cDNA positioned between nucleotides 88 and 89

These describe mutations (SNPs) in introns.
IVS stands for intervening sequence (which is another term for intron).
The number following IVS specifies which intron the mutation occurs in (intron 1 follows exon 1, etc).
The +n or -n, where n is an integer, gives the location of the nucleotide. +n counts 3' from the preceding exon whereas -n counts 5' from the following exon. I think that the first and last nucleotide of each exon is given position 0 such that, for example, +1 refers to the first nucleotide of the intron and -1 refers to the last.
X>Y, where X and Y are nucleotides, describe what mutation has occurred.

IVS11+6G>A means a G to A transition at position +6 of intron 11
IVS11-4G＞A means a G to A transition at position -4 of intron 11


text:
Why would Aspergillus Oryzae produce lactase when no lactose is present?
Studies [1] have shown that lactase is produced by A. oryzae when grown on wheat bran and spent beer grains.

Why would A. oryzae produce lactase when these substrates have no lactose?
In [1], it's shown that A. oryzae produces more lactase when grown on wheat bran vs when grown on whey, which has lactose in it - what might explain that?
Since lactose is found in mammals and is not common elsewhere, how/why could A. oryzae have evolved the ability to produce lactase in the first place?

[1] Bailey, M. J., & Linko, M. (1990). Production of β-galactosidase by Aspergillus oryzae in submerged bioreactor cultivation. Journal of Biotechnology, 16(1-2), 57–66. doi:10.1016/0168-1656(90)90065-j

"Although beta-galactosidase is mainly produced for utilization in the hydrolysis of lactose in milk or whey, in natural systems this enzyme is also involved in the breakdown of galactan-based hemicelluloses. Wheat bran contains almost 30% hemicellulose, including considerable amounts of galactose residues (Salo and Kotilainen, 1970). Similar residues are presumably also present in spent grain (wheat). "

From the paper linked in the question.


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How can Haemophilus influenzae survive and grow alone in the human body?
Haemophilus influenzae gets its name from the fact, that it requires nutrients from blood in order to grow. More specifically, I see it mentioned that in vitro they often exhibit the pheomenon that they don't really grow in plates with blood alone. They do, however, grow when other bacteria are added that causes haemolysis (like Staphylococcus aureus).
H. influenzae is known to cause otitis media, meningitis and pneumonia. How does it get its nutrients in these places? Is there a coinfection with other bacteria that do haemolysis?


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Help with histological cell identification in colon
I have scans of a histology slide of tissue of colorectal cancer and its surrounding tissue. This slide has been stained with the typical Hematoxylin & Eosin (HE) staining then unstained and stained again with two immunehistochemical markers, one for each B- and T-Lymphocytes. Those markers are CD3 for T-cells (which appears red) and CD20 for B-cells (which appears brown). The two scans were then aligned so that it is easy to identify a lymphocyte on the immunehistochemical stain (IHC stain) and find that exact cell in the HE stain.
After looking at these scans for some time I noticed, that there was a cell type that, to me, looks indistinguishable from a lymphocyte on the HE stain but clearly expresses neither CD3 nor CD20 when referencing the IHC stain. These cells are mostly found inside colon epithelium or cancer. Below are two images (one in the HE stain and one in the IHC stain) with two example cells marked with red arrows.
My question is what type of cell this is? Could it be some sort of precursor cell or sub-class of T- or B-cells, that expresses neither CD3 nor CD20? Is it even an immune cell at all?

There are immune cells, such as monocytes, macrophages, and dendritic cells, that don't express CD3 or CD20. I'm not enough of a histology expert to identify them on this slide, though.

Monocytes are, by definition, only present within blood vessels, macrophages have a large diameter with slightly uneven borders and a large amount of cytoplasm and dendritc cells aren't found inside epithelium to my knowledge. So I'd be very surprised if it was any of these cells.


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Centrifuge after sonication
I follow a protocol to get protein from E.coli cells after sonication.
I used to grow 6 litres of large cultures and add IPTG to express the protein. I centrifuge for 10 mins at 8,000 rpm and get the pellets.
Then I do sonication and centrifuge again at 20,000 for 1 hr.
My question is: can I do the last step of centrifugation at 4000 rpm for 2 hr? The centrifuge is no longer working at high speed (20,000rpm)
Thanks

It is better to indicate centrifugation speeds in terms of g instead of RPM. We basically want to know the centrifugal force acting on the sample. The RPM required for a particular amount of centrifugal force depends on the rotor radius.

No, if you use only centrifugation to separate proteins from other parts of the (bacterial) cell, you need very high centrifugal forces. The actual speed (in rpm) you need to separate soluble proteins from the rest of the cell is mostly dependent on the rotor of the centrifuge, because both together determine the acceleration you get, which should be
in the order of at least 10,000 - 100,000 g.
If you do not have a (working) ultracentrifuge available, you could try to precipitate your proteins from the lysate, which would allow you to use a normal centrifuge to collect it. However, this won't be an option if your protein can't be properly re-folded and you need it functional.


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The threshold of Ki
Is there any threshold (Ki) between strong and week small molecule inhibitors?
When I see the (Ki) values in any published work, how can I decide if this good or bad inhibitor?

K$_i$ values represent the binding affinity of an inhibitor and are typically in the picomolar to micromolar (10$^{-12}$ to 10$^{-6}$ mol/L) range (ref: (a), (b)), but have also been seen as low as femtomolar values, albeit rarely (10$^{-15}$ mol/L) (ref: (c)). A small K$_i$ value (e.g. femtomolar) represents an enzyme with a high affinity, i.e. a "strong" inhibitor. But your decision of whether an inhibitor is "good or bad" or "strong" will depend on context, and how well the inhibitor fits its purpose and compares to other inhibitors. There is no standardized "threshold".
Furthermore, other factors apart from the K$_i$ value could affect how "strong" the inhibitor is. The K$_i$ value just tells you how well the inhibitor can bind to the enzyme, but other factors that affect how well the inhibitor is able to inhibit the enzyme:

What type of mechanism does the inhibitor display? Competitive? Noncompetitive? Other types? Different mechanisms of binding could change qualities of the inhibitor, such as whether it is surmountable or not. Also, if the inhibition can involve binding to the enzyme-substrate complex, does this binding have a different affinity constant to K$_i$?
Does the inhibitor interact with the substrate? Two inhibitors could have equal K$_i$ values but a different strength due to interactions with the substrate.

Lastly, the IC$_{50}$ is practical measure of the potency (i.e. the strength) of the inhibitor. It describes the concentration needed to inhibit enzyme activity by 50%. However, the IC$_{50}$ is dependent on the experimental conditions, such as enzyme and substrate concentrations. For some competitive inhibitors, the IC$_{50}$ may relate to the K$_i$, [S] (substrate concentration) and K$_M$ (Michaelis constant of the enzyme) with the Cheng-Prussoff equation:
$$K_i=\frac{\text{IC}_{50}}{1+\frac{[S]}{K_M}}$$
Reference K$_i$ values:
(a): Flurbiprofen at PGHS1 or PGHS2: K$_i$ = 0.5 uM to 0.6 uM
(b): Methotrexate at DHFR: K$_i$ = 7.3 pM to 2.3 nM
(c): Ribonuclease inhibitor protein at ribonuclease: K$_i$ = 1 fM.

Could use more explanation for context. Like, is mechanism is a type of context?

Not sure about point 2 (that the IC50 is a function of temperature).

@xusr Thanks for the (+1)! I added notes about the tight binding of femtomolar Ki inhibitors and that the IC50 is dependent on experimental conditions - I agree, it has its limitations, but it's nice to have practical models of the theory :)


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What are the advantages using SUMO vector for expression?
My question is : What are the advantages using SUMO vector for expression?

As the pET SUMO info page states

It utilizes a small ubiquitin-related modifier (SUMO) fusion,
  belonging to the growing family of ubiquitin-related proteins, to
  enhance the solubility of expressed fusion proteins.

So, in general, you could consider using SUMO vectors to improve the solubility of your protein.


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Is QIAPI 1 a scam?
I find it strange that there isn't a wikipedia article on a drug that allegedly modulates human photosynthesis. I thought I might get a virus from some of the sites selling it, but others seemed decently official. I couldn't find any logs about it but there seems to be a lot of papers supporting the claims of its developers. The only testimonials I found were in spanish and I wasn't sure if they were real. Anyone heard about this stuff?

Regulating human photosynthesis? This is nonsense since humans don't do photosynthesis. Additionally it is unclear what you are asking about, so please add some references.

Based on what you are saying, yes. It is a scam.

Total Fraud
It's not true.  As things stand now, it is absolutely impossible for human beings to photosynthesise.  If you want a rather technical quote from D. C. Smith and E. A. Bernays:

A survey of modern associations in which protists or invertebrates are hosts shows that very few of the many species of photosynthetic microbes are adapted to an endosymbiotic existence. None occurs as intracellular symbionts in animals structurally more complex than cnidarians and platyhelminths. Photosynthetic symbionts are not usually capable of being the sole food source for hosts because they do not provide a balanced diet; most hosts therefore retain holozoic feeding. Interactions between hosts and intracellular symbionts are complex, and have to include mechanisms for inducing release of photosynthate from symbionts as well as controlling symbiont cell division. Possession of symbionts imposes a measurable cost on hosts. For the great majority of animals, the costs of adapting to herbivory or other forms of nutrition are probably less than that of hosting photosynthetic symbionts, especially when the need for exposure of a large surface area to light is borne in mind. Once hosts become multicellular, it is virtually impossible for any photosynthetic symbionts they possess to evolve into organelles because they are restricted to specific host cell types.

Otherwise, the simple link is: http://www.bbc.com/future/story/20120906-will-humans-ever-photosynthesise.
Short answer: no complex organism truly uses photosynthesis to produce its energy because of the major loss in efficiency of gaining energy from the sun on a multi-cellular level.  Too, the amount of energy that a human being needs for survival is so massive that we would have to have leafy protrusions all over ourselves to collect enough energy to make any difference whatsoever.

Two things: 1. Is this drug about photosynthetic symbionts? If not, your answer does not fit the question. 2. I am unsure if your short answer is correct. Plants use photosynthesis to create a carbon source for "producing" (rather making it available to them) energy in cellular respiration. Accordingly, photosynthesising humans would not need to convert all their energy from photosynthesis but rather supplement their carbohydrate uptake internally. Don't get me wrong, I also think this is a total fraud. Still, I am not convinced by this argument.

Sure, that's valid, @AlexDeLarge.  I'd just encourage you to read the article on BBC that I shared.


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Senescence, immortality and evolution?
Many have heard about the fabled "immortal" jellyfish, Turritopsis dohrnii, which doesn't die from aging (senescence) and can revert the aging process indefinitely. It is rather remarkable that only one, or very few species show this type of behavior.
I wonder if at some earlier point in evolution, when life was predominantly simpler and sea based, there were more species with this feature, but this "immortality" caused overpopulation and/or didn't allow for proper action of natural selection, meaning that "immortal" species didn't evolve much and got wiped out almost entirely by whatever phenomenon.
In this scenario, aging and dying from old age would be an important evolutionary trait which would allow for populations to maintain reasonable sizes and would allow for natural selection to impart changes.
I was wondering how plausible all of this is, since I'm not an expert in the area and know little about the appropriate technical concepts behind these things.

Are you asking what the drawbacks of cellular immortality are to the individual or the species? They're slightly different. Try http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer?rq=1 for more information on aging and evolution.

You will find here a very good overview of the main hypotheses that explain senescence.
I am not sure I will answer your question but here are some reactions to your post..
What you say has to do with species selection. Selection selects between various objects/units that differ. These objects may be genes, individuals, populations, species, etc… In other words, there are various level of selection or different units on which selection acts. Wiki
Generally speaking, it is often assumed better to think in terms of selection acting on alleles (gene variants) or on individuals. Therefore, we tend to think that selection acting on genes or on individuals is more effective than selection acting on species. However, selection acts on species and we should not necessarily discard explanation using the concept of species selection.
What you say, if I am not mistaken, if we consider a set of species that are either mortal or immortal, we would predict that selection would benefit the mortal ones. Stating differently, mortal species have some advantage over immortal species that allow them to not get extinct or eventually to speciate more.
However, I don't quite understand the reasons why immortality would be deleterious to species. You say that it leads to overpopulation. So would you expect that a population is lead to overpopulation due to immortality and suddenly disappear because it is overcrowded. It doesn't sound like a well formulated argument to me. You could however argue that mortal species have a much greater individual turnover allowing them to adapt faster to environmental change than would immortal species.


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Cysticercoids of Eucestoda
I have found the following pictures representing cysticercoids of Eucestoda.
If I correctly understand the right part of the picture, I would say that the development of the scolex is portrayed on the right, as the formation of what I think to be two acetabula shows. Nevertheless, with respect to the images on the left, it is totally unclear to me, since the text says nothing about it, what the structure that seems to be encapsulating the animal is.

I know that cysticercoids develops from an oncosphere, but I do not know whether that sort of capsule that seems to be enveloping the animal is a part of what was the oncosphere's tegument -the embrionophore- that it can have gone out of and is entering again...
Does anybody reading this question know more about it? I thank you very much for any answer!

I would say that the left part of the picture depicts 2 stages of the development of cysticercoid, while the right part shows the consecutive stages in the development of cysticercus. These two parts represent different species of tapeworms in the same stage of their developments.

To say the truth, the cysticercus is drawn in another picture elsewhere, while the legenda under this one says cysticercoid... As to that sort of tailed capsule which seems to envelopes the animal on the left, what is it? Thank you so much again!


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Founders of Cnidarian colony
I know that colonial Cnidaria enlarge their colony by the means of asexual reproduction and sexual and asexual reproduction can originate individuals that will be part of other colonies.
Nevertheless, I cannot find any precise information about whether the individuals of a certain colony are all descendants of one founder or not. I thank you anybody for any answer!


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Re-solidify disturbed agar plates
I am stuck in trouble while pouring LB agar onto my petri dishes. I had to add kanamycin to my plates just before it started to solidify, out of forgetfulness, which I tried to mix using the tip. The plate was such a disaster! Is there a way to melt the agar in the plate and re-solidify it evenly.
I use falcon sterile plastic petri dish.

Yes. It is quite simple actually. Do this inside a clean laminar hood:

Take a clean sterile scalpel blade or any other sterile long object. 1ml pipette tip would also do.
Cut the agar on your plate. Scrape off cleanly.
Put it in a sterile glass bottle.
Heat in microwave
Add kanamycin
Pour back

Another solution is to coat the agar surface with kanamycin just like spread plating. Check the appropriate concentrations.

If the agar has solidified with a nice surface, I would prefer the spreading technique. Works pretty nice and is definitely much less hassle (and contains less contamination problems) than removing and remelting. Before spreading, dry the plates open so they can take up the liquid.


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Pink E.coli cell pellet. Reasons?
I've harvested IPTG induced E.coli BL21DE3 cells' suspension culture by spinning at 5000 rpm/15 min/4 degrees C. The pellet after spin looked pale pink colored. What could be the reasons?

If you induced them with IPTG what additional genes had you added to induce?

That would be my question as well: What do you overexpress in the cells?

I've seen E. coli colonies with red fluorescent protein that were visibly red even without UV light. That assumes you have cells with RFP. I've heard of carotenoids making bacteria red too, but I don't know what would happen to make E. coli produce them.

There are a few possibilities why the cells can be pink, so it would be important to know which gene is overexpressed.


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Can protein sample be made 2% Triton X-100 free?
The protein I am purifying needed an elution buffer with 2% Triton X-100. I formulated the elution buffer not keeping the CMC in mind. My goal is to make my protein sample triton free to check its stability and quantify its concentration. Lately, I learnt that micelles can be broken down upon dilution. So, I've diluted my protein sample below triton's CMC and tried concentrating it using Sartorius Vivaspin 5K (PES resin). I loaded 500 ul of diluted sample and was left with 100 ul after concentration using vivaspin. But, this sample gave an abnormal reading of above 3 OD after blanking against the buffer it is in. I presume, triton's interference is causing these discrepant readings.

You'll probably have to do multiple buffer exchanges if using a centrifugal filter. Dialysis is another option.

This is a dialysed protein sample against Tris-HCl. Multiple buffer exchanges meaning, re-adding fresh buffer to the remain on filter?

If dialysis didn't remove it, I doubt filtration would. You can get beads specifically designed to remove Triton X-100 by adsorption.


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On the selection coefficient
I'm reading  Williams' Adaptation and Natural Selection:
A Critique of Some Current Evolutionary Thought.
In this book the author talks about selection coefficients which, if I understand it correctly, can be calculated as finiteness arithmetic means (for each allele).
My question is: should this calculation be made assuming a ceteris paribus condition?

Definition of selection coefficient
A selection coefficient is a difference in fitness between two genotypes (or haplotypes). Let the two genotypes be A and B. Let's use relative fitness and say that the fitness of A is $w_A = 1$ and the fitness of B is $w_B = 1 - s$, where $s$ is the selection coefficient. As a consequence $w_A - w_B = s$.
The question of long-term fitness is unrelated to the definition of selection coefficient, as the selection coefficient is defined as a difference in fitness. A question of importance is "What measure of fitness should one use for a population where selective pressures are changing over time and/or space".
What measure of fitness should one use for a population where selective pressures are changing over time and/or space
Roughly speaking, if changes in fitness are over space, then you should use arithmetic mean fitness and if changes in fitness are over time, then you should use the geometric mean fitness but it is not quite that easy.
The real interest is whether fitnesses are correlated among generations. In other words, do individuals within a generation tend to have a more similar fitness values than the individuals of another generation? When variation in fitness is spatial than one should not expect such correlation. When variation is temporal one should expect such correlation.
Hoping you can read a code in R, the easiest is probably to read some code that make a simulation and look at the output. So here is a code that performs simulations. The key difference between simulations with spatial and temporal variation is the line that gets fitness value (runif).
set.seed(43)

temporalVariation = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        fitnessPerIndThisGeneration = runif(1,lowestFitness, highestFitness) # All individuals have the same fitness in a specific generation
        N = N * fitnessPerIndThisGeneration
        Ns[generation] = N
    }
    return (Ns)
}

spatialVariation  = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        FitnessOfEachIndividual = runif(N, lowestFitness, highestFitness) # Individuals differ in fitness within a generation
        N = sum(FitnessOfEachIndividual)
        Ns[generation] = N
    }
    return (Ns)
}

N = 1000
lowestFitness = 0.95
highestFitness = 1.08
nbgenerations = 200

spatialNs = spatialVariation(N, lowestFitness, highestFitness, nbgenerations)
temporalNs = temporalVariation(N, lowestFitness, highestFitness, nbgenerations)

plot(y= spatialNs, x=1:nbgenerations, col='blue', xlab = 'generation', ylab = 'N')
points(y= temporalNs, x=1:nbgenerations, col='red')

In blue is the simulation with spatial variation. In red is the simulation with temporal variation. You will note that the geometric mean is always equal or lower than the arithmetic mean.
Whether the arithmetic or geometric mean fitness matters most will affect the reproductive system that will be most successful. In this regard, you should read Ripa et al. 2009 about bet-hedging

"Roughly speaking, if changes in fitness are over space, then you should use arithmetic mean fitness and if changes in fitness are over time, then you should use the geometric mean fitness but it is not quite that easy."  Remi, would you explain/elaborate on this?

@sterid See edit. I am not 100% sure how to explain it, so I decided to write and show results of a simulation. Hopefully that will make sense when reading the code.

I appreciate your writing the code, but I don't know the R language.  I have a couple questions if you feel like indulging:

Never mind.  I understand the program.  Will study it & probably have questions.  Thank you.

OK I see why that result was obtained.  Would you please explain the relevance of "You will note that the geometric mean is always equal or lower than the arithmetic mean." ?

It means that environmental variance on fitness causes a greater decrease in long term fitness if this variance is temporal rather than spatial. This whole subject is very interesting especially in the bet-hedging literature. The first one to point out to this effect was Richard Levin. His book evolution in changing environment is all focused on that (IMO it is old and not very pleasant to read though).

But isn't it true that if you consider the effects of selection, you must have spatial variance in order to have temporal variance and vice versa (as long as heritability is high)?


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Do users of CRISPR/Cas iterate or parallelize to try multiple guide sequences?
I've read about on-target efficiency and off-target effects in use of CRISPR/Cas9, and about tools that suggest good guide sequences. I am wondering: how many guide sequences do typical CRISPR users try -- i.e. is there any iteration or parallelism involved?
I think the answer is yes for some use cases, but I am not sure:

Knocking out one particular locus: There are only a few possible guide sequences, so you can just make a library that includes all of those and run one experiment, without iteration. You would not know which guide sequence worked best, though, but users may not need this information.
Knocking out one gene, no matter at which loci: Since there are many possible loci for indels, the key is to choose a locus for which the guide sequence is effective and produces the last off-target effects elsewhere in the genome. This would mean iterating/trying several of the top suggested guide sequences individually. These could be tried in parallel across several experiments.
Knocking out multiple genes, aka multiplexing: The user would want to find good guide sequences for each gene separately to avoid any interactions. This would reduce to the previous example above.

Is my understanding above correct?

I usually do 2-3 parallel guides for a single gene, but I'm not sure on how common it is.

@MarchHo Thanks! Do you just use the 2-3 top guides from a guide selection tool like http://crispr.mit.edu/ in parallel, and then report whichever worked best?


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Why didn't Mendel ever see the recombination?
I saw a video on youtube of a professor saying it's because of the quantity of peas. So Mendel would never have published his work if by any chance he had found a pea with recombination.
Someone can explain to me in a dummie way the reason?

Mendel did not do sufficient number of experiments. :P

Both are real biologists. Mendel pioneered genetics and his findings provided leads for others. In the process of science there is continuous validation and re-examination of facts. Some may be proven false; that doesn't mean that the initial scientists did not contribute anything.

But the reason is because he did not do sufficient number of experiments. Do you have some biological way to explain this to me?

Before Mendel, humans has been trying to figure out heredity for over 2000 years without being able to reach any conclusions more specific then that offspring tend to inherit the traits of their parents. This is because the full process of inheritance is staggeringly complex. Mendel's contribution was to demonstrate that there were least a few traits that were inherited in specific and quantifiable patterns. He had to look very hard to find those traits. As @swbarnes2 suggests, his search may have led him to traits on separate chromosomes, eliminating the complication of recombination.

Of course, it's also possible that he looked at more than 7 traits, but didn't publish on traits which violated his laws.  The probability of randomly picking 7 traits on 7 chromosomes is quite low.

I'm not sure what you mean by "recombination".  Peas have 7 chromosomes.  Mendel's seven published traits are each on a different chromosome.  Mendel's second law states that all genes assort independently.  This is wrong, but it is correct for genes located on different chromosomes, which Mendel's were.