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miRNA targets mRNAs
If we observe that a miRNA, say hsa-mir-233, targets a mRNA, say XXX, in a given tissue in disease condition, can we say that always hsa-mir-233 targets mRNA XXX regardless of type of tissue and disease condition?

miRNA's can be tissue-specific, and their mRNA target can also be tissue-specific. I'd be careful about generalizing.

by tissue-specific, you mean miRNA may target mRNA in tissue A, but not in tissue B?

To avoid confusion, yes, the miRNA can be targeted to it's specific mRNA if it ends up in another tissue. To me there are some confounding factors that may alter it's net effect in different tissues or disease states.

First you have to define what you really mean by miRNA-X targets mRNA-Y. If you mean direct targeting then there are assays to verify it.
To verify if the miRNA can potentially target the mRNA independently, what is routinely done is a reporter downregulation assay (usually luciferase). You clone the 3'UTR of your target mRNA downstream of the reporter gene and check the activity of luciferase in the presence and absence of miRNA. You do that by co-transfecting the miRNA and the luciferase construct, collecting the cell lysate after some time (typically 12/24/36h post transfection) and measuring luciferase activity using bioluminescence counter. This just establishes the molecular possibility of targeting but does not really say if the same actually happens in a given tissue.
Reporter assays like this can be modified for in-vivo conditions too. Express the reporter-3'UTR construct in your organism (or specific tissue). Use another reporter with a mutated target site in the 3'UTR which abolishes miRNA targeting and compare the activities of the two. In zebrafish, people also use modified-backbone oligonucleotides (morpholinos) to mask the target site such that the miRNA can no longer target the mRNA. This assay is called target-protection assay.
There are other assays which do not involve reporter genes but actually capture miRNA and mRNA bound to the Ago-complex. This is done by protein-RNA crosslinking followed by immunoprecipitation of the protein (Ago) which is then followed by sequencing of the bound RNA. See this post for more details. These assays will give you tissue specific information but they only tell you if a miRNA and mRNA are bound together. They do not tell whether the mRNA activity is downregulated or not.
Targeting of the mRNA by miRNA, in-vivo (which has already been established by ectopic reporter assays) depends on many factors, the foremost of which is the relative concentrations of these molecules and the competitors. To produce an effect, the miRNA has to be in sufficient concentration for each of its target (if the miRNA has many targets then the per-target availability will go down).
So, if a miRNA-X actually targets i.e. downregulates a mRNA-Y in a specific condition, it need not do it in another condition. However, we would still say that mRNA-Y is a valid target of miRNA-X if it is so in at least one condition and better if it has been validated using reporter assays (ectopic).

mRNA targeting mechanism is highly specific and depends on various factors. the target mRNA and miRNA complex is highly conserved even from an evolutionary point of view.There are many in-vitro studies which shows the importance of miRNA concentration.Now under any kind of disease state the normal functioning of cells is hindered and this directly effects the level of transcription. the rate can either increase or decrease.
mRNA target region for miRNA in the 3'UTR region is highly specific, and its dependent on base pair complementarity between mRNA and miRNA, due to which the miRNA-mRNA duplex remains exclusive. there are multiple miRNAs which have been found for one particular mRNA, if u go through the database TargetHumanScan database(http://www.targetscan.org/) u will find many miRNAs for one particular mRNA, and vice-versa.
The concern here is not weather any mRNA can be regulated by the particular miRNA, but, whether its positive regulation or negative regulation which is needed by the cell at that particular diseased state.

miRNA hardly ever cause positive regulation. They are primarily repressors.

As well as the above, it's worth noting that the usage of 3' UTRs and polyadenylation sites can vary from tissue to tissue, so that an mRNA might have the cognate miRNA binding site in one tissue, but not another.


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Why do provitamins-A do not cause Vitamin-A toxicity?
Why do beta-carotene and other provitamins like alpha-carotene not cause vitamin-A toxicity but rather carotenosis (Orange skin) whereas retinal, retinol, and retinoic acid cause vitamin A toxicity with dosage as low as 4000 IU?

Retinoic acid is a signalling molecule whereas the provitamins are merely precursors.

Since, you didn't state whether you were referring to a concentrate or not, i'm assuming the following forms of Vitamin A were obtained via pill or topical suspension - except for the Carotenoid.
α-carotene and β-carotene are (primary) precursors to Vitamin A. Likewise with, Retinal, Retinol but not with Retinoic Acid (irreversibly metabolized/end point) however, i'm assuming that these first generation Retinoids are produced via ex situ (a facility) metabolism and hence, they do not contain the carotenoid component that cause yellowing of the skin due to the absence of lipid soluble orange/yellow pigments (Xanthaemia). Albeit, the color of the aforementioned FG retinoids when in a concentrated solid state are all yellow still due to molecular structure - explained in midsection.
For example:
Retinal:  Otherwise known as Retinaldehyde, is ingested via meat (as a single/complete molecule) or produced by ingestion of carotenoid containing food-stuff (e.g. carots). The pigment causing the color are, Carotenes. Carotene is a component of the Carotenoid molecule; α-carotene and β-carotene.
Alternatively, Retinal can be produced from the metabolism of β-cryptoxanthin, a Xanthophyll containing compound. Xanthophyll and Carotene are similar in terms of molecular structure, however, a Xanthophyll molecule contains Hydroxyl groups and hence, Oxygen atoms - Carotenes are hydrocarbons.
On that note, hypervitaminosis A can be caused by an over ingestion of α-carotene and β-carotene sources e.g. Carrots, due to the process of metabolism; over an extended period of time.
Generally;
Retinyl ester <=> Retinol <=>  Retinal => Retinoic acid

What causes Xanthemia in this context?
α-carotene and β-carotene, are absorbed via (passive) diffusion within the gastrointestinal tract. From there, they are metabolized (not fully/partially) at the the mucousal layer of the intestine for the substance to be transported into the liver. Next, the metabolite is diffused into the peripheral tissues by the blood plasma. This is were the "issue" is: Excretion. Carotenoids are excreted via bowel movements (gastrointestinal secretions), Urination, through the secretion of sebum and by sweating.
If very high levels of Carotenoids are being ingested, the pigment tends to show itself when a "build up" occurs, in the sweet glands of our dermis and more noticeably, in areas of which there are a large amount of sweat glands e.g. nasolabial folds.
The orange color is defined is due to the classification of what Carotenoids are. All carotenoids are tetraterpenoids: essentially being tetraterpenes that have been modified by chemical transformations such as oxidation or cyclization. Furtherly, tetraterpenoids are made up 40 carbon atoms and contain 8 isoprene molecules. α-carotene and β-carotene, are bicylcic tetraterpenoids. This molecular classification may have an affect on the amount of energy that the molecule can absorb, and more formally, the colour. Albeit, the greatest majority of reasoning in regards to the orange color, is in favor of the long conjugated chain'ed structure of the molecule.
Carotenoids absorb light in the blue-green and violet region and reflect the longer yellow, red, and orange wavelengths; these pigments also dispose excess energy out of the cell.

Conclusion
Retinal and Retinal are preformed retinoids and are not obtained by means of carotenoid metabolism so, they won't contain the the yellow/orange dark pigment that is found within some plant-based food (Carotene).
Retinoic Acid, is a retinoid although it's function is as a cell signalling molecule. The difference between it and the other retinoids is the functional group present of the tail of the carbon-carbon backbone
Theoretically, speaking, and due to retinoids having a shorter/less extended  conjugated system with less unsaturated (multiple) bonds in the molecules it will have shifted the absorption to shorter wavelengths (The two carotene precursors have 11 conjugated bonds and the latter retinoids contain 5).
Furtherly, I don't think that the carboxyl group attached to the Retinoic acid molecule could be classed as an Auxochrome although the remainder of the retinoic acids carbon-carbon chain is still the molecules Chromophore - likewise with the other retinoids.  For example, this would mean that there is possibility that the retinoic acid molecule will be more inclined to absorb shorter wavelengths and hence, less orange/yellow. This is relevant as, you will often find retinoic acid in topical preparations that are used to treat certain dermatological conditions.
I don't think that there is a 100% correct answer for this question as there is no evidence to prove that it would be true in this particular case.
So, you are susceptible to toxicity at lower levels in regards to retinol, retinal and retinoic acid because, of the fact that they are metabolites/concentrates and you need ingest less in order to get to the same point of toxicity. Carotenoids are "raw" in contrast to the preformed retinoids   and require breakdown. Look at the image below to get an idea of how much the molecular mass will have reduced when the carotenoid is metabolized into a useful form of Vitamin A.
Another example would be, you needing to eat more daffodil bulbs to get the required dose of Galantamine hydrobromide (used in Alzheimer's disease treatment) - that's a bit different though, to be fair.

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Why is binding energy the difference between ∆G catalyzed and ∆G uncatalyzed?
I think the title explains it pretty well -- I'm confused on what 1) exactly binding energy is 2) and why it's the difference. Like in this diagram:
my teacher sort of said it was the energy the enzyme uses to make interactions to the substrate, but that doesn't really click for me.

A catalyst does not change the free energy i.e. ∆G of the net reaction. It only changes the activation energy. The catalysed reaction can be expressed as a series of many reactions and the overall ∆G can be expressed as a sum of that of the individual reactions.

yeah I know that. where was binding energy in your explanation?

binding can be considered one of the reactions (binding-unbinding reversible reaction). So totally there would be two reactions 1. binding and 2. conversion

There's two binding energies in your diagram, and it's the difference between them that's the critical point in understanding enzyme catalysis and the difference between $\Delta G$ catalyzed and $\Delta G$ uncatalyzed?
$\Delta G^R_{bind}$ is the binding energy of the enzyme-substrate complex. That is, it's the difference between the energy of the apo-enzyme and substrate in the non-bound form ("$E+S$") and the enzyme and substrate in the bound form ("$ES$").
The other binding energy is $\Delta G^T_{bind}$. This is the (theoretical) binding energy of the transition state. That is, it's the energy difference between the enzyme-transition state complex (here labeled "$T_{uncat}$", for some reason; it probably should be "$ET_{cat}$") and the apo-enzyme and the unbound transition state ("$E+T_{uncat}$").
Now remember that free energy is a state function. A free energy change ($\Delta G$) is simply the difference between the free energies of the starting state and the ending state - it doesn't depend on the path you take to get there. (The absolute free energies of any given state are unmeasurable, but you can infer information about relative free energies by measuring the $\Delta G$ of transitions between them.)
The two equations at the bottom are derivable from this definition of free energies as a state function. You know that the free energy difference between the $ES$ and the $E+T_{uncat}$ state is the same regardless of the path you take. So if you go first through $ES$ the free energy change ( $- \Delta G_{bind}^R  + \Delta G_{uncat}^\ddagger$) will be equal to that if you go through "$T_{uncat}$" ($\Delta G_{cat}^\ddagger - \Delta G_{bind}^T$) - you don't necessarily need to have physically realizable reactions for the state function property to hold. The second equation is then simply a rearrangement of the first.
In looking at the rate of catalysis, you're primarily interested in how big a free energy change it is to the relevant transition state from the previous state. (This is a basic principle of Transition State Theory.) To speed things up, the enzyme needs to make that energy change smaller - that is, to make $\Delta G_{cat}^\ddagger$ smaller than $\Delta G_{uncat}^\ddagger$. If the enzyme binds the substrate and the transition state equally well, $\Delta G_{bind}^R$ and $\Delta G_{bind}^T$ are the same, and $ES$ and "$T_{uncat}$" are lowered by the same amount, such that $\Delta G_{cat}^\ddagger$ and $\Delta G_{uncat}^\ddagger$ are equal: no catalysis.
But if instead $\Delta G_{bind}^T$ is greater than $\Delta G_{bind}^R$, then the "$T_{uncat}$" state is lowered more than the $ES$ state, making the gap between them ($\Delta G_{cat}^\ddagger$) smaller than the gap between $E+S$ and $E+T_{uncat}$ ($\Delta G_{uncat}^\ddagger$): the enzyme thus speeds up the reaction. This is what that second equation is saying.
This sort of thermodynamic analysis is what leads to the "transition state stabilization" hypothesis of how enzymes work: enzymes speed up reactions because they bind to the transition state more tightly than the substrates or the products.
(P.S. You may be wondering why we have the enzyme hanging around in the uncatalyzed reactions. This is simply a bookkeeping measure to make sure we're using the same reference state for the very start of the reaction ($E+S$). In the uncatalyzed reaction the enzyme doesn't change, and so doesn't really contribute to any free energy change.)

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How do cell repair mechanism ratios change as they age?
I have seen that embryonic stem cells are shown to use homologous repair for double strand breaks rather then non-homologous end joining (NHEJ). [1]
I am wondering if something also happens to a cell's usage of certain repair mechanisms after diversifying.
For instance, is there any evidence that two cells in the same lineage but of different ages (one from a person who is 20, another from someone who is 80) use different ratios of repair mechanisms? Has there been any research on this or is there any indirect data that could support such an idea?

The mechanism of DNA repair depends on the stage of cell cycle. Different cell types spend different relative times in different stages of cell cycle and so their preference for the DNA repair mechanism varies.

Yes I know this but I am asking about two cells of the same type but in organisms of different ages.
Has there been any comparison between two cells that are the same type, from the same species, but from two organisms that are at different stages of life to see if there is a difference in what repair mechanism type that they prefer?

I haven't come across any such studies but if the cell is self renewing at the same rate at both the ages (and has no other accumulated mutations), the preference ratio should remain the same.

I'm mainly wondering since we know that mutations occur more often as an organism ages and if perhaps there is more at play than telomere shortening, build-up of junk, etc.
The most I can find is this study http://www.nature.com/cr/journal/v18/n1/full/cr2007111a.html
However it really focuses on the decision between choosing NHEJ or HR and pretty much said what you said about there being differences during cycle and between types of cells. It'd be interesting to study but right now I can't find any evidence that would lead me to think it is happening or deserves investigation.

Also this http://www.fasebj.org/content/14/10/1325.full, but other than that I can't really find anything that could lead someone to support this idea.

This choice would probably depend on specific mutations (for e.g. XRCC which is mutated in some cancers) which down/up-regulate the activity of one type of repair pathway.

More of the emphasis of degeneration and aging has been placed on mitochondria these days. Telomere length usually almost never enters the equation as most tissue is replenished from Adult Stem Cells that continue to express telomerase. 2) If the information you are interested in has been researched and published, it will have likely been done in either Yeast, C. elegans, or Drosophila, so your best bet is to look for data on studies from those model organisms.


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Do vitamins protect you from common cold?
Do vitamins (taken as pills) boost your immune system, and make you less likely to contract diseases such as common cold or flu?

Welcome to Bio. Consider posting this on Health.SE

Sorry. I wasn't aware of "health.SE".  Maybe it's better to close this question then.

I'm voting to close this question as off-topic because it may be better of at Health. SE

@Christiaan the OP has already reposted it there...

@Nemo please don't post questions on two different sites. If it doesn't belong on the first site you post it at, it will be migrated to the better fitting one.

There are two answers to your question, "emphatically yes" and "sort of."  Vitamins play a critical role in immune function, and a deficiency of certain vitamins can lead to a higher risk of developing an infection.  Specifically, vitamin A, B2, B6, C, D, and E deficiency are linked to depressed immune function.  However that is deficiency, not supplementation above what most people need.
There's a popular idea that megadosing with vitamins, usually vitamin C, lowers the risk or length of common upper respiratory infections (eg the common cold).  The evidence on that is much less convincing.  A metanalysis of studies finds weak or no evidence that it is effective, but may be associated with a small effect.  More study is recommended by the researchers, but they don't go as far as recommending large doses of vitamin C.  (It is also worth noting that large doses of fat soluble vitamins, A, D, E, and K, can be quite toxic and should be avoided).
The magnitude of the first effect is quite large: people with a vitamin deficiency certainly have a depressed immune system.  However it is not clear that larger doses are helpful.


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How do electrons destroy DNA bonds in radiation?
Malignant tumors can be treated by radiation therapy. Most commonly it's radiotherapy with photons, or protons and so on. The common denominator for both types is that the radiation creates electrons inside the body via different effects.
What I haven't quite understood is how these electrons destroy the DNA bonds in the tumor and how this aids in killing off the cancer cells? Is it due to the generation of heat, or otherwise?

(1) Molecules are held together by bonds. Jamming energy (not necessarily heat) into the bonds causes them to become unstable and behave differently (electrons jump to different energy shells). (2) Cancers propagate through modified cellular pathways. To do this, the DNA needs to be functioning. Not properly, just functioning. (3) DNA functions by producing RNA. It's all about the sequence! Damaged sequence = damaged tumor pathways = death. Relevant mechanistic paper on direct damage by ionizing radiation.

I think you have a fundamental misunderstanding of the chemical reactions involved in radiation therapy. Neither photon based or proton based therapies "create electrons", but they do cause ionization by adding enough energy to existing electrons around atoms so that the electron is ejected from the atom, creating an ion or free radical, which can then undergo chemical reaction.
Photons, typically gamma rays, X-rays, and high energy UV, typically interact with water molecules and produce free radicals, including the dangerous hydroxyl radical. The hydroxyl radical can interact with proteins and DNA and damage those molecules, but has a very short half-life. Molecular oxygen can help increase the damage by reacting with the hydroxyl radical to produce Reactive Oxygen Species, ROS, which can also damage DNA or protein. However, many tumors have low oxygen concentration that reduces the effectiveness of photon based radiation therapy.
To overcome this, many patients receive proton based radiation therapy. Protons are much heavier than photons (I guess infinitely heavier than a photon, since photons have no mass) and therefore scatter to a much smaller extent. They just sort of plow through tissue and knock electrons out of orbitals as they collide with molecules such as DNA or protein. They don't rely so much on free radical generation or ROS, so low oxygen levels don't reduce their effectiveness.
The goal is damage the DNA to induce double strand breaks which are hard to repair in fast growing cancer cells. Because they grow so quickly, they are already stressed and their DNA repair machinery is less effective than in healthy cells. If their DNA can be sufficiently damaged, the cell will die.
For more information about these processes, please see these wikipedia articles on Radiation Therapy, Radiolysis, Linear Energy Transfer, and Free Radical Damage to DNA.


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Do intestinal flora have the same DNA as their host?
Please bear with me, this is not my professional field and I might be mixing things up. In an explanation why seeds won't start growing in one's intestines, the explanation given was that foreign bodies are detected by the DNA they carry and get attacked and digested, separating all strands of amino acids so they can be reused by the host and no DNA mixture can occur.
I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).
I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

Welcome to Biology.SE. Is your question "How come our gut endosymbionts don't get killed by our immune system?" or is it "Are gut endosymbionts inherited from the mother or are they acquired by the baby through food?"

I think he's asking "Where does the gut microbiotia start from?"

@swbarnes2 Could you suggest a good source for beginners. The wikipedia link that m1clee provided was helpful, but I guess a more ordered source that starts at basics and builds up would be more appropriate. Unfortunately I don't have the time or money to go back to high school (there are many additional subjects I'd love to study if I could :-).

I saw this link tonight. It is related to an exhibit at the American Museum of Natural History about the microbiome. http://www.amnh.org/exhibitions/the-secret-world-inside-you?utm_source=online&utm_medium=banner&utm_content=paid-placement&utm_campaign=SWIYcampaign2015 There are a few movies and it is likely curated for the general public, so you may want to start there before you delve into some of the links in my answer below.

Could you suggest a good source for beginners. - Louis Somers

The interactions between the human body and its microbiome are quite complex. I am going to provide you with an answer that will be based on your comment that you would like an answer from a beginners perspective.
For simplicity sake I will keep the answer to humans as the host organism, though pretty much any multicellular organism can act as a host for microscopic organisms.
Note: A number or the references I use come from Janeway's Immunobiology. The links provided are to the 2001 edition that is on the NCBI bookshelf. The issue, however, is that over the past decade we have learned a great deal more about the immune system since then, and some of the things I refer to were not represented in that edition of the text.

Do intestinal fauna have the same DNA as their host?

The short answer to this question is no. Also, we generally identify microbes of this nature as flora instead of fauna, so you would say intestinal flora.
The human microbiome (microbiota), as it is often referred to, is made up of hundreds of trillions of microorganisms that live in the niche of our digestive tract, airways, urogenital tract, and skin. In fact, the estimate is that there are 10 times as many microbial cells that live on the human body than there are human cells that make up the body itself (1). The difference is that human cells are immense when compared to most of the microbial cells that colonize us (2).
The vast majority of the microorganisms that populate us are single-celled organisms, such as bacteria or fungi (yeasts). Each of these cells is its own entity, in other words is an independent living organism, and they have their own genome (the complete genetic material of an organism) that encodes for their own proteins.
There is a good reference tool, though maybe a little advanced from The University of Utah, The Human Microbiome. This interactive presentation gives a layman's overview. The American Museum of Natural History has also curated an exhibit called The Secret World Inside You.
To add a point for clarification, while the genetic codes of these microbes are different in different species and are different from that of the human host, the molecules that hold the information, namely DNA, are all made of the same nucleic acid building blocks (5). To use an analogy, it is like using the same letters but writing in two different languages. We may use mostly the same characters, but the way we arrange those letters to form words in Spanish or words in English create different meaning.
When these single-celled organisms reproduce, they copy their own DNA and they divide into two new cells, each receiving one copy of that DNA (6).
Since yeast and other fungi are evolutionarily closer ancestors to humans than are bacteria, some of their genes, the sections of DNA that are functional and encode for proteins and RNAs, have a very similar sequence to our own (referred to as having homology) and often perform similar or the same function (7). When this is the case, we say that the genes are evolutionarily conserved, but for the most part evolutionarily conserved genes will vary in sequence from organism to organism, and the variation will usually increase the farther back you go in order to find a common ancestor between the organisms.
The human body is made up of about 37.2 trillion cells, on average (8). Almost all of these cells, with the exception of Red Blood Cells, have a copy of the hosts genome (9). All of these cells arose from a single egg produced by the mother and fertilized by the father's sperm (10). The egg and the sperm contained half the genome necessary for the embryo to develop. The DNA from the mother and the DNA from the father come together when the nuclei fuse. So we have our own genome that came from our mother and father, and the microbes have their own genome which they inherited from the ancestral cells that gave rise to them.
That is a slightly simplified answer as there can be different ways that the DNA can be passed between the organisms, but for the most part, we have our own DNA and, even though they live on us and in us, the microbes have their own DNA.

Your first paragraph.

I cannot tell you necessarily why seed that we swallow and digest do not germinate inside of us. It is likely that the seeds are not receiving the proper signals from the environment of our digestive track to initiate the genetic program to begin germination and development into a plant.

I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).

The vertebrate immune system is a diverse, highly-tuned system of surveillance that monitors for pathogens or foreign bodies that are introduced into the body that may be dangerous to the survival of the organism (11).
For humans, the first set of defense are barrier defenses (12). The surface of our skin consists of several layers of dead, keratinized cells that form an impermeable barrier. As long as this layer is not breached, it does an excellent job of keeping yeast and bacteria outside, away from tissue that they could damage.
On the interior surfaces, our airways, gastrointestinal tract, and genitourinary tracts contain specialized cells that produce large amounts of mucus that will coat the surfaces of these tissue. Mucus serves multiple roles. First it keeps the tissue moist, so that it does not dehydrate. Next it keeps the microbes at a distance from our cells, so that they do not come in direct contact with our epithelial cells (The cells that make up the linings of our digestive tract, genitourinary tract, and airways). Third, it can trap microbes in it. The epithelium is able to "sweep" the mucus along and as a result it is able to clear bacteria out of the body (13).
Included in the barrier defenses are actually the microbial organisms themselves. The interaction between the host and an organism which is neither detrimental or actively beneficial is known as commensalism (13). Basically, all of these trillions of microorganisms that life on us do not hurt us. In return, they get an environment in which they can live. As a result of this, commensal organisms will grow on these surfaces, will take up all of the space, and will use up the nutrients that could be used by pathogenic organisms (organisms that are actively able to cause an infection) to establish an infection.
The next level of defense comes from the cells of the innate immune system (14). In innate immunity, specialized cells monitor the area they are in for Pathogen-Associated Molecular Patterns (PAMPs). PAMPs can be sugars that make up the cell walls of the microbe or proteins that get expressed on the surface of the organism, such as Flagellin, a protein only found in the flagella of certain pathogen. The innate immune cells have pattern recognition receptors (PRR) that have a general specificity for recognizing and responding to the PAMPs. Our cells even have PRRs for DNA and Double Stranded RNA's, however those are usually found in vesicles on the inside of the cell. These interactions are very general, however once PRRs bind to the PAMP, they are able to signal into the cytoplasm, which can lead to the production of proteins, among other possible responses.
Here you can think of PRRs like a motion detector in a security system; the dog, or your two year old, or an intruder are going to set off the alarm just the same. It is not specific. The motion sensor "knows" that something that it is supposed to recognize, i.e. a moving object larger than a mouse passed by and it triggered the response, but it cannot tell you which moving object triggered it, only that it was triggered.
The innate immune cells are also able to respond by "eating" the pathogen in a process called phagocytosis. Here, they break up the bacteria, yeast, or the remnants of other dead host cells or large pathogens, things like worms, and put the broken up pieces on protein molecules on their surface.
When innate immune cells do this, they are presenting molecules to specialized immune cells (adaptive immune cells (14)), B-Cells and T-Cells, that are highly specific as to what they will react to. These cells can also cause a lot of damage to the host, so they are tightly regulated. Think of the interactions as keys and locks. A protein from a bacteria should turn a few of these cells on, but a protein from the host should not fit the lock.
All of these immune cells also respond to diffused chemical signals called cytokines. These molecules are secreted by some cells and are received by receptors on the host cells. Sometimes the secretion is by another immune cell, sometimes it is from a non-immune system host cell, and sometimes these molecules can be secreted by the bacteria, fungi, or worms themselves.
Depending on the chemical signals that are secreted, and how the cells are interacting at the time of the message, and which cells are receiving the message, will determine the response to the message. It is contextual. Think of the phrase "You're killing me." If someone says it, while laughing, to a good friend who is telling jokes, it means one thing. If it is screamed as someone is being choked by an attacker, it means something very different.
To summarize, the immune cells are surveilling the environment and trying to pick up what is friend and what is foe and they try to respond accordingly.
Over time and coevolution, our microbiomes have developed ways of communicating with our immune system to let it know that these microbes do not mean any harm. They are able to "train" the immune cells using chemical signaling to temper the immune systems response to them (15), and this is how they are able to coexist within our body and with an immune system that is constantly on seek an destroy missions. Also because of the mucus, our microbiome usually isn't in direct contact with our cells, so it is a different kind of interaction than if an infecting pathogen were to breech the barriers and gain access to sterile areas where no bacteria or fungi should be found, and as a result, the immune system reacts differently.
As for organ and tissue rejections (16), the issue here is that each of our cells, except for Red Blood Cells, present molecules on their surface that identify it as being a cell that was made by the body itself. You can almost think of it as a sport's teams jersey. The immune cells can survey the proteins displayed on the surface of our cells and tell that they are ours instead of from a pathogen. The problem is that each person makes a different array of these proteins, so if I were to give you a kidney, the proteins that the cells from my kidney make and put on their surface for immune cells to look at will be different from yours. In this case, because the keys do not fit the locks, the immune system reacts to the donated organ as an intruder and begins to attack it. Immune cells are extremely lethal and will kill the donated organ if they are not suppressed. That is why transplant recipients need to have their immune systems suppressed in order to survive with the donated organ. You might ask "well what if we just took all these proteins off of the surface so that they don't get recognized?" Well, the problem is that we have another class of immune cells known as Natural Killer Cells that patrol the body looking for cells that are not presenting these proteins, so the immune system is pretty adept and finding and killing things that it does not recognize specifically as self.

I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

To be honest, the majority of the microbiome is laid down during vaginal birth and breast feeding. Passing through the birth canal, microbes from the mother's vagina and feces are ingested by the newborn and this is their first real dose of microbiome, though some research is suggesting that the microbiome begins to form in the fetus before birth and is transferred through the placenta from the mother to the fetus.
Assuming we do not kill these bacteria with antibiotics, have other pathogenic bacteria take over the territory (yes, bacteria and fungi, like gangs, have turf wars; that is why we often find our antibiotics as compounds secreted by these organisms), or have a disease that wipes out the microbiome, and provide it with a health diet, then the microbiome pretty much is maintained by the microbial cells reproducing by cell division.
Also we will pick up these bacteria from the environment. We are constantly shedding enormous amounts of these cells into our environment. Babies touch things and put their hands in their mouths. This transfers good microbes as well as bad ones, and it is really just a natural part of the process. That is why the overuse of antibiotics and antibacterial soaps can cause unintended consequences. We are killing the good as well as the bad.
This reference, Your Changing Microbiome, again from The University of Utah is a good resource.
So to summarize, babies get the microbiome at birth through vaginal flora and maternal feces. They are also getting daily doses from the microbes that colonize the mother's skin when she nurses the child. Then these bacteria are also in the environment, so babies touch things, then they put their hands (or feet, the little contortionists) in their mouths and they get doses this way. Raw fruits and vegetables will also have microbes on them that will be taken in. As for the microbes, they have cell walls that allow them to live in environments that would be hostile if they did not have the cell walls. They also communicate with our immune system and "train" it not to kill them, and as long as nothing that we do, such as take antibiotics or get a disease, the microbiome will pretty much maintain itself through replication.

Wow, Thanks for all the effort you put into this! It is allot more complicated than I thought. I have yet to follow the provided links, but the text has been an enjoyable read! Thanks again!

@LouisSomers Always willing to put in effort to help someone who expresses a sincere and honest interest to learn. I could see from the comment on your question that it was worth the time to put together as complete a response as possible. As you work through the references, don't hesitate to raise questions about things that might be confusing. I, or one of the other contributors here will be happy to clarify. Best of luck on your journey. Biological knowledge can be truly mind-blowing when you start to see its complexities and its interconnectedness.

3k! Congratulations :D Close voting is all open up now :-)

@Christiaan Thank you. I'm in it for the knowledge... I figure the blood, sweat, and tears I put in to acquiring it should benefit someone other than me.


text:
How to find conserved residues across species?
I want to identify if certain phosphorylation sites are conserved for protein X across humans and yeast. I know from MS data that there are 4 phosphorylation sites in Human protein X. In order to identify if these residues, and therefore potentially the phosphorylation sites, are conserved, is it correct to align both sequences using pairwise comparisons by using software like Needle? Or should I rather perform a bigger alignment and use clustal omega? Are there better approaches?

I'd perform a bigger alignment using clustal or mafft or something. Pairwise alignments will give you a lot of noise from random chance and the set of pairwise alignments will be really large. Multiple sequence alignment will detect smaller conservation signals.
Compare against several species of yeast and maybe other mammals for context. When the alignment is done, perhaps draw it? I like logos for vertically large alignments.


text:
Time needed for transcription of DNA
How much time would it take to complete the transcription of an average-sized human gene?

Welcome to Bio. Answer: 4 'o clock in the morning! What do you mean with time? Time to do what?

Which organism? Did you try searching anything at all?

I'm interested in human cells. I would like to know the order of time taken to complete transcription of a medium-sized gene in particular.

From Bionumbers, the average transcription rate of RNA Polymerase II is about 3.8 kb/min. Other researchers measured it as 6.3 nucleotides/sec, or 378 bp/min, a 10-fold decrease. In the same paper, however, they measured the maximum rate at 71.6 nucleotides/sec, or 4.3 kb/min. To figure out the differences between the measurements, I suggest reading the paper, but since it's from Nature Publishing Group you'll have to pay for it, unless you're at a subscribing university or institution (or someone posts the paper in the comments <hint hint>).
So, the answer to your question, like most simple questions in biology, is it depends. It likely depends on the size of the gene, its structure, what transcription factors are necessary for the assembly of the polymerase complex, and, last but not least, exactly how and when you measure. Transcription likely initiates in fits and starts, then gets going faster. This is similar to (but not exactly like) measuring the speed of your car from Point A to Point B. Are you starting from a dead stop, or passing the starting marker at speed? Do you have to start the car first, or is it already running? How many turns and other slowdowns are on the road? Do you stop measuring as the car passes the finish marker, or when it comes to a complete stop? All of these things figure into the final answer, and the result given is entirely dependent on the scientists' choices of methodology.
If you are interested in a broader discussion, I got started on this page at Bionumbers.


text:
Why are human immune systems comparatively weaker than other animal immune systems?
Humans get sick on such a regular basis and animals will hardly ever get sick. Animals are typically exposed to the same pathogens as humans, yet a dog won't have a cold or the flu twice a year, with other miner health issues occurring regularly in between. I understand that humans are very structurally flawed due to some evolutionary processes, and I'm just wondering why our immune systems seemed to have taken a pretty big hit as well.

Sorry, but this is opinion based nonsense. Animals get sick as well and our immune system actually works pretty well in protecting us from the world.

Your pet dog likely isn't exposed to the hundreds/thousands of people a day that you are as you commute, perform your job, run errands, and just live your life. Your claim that humans are "very structurally flawed" is silly: compared to what? In what way? Do you have a citation for that statement? Do you have any evidence to support your claim that our immune systems are weak?

If animals could complain loudly in human languages, you'd probably hear a lot more about the illnesses they get.

@Chris that was very harsh.

The question probably has a mistaken premise.  Human immune systems are pretty similar to other species, at least in major structural elements. Our differences in adaptive niche have led to differences in some aspects; humans don't fare well with rotting meat, for example, while a scavenger can eat it without a problem.  Many scavengers have unique adaptations for dealing with this.  Dogs do not, however. Humans too have a unique niche, which is highly social, and thus have a well-developed social immunity (sometimes called a behavioral immune system).
Many animal populations have endemic diseases at fairly high levels.  Koalas, for example, famously have a very high level of chlamydia.  Sea lions rookeries often have infections, bats can have high levels of rabies, and so forth.  Lots of animals do get lots of infections.
However your question specifically on dogs is interesting, and probably gets to a risk factor which is very human.  Humans come into contact with far more other humans (and thus, likely more infected humans) than dogs encounter other dogs.  Diseases which spread through close proximity, such as airborn upper respiratory viruses, spread more readily in humans than these relatively isolated animal populations.  Combine that with a concerted effort to wipe out in animals any diseases which can transmit to humans, and pet infections are indeed relatively rare.  This is not due to the immune system per se, but the social factors associated with each organisms' niche.

+1 - I agree with most of this, but not the last paragraph. (My vet bills speak volumes; only $240 says "anaplasmosis.") Pet infections aren't rare; house pets are vaccinated against many illnesses, and aren't exactly vocal about the rest (just as the koalas don't complain about chlamydia.) The feral population are a pretty mangy, parasite infected, ill (esp. cats) bunch. Dogs are interesting because of their close association with man for most of their existence.


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How does RNA polymerase achieve higher processivity?
DNA polymerase uses a sliding clamp in order to replicate DNA. RNA polymerase does not require one. What allows RNA polymerase to hold on to DNA just like DNA polymerase?

Hi @notorious. Could you add a citation for this sliding clamp usage? I'm rather intruiged!

The structure in the presence of s (holoenzyme) is on the right; note the open channel for DNA binding. The structure in the absence of s (the core enzyme) is on the left.  Note that the channel is now closed, as if the fingers and thumbs of a hand now closed to make a circle. This striking conformational change that occurs when s dissociates is thought to confer high processivity on the RNA polymerase.
SOURCE: http://biowiki.ucdavis.edu/Genetics/Unit_III%3A_The_Pathway_of_Gene_Expression/10%3A_Transcription%3A_RNA_polymerases

DNA Polymerase III Holoenzyme has processivity of 500,000 bases. High isn't a number,

If you have nothing to add to the discussion and if you continue criticizing other people's answers without giving a proper explanation to the question, then you really shouldn't be using StackExchange. Also, you still haven't corrected the error in the question.

And here is another point that you are missing. RNA polymerase need only associate with the template strand of DNA and transcribe from that, where as DNA polymerization is a far more complex process involving leading and lagging strand synthesis, laying down or RNA primers, producing Okazaki fragments and performing exonuclease error correction with DNA polymerase working with both strands of DNA at the same time.

Perhaps you can add some details on processivities of DNA and RNA polymerases. This will clarify the point. Also cite references for those. BioNumbers is a good place to look for figures such as these.

@AMR DNA-polymerase, unaided by sliding clamp has a low processivity. Highest seems that of viral polymerases (7200 for EBV).

@AMR I remember being scorned for almost exactly the same thing in a college (UK) biology class. I said there was a "high amount" of something I can no longer recall. I now fear the words "high" and "amount". Specificity is key for, if nothing else, not angering teachers and biologists.


text:
Proof of the equivalence between two ways of defining ESS
Background
Two common ways of defining what an Evolutionary Stable Strategy (ESS) are:
First definition:
Consider a population composed of populations playing two strategies, $\mathbf{p}$ and $\mathbf{q}$.
Let us denote $W(\mathbf{p})$ the average fitness of the
strategy $\mathbf{p}$. A population consisting of individuals playing $\mathbf{p}$ will be an ESS if, whenever a small amount of deviant individuals playing $\mathbf{q}$, the old type $\mathbf{p}$ fares batter than the newcomers $\mathbf{q}$. This means that for all
$\mathbf{p}\neq \mathbf{q}$,
\begin{equation}
  W(\mathbf{p}) > W (\mathbf{q})
\end{equation}
Second definition: $E(\mathbf{p},\mathbf{q})$ is the payoff for $\mathbf{p}$-strategist against a $\mathbf{q}$-strategist. The strategy $\mathbf{p}$ is an ESS if and only if the following conditions are satisfied:

$E(\mathbf{p},\mathbf{p})\geq E(\mathbf{q},\mathbf{p}) \quad \forall
  \mathbf{q}$
If $\mathbf{q}\neq \mathbf{p}$ and $E(\mathbf{p},\mathbf{p}) = E(\mathbf{q},\mathbf{p})$, then
$E(\mathbf{p},\mathbf{q})> E(\mathbf{q},\mathbf{q})$

Question (shorter version)
The above two ways of defining what an ESS should be equivalent. How can I prove such an equivalence? Alternatively, do you know of a book (or a paper) that has this proof?
Question (longer version)
I understand that the first definition implies the second. According to the first definition:
\begin{align*}
   W(\mathbf{p}) - W (\mathbf{q}) &>0\\
   (1-\epsilon) [E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]
   + \epsilon [E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})] &>0
 \end{align*}
where $\epsilon$ is frequency of individuals playing $\mathbf{q}$. Since $0<\epsilon<1$, if the above inequality is true, the conditions 1 and 2 in the second definition must be true. The part that I find less clear is how the second definition implies the first definition. More specifically, that if $\mathbf{p}$ is a strict Nash equilibrium (i.e., $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$), then $W(\mathbf{p}) > W (\mathbf{q})$.

Aren't these definitions applicable to different models of evolution?  It seems like the first is applicable in a case where each strategy has, regardless of the other strategies, a known distribution of payoffs.  The second seems to have a payoff which is dependent not only on the strategy but also on the other players' strategy.  If they are different models, I am not sure what it means to be equivalent.

@Hans The equivalence between these defs is mentioned in a few textbooks, such as p.232 of Gintis Game Theory Evolving and on p. 63 of Hofbauer & Sigmund's Evolutionary Games and Population Dynamics.

We need to show that if $\mathbf{p}$ is a strict Nash equilibrium, $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$, then $W(\mathbf{p}) > W (\mathbf{q})$ for some sufficiently small $\epsilon$. When $E(\mathbf{p},\mathbf{q}) \geq E(\mathbf{q},\mathbf{q})$, $\mathbf{p}$ clearly dominates $\mathbf{q}$.The less obvious case is when $E(\mathbf{p},\mathbf{q}) < E(\mathbf{q},\mathbf{q})$.
Since $E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})>0$, there should be a strictly positive number $k$ such that
$$k[E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]+ E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})>0$$
is true. Whatever this number is, we can write $k$ as $(1-\epsilon)/\epsilon$ for $0<\epsilon<1$. Substituting this into the equation above gives us the desired result.


text:
When does lactation occur?
High levels of estrogens and progesterone antagonize prolactin’s effect on the mammary glands, and it’s only after the placenta has been removed and the levels of estrogens and progesterone has decreased that prolactin effectively stimulates milk production in the alveoli. However, I’m also aware that many hormones cause the maturation of the breasts and mammary glands during pregnancy—is anything produced then? When does lactation really occur—before birth or after birth? I ask this because I’ve heard things about milk leaking out of breasts during pregnancy, and there’s also the fact that the breasts seem very heavy and laden with milk during parturition.

See prolactin..

@WYSIWYG - don't forget estrogens, progesterone, adrenal corticoids, insulin and growth hormone... it ain't just prolactin.

@anongoodnurse I was just giving a hint.. Not answering the question because I feel it is a bit broad. Hypothalamic control etc is also important.

@WYSIWYG It's not too broad at all. Geez, we get questions about why we didn't evolve wheels, wings, etc. This one is a walk in the park comparatively.

Stage I lactation occurs from midpregnancy onward; stage II is the onset of substantial milk secretion associated with having given birth.

In humans, stage I occurs at approximately midpregnancy... the gland is sufficiently differentiated to secrete milk, but secretion is held in check by high circulating plasma concentrations of progesterone and, possibly ...estrogen.

You ask,

...is anything produced then?

Yes. The mature primed breast produces colostrum, containing sodium, chloride, immunoglobulins, lactoferrin and other substances.

I’ve heard things about milk leaking out of breasts during pregnancy...

Not at all common that I know of. I'm sure one can manipulate the breast to get a small amount of milky discharge, but that's a big leap from leaking. More common (again, that I'm aware of) is galactorrhea associated with early oral contraceptive pills, prolactinomas, and other conditions.

the breasts seem very heavy and laden with milk during parturition.

The breasts mature during pregnancy in preparation to make milk; that's why they get bigger. They can get even bigger when they are actually full of milk. It may not be as obvious in a human, but in milk animals (goats, cows, etc.), well, a full udder is pretty obvious.
Different researchers divide lactogenesis into a different number of stages; this is a simple two-stage approach.
Lactogenesis: The Transition from Pregnancy to Lactation


text:
Colorblindness in females and random X chromosome inactivation
From Annenberg Learner:

Because the X is inactivated randomly in cells, one cell could have the maternal X inactivated, while the adjacent cell could have the paternal
  X inactivated. This causes a pattern of gene expression called mosaicism, which occurs when different alleles of X-linked genes are expressed in different cells.

However, this seems at odds with colorblindness being more likely in males.  From Wikipedia:

The genes that produce photopigments are carried on the X chromosome; if some of these genes are missing or damaged, color blindness will be expressed in males with a higher probability than in females because males only have one X chromosome, whereas females have two and a functional gene on only one of the X chromosomes is sufficient to yield the necessary photopigments.

Question: If X chromosomes are randomly inactivated cell by cell, shouldn't the fully functional photopigment-producing gene be inactivated approximately half the time?  In which case, wouldn't we instead see females with colorblindness with higher frequency as males, but experiencing colorblindness to a lesser extent?  (After all, two X chromosomes means two chances for a dysfunctional gene.)
I'm guessing I'm missing a piece of the puzzle here, e.g., perhaps the relevant cells "know" to inactivate the dysfunctional X chromosome, or perhaps it's to do with X chromosomes only being incompletely inactivated.

@Christiaan. I was thinking the exact same thing about the tags. But it had a part about sex determination in it, and while not what I would consider sex determination it was related to sex-linkage... I agree with your decision.

@AMR - I just posted in chat. Will ping

In heterozygote females with colour defect genes on the X-chromosome, even if approximately half of their photoreceptors are dysfunctional they usually have enough functional cone photoreceptors to have normal colour vision.
From Molecular genetics of colour vision deficiencies:

Due to X-chromosome inactivation during early development,
  heterozygotes are mosaics for two populations of cones, one expressing
  visual pigment genes encoded by an X-chromosome that would cause
  colour vision defects in males, and the other expressing genes that
  would confer normal colour vision on a male. In support of this,
  patches of defective colour perception were detected by shining a very
  narrow beam of red or green light into the retinas of female
  heterozygotes for X-linked colour vision defects. The majority of
  heterozygote women (carriers of colour vision defects) have normal
  colour vision.

This means that  – in most cases – for a female to be colourblind, her father must be colourblind and her mother must be either a heterozygote (carrier) or homozygote colourblind. In a male, only the mother's X-chromosome determines whether he inherits the defective genes, so he is more likely to have the colourblind trait.


text:
Does neural network in brain form cycles?
In other words is it possible for dendrite of neuron A to be connected with axon of neuron B and at the same time dendrite of neuron B to be connections with axon of neuron A (or similarly for any larger number of neurons)?
If so, are there any statistical data on number of such cycles in average human brain?

I don't think such direct loops exist. I haven't even heard much about small indirect feedback loops in neurons though feedforward are well known.

I wouldn't call them "cycles". "Both inhibitory and excitatory coupling were observed between pairs of mitral cells." from Reciprocal intraglomerular excitation and intra- and interglomerular lateral inhibition between mouse olfactory bulb mitral cells. It's dense reading but I think it's giving an example of your A and B.

In general neural networks are a lot less simple and directed than ANNs or artificial circuitry - connections can be inhibitory or excitatory, vary widely in strength etc etc. So unsurprisingly yes, recurrence is observed in actual neural networks. I don't know of any statistics on the frequency of such network structures, or even if such exists. Our knowledge of the brain at this fine level is still limited I think, the more global attempt to map 'the connectome' generally consider things at a higher resolution.

"...inhibitory or activating." I believe the official term is excitatory, not activating.

@CDB - true, fixed


text:
Lysosome function
Does any cell have lysosomes in it? Or maybe there are other organelles that do the same function. I read about it a lot and I can't find a good answer.

Yes, lysosomes (note spelling) exist. see https://en.wikipedia.org/wiki/Lysosome

The very first sentence of the Wikipedia article on lysosomes: "A lysosome (derived from the Greek words lysis, meaning "to loosen", and soma, "body") is a membrane-bound cell organelle found in most animal cells (they are absent in red blood cells)." So yes, any cell except RBCs would have lysosomes, as they are essential to the function of a metabolizing cell (which RBCs are not).

The function of a lysosome is to essentially digest and break down molecules (often compared to the stomach of the cell).
For example, a cell with high proportions of lysosomes would be a macrophage, as its function is to neutralize pathogens. After the pathogen is engulfed by the macrophage, the vesicle formed, called a phagosome, fuses with a lysosome, and the lysosome's digestive enzymes work on breaking down the pathogen into harmless bits and pieces.
In most cells, however, lysosomes also function to recycle the cell's own components, called autophagy. Damaged organelles are broken down by the lysosome and recycled.
So, yes, there are many cells that do have lysosomes.
The importance of the lysosome is shown when there is a malfunction in the lysosome. These diseases, called lysosomal storage diseases, occur when the lysosome does not function properly and the cell eventually is impaired by the buildup of a molecule that should have been broken down by the lysosome (e.g. Tay-Sachs disease).
References
The AP Biology textbook

Campbell Biology 7th Edition, Chapter 6 - "Lysosomes: Digestive Compartments", although this is pretty much the same in any edition of this textbook
Campbell Biology in Focus, Chapter 4 - "Lysosomes: Digestive Compartments"

Welcome, and thank you for your answer. You may want to consider an edit to provide some references to the information in your answer. It can help to provide the person who asked the question or others reading your answer who would like to research further a starting point.


text:
Large congregation of birds?
This year in October, I saw a lot of robins, male and female, finches and chickadees, and geese flying south.
Surprisingly I didn't see many juveniles from previous broods. My guess is that juveniles are harder to see.
And the robins were flying above me, looking for worms below me, and most ended up in tall shrubs. The finches stayed in place longer than the robins.
So why this big congregation of birds when it is still going to be relatively warm for most of the fall(which it ended up being)?
I live in ohio where it usually gets down to -4 in January and 90+ during the summer.

So, we typically think about migrating birds as living somewhere (North) and then traveling South for the winter. This way of thinking is actually not accurate according to a number of ornithologists, including many I used to work with/for. Thy suggest that the birds live in the South and migrate North to breed and to avoid overcrowding of Southern locales. (Though see this article that found support for the more often assumed N-to-S direction of migration). If 'South' is in fact their 'home,' then perhaps they will venture there regardless of weather patterns. However, perhaps neither of these thoughts applies to short-range migrators like robins.
Also, many birds migrate during the dark hours of the night, so I wonder if the birds you saw were even migrating, per se, or just moving about regionally.


text:
What are the tests performed by NASA's Mars rovers to establish that life could survive on the planet?
I am particularly interested in the Mars Rovers, which are out there trying to find life. Do they believe that the tests they perform are sufficient to verify the existence of life (Also please mention about the tests). How do they accommodate for the possibility of life forms different from the conventional carbon based as that of Earth?
I am really curious to get these answers, please explain.

You can check on NASAs website, as each mission has a page dedicated to it. If I remember correctly, I do not think that any of the rovers to date have technology to directly test for martian life forms. I think that the current missions are only able to test indirectly for conditions favorable to life and also possibly the evidence of organic molecules.

"How do they accommodate for the possibility of life forms different from the conventional carbon based as that of Earth?" - a very important question, life is just a human concept/definition applied to natural things, just like species. We could end up redefining life.

@rg255 I think that you need to remember that there are two things going for carbon as the basis of all organic life. The first is that it is the first element able to form 4 covalent bonds, which leads to the incredible diversity that we see in carbon-based molecules. Second, the second period elements are more abundant in the universe. There is still a good amount of silicon (The group four element below Carbon) but I would check the bond energies of silicon compounds and compare stability to their carbon counterpart.


text:
Where exactly is 'Colloid' with regards to synthesis of thyroid hormones?
I've researched colloid and it seems to be a substance of microfibres and thin films in which thyroid hormones may be synthesised, but I was wondering where this exactly is... I think it could be in the inter membrane space but I have no evidence of that, or is it just surrounding all cells?

Colloid is found in thyroid follicles and is composed of the protein from which thyroid hormones are made.
This link below states: "Follicles are filled with colloid, a proteinaceous depot of thyroid hormone precursor."
That precursor is called thyroglobulin.
The image below shows micrographs of the thyroid.
In the image, the colloid is surrounded by thyroid epithelial cells, which collectively form a follicle. The lower mag on the left shows many follicles filled with colloid.  The image on the right shows one follicle. The white areas inside the follicle near the epithelial cells show uptake of colloid by the epithelial cells, which are activity synthesizing thyroid hormone.

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/anatomy.html


text:
Can an argument be made that humans are 90% bacterial?
On the blog, All about Scientist in Microword: Microbiology, I read the post We are 90% bacteria, actually, which says that humans are 90% bacterial cells.
If this is the case, then why don't we behave like them and why isn't the bacteria genetic material more dominant?
As bacteria helps us in making many enzymes for us, can we say that we are symbiotic creatures?

Can you please cite the source you are talking about? Your point is not completely wrong, since we harbour indeed a lot of bacteria in our gut and on our skin and their numbers (depending on the source) outnumber the number of our cells by about one magnitude. Still, they are not part of us.

The bacteria within and on our bodies do engage in a symbiotic relationship – defined as an interaction between two different organisms living in close physical association. It can even be said that the relationship between certain bacteria and humans is mutualistic. For example, the bacteria residing on our skins and within our intestines benefit nutritionally, while we benefit from the bacterial "barrier effect".

One could consider energy: If you count human somatic cells as zero percent bacterial (you cheater!) then you ask what fraction of heat comes from those as opposed to bacteria. I think it is ~8% bacterial, almost all form the gut, but am not sure.

I am not sure what you read as you have not supplied any references, but humans are not 90% bacterial cells. (OP subsequently provided; see Edit 2)
Humans are 100% human cells, however for every one human cell, approximately 10 single celled organisms (Bacteria or Fungi) live in (colloquially) or on the human body. This is referred to as the microbiome. You can find more information in the link I provided or in the answers to the following questions on Biology SE.

Do intestinal flora have the same DNA as their host?
How many diseases can be linked to disruption in the microbiome of a human?
What is the function of E-coli bacteria in our stomach?
How heavy are all foreign microorganisms in and on the human body?

Think of it this way; just because the human body provides these organisms with a home does not mean that it is composed of them, that would be like saying an apartment building is made up of x percent of humans or pets or mice or insects just because that is where they live.
You may also find some interesting information at The Secret World Inside You from the American Museum of Natural History.
Edit

As bacteria helps us in making many enzymes for us, can we say that we are symbiotic creatures?

The definition of symbiosis is:

The interaction between two different organisms living in close physical association, typically to the advantage of both.

Given that definition, and given the fact that there are some bacteria in our microbiome that are able to produce metabolites that our cells cannot, and we provide them with a "home" with the necessary nutrients for their propagation, then you can say that this is in fact a symbiotic relationship.
The more technical description that is often used for the microbiome is that these organisms that populate the human body are commensal.
Commensalism is defined as:

An association between two organisms in which one benefits and the other derives neither benefit nor harm.

In this respect, the majority of our microbiome are commensals, they live on us, but give us nothing in return, and for the most part do us no harm.
Some of the organisms can be opportunistic pathogens in the sense that if they are able to gain access to normally sterile areas of our body, such as in peritonitis arising when the intestines are perforated, then they can be harmful, but in their general niche, they are just there.
As we learn more about the microbiome, we are beginning to see that there is a far more complex relationship between host and microbe than we anticipated, so over time, the views on the microbiome are likely to change from the understanding that we have today.
Edit 2
To address the source that you added All about Scientist in Microword: Microbiology, I would say that the blogger is guilty of hyperbole. While Steven Gill, the molecular biologist that the blogger quoted, may not have chosen his words carefully, he was not implying that humans are 90% bacteria, as the blogger then posits.
Gill makes the mistake of using the word "in" when he states "There are some estimates that say 90% of the cells in our body are actually bacteria...." The microbiome exists on the surfaces of our body not in it.
We forget that the gastrointestinal tract, urogenital tract, and respiratory tract are lined with epithelial cells and are thus external surfaces, just as our skin is an external surface. So the microbiome lives on our body, and not in it or as a part of it.
No place in our body do we have organs or tissue that is a homogenate of human cells and bacterial cells functioning together normally. And while there are bacteria that are able to infiltrate cells and live within vesicles or the cytoplasm, this is a pathogenic condition and not what we would normally expect to see in a healthy human.
We know that this is the case, because developmentally all of our body cells and germ cells arise for the fertilized egg. It isn't until much later in development or at the moment of birth (there are some reports that microbiome begins to cross the placenta prior to birth) that we acquire our microbiome. If it were the case that humans, or any eukaryotic organism for that matter, were 90% bacteria, then we would not develop in the sterile environment of the amniotic sac. The lack of bacteria during development would be fatal.

http://microbioresearch.blogspot.in/2008/06/we-are-90-bacteria-actually.html

this is the link where you will find about the fact I discussed.

@user101184 Please edit your question to include the reference. Also, you should quote what in the site brought you to your conclusion.

But we can say that 90% of human weight is actually bacterial. "and for the most part do us no harm." - we weigh more, so we are less enduring. We run slower and jump lower. Isn't it so? Then don't they cause us a disadvantage?

I just wanted to tackle the interesting numbers here.  So there are roughly 10^13 human cells in our body, and 10^14 bacterial.  That is where your 90% bacteria number comes from.
But remember that bacterial cells are much, much smaller than human cells.  E. coli ranges from 0.5um to 2um.  Human cells are ~100X larger at 0.1mm or 100um.  That translates to:
Surface area - E. coli is ~3.14um^2, human cells are ~32,000um^2.
Volume - E.coli is ~0.52 um^3, human cells are ~524,000um^3.
From an information content point, each of your cells contains 3 billion base pairs of genetic information, an e. Coli cell is ~4 million base pairs (bp).  So your cells contain 3^23 bp, while the total bacterial content is closer to 4^21 bp.  There is almost 100 times as much of your information as bacterial information.  Also yours is all the same, vs the different types, colonies, and progeny of bacteria in your body.  To put in similar terms as your question, while bacterial numbers account for 90% of your total cell numbers, their genetic information accounts for ~1% of the total.

Nice analysis and good insight.


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How do you calculate the charge on a polypeptide chain with changing pH?
I understand the charge placement on the N & C-terminus and also the utilization of the R-side groups in the amino acids.
For example,
What is the overall charge for a chain Glu-Cys-Arg-Asp with pH 11.0 buffer?

In theory, you can calculate the charge on every individual ionizable group (i.e. looking up their pKa and calculating charge by henderson hasselbalch) and just add them up to get the total net charge.
In practice you would need to measure it with something like isoelectric focusing, since polypeptides fold and certain groups end up interacting with other groups/being shielded from solvent, meaning you really can't calculate it accurately unless you had structural data and even then it would be extremely difficult.

This is about as straightforward as you can get for addressing a homework problem. For this, though, I think you can just eyeball the net charge if you know the R groups and pKa values: NH2(-1)(-1)(+1)(0)COO- = -2, for example. This may get a close vote due to the homework nature of the OP question, however.


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What effect is seen when the extracellular concentration of sodium is increased?
I can't seem to figure out how this would effect the cell since sodium is not very permeable.

Welcome to Bio. What cell? A human neuron behaves very differently than a bacterium at the bottom of the sea.

Don't expect tags to provide question background; they are basically not more than search terms. The answer below is likely not what you are after, but it answers your question perfectly. Vote to close.

The membrane isn't sodium permeable but it is water permeable.  Water will move from areas of high concentrations to low.  So when you increase the extracellular concentration of sodium, water will move out of the cell and into the extracellular matrix.  This causes the cell to shrink.

The question is closed, so answers can't be added, and existing answers generally should not be edited to add material.  Welcome to Biology stackexchange Patricia; try adding an answer to an open question instead of this closed question.


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How does the pancreatic beta-cell know how much insulin to secrete in response to glucose?
How do $\ce\beta$-cells know how much glucose is in the blood?
I know that when glucose enters a beta cell it triggers the cell to produce insulin. $\ce\beta$-cells trap glucose by converting it into glucose-6-phosphate, this means $\ce\beta$-cells actually consumes glucose.
So my question is: how do $\ce\beta$-cells decide when to stop producing insulin? (To do that the cells must know the level of glucose in blood, right?)

Yes, pancreatic beta cells can indeed sense the level of blood glucose. They respond to high glucose concentrations by secreting insulin, and stop (or reduce) secreting insulin when glucose concentration falls. This is a classic example of feedback regulation (homeostasis) in physiology.
Exactly how the glucose sensing in beta cells has been the subject of much research for decades; a freely available review is here. You are correct that phosphorylation and further metabolism of glucose by the beta cells is required for sensing. The current theory is that mitochondrial oxidation of glucose leads to increased ATP levels, which is detected by ATP-sensitive potassium channels at the plasma membrane, which in turn leads to secretion of insulin.
When glucose levels fall, beta cells reduce their glucose metabolism because they use the glucokinase enzyme to phosphorylate glucose, and glucokinase is a low-affinity enzyme that becomes inactive at lower glucose levels. Therefore, uptake and oxidation of glucose is reduced, ATP levels fall, and insulin secretion stops.
This is the current consensus I believe. But these metabolic processes are difficult to study, and the precise nature of the connection between glucose metabolism and the ATP-sensitive channels is still somewhat controversial.


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What does it mean to clone a gene?
When I look up information related to the identification of disease genes, texts will often refer to the gene being "first cloned." What does "clone" mean in this context? Is it simply a synonym for discovery?

Wiki > molecular cloning might help you.

Possible duplicate of Are there multiple meanings to "clone" as in "clone a gene"?

@Christiaan I would rather close that question as a duplicate of this one. Chris' answer below is much more informative than the one in the linked question. And yes, it is perfectly "legal" to close older questions as dupes of newer ones - we do it on Stack Overflow all the time.

@MattDMo, agreed. I retracted my vote.

@Christiaan I just submitted my duplicate/close vote on the other one - feel free to join in :)

@MattDMo - done :)

Usually this is used in the context of gene analysis and further characterization. What is done, is that a piece of foreign DNA (either generated by digesting genomic DNA (from human or mouse for example) or by PCR amplification) digested at the end of the DNA to have matching open ends with a bacterial vector.
The DNA of interest is then ligated with the vector and can then be replicated in bacteria and isolated easily in great yields. This plasmid can then further analysed (by restriction analysis, sequencing etc.), the gene or its promoter manipulated and mutated, or in case of protein coding genes the gene overexpressed in the cells. All this is useful to analyze the function of unknown genes. See the figure for a schematic overview (from  Campbell AP Biology Book 8th edition, via this website):

Technically making a clone means that you generate multiple genetically identical daughter cells from one precursor.

I think that might be a figure from Campbell Biology. I know you put a link, but you may want to attribute it... as it is copyrighted material. Figure 20.2 in the Ninth Edition, page 397.

Oh, I didn't know that - I have adjusted the information.

I have seen Campbell so much in my life that I can pick their graphics out from 150 meters... :-) Same with Molecular Biology of the Cell and Janeway's Immunology. I can usually spot Nature's cell biology graphics as well. They are all very branded and distinctive.

That's right. I never used the Campbell very much...

So basically, the act of cloning the gene is more or less necessary to sequence and characterize it, thus when people say that a gene is first cloned, they're effectively referring to its full characterization?

In the lab it means that you identified and isolated a certain sequence.


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Cause of a extra vertebra in the human body
Most people have five vertebrae in their lumbar (lower back) region, which are named L1 to L5. However, some people possess an additional lumbar vertebra located below the L5. This extra vertebra, known as the L6, is called a transitional vertebra. About 10 percent of adults have some form of spinal abnormality caused by genetics, and a sixth lumbar vertebra is among the most common of these abnormalities.
Question- What is the current explanation to why some humans have developed this extra vertebra in the spine?

What do you mean by genetic link? Are you looking for the names of the genes which variation explain variation in number of vertebrae? Or are you looking for the fraction of the phenotypic variation that is explained by genetic variation (namely, the heritability)?

Your phrasing suggests some confusion on these concepts and you might want to read on the concept of heritability (even if it may seem unrelated to your right now). On this post I linked 4 other posts (and the wikipedia article) that talk about heritability.


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What does it mean to have a Y-DNA Haplogroup "R-M512"?
I did a DNA test to learn about my origins, but the results are highly technical.
I see I have a Y-DNA Haplogroup R-M512 and a mutation (zero marker in DYS448). I Googled these terms and came across a bunch of technical papers, but I don't have the expertise in Genetics to make much sense of them.
I wonder if one of you can shed light on this?

Normally Humans inherit from each parent one sex determine Chromosome. If you have a XX chromosome pair you are female. If you have a XY pair you are male. Therefore the Y-Chromosome get only passed on from father to son. The Chromosomes itself consist of DNA. The DNA consists of base pairs in which an A only pairs with a T and a C only pairs with a G. The Y-Chromosome has about 57 million of these base pairs. DNA is normally relative stable but from time to time only one of these base pairs randomly changes from a C-G base pair to an A-T base pair. This phenomenon is called a pointmutation. So imagen two brothers. One has the unchanged Y-Chromosome of their father the other has one this pointmutations. So the descendants of the one Brother have the same Y-Chromosome, with exception of the pointmutation, the same Y-Chromosome. This is called a Single Nucleotide Polymorphisms (SNP). In the millennia the Y-Chromosomes acquire more and more of these SNPs. One combination of these SNPs is called a Haplogroup. By the amount of SNPs and the kind of them you can reconstruct which Haplogroup descended from which one. You have the Haplogroup R-M512 which is a rather old one (https://upload.wikimedia.org/wikipedia/commons/d/d4/R1a._Info-19.05.2014.jpg) and could be found in great area. M512 is actually the name of the last SNP that defines your Haplogroup. Here some people had write down which Haplogroup they belong to. By the ethnicity of the name you can assume how far it is spread ( https://www.familytreedna.com/public/R1a?iframe=ysnp ).
Another Name would be R1a1a. Maybe these papers help you more to understand the nomenclature ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155271/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288547/ ).
Short tandem repeats (STR) are small DNA sequences that repeat multiple times.  On the Y-Chromosome these STR can be referred to as DNA Y-chromosome Segments (DYS).  DYS448 has the sequence AGAGAT  with 20 to 26 repeats. Here ( http://cstl.nist.gov/strbase/ystrpos1.htm ) is visualized where actually  it is located on the Y-Chromosome.  In your case the laboratory was not able  to measure any repeats.


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Extraction of RNA from algae
I have used a standard protocol (I will give the bibliography below) to extract RNA from an algae (Posidonia) but I have get literally nothing, since I could not even see traces of the two rRNA. I think that I have failed because the huge quantity of salt and/or carbohydrates in algae in comparison with terrestrial plants. My final objective is to get mRNA and then sequence it, so I need a very good extraction.
Any ideas of paper I could read to go above this problem?
Gambino, G., Perrone, I., & Gribaudo, I. (2008). A rapid and effective method for RNA extraction from different tissues of grapevine and other woody plants.Phytochemical Analysis, 19(6), 520-525.


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Are carbohydrates an essential component of human diet?
Are people able to satisfy all the needs of a healthy diet without consuming carbohydrates?
My question includes the assumption that a person has no health condition that would prevent them from meeting their caloric needs with only fat and protein.
I'm also not asking about the practicality of eliminating all carbohydrates.  If a person could consume no carbohydrates whatsoever, this other question would clearly matter a lot, but I'm not asking it.
If there are essential dietary components that happen to be carbohydrates, but are not converted into glucose, I'll say up front that it wouldn't satisfy what I"m asking.  However, it would be interesting footnote on an otherwise correct answer.

While it's possible to live that way for some period of time, your body will be dying of stress. Your liver and kidneys will be first to fail. Your brain and muscles will struggle as well. Regarding your last paragraph, dietary fibers (comprised of different carbohydrates) are essential to maintain healthy digestive system and microflora, and the later has a tremendous impact on your immunity.

@Christiaan it won't. Beta-exidation of fats produces acetyl-CoA that fuels the citric acid cycle when there are no sugar resources left.

@EliKorvigo, thats interesting. Will look into that, thanks.

@Christiaan sorry for the typo, it was supposed to be "beta-oxidation".

http://ajcn.nutrition.org/content/75/5/951.2.long Check this out.

@243 interesting article from Journal of Nutrition - I've never though of carbs as being essential - given that fatty acids can supply power via beta-oxidation and all the amino acids are either ketogenic, glucogenic, or both - and thus can supply the TCA cycle via anapleurotic reactions. Sounds like the Inuit populations with almost no carb intake do just fine - suggesting that dietary carbohydrates are not required for life - very interesting

I've heard (link missing) that our brain functions on sugars and only after one day or two of real fasting the metabolism can switch to using ketons derived from (more compactly stored) fats.

From a theoretical perspective this is a very interesting question, mostly because it is difficult to completely abstain from carbohydrate intake on a normal diet. Even the popular low carb diets of the late 1990s and early 2000s (e.g. Atkins Diet, South Beach Diet) were just that, they were Low Carb, Not No Carb.
We know there are essential dietary nutrients for humans, like essential fatty acids and essential amino acids. The reason that these must be obtained in the diet is because humans do not have the enzymes to synthesize these nutrients de novo (aka, "From Scratch").
From a biochemical perspective we know that fatty acids and acetyl-CoA cannot be converted back into glucose or other carbohydrate intermediates. This is because of the irreversible biochemical reaction catalyzed by pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA. Thus, fatty acids (lipids) can be oxidized to acetyl-CoA (for the TCA/Krebs Cycle) but cannot be further converted to glucose within the body.
In terms of protein, however, amino acids are either glucogenic, ketogenic, or both. If amino acids are ketogenic, then this means they can be converted into acetyl-CoA for the Krebs Cycle. If amino acids are glucogenic, then it means that they can be broken down into glucose. The breakdown of amino acids can be used to synthesize glucose or for anapleurotic reactions of the Krebs Cycle.
As stated in the editorial noted in the comments of this question (From the American Journal of Clinical Nutrition), there are daily "requirements" for carbohydrates. However, it does not appear that any diseases are unmasked by very low to zero carbohydrate absorption (which is most closely occurs in the Inuit populations whose diet is entirely fat and protein).
So, if you ask the question "are carbohydrates essential components of a human diet?" the answer would be probably not. However, as mentioned above, carbohydrates are ubiquitous and it is impossible to abstain from all carbohydrate intake.

Below is a picture freely available online from this website (from Lehninger Principles of Biochemistry, 5th Edition) of the glucogenic and ketogenic amino acids and the metabolic intermediates to which they can be converted. This is how Krebs Cycle intermediates can be generated from amino acids and are not dependent on dietary carbohydrates.

Wouldn't ketogenesis on such a scale (for all glucose needed) lead to severe ketoacidosis?

@YviDe at first thought you might think so... but according to the article from American Journal of Nutrition it sounds like the Inuit populations live virtually as close to zero carbohydrates as you can get. It doesn't sound like they have any 'problems' like ketoacidosis. Prolonged starvation would also be a similar state - check out this great review from George Cahill...(http://www.med.upenn.edu/timm/documents/ReviewArticleTIMM2008-9Lazar-1.pdf)  I would guess that the development of ketone bodies would be gradual enough in a conversion to fats and proteins that the body could buffer it

Interesting. Is there data on the actual carbohydrate content of the Inuit diet? Meat does contain some carbohydrates, e.g. muscle and liver tissue contains appreciable amounts of glycogen, and all animal cells are thought to have a few % carbohydrate content in the form of ribose, glycoproteins, etc.

@Roland I don't think there is specific data on Inuit... but that American Journal of Nutrition article referenced above in the comments to the question is kinda interesting - I agree with you, though, some carbohydrates are everywhere

For completeness, it should be noted that the irreversibility of the pyruvate→acetyl-CoA reaction does not, in and of itself, preclude the conversion of fatty acids and acetyl-CoA into carbohydrates; plants do just that by short-circuiting the Krebs cycle into the glyoxylate cycle and releasing the extra two carbons as glyoxylate (which can then combine with acetyl-CoA to form malate, which can be turned into oxaloacetate, which can be used for gluconeogenesis) rather than carbon dioxide.  However, as almost all animals lack functional (1/2)

versions of the two enzymes required for the glyoxylate cycle to proceed, it is true for most animals that fatty acids and acetyl-CoA cannot be converted into carbohydrates.  (2/2)


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How are isovolumetric contraction and afterload related in the cardiac cycle?
In the cardiac cycle isovolumetric contraction occurs and causes a pressure gradient. The "afterload" is the pressure exerted on the ventricle from the artery.
Is the afterload the cause of isovolumetric contraction, or what is the exact relationship between them?

The important thing to remember is that the "afterload" on the heart is the diastolic blood pressure in the aorta. In other words, the pressure in the aorta that the heart must overcome to open the aortic valve and create a pressure gradient to force blood into the aorta and generate flow. The isovolumetric part of the contraction is the generation of pressure up to the afterload 'pressure'. Once the pressure in the heart is higher than the pressure in the aorta a pressure gradient is generated and the aortic valves open and blood flows out of the heart into the aorta. During this movement of blood the heart is contracting again and changing volume (i.e. not isovolumetric anymore).
If the afterload is higher (i.e. higher blood pressure or hypertension) it increases the work on the heart because it has to generate an even higher pressure within the heart to open the aortic valve to generate the pressure gradient and flow.
If the afterload is lower (i.e. low blood pressure or hypotension) the work on the heart (with all other factors remaining constant) would decrease because the pressure to open the aortic valves and create flow is lower. The diagram below is available online at this link. This is a very common picture/diagram that can be found in any cardiovascular physiology textbook.
Note: In the picture below the isovolumetric contraction is only the time between the two vertical lines as indicated. During that isovolumetric contraction you can see that the volume (i.e. the red line) stays the SAME, but the pressure in the ventricle significantly increases up to the point of aortic pressure.


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Why isn't the DNA in bacteria always split up and replicating?
Isn't helicase always free floating in bacterial cells, and the DNA without a nuclear membrane and uncoiled and freefloating and so why doesn't the helicase keep breaking the double helix of DNA? Also, since other DNA synthesizing enzymes like polymerase and RNA primer and other replication enzymes also free floating, so why doesn't the DNA in bacterial cells keep replicating at all times?

Bacterial DNA replication is initiated at the oriC by DnaA in E. coli. Think about ways in which DnaA binding or activity can be regulated in a way that inhibits or permits DNA replication. In recently replicated bacterial DNA, the DNA is hemimethylated (parental strand has a methyl group, daughter strand doesn't): An inhibiting protein binds to hemimethylated DNA, that can block DnaA activity at the oriC. A DAM methylase adds methyl groups after a while to the newly synthesized DNA, in which case DnaA may bind. Due to the lag between replication and methylation, DNA replication can't be continuously initiated! This is one of many examples (for example, DnaA must bind ATP for it's mechanism of action), but the take home point is DNA replication must be initiated and if it can't be, then it doesn't take place!
THE INITIATION OF BACTERIAL DNA REPLICATION
Breaking that down: (note, this is in E. coli)

DnaA is a protein with DNA-binding activity. When many DnaA bind at the oriC, it causes the DNA to bend open and loop. At this point, DnaB would have access to the DNA, and this is the helicase that unwinds everything for replication (you'll also see that DnaB must be loaded onto the DNA by DnaC, a helicase loader). So blunty enough, oriC is an origin of replication, everything starts here. There are repeats of AT rich regions denoted 13mer and 9mer in the oriC (number of bases in the region if you will). We know that this is beneficial because AT rich regions are easiest to pull apart due to the number of hydrogen bonds between A and T.
In the example I provided, the assumption is that the DNA of E. coli is methylated on adenines on both strands. When replication occurs, the new DNA doesn't have this methyl group on it's adenines like the parental strand. A protein that recognizes and binds so-called hemimethylated (half methylated) DNA, SeqA, binds where it can, including in the oriC. It blocks DnaA subsequently for a short time, and falls off the DNA on its own. The DAM methylase adds the methyl groups when it can, and once it does the SeqA can no longer bind, but the replication-initiation complex thus can.
There are other modulators of DNA replication, and the concentration of the DnaA itself is a big factor because you need many units of DnaA to bind to facilitate initiation. So then you have to consider is DnaA being expressed strongly enough? And this has it's own pathway outside the scope of this question.

Ok, I get some of it. Could you explain it at a little lower level (keeping in mind that I am still a highschool student but I have done extended research so you can use some jargon). What is DnaA? and oriC? So when the DNA is methylated, it can replicate? then what does the inhibiting protein does (what does blocking DnaA activity do?)? So according to the lag point, the DNA, methylation activates replication? I get the core point though :P

@SarthakGarg I made some edits that explain it a little more detailed. Always keep note that this is in E. coli and other families may adopt different strategies, but the take-home point is there (you need the initiation complex).


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Why do bacteria need messenger RNA?
Why do bacteria need mRNA? Isn't the DNA free floating without nuclear membrane so why doesn't the tRNA read the code directly off of the split DNA strands? (ofcourse after helicase splits them). Wouldn't this be more efficient?

DNA in bacteria does not float freely in the cytoplasm.

Ribosomes don't read DNA.
Transcription adds several layers of regulation tactics: you can control transcription itself, you can control mRNA.
mRNA amplifies genetic information that you need at the moment. Having many copies of a matrix really helps.
Some prokaryotes have splicing. It's not a good idea to splice your DNA.

EDIT per your request of some elaboration.

Why did they evolve to read RNA in the first place as they are primal
  to all other organisms, why did they develop this

The "RNA world" hypothesis (which is the most realistic early life model, considering the ever-growing body of evidence) postulates that RNA had been the main thing long before DNA was introduced into cells. The ribosome (being an RNA enzyme that doesn't require any proteins to bind amino acids together), along with many other RNA enzymes and regulators, is believed to be a relic of that world. Wiki has a good page with all the references you might want to read.

Also, the regulation tactics, isn't DNA free floating and so are all
  the replication enzymes like Helicase, primase and RNA primer etc. So
  how do they regulate the action of these enzymes as they are just free
  floating?

First of all, it's a common misconception that prokaryotic cells are mere bags stuffed with enzymes and whatever. Prokaryotes posses highly complicated compartmentalisation systems (some even possess nucleus-like compartments). Second of all, DNA is not "free floating": it's located at a specific site with a special molecular environment. If you want details, ask a separate question, or better a series of questions with narrow scope, because bacterial regulation is too diverse, bizarre and sophisticated to cover here (we had a 3 years-long course on this matter when I was a student).

Could you explain a bit of how the extra copy helps as is it not just
  more data to deal with?

When you have many copies of a matrix, many ribosomes can synthesise a protein at once. This comes in handy when you need to make tons of something as fast as possible. Remember, ribosomes are quite ubiquitous in all active cells for this very reason: to facilitate fast protein synthesis (at least as far as copiotrophic organisms are concerned).

What exactly do you mean by splicing?

I mean splicing: a group of processes by which introns are excised from primary transcription products.

Why did they evolve to read RNA in the first place as they are primal to all other organisms, why did they develop this? Wouldn't it have been more convenient to just have the the tRNA in ribosomes to just read the DNA? Also, the regulation tactics, isn't DNA free floating and so are all the replication enzymes like Helicase, primase and RNA primer etc. So how do they regulate the action of these enzymes as they are just free floating? Could you explain a bit of how the extra copy helps as is it not just more data to deal with? What exactly do you mean by splicing? @Eli

@SarthakGarg you're welcome

I find most of these arguments unconvincing and undermine the only reasonable argument, i.e. that the translation system developed in organisms with an RNA genome, with ribosomes and tRNAs already tuned to work with RNA messages. For reasons that we cannot know, a transcription system evolved rather than a DNA translation system.

@David I see your point, yet I believe you are approaching this question from a different perspective. From my perspective, the original question was about mRNA's utility in modern cells and not about the process that had resulted in this functional separation between RNA and DNA. Only later (in the comments above), this additional question had been raised and later addressed in the Edit section.

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


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Homework Question: Confused about figure related to cDNA and gDNA

what is the answer in blank?
I think the loop structure for the top blank is an intron.
I think RNA is the answer for the bottom blank, but it is cDNA, so it can't be RNA.
I cannot figure out what the question is asking. Please help me.

I think that the OP has tried to answer the question himself, so why close?

You are correct about the top loop being the intronic region of the gene that would be spliced out of the mRNA that was used to make the cDNA and will not have complementarity to the sequence found in the cDNA.
You are also correct that because it is cDNA, then it cannot be RNA for the bottom box. Remember that the cDNA will contain what the mature, spliced mRNA contained, 5'-UTR, coding sequence, 3'-UTR and Poly-A (Poly T if this is first strand cDNA) tail, so the bottom answer is likely an exon, as there is complementarity between the genomic DNA and the cDNA at that position where the arrow pointing.