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how does DNA and RNA work
How do the DNA modules tell the cell what to do?

Since this is pretty broad, have you tried looking it up in the Wikipedia and then ask some more specific questions? This stuff fills a few pages in biology books and probably no one wants to write this down here...

This question is too broad (and also a bit poorly defined). I will try to give few concepts to help you in your exploration of wikipedia articles. If then you have more specific question, we'll be delighted to help you answering them.
In very short...
The genetic information contained in DNA in coded through codons, which are series of three base pairs, there are 4 different base pairs, namely, A,T,C,G. Therefore, there are $4^4 = 64$  but these 64 codons codes for only 20 amino acids (in most species). By analogy you may consider a base pair as a letter, a codon as a word (all words are made of 3 letters) and genes are sentences. But many words are synonymous. The genetic code is said to be redundant.
DNA is a double stranded molecule, which splits in two around a coding region so that a RNA molecule can be created by copying the DNA template. This process is called transcription. This RNA is called pre mRNA. It is then spliced to become a mRNA (messenger RNA). The mRNA exit the nucleus. Two rRNA (ribosomial) RNA (which forms the so called ribosome) attach to the mRNA and tRNA (transfer RNA) will recognize the RNA sequence and paste amino-acids the ones to the others according to RNA sequence. This process is called translation. The molecule that is constructed is a polypetpide (a protein).
The quantity of proteins that are produced can be regulated by various mechanisms at different "moments": pre-transcription, pre-translation, post-translation.

Great answer Remi.  Along these lines, I wanted to impart an important concept to understand as you read.  Most proteins become either enzymes or structural components in the body.  The key to conceptualizing the DNA-->RNA-->protein process is this: shape determines function.   A strand of DNA is a template for which the Amino Acid (AA) subunits will be strung together in a chain.  That chain will fold into a complex shape.  The shape is determined by the interactions between the different amino acids.  Each AA has unique effects, causing the chain to twist, bend, loop, link together, etc.

Once the AA chain is done bending, it's a shape that is pretty much unique to that protein.  For enzymes: the shape of the enzyme determines what it can do, how it interacts with molecules, and where it can go in the body.  Shape is everything.  For structural components, shape is everything too.  Think of an engine - the shape of each component is critical to its ability to function.  Because the order of Amino Acids in the chain causes it to form a specific shape, that is why the DNA sequence is a template for the protein's shape - and ultimately, its function.

I agree with Chris that this is way too broad a question.  But if you want a very broad answer...
DNA is a long molecule consisting of a sequence of 4 different subunits.  The sequence of those subunits determines the shape of the DNA, and its shape determined how it interacts with other molecules, based on their shapes.
Computer code doesn't work like that at all, so I think you need to really strongly question your premise that knowing anything about computers is going to tell you much about biology.


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What does "substoichiometric amounts" mean in the context of molecular biology?
Recent paper:

PRC2 is composed of the histone methyltransferase EZH2, EED, SUZ12,
  and the histone binding proteins RBBP4 and RBBP7. JARID2, AEBP2, PHF1,
  MTF2, and PHF19 are also present in PRC2 in substoichiometric amounts.

Does this have a more specific meaning than "very little" or "very small amounts", which I presume is what it means?
Paper (paywalled): http://genome.cshlp.org/content/26/7/896.abstract

It possibly refers to fractional stoichiometry i.e. less than a molecule of these proteins per molecule of PRC2. Obviously, you cannot have half a molecule and this statement means that in a gross sample, the concentration ratio of these proteins with respect to PRC2 is less than 1:1. At a molecular scale, it would mean that these proteins may not be always associated with PRC2.
This is also in agreement with the known fact that PRC2 core components are EZH2, EED, SUZ12 (along with RbAp46/48) and the others are accessory factors (Margueron and Reinberg, 2011).

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recolonize earth desert with plants : which plants first?
if willing to recolonize earth desert , let's say sahara or any dehydrated and sterile land, without intensive human intervention, what would be the first plants / algae / fungi /bacteria to grow ?
what could be the strategy to slowly bring back biodiversity and trigger new water cycles ?

I think this is far too broad since you cover recolonization (for humans?), restoring biodiversity (from where/what?) and water cycles. Ask several smaller questions instead, preferably including your own ideas and preliminary research to answer them.

this question is answerable, but it just needs a longer answer...

This is a big idea that's gaining momentum in many people's minds across the world.  This is a brief and probably inadequate survey and hopefully other answers / comments will fill out a better picture.
Most of the plans to reclaim arid regions are not completely hands off.  It seems that the current thinking is that if we waited for microbes and lichen to reclaim arid soil, it would take too long.  Most of them focus on trees.
Trees are fantastic because they can grow in climates that have minimal water once they are established.  They can claim moisture from the air, remove pollution from the air, reduce the ground temperature, sequester carbon, prevent erosion, and make the environment more accommodating to other plants.
Some estimates are that to curb the expansion of deserts worldwide, 30 billion trees should be planted every year for the next decade.
The tree one plants varies depending on the place and application, but the selection of the plant is more than just a climatic choice.  Trees are grown in nurseries when their needs for water are most intensive, and then need to be cared for until they are established enough to survive on their own.
The Green Belt project was the focus of the 2004 Nobel Peace Prize.  Its success in rolling back desertification was because of its understanding of the causes of desertification in many cases as a social effect.*  People harvest the trees, graze the land dry, burn grassland etc.  Green Belt created networks of local people and incentivized them to grow trees, selecting trees which had agricultural and economic value so that they would help the local economy.
The Great Green Wall project is a successor to this idea.  Attempting to contain the Sahara desert's spread across the continent of Africa.   Their plan is to have a different organization in each country, including automation of sorts to collect water from the air and rain for more continuous support of young trees.

there are arguments that ultimately the animal ecosystem needs to be involved.

i suppose a strategy would be :
-find among xerophyte plant ( http://en.wikipedia.org/wiki/Xerophyte ).
-selecting plants that needs the less water, grow fast and expand on surface, and produce the maximum biomass.
-the soil produced by the pioneer plants would allow other plants to grow.
-these last plants would be selected for their better ability to condensate water and cool the atmosphere down and humidify it, and for producing more biomass that would allow a third pool of plants to grow

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In genome research, what is the problem in Mapping that may be caused by reads being too short?
In the following scenario: You were given short sequence reads of plant RNA obtained from a next-generation sequencing machine (fragments of 20–30 nucleotides in length). You attempt to map them back to the genome, but a significant proportion of them do not align.
The question is: give some obvious explanations why the alignment of short sequences can fail, apart from possible contamination or technical difficulties during the preparation of the RNA.
I would answer it as because reads are short, and because of introns(since it is RNA)
Another scenario: There are some indications that the problematic sequences come from an uncharacterised plant RNA virus. What would you do next? What are the specific caveats with short sequence reads?
I got the above questions, I am a computer science student doing bioinformatics, any biologist could answer it will be well appreciated

Welcome to StackBiology! Your question very looks like a homework question. You should have a look to the homework's questions policy. Because you haven't really showed attempts to answer the question, it is likely that nobody will answer it. Also, you should always try to limit your posts to one question only.

@Remi.b It is not a homework question, it is a past exam questions. I have attempted several answers. Thank you

There is no correlation of fragment size with its likelihood to arise from an exon-exon junction.
Some reads may arise from the adapters. They are generally filtered out.

You may also be interested to look at RNA editing in plants. Again, this doesn't connect to the small reads issue.

Being a bioinformatician as well, I am not really what you asked for, but I work with plant genetics so I'll try and answer anyway.
What you are mapping is RNA. So, as you already figured out, splicing events will be a problem for end-to-end mapping of the reads. There are tools managing that, though, so let's assume you used one of them and still a lot of your reads do not map. To put in WYSIWIG's good point: Another event that can mess up with your alignments is RNA editing, although this is not too likely to cause a high proportion of reads to not align at all.
Some aligners might filter out "too short" queries, so make sure you are not using one of them.
Then, have you preprocessed your reads? If you have not, there might be adaptor sequences left. Or may reads have very poor quality, thus are also aligned with poor quality, thus might be counted as unaligned.
And then check what you are aligning to. Many published plant genomes are also of minor quality, including lots of unassigned bases. So, there could be large proportions of your reference genome that count in the genome length, but are only Ns and nothing will align there.
Last but not least, your thought about a virus could also be right. Depending on the experiment, there might be pathogenic RNA in your sample, so check against a suitable database.
If the problem is only that the reads are "too short" for whatever reason, try doing transcriptome assembly before comparing to your reference.

Dear @skymninge, the question is indeed a exam question, I am not actually doing the experiment but trying to answer them.

Well then all of those are possibilities and the exam question as such is fairly broad. To get an example answer, you will have to ask the person that held the lecture and graded the exam.

I don't think it's possible to answer part 1 without more information.  Specifically, are you using a splice aware mapper, like Tophat?  Are you using a predetermined gtf with putative exon coordinates?  If so, is it for an extremely well studied plant, like Arabidopsis, or something brand new?  Your answer isn't right, introns would align to the genome fine.  The aligner doesn't know or care that those sequence shouldn't be in the sample, that won't affect mapping.  Personally, I don't think there is a very good answer to the question.  Short reads aren't more likely to fail than longer reads.  They are more likely to map to the wrong place, but that's not failure to map.


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Are human males and females more genetically different than members of other species?
I'm looking at this Ted talk about a Saudi Arabia woman who dared to drive a car in the last few years. This reminds me that until the last century or so, women (all over the world?) enjoyed less rights and might've been pigeonholed into roles predetermined by society. Those roles might've encouraged certain traits, and discouraged others. Those who did not conform might've been punished, like the woman in the talk above received death threats and was jailed.
This sounds to me like selective pressure, did it really exist, and did it have any effect on the genetics/traits of modern women?
This makes me interested in the question - compared to other species, are men and women more genetically different because of selective pressure put on women to conform to male-dominated world for thousands of years before 19th century?

Males and females have essentially identical genomes (differing only in the very small Y and mitochondrial chromosomes), so they essentially don't differ at all.  This is true in other mammals too.

Since asking this question, I've learned that there's a massive amount of differences between male and female cognition, as explained by Evolutionary Psychology.

Females eating male spiders puts a lot of pressure on genetics too. Sea lions, lions, peacocks and hyenas also have probably as much pressure... sharia law is one of the most extreme sexual religious laws that has existed for only 1300 years, not all of human evolution. Chinese, African, etc law is 90% tribally moderate with plent of ancient civilizations having female leaders and warriors.

humans in general are incredibly genetically similar, its obvious we lost most of genetic diversity during a bottleneck.

I'm not sure I buy your premise: firstly, the degree and form of male-female differentiation in social roles has varied widely across time and culture in human history so I doubt it forms a uniform evolutionary driver such as you describe. Secondly, the degree of male-female differentiation appears to me to be much greater in species such as gorillas, lions and peacocks than it does in humans so I'm not convinced that humans would stand out on this front as a species we'd expect to have greater genetic differences.
Even so, the only genetic difference between male and female humans is the Y-chromosome. The X appears in both males and females and doesn't have exclusively female lineage so it can't acquire separate genes for male and female. The Y chromosome contains very few genes so its not capable of manifesting a major genetic gap and because there is no recombination in the Y chromosome it is not a fertile ground for new genes anyway.
So males and females have essentially the same genes. However, this isn't the whole story because how, when and whether genes are expressed is about as important as what genes are encoded anyway. It is these differences that enable big differences between the sexes not actual coding differences.

It would be interesting to check (maybe someone has already, I don't know) whether the epigenome of men and women is different!

They are different. Google 'sex differences in epigenetics' and you'll see there's quite a few papers on the subject. It's not my area so I won't claim to know the details.

If I understand your answer correctly, because most of the genes(that matter) are in the X chromosome, then selecting for a specific trait in females would also produce it in males, because it's most likely that the X chromosome would be involved. Is this correct?

Almost. Because genes can be differentially expressed you can still get differences in males and females even though they both share (almost) the same genes but there can't develop a major gap between male and female genomes because they share almost all the chromosomes. The Y chromosome is the only exception but it's not a healthy chromosome because it is exclusively passed down the male line and thus can't rely from recombination to "repair" damaged genes and shuffle genes into new contexts.

Essentially, what makes a (mammalian) man a man is a small region on the Y-chromosome called SRY. If this region is deleted, a female phenotype having XY-chromosomes develops. If this region is translocated to an X-chromosome, a male phenotype with two X-chromosomes develops. Other than that, the Y-chromosome does not carry a lot of genes.
So apart from the Y chromosome, males and females are genetically very similar and more similar compared to other species.

Are men and women not identical except the Y-chromosome (Not only similiar)?

Similar in the sense of interindividual differences in the genotype. If we were identical, we'd be clones.

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Can cerebrospinal fluid deliver nutrients/drugs to neurons during sleep?
I'm looking at this article on the possible mechanism of detoxifying brain during sleep using cerebrospinal fluid. It states that at night, the space between neurons may allow better (up to 20x) circulation of cerebrospinal fluid within the brain to clean out metabolic by products of daytime activity.
My question is if this may also work in reverse and allow to deliver drugs within the fluid to the brain.  If a person ingests a drug or nutrient before sleep, would the increase in circulation of cerebrospinal fluid deliver the drug to deep regions of the brain? Or does the blood-brain barrier prevent drugs from entering cerebrospinal fluid?

Certain drugs can cross blood-brain barrier. In such cases your hypothesis should be correct.

Only certain drugs can cross the blood brain barrier (BBB). However, there exist techniques to deliver drugs to the brain that otherwise cannot permeate through the BBB.
One such technique is called intrathecal delivery that injects drugs directly into the cerebrospinal fluid, avoiding the BBB problem and allowing the drug to reach cells, including neurons, in the brain. It has been used for certain kinds of chemotherapy, pain management, treatment of spastic cerebral palsy, and more recently for enzyme replacement therapy.
However with intrathecal delivery there is a risk of infection.
Having said that, if a drug reaches the CSF then your hypothesis should be correct. There is no experimental evidence for it yet.


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Help identify this awesome climbing plant with velcro like stem
I got this plant sprouting in my window box this spring. Starting from a single seed, it has grown into an impressive array of branching climbing vines, reaching 6 feet tall. The stem turned red as it matured. The most awesome feature of this plant is that the stem is covered in micro hooks that cling to everything. I've seen it cling to a paint on a metal gutter pipe I can think of these hooks as velcro or gecko feet.
Can someone help me identify this plant?

climbing vine
stem is covered in tiny hooks that are very clingy
grows to 6 feet tall
stem turns to red as it matures
segmented leaves
leaves grow to palm size
new leaves sprout from stem where old leaves were connected
 -

In what general region of what country is this plant? Do you know if it is native or if it cultivated? Also, check in with Gardening and Landscaping.SE as someone there may be able to help you.

I don't know its name, but kill it now! Some bird dropped it. This plant appeared in my yard five years ago and now it's choking everything. It is the most invasive weed I've ever seen.

I think this might be Japanese hops. Well, what I have in my yard is Japanese hops.

As I said, it's horrible.
Description and Biology:

Plant: herbaceous annual, twining, shallow-rooted vine that can climb to heights of ten or more feet with the help of rough-textured stems covered with short, sharp, downward pointing prickles that can be very irritating to the skin.

Leaves: leaves are rough-textured, paired, simple, palmate (like a hand) with typically 5-7 lobes; leaf margins are toothed.

Flowers, fruits and seeds: flowering occurs in July and August; male and female flowers are borne on separate plants; male flowers are very small, greenish yellow and occur in branched panicles; female flowers are in pale green, plump, drooping, cone-like structures with overlapping scales that become ‘hops’; hop scales and the seeds are covered with yellow glands; seeds are about 1/8 in. in diameter, roundish with a blunt tip, and light brown with darker specks; seeds mature through September.

Spreads: by seed which begins to germinate in early spring, but new plants may continue to emerge as the season progresses if sunlight and moisture are available; seeds are dispersed by animals (including people), machinery and floodwaters.

Look-alikes: native common hop (Humulus lupulus) looks very much like Japanese hop but it is usually 3-lobed or unlobed; native bur cucumber (Sicyos angulatus) lacks prickles, has tendrils, and the leaves have much less pronounced lobes.

Prevention and Control: Do not purchase, plant or transplant this species.

@Alex Stone - sorry it took me so long to edit with more info. Really, trust me, kill it before it sets seed (which it's doing right now.)

Thanks for the description. The plant never had a chance to flower and is mostly dead now. I will dispose of the rest of it.

The Velcro Vine, known variously as Cleavers, Goose Grass and Bedstraw is botanically known as Galium aparine. New spring growth can be juiced or eaten in salads or on sandwiches. It can be used to stimulate and decongest  the lymphatic system and as a diuretic to remove excess H2O.

Can you add sources and an identifying image of the species so people can background read on your answer?

That plant clearly is not galium aparine. Leaf morphology is completely different. Not sure what it is, but it grows as an invasive weed in my garden in Burlington, VT. Please DO NOT try to eat it.

This is not cleavers. Not by a long shot!


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Are there specific features of birds that cats/small predators are attracted to?
I've recently heard a podcast, in which a professor describes one of the theories as to why we like abstract art. In his talk, he mentions an experiment with seagull chicks, in which the seagull chicks mistake a stick with a red dot for their mother's beak, and in the case of stick with 3 stripes actually preferred it to their mother's beak. When a stick like that is waved around a chick, it starts to peck at it, believing it is mother bird:

This experiment suggests that birds are imprinted to recognize specific patterns and interpret them as mother.
I'm in trying to create a similar experiment for cats. To do so I'm trying to understand if cats other small predators (ferrets,etc) are imprinted in a similar way - do cats recognize specific features of a bird to identify it as "bird", "prey" or "can hunt and eat"? I'm talking about stuff like - do they recognize eyes, beaks, wings or tail in a special way?
To paraphrase the question: If I'm to create a stick like above, but for cats, what features would be painted on the stick?
I know that butterflies, caterpillars and other insects have evolved to mimick "eyes" on non-vital organs to confuse birds. I'm interested if same stuff exists for small mammal predators.

Heh, what an interesting idea! I suspect you won't succeed (though I hope I'm wrong), I think that cats are more attracted to movement than anything else. They seem to jump at anything that moves.

insects and birds with tiny brains are easier since they have small brains.  larger brained creatures are harder to hack.  cats might not be so easy to fool. also depends on where the wiring is.  bats use scent primarily, which is hard to hack.

@shigeta they do? I would have guessed they use their echolocation.

to identify their young ones - in some cases - when the ceiling of the cave is crawling with baby bats... sorry i don't have a reference - saw it on a documentary on carlsbad caverns.  some bats see just fine - not sure if scent is always important... mice, closely related to bats do as well, so this may be the result of adaptation as well as limitations on brain size etc..

Movement is definitely part of it. I noticed that my cat likes to chase dried cranberry more than a similar sized plastic ball or a rock. The cranberry bounces in a different way, or maybe it's the seeds rattling inside.

Texture might be a part of it. Cat responded with surprise to a still piece of artificial fur. It seems the cat knew that fur might be an animal.

Maybe a random approach could get some answers, if you had a computer program output random patterns to a screen and some method to watch the cat and record when it's interested.

My cat ignores the last pointer but loves to play with a real dark red cranberry. Red might be a clue

Not all cat predatory behavior is innate. Researchers found that cats predatory behavior for birds vs. mice depends to a significant degree on training by the mother: if the mother taught predatory behavior with birds, the kittens grew up to be better at catching birds than at catching mice and vice versa. Supportive data shows that aside from monkeys and other primates, cats are among the most adept at learning by observing the successes and failures of other animals attempting to complete tasks to obtain a reward. This might influence, therefore, a cat's response to and attraction for objects in the air or on the floor.
Blindfolded cats can hunt mice by vibration. Paul Leyhausen, a German animal behaviorist studied domestic cats (and related felines) from the 1950's through the 1970's, and much of what is known about their predatory behavior is thanks to him.
Although their vision is not especially keen, domestic cats see well in dim light and readily perceive motion. According to Leyhausen, prey movement and the direction of movement are the only factors which innately release crouching, stalking, and catching behaviors in cats. When presented with quail, cats were far more likely to go after active quail than those stilled by tonic immobility. Cats are also more likely to go after smaller prey (mice > rats) and mice were much more likely to elicit play pawing.
Leyhausen also demonstrated that rodents were probably the natural prey of cats.
Though there has been much study of cats and predation, little is available on detail of the kind you are interested in.  My best guess for a good toy for a cat would be a smaller object that moved along the floor.
More information can be obtained from Leyhausen's book, Cat Behavior: The Predatory and Social Behavior of Domestic and Wild Cats.
Effects of the mother, object play, and adult experience on predation in cats
The effects of experience on the predatory patterns of cats
Tonic immobility in Japanese quail can reduce the probability of sustained attack by cats
The behavioral bases of prolonged suppression of predatory attack in cats


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How quickly can the human heart rate rise and fall?
How quickly can the human heart rate rise and lower?
For example lets say a human heart rate is rested and is at 60BPM and that person is suddenly scared to trigger their fight or flight reaction. Lets say their heart rate rises to double (120BPM).
From the above example their rate has gone from 1000ms between beats to 500ms between beats. Can the human heart instantly in one heart beat go from the 1000ms to 500ms between beats or does it need to ramp up? If yes how quickly can the heart rate ramp up?
I understand that each human heart is different, and that the speed increase and decrease will be different from person to person. What I'm looking for is a value that I can safely say the human heart won't exceed.
Similarly the same question goes to your heart going lower.

Heart rate is controlled beat by beat by the brain. Infact the native rate of the heart (the sinus nodal rythym) is around 100 beats per minute. The parasympathetic supply to the heart (through vagus nerve) supresses the rate to around 70-80. So if the parasympathetic flow is supressed, the heart rate will accelerate. Nerve conduction speed will then be the limit of speed at which the heart rate can be regulated.

According to the Wikipedia page on Supraventricular tachycardia the heart can go to a new faster rate in the space of a single beat, and then come down again just as quickly, as shown in this image taken from the Wikipedia page.

Thanks for the evidence. I was hoping the above not to be the case so I could apply some sort of validation off the readings from the pulse sensor I am using.


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What is 'calcium conductance'?
What is the meaning of calcium conductance in ion channels. I encountered this in the following text:

It was established that the µ and δ opioid receptors open potassium
  channels, which results in reduction of calcium conductance (Simon, 2005).

Also why should opening a potassium channel reduce calcium conductance. How are they related ?
Reference:
Simon, E. J. (2005). Opiates: Neurobiology. In J. H. Lowinson, P. Ruiz, R. B. Millman & J. G. Langrod (Eds.), Substance abuse : a comprehensive textbook (4th ed., pp. xxiv, 1421 p.). Philadelphia: Lippincott Williams & Wilkins.

This might be a mistake in the text you read or the referenced book. Opioid receptors can regulate calcium channels as well as potassium channels.

@MadScientist you're right that opioid receptors regulate both calcium and potassium channels but the snippet is about mu and delta receptor types. The text also says:
The activation of κ receptors was found to reduce calcium conductance by closing calcium channels. It was recently found that all three types of opioid receptors can act by both mechanisms; i.e., they can open potassium channels or close calcium channels

Conductance is the inverse of resistance, and measures how much of a given substance flows throught a channel. In this context, it means how many calcium ions enter the cell in a period of time.
There are at least two ways potassium channels may prevent the calcium to enter in the cell.
1) Potassium intake by ion channels decrease the membrane potential, restoring it to its rest state. Since many calcium channels are voltage-dependent, a reduction of the membrane potential would close them, effectively decreasing the calcium conductance.
2) Potassium channels may be coupled to different signaling pathways (i.e. G proteins), wich may affect indirectly other calcium channels.
In the case of opioid receptors it seems to be the first mechanism. With potassium channels open, the neuron is less likely to be activated, because it needs higher stimulation to reach the action potential. Calcium channels open in neurons mainly during action potential events (althought they may exist other calcium channels that open in other conditions, i. e in response to hormones or neuromodulators).


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What is a good list of unsolved protein structures?
I'm trying to get a list of unique soluble structured proteins that don't have a solved structure. That is, they aren't the usual membrane proteins or some derivative of another protein.
Things that I've been able to think of are low producing transcription factors and novel fusion proteins.

You can build it yourself by comparing protein names (of the species of your choice) and PDB records. UniProt flat files have PDB accessions for some, not all proteins. Extracting the entries with no PDB should be a good starting point. Let me know if this interests you and I can write up an answer with the details.

@terdon, that pretty much sounds like what I'm looking for. Unfortunately, there might be a significant number of proteins that have analogs in other species but essentially the same structure. Probably the safe test would be to look at the unsolved structures in ecoli.

@leonardo, well that seems to be a challenge.

There are some funded projects and analyses available just for this purpose.
Structural genomics or high throughput structure projects take all available peptide sequences group them into families and make sure sequence families pointing to most likely novel folds were available.
Here are the status and target list for the joint center for structural genomics. This list is filtered by species as well as by project status.
Their analysis is availble for us to browse through.  http://www1.jcsg.org/prod/newscripts/psca/help/document.cgi
Sorry this isn't so thorough.  Nature also hosts Target Track, which allows several high throughput structure centers to coordinate their efforts.  Each might have resources which could do your work for you.

Try looking at structure homology databases - the sequences that they have no annotation for are likely the kind of sequences that you are seeking.
SUPERFAMILY has a comprehensive annotation across almost 2500 fully sequenced cellular genomes. this would be a good place to start ...

This is how I would do it:

Download the UniProt/SWISSPROT flat file for bacteria from here.
After decompressing the files, extract the E. coli protein IDs for which there is no PDB annotation in the file (I am giving you a command line that will work on *ix systems (Linux/Unix/OSX etc)):
zcat uniprot_sprot_bacteria.dat.gz | gawk '{if($1~/ID/){if($2~/_ECOLI/){id=$2; frag=0; eco=1; want=1}else{eco=0}}  if($1~/DE/ && $0~/Flags: Fragment/){frag=1;}if($1~/DR/ && $2~/PDB/){want=0; } if($1~/\/\// && want==1 && eco==1 && frag==0){print id}}' > no_pdbs.txt

Explaining the details of this command line is clearly off topic here :). Suffice it to say that it will print those UniProt IDs from the flat file
whose name ends in _ECOLI and for which there is no PDB annotation in the file. It also ignores protein fragments. If you need help understanding it, let me know and we can chat or something.

The result of this quick and dirty analysis is a list of 2694 E.coli proteins with no PDB annotations in the UniProt flat files.
CAVEATS:

These are only the curated SWISSPROT proteins, you may want to also get the UniProt/TrEMBL proteins from here. I would recommend you stick to SWISSPROT though.
As others have pointed out, you should filter this list for homology to other known structures.
The fact that there is no PDB annotation in the flat file does not necessarily mean that there is no known structure.

So, this is not perfect but it should serve as a starting point. Good luck!

You can also filter for different protein model databases like "ProteinModelPortal" to get rid of proteins that can be modelled based on homology.


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Gene perturbation, what is it used for, explain to computer scientists?
I am trying to build a gene regulation network, and I need some basic knowledge of it.
So, in gene research, we perturb genes. Such as knock down them?
Can people tell 2 or 3 experiment methods to perturb genes?
And 3 or more observations (phenotypes) after perturbation?
If it could be explained in the context of Microarray, it will be well appreciated.
The question is not that organised, if you can tell a whole story before the computational work started, I will thank you so much.

I'm afraid this is really a bit too broad. Perturbation can mean very many things from changing the expression level, to switching genes on or off, to altering the protein produced. The phenotypes will depend both on the particular perturbation applied and on the specific gene perturbed.

@terdon Thanks for your comments, What I am asking is how to perturb genes ? How to do experiments to perturb genes ? and what are the possible phenotypes/outcomes after perturbing ?

This questions doesn't fit the SE format too well. While there are several ideas that could be good questions on their own ("how can genes be perturbed?", "what phenotypes result from gene perturbation?", "how is gene perturbation used for microarrays?"), it seems like this question wants someone to write a report tailored to this person's research needs (how many future visitors will benefit from such an answer?).

@GeekCat, currently your question is too broad and actually includes several sub-questions. You are more likely to get a good answer if you break it down into distinct separate questions. For a start, I would recommend that you ask "What does gene perturbation mean in the context of gene regulatory networks and how is it achieved practically?" as this will help you to understand what else you need to ask.

Here are 3:
1) gene knockout.  Just delete the gene from the genome.  The function is gone - useful for demonstrating a direct involvement of the gene in the phenotype.  As a phenotype, the microarray will register all sorts of reactions to the loss of the gene in addition to the RNA in question being gone.
2) use selection to find mutants for the gene.  Expose the organism to a mutagen or high amounts of UV radiation.  Useful mutants vary by what the function of the genes are.  Temperature sensitivity - the gene doesn't function above 30 deg C is an example of a phenotype for a mutant that has been used classically.  In this case the functioning of the gene itself is a phenotype.  This is an example of a weaker perturbation.  Can be used when knockouts are fatal or when the system is too sensitive for a knockout.
3) change the environmental conditions. increase the concentration of a substrate or lower the availability of nutrients.  Phenotypes can be rate of growth/division, production of a given metabolite from the cells, but it goes on and on.
The affect on whole genome microarray data can be quite complex in such perturbation experiments because the coupling of many genes, even in bacteria can be broad and significant.

Thanks, @shigeta, could you please give 3 possible phenotype outcome of it ?

well the microarray itself is often the phenotype itself - RNA production.   That's why its so popular as a technique.  Mutant studies have a measurable phenotype such as a the amounts of a chemical that is produced in the cell, or the rate of growth.  Phenotypes are a very broad topic - they are essentially ANY observable w.r.t. a cell or an organism.  that's a very large list if you include observations by instrumentation.  Its akin to asking a mathematician to list all the properties of numbers.

Perturbation is when you either introduce a gene or gene product or inhibit it using a variety of approaches to see what other genes show changes in expression or other epigenetic modifications, which can be measured using a microarray.
If genes A,B,C,D,E are expressed more due to the activity of Gene X while F,G,H are unaffected, when you compare microarray data from samples where X has been turned off to those where it hasn't, you will see decreased expression of A,B,C,D and E - you can represent this as a graph with Gene X being the hub.
Hope this helps,
Ankur.


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How to calculate the LOB, LOD and LOQ of an enzyme assay
I understand how to calculate limit of blank (LOB), limit of detection (LOD), and limit of quantitation (LOQ) in the traditional way i.e., average and SD of raw analytical signal of blanks and low concentration samples. But the enzyme assay makes things unclear. I am not sure what measure to use in my calculations.
The enzyme assay with seven calibrators produces a very nice dose-response that I fit with a nonlinear regression model (4-parameter aka. Hill equation). Running blank samples gives three relevant measures that I could use to calculate LOB, LOD, LOQ:

Raw absorbance at 405 nm

Problem here is absorbance increases over time as the enzyme goes to town on substrate. Results across multiple experiments are not comparable. Not a good candidate.

Normalized enzyme activity (as a % of uninhibited control)

I like this option the best because it's not time-dependent. Blanks run on various days are comparable.

Concentration (ng/mL)

Concentration is interpolated on calibration curve using % activity as the input. Problem here is sometimes the nonlinear model cannot calculate results that are beyond the upper asymptote (parameter A for those familiar with the Hill equation). So roughly half of my blanks don't get a concentration.

I feel like I want to proceed using % activity as my measure for calculating LOB, LOD and LOQ but it just doesn't feel right.
For example, my 20 blanks run over 8 experiments have an average enzyme activity of 99.4% and standard deviation is 2.2%. If I calculate LOB the traditional way LOB = mean of blank + 1.645*SD of blank, I get 103% which doesn't make sense (it should be mean - 1.645*SD instead, which gives 95.7%). First red flag.
I need to report my LOB, LOD and LOQ to external stakeholders. No one is going to understand what it means when I say my LOB is 95.7% activity, LOD is 92.1% activity, and LOQ is 77.2% activity. They'll want the limits expressed in terms of analyte concentration.
But... to go from % activity to ng/mL, I have to interpolate on my calibration curve. But I got the data from 8 separate experiments. Am I supposed to average out the curves for the 8 experiments and use that to turn % activity into concentration?
I would really appreciate some help on this one. Everyone in my lab is pure analytical chemistry and they don't get the whole enzyme thing.


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How do non-dimorphic birds distinguish sex of possible partners/rivals?
Some birds, such as my pet Pionus chalcopterus, are not sexually dimorphic.  People can't tell them apart, and even trained avian vets are not 100% certain with an inspection probing the vent.
I understand that when not "in season" there is no physical difference as internal sex organs are atrophied to save weight.
But how do they tell the difference?
Do they have dimorphic markings that bird eyes (but not humans eyes) can see?

Since we're not birds there's no way of knowing for sure, but I would imagine calls/songs and possibly pheromones have something to do with it. There may also be anatomical differences as well that humans haven't discovered yet.

Behavioral differences are likely a part of it, at least for some species.

As very well explained also in Wikipedia https://en.wikipedia.org/wiki/Sexual_selection_in_birds , visual signaling is only one of the way birds uses to pick a partner, olfactory and acoustic signals also play a major role.

Thanks for the link. I would still like to know about Pionus specifically though.

I can't find anything about Pionus specifically, but I don't see why it should be different.


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How to measure the biomass of hydroponic plants in netpot/rockwool DWC system?
I'm doing an experiment with 4 kale plants, each in their own small deep water culture (DWC) system. Each plant was transplanted in rockwool with netpots and clay pebbles. But I need to periodically and accurately measure the biomass of each plant. The roots have grown through the rockwool and netpots and I don't want to rip out the roots.
Is there an easy way to do this?

If you did enough replications in your experiment, you could harvest one or more plants and measure fresh weight, and then gently oven dry for about 48 hours at like 160 degrees F and then take a dry weight as a measure of biomass. I don't know a non-destructive way to do it. A lesser alternative would be to measure plant height and number of leaves, though this would be less accurate. There are devices that measure leaf area, and I know a simple, low-tech way to measure leaf area.

we appreciate references to all answers to allow all users a chance to try and understand the answer and go for more information - you might want to add some references as this would strengthen your response


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Accurate Human Skull Model for Educational Purpose
I want to buy a model of Human skull for education purpose. However, I really want a very accurate model and at a decent price. I got the info that many of the available skulls in the market are not accurate.  Can anyone suggest me one?
Also I want to know is there any regulatory body that certifies such
educational models regarding the accuracy etc.? If not then what is the way I can ensure that I am buying an accurate (or most accurate) model.

Product recommendation are often seen as not strong questions across the network, however the second part of your question is very interesting

Maybe you can find and print a 3d model near your location?

I am unable to understand why is location important, when I can order online

@gpuguy this is very difficult to answer without knowing: what models you have been told are inaccurate, how/why they are insufficiently accurate, what you need the model for, how accurate you need the model to be, what features you need to be accurate... There is never going to be the perfect skull model because everyone's skull is different and there is considerable natural variation in skull morphology, illustrative examples: http://www.understandingrace.org/images/482x270/science/early_class.jpg and http://news.nationalgeographic.com/news/bigphotos/images/070718-african-origin_big.jpg

The best way to ensure you're getting an accurate skull, near as I can tell, is striking the "model" part of your question, and go straight for a real skull.
A cursory search revealed, for instance, Skulls Unlimited International, The Bone Room, and The Evolution Store although other providers probably exist as well.
A regulatory board for model skulls probably doesn't exist, given the apparent ease with which real skulls can be obtained and kept.


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If I built a concrete pool, would it ever contain fish?
Imagine that I built a concrete-walled pool the size of a football field and filled it with fresh water - obtained from another lake but free of bacteria, plantlife, eggs, etc.
Would it ever, over time, become a life-filled "lake" - with fish, amphibians, algae, plants and other water-dwellers?
If yes, how?
What would the chain of events look like?  I'm assume plant-life would get there first but how would it develop an established eco-system?
Please re-tag as appropriate as I am new to this SE site.

The short answer would be yes, given enough (long++) time. The situation would be similar to e.g. newly formed volcanic islands or when bare rock is exposed after a glacier disappears. However, the specifics are really hard to answer and would depend on the geographical location and stochastic colonization events, and you won't get a definite answer on a Q&A. Look into the vast ecological litterature on colonization and succession. A likely chain of organisms would be someth. like: Bacteria & phytoplankton-> zooplankton-> invertebrates & plants-> vertebrates (e.g. birds and amfibians first).

Also look at Hydrosere succession, which describes long term succession in fresh water bodies.

@fileunderwater Assuming that you don't also build a bunker around the pool, and that you live near or in the path of migrating species (especially birds, and you probably do), it actually doesn't take long at all.  Higher level animals are going to land/bathe/drink it, as they do they are going to bring a whole host of life with them, including the possibility of fish through eggs.

@AtlLED The "long++" part was referring to fish. I agree that birds and flying insects will visit quickly (they will spot a fotball-field sized pool). I read the questions mostly as asking whether a natural lake ecosystem will develop over time.

If the pool was stagnant, I can imagine that algal spores would be among the first to reach the lake. The algae could 'suffocate' the lake and make it very cold and even poisonous if certain species of algae bloom. I hope one/some of the answers discusses this.

@goodgravy your scenario requires a healthy dose of nutrients

@Abe A very good point about nutrient rich water, especially considering we are starting from a blank slate. There many are trace elements in concrete, notably calcium. This is usually one of the limiting factor in algal growth. The other problem is nitrogen. This is where my theory has a weak link, yet I don't think we should dismiss that algae could thrive on whatever other micro organic matter found itself in the lake. Obviously if we were to discuss this further we would need more specifics on types of concrete, geographic location, animal contamination, pollutants etc.

@goodgravy algae don't thrive on organic matter, they thrive on mineral nutrients, N and P in particular. Ca is important but rarely limiting.

@Abe If you are intentionally trying to grow algae, you get a pot of water and leave it in the sun. Algae will grow. This is sped up by the nutrients, but there will be enough for slow growth from microscopic spores, fish eggs, seeds bacteria etc. This question is a scaled up version of growing algae in a pot.

if the pool were just sitting out in open air, on earth and all that good stuff, it certainly would, given enough time.
This thought experiment is in the same vein that inspired Darwin when he reflected on his experiences on his visit to the Galapagos islands.
Think about it - the many islands which are formed by upheaval were lifeless when they first emerged from the ocean.  Over time, the winds or storms eventually populated them all - just about every island has animal life on it.  Not all animal types are found there that are best for the climate; its a matter of accident that some birds or lizards are found on the galapagos islands.  These accidental landings don't happen very often and sometimes a single animal will generate many species which will fill the role that other animals would normally fill on the mainland continents at the same latitude.
This is what happened on the islands- in different islands, Darwin found finches of sizes and shapes would be eating insects from bark or ant hills that might be done by an animal
Eventually, if you wait long enough a frog, then maybe a couple of fish will find their way into the pool from a nearby waterway (yeah that could take a long time I know).  If it takes too long then a new species will show up.  If you build walls around the pool it might not happen.  These accidents of animals showing up by accident can take millions of years.
This experience of Darwins' has inspired an entire field of biology - Island biogeography.  Each island is an experiment and ecological niches can be observed by taking a series of islands and seeing how different animals take up the various ecological roles on each.  A famous experiment EO Wilson and colleagues did was to fumigate some mangrove islands and watching them repopulate.

I recently dug a pond in a forest, and the first things to happen was not actually plant life. First I found small aquatic animals that lived in the mud, then I found salamander axolotyls and water striders, and crawdads. Salamanders (especially newts), water striders, and crawdads all migrate between ponds to breed and when old ones dry up, as well as various other aquatic animals. The aquatic mud dwellers might have been washed there by rain, or they might have migrated there like the others. In the case of a lake, all of these will happen, although slower because of a lack of sediment with concrete walls. The fish would depend on whether or not there is a waterway connecting the lake to an area where fish already live. These events would happen in the first year except for fish, and pretty soon algae will be growing right after the animals moved, or during, and plants will start to grow as well, their seeds or whatever they use to spread will make their way to the lake. I have found though that lakes, especially man made ones, often contain very little large plant life. As for the time it takes, one year will start it off with basic predator prey relationships, and will slowly grow from there over the course of years.

I believe that's why the question used concrete, to avoid the fact that a pond/lake in the dirt is actually still quite open and in contact with life.

I did mention the fact that it would occur slower with concrete, but eventually enough debris would fall in the water that there would be sediment.

The answer is yes, absolutelyvne enough time. You can do this experiment yourself. Get a clean glass jar, hell even sterilize if if you like (your oven overnight at 250 F will do it).   Fill it about 3/4 with clean (or even sterilized) water, and leave it outside in a mixed sunny shady spot for a few weeks, in moderate weather. It's small volume will get cooked by constant direct sun, which will impede the results.
After a few weeks (might be faster), look closely into the water (through the sides of the jar) with a magnifying glass, or better still, sample the water and look under a microscope. You won't see, but they are there, multiple bacterial species.
You will see single celled algae, small pond creatures (hydra, rotary-topped species (multiple)), paramecia, and multi-celled algal forms in strings. These are all fallen in from airborne dust and windblown particles.  You likely won't get fish, but if you are lucky, you might get a few brine shrimp.  And yes, particles of blown or bird-carried dirt etc can easily carry shrimp, amphibian, or plausibly, viable fish eggs.
But what do they feed on?  There's no food in the water you put in !!  CO2, nitrogen, Oxygen, etc are readily available from the air. A few cells of bacteria or algal forms seed the clean water, and begin fixing CO2, nitrogen etc, and now you have a food source. Wind-carried (or bird-carried) small organisms can now survive in a web of bacteria-plant-animal interactions.
By the way, you can also run a control jar, where you sterilize the jar, fill it with boiling hot water, and quickly cover it tightly with foil. Place it beside your open jar, and it will grow...nothing.
As a side note, "toxic" algae are often not toxic to small organisms and other algae. Their toxins (neurotoxins usually) affect mostly only higher organisms, such as fish and humans. Algal blooms kill fish and birds, they seldom sterilize the pond.


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Can a human survive without ACE2?
I guess not, but it was discovered in 2000 so I don't know if we know enough about it. Are there people without ACE2 (angiotensin converting enzyme 2)?
It seems mice can survive, but that's not a proof on humans: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829150/

No obviously inactivating variants are found in this gene, which provides at least negative data (humans generally seem to have at least somewhat functional ACE2). Exome sequencing across >200K humans has found a series of variants, mostly low-frequency, in the population.
Some of these variants may affect gene function, but it is not clear how, and none of them are obviously complete loss of function variants (e.g. nonsense mutations).
A more complete analysis of the data, including e.g. CNVs, might be necessary to fully address this question.

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


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Bio-fuel efficiency as aviation gasoline
Can biofuels replace petroleum for aviation fuel?
I've read in the news that Alaska Airlines was flying with 10~20% biofuel and 80~90% petroleum. Is biofuel efficiency comparable to the efficiency of petroleum? I am curious whether or not the maximum speed of the airplane is same when it uses bio-fuel 100%.

The term biofuel refers both to the source of the fuel, as well as (currently, at least) the compounds contained in it. If the production quality is strictly controlled, eventually there should be no detectable difference between a fuel mixture derived directly from biological sources, and one derived from petroleum products (which, technically speaking, are of biological origin themselves, just a few million years removed). However, due to technological limitations, biofuels and petroleum-based fuels do have different chemical components today.
The reason we hear of differences in mileage or "energy density" in biofuels used to power automobiles as compared to gasoline/petrol is because they are not the same mixture of chemicals. This page goes into detail (the whole site is actually quite clear with its explanations), but the basic difference is that petroleum products are essentially 100% hydrocarbons (only containing hydrogen and carbon atoms) while nearly all biofuels contain oxygen as well, which has numerous effects on the fuel's physical and chemical characteristics, altering everything from polarity to reactivity to stability over time to the types of byproducts (and pollutants) produced during combustion.
There is much more to the story, but the basic answer to your question is yes, biofuels could replace petroleum-based products for aviation and many other types of fuels, and not impact the maximum speed of the aircraft. It may require engine modification, and the energy density may not be exactly the same (possibly reducing range), but for the long-term health of our planet we MUST reduce and eventually eliminate our use of petroleum.

By the way, the Aviation or Chemistry StackExchange sites would likely be able to provide you with much more in-depth answers, as ultimately this question is better suited to either or both of those sites than Biology, which would be more concerned with the production of biofuels by living organisms.

Thanks a lot for your great answer and guidance to the aviation stackexchange. I will check it out to find the detail.

@Trailblazer glad I could help. If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.


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How do exon tandem exon duplications occur in the genome?
By this I mean in cases where tandem exons are introduced by replication slippage how would a DNA polymerase by chance duplicate an entire exon cleanly (i.e. from exact start to exact end) when it doesn't even know what an exon is?

I dont think it would happen because of slippage. It should happen via recombination. Can you indicate the source of this information ?

i guess I was thinking of somatic cancers but the question still stands: how does the recombination machinery know what an exon is?

There is a section in the Human Molecular Genetics textbook about how such repeats do occur. Like the commentor said, it is likely a result of recombination. If there are repeats flanking a gene or an exon there can be paring between sister chromatids / chromosomes, which can result in the duplication. See Figure 9.7 here http://www.ncbi.nlm.nih.gov/books/NBK7566/#A1095
As for how does it "know": It doesnt. Its not just the exon that is duplicated though. It is also the DNA before and after the exon, which contains cis-elements that splicing factors bind to, which results in the exon being spliced into the transcript.
Splicing is pretty complicated but if just 50 bp upstream and downstream of the exon was also duplicated, it would probably be enough to cause some splicing of the exon. U1 and U2 snRNP bind immediately at the exon-intron junction, and the polypyrimadine tract is about 30 bp or so upstream from the exon. U1 and U2 and the polypyrimadine tract are all vital to splicing. I dont know of any work that shows the minimum requirement for splicing but if you have those 3 you will probably splice the exon at least part of the time. So in sum, its probably not just the exon that is duplicated. It is probably the exon plus the cis elements involved in splicing.

I'm going to speculate that exons that are not cleanly duplicated activate the cell death machinery. We see the clean exon duplications because they are able to survive.


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How long can a unicellular organism live without nutrition? What happens after that? Does it depend on the domain?
Say I have three unicellular organisms: a eukariote, a bacterium and an archaeon. If I cut off nutrition from them at the same time, how long will it take for them to die? What will their death look like, and do they actually need to die? If so, why?

This is very dependent on the organism within each of the groups you mention. While for the most part, archea are the extremophiles and have the ability to withstand many extreme conditions, nutrient limitation survival greatly varies. I think you could easily find organisms in each group that could withstand nutrient limitation well.
A good example would be yeast, which is a single celled organism you may have actually worked with. If you take laboratory yeast, in their diploid state, and starve them, they will undergo meiosis, and in their spore form, live for a very very long time without nutrients, protected by their ascus (which is actual their dead mother cell).
Yeast can also completely desiccate and still live. When you pick up an active yeast packet for baking, those yeast have not only been starved, but have been completely sucked dry of their water. Yet when you add water back, they live (though a great number of them will die).
I think in general, most single celled organisms have a certain tolerance for low nutrient conditions. This does happen to them a lot. All it means is they slow their cell cycle down, stop dividing, and just undergo a caution period. There is all sorts of signaling in the cells that sense the nutrients, and slow growth based on their conditions.

Thank you. But why will they (some of them?) eventually die?

Why will they die? That's kind of difficult to answer. There are some hypotheses that unicellular organisms to a certain extent have multicellular characteristics. And this includes the ability to altruistically die for the benefit of the rest of the colony or species. By dying they would free up the limited resources, as well as allow their own proteins and cellular components to be taken up. Others believe it is just random, and some cells live a bit longer making them able to take advantage of what I said above, making the death in no way planned or organized.

I'm planning to ask about cell death later. But I would like to know what it is that actually kills those cells that don't commit suicide. Is it just random damage, or is there something else? And is there a criterion that allows to pronounce a cell dead as we can do with humans?


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Is there any advantage to one blood type over another?
All humans can be grouped into ABO and Rh+/- blood groups (at a minimum).  Is there any advantage at all to one group or the other?  This article hints that there are some pathogens that display a preference to a blood type (for example Schistosomiasis apparently being more common in people with blood group A, although it could be that more people have type A in the areas that the parasite inhabits).  Is there any literature out there to support or refute this claim or provide similar examples?
Beyond ABO-Rh, is there any advantage or disadvantage (excluding the obvious difficulties in finding a donor after accident/trauma) in the 30 other blood type suffixes recognised by the International Society of Blood Transfusions (ISBT)?
I'd imagine not (or at least very minimal) but it would be interesting to find out if anyone knows more.

Do you mean advantage in an evolutionary context?

That reminds me about the sickle-cell disease where the malformed red blood cells show much higher resistance against the malaria plasmodium.

I've been doing a little more digging myself and have found a couple of other advantages:
Risk of Venous-thromboembolism (deep vein thrombosis/pulmonary embolism (1)).  Blood group O individuals are at lower risk of the above conditions due to reduced levels of von Willebrand factor(2) and factor VIII clotting factors.
Cholera Infection Susceptibility & Severity.  Individuals with blood group O are less susceptible to some strains of cholera (O1) but are more likely to suffer severe effects from the disease if infected (3).
E. coli Infection Susceptibility & Severity. A study in Scotland indicated that those with the O blood group showed higher than expected infection rates with E. coli O157 and significantly higher fatality rates (78.5% of fatalities had blood group O).(4)
Peptic Ulcers caused by Heliobacter pylori which can also lead to gastric cancer.  Group O are again more susceptible to strains of H. pylori (5).
Whether blood group antigens are displayed on other body cells or not has been linked to increased or decreased susceptibility to many diseases, notably norrovirus and HIV.  This is fully explained in the article that I was above summarising - "The relationship between blood group and disease" in addition to extended descriptions of the other two answers.

The less antigens a woman (or in fact a female of any species close enough to humans for this phenomenon) has, the higher are the risks of triggering an immune reaction during her pregnancy, if the child has those antigens.
The Rhesus incompatibility is probably the most common case of this problem.
One could thus assume that in populations that are genetically diverse in respect to blood groups, absence of antigens has negative effects on reproduction (unless countered by medicine).

People with blood type O are more resistant to malaria and syphilis
  than those with the A and/or B proteins.

From the Encyclopedia of Evolution, Stanley A. Rice, page 40.

Can you provide references to the original research showing that? I cannot really find any on Pubmed. What I found is that individuals of Duffy- blood group are resistent to Plasmodium vivax invasion (Langhi and Bordin, Hematology 2006), but I cannot find anything on AB0. Also see: http://www.ncbi.nlm.nih.gov/books/NBK2271/


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What limits the maximum spacing of Nodes of Ranvier and which organisms tend to have the widest gaps?
Assuming that a longer distance between gaps in the myelin sheath is beneficial for an organism due to the increased propagation speed, what is the limiting factor in determining the maximum spacing between nodes?  I have previously encountered the analogy of the Nodes of Ranvier as forming a circuit between themselves and the previous node in order to pass on the action potential, which leads me into thinking that it is simply electrical resistance that is the cause however I assume the analogy is an over simplification and would be very interested in any alternatives.
Also, is there a significant variation in node separation between organisms?  Which organisms have the greatest gaps?

This is best answered via something called cable theory.  Basically, as the action potential (AP) propagates along the membrane of the axon, it's tripping voltage gated channels that "renew" the flux of ions into the stream at the nodes. There are no ion channels under the sheathing (or they are there anatomically and inactive, but I don't remember), so the current is able to zip through that area.  There's no renewal of AP, but there's no loss due to leak of ions either.  Since there's no influx of ions from outside of the membrane until the next node, the capacitance and resistance of the membrane is exponentially decaying the voltage.  So, if the distance between the nodes was too long, the voltage would just die off and the AP wouldn't propagate.
I don't have any anatomical data about individual species, but know that only the smaller diameter axons require sheathing to compensate for the slower ion flow due to higher resistance (e.g., the squid giant axon(not to be confused with the "giant squid" axon) has no myelination due to its large diameter).

Right on. The only thing I would add is to explicitly mention the distinction between axial resistance and membrane resistance in cable theory. The axial, or longitudinal, resistance is what is relevant here as it determines how much current flows down the center of the axon. As you say, this parameter is mostly affected by the axon diameter (larger axons have a lower axial resistance). Thus, the decay of voltage along a large diameter axon will be less severe than along a small diameter axon.


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What are the units of Q10 (temperature sensitivity)?
$Q_{10}$ is the increase in a rate (e.g. activity of an enzyme) observed with a 10° temperature increase.
According to Wikipedia:
$$Q_{10}=\left(\frac{R_2}{R_1}\right)^{{10}/\left({T_2-T_1}\right)}$$
It is apparent that the units of $R$ (e.g. $mol/g/s$) cancel out, but what about the units of temperature? Does $Q_{10}$ have units? It seems the units would be "per 10 °C", but it is not clear how this comes from the referenced equation

Figure. A schematic diagram showing the effect of the temperature on the stability of an enzyme catalysed reaction. The curves show the percentage activity remaining as the incubation period increases. From the top they represent equal increases in the incubation temperature (50 °C, 55 °C, 60 °C, 65 °C and 70 °C).
The $Q_{10}$ is a unitless number, that summarizes the effect of raising temperature 10°C on the rate of a chemical reaction. A $Q_{10}$ of 2.0 suggests that raising the temperature of a system by 10 °C will effectively double the rate of the reaction. This value would be expected for most chemical reactions occurring within normal physiological temperatures.
Mathematically, $Q_{10}$ can be represented by the following expression:
$$Q_{10}=\left(\frac{k_2}{k_1}\right)^{\frac{10}{t_2-t_1}}$$
$t_2$ = higher temperature
$k_2$ = rate at $t_2$
$t_1$ = lower temperature
$k_1$ = rate at $t_1$
Usually the temperature difference is about 10 °C, then you can simplify the equation
$$Q_{10}=\left(\frac{k_1}{k_2}\right)^{\frac{10}{10}}=\frac{k_1}{k_2}$$
Edit: You can easily calculate $k$ form Arrhenius equation
$$k=Ae^{\frac{-\Delta G^*}{RT}}$$
where $k$ is the kinetic rate constant for the reaction, $A$ is the Arrhenius constant, also known as the frequency factor, $-\Delta G^*$ is the standard free energy of activation ($kJ/mol$) which depends on entropic and enthalpic factors, $R$ is the gas law constant and $T$ is the absolute temperature.

how do you calculate k, are the curves in the figure something like e^{-kt}?

Here k is a rate constant like R in your wikipedia example, and for the figure the curves show the percentage activity remaining as the incubation period increases.

But how do you estimate the pre-exponent factor A?

My understanding of Q10 it that it is the ratio of the rate of a chemical reaction at a specified temp to the rate of a chemical reaction 10 degrees higher.  For example if the rate of an enzyme-catalysed reaction at 37 C is twice that at 25 C, then can speak of a Q10 being equal to 2.  Q10 makes no assumptions about the underlying mechanism which, for an enzyme catalysed reaction, is likely to be complex, and to involve temperature effects on multiple rate constants (both first-order and second-order).  I find your diagram of (first-order) decay curves misleading. These may be used to ...

calculate the half-life of an enzyme at different temperatures, but surely have nothing to do with Q10?

This is a nice example of mathematical sloppiness which is more often present in textbooks on biology than on chemistry or physics where perople are more careful about dimensional analysis*.
The correct form of equation (with your notation) is
$$Q_{10} = \left(\frac{R_2}{R_1}\right)^\frac{10\,^\circ\mathrm{C}}{T_2-T_1}.$$
From this form, it is clear that the units of temperature cancel out, and that  $Q_{10}$ is therefore unitless.

* For example, exponential function – such as the one present in the equation for $Q_{10}$ – cannot take units as an input, only dimensionless numbers.


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What does "developmentally programmed" mean?
What does the term "developmentally programmed" mean? I can't seem to find a definition anywhere.
What would the alternative (i.e. not developmentally programmed) imply?

Where did you find this expression? That will probably help a bit.

Agreed, this phrase can mean different things depending on the context - the answer still wouldn't be pages long if it included all contexts but it would make it a lot easier if you could provide that background information :)

As in "development of secondary lymphoid organs happens during embryogenesis and is thought to be developmentally programmed"

The link to your source would help, not only the sentence.

Sorry yes I should have posted that in the first place --> doi:10.1038/nature13158

Yeah, it looks like just bad phrasing, probably caused by word count restraints.

The term could mean two things depending on the emphasis:

"developmentally programmed" would seem to emphasise the "programmed" nature of the development of something, implying that it is under specific regulation and the result of targeted energy expenditure ("Here, we describe widespread developmentally programmed nuclear destruction (PND) events that occur during yeast gametogenesis").
"developmentally programmed" would be intending to distinguish from other means of being programmed, i.e. this would go in the direction of a nature vs. nurture statement ("Hair colour is developmentally programmed and does not depend on external influences after fertilisation").

The first of the two appears to be the more common use of this phrasing if one wants to trust Google to be representative. Something along these lines might be intended in your example, though I don't see why this statement is necessary as it seems quite obvious that any organ that develops during embryogenesis is "developmentally programmed"...
I suppose the alternative ("not developmentally programmed") would imply that the development of secondary lymphoid organs is an accident which is not driven by specific mechanisms that exist for the particular purpose of developing them.
In any case, there is no magical scientific meaning to either of these two words, to me your example seems to be rather a mishap of phrasing.


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Can all biological processes be understood as computations and studied as such?
Can we understand a cell as an organic computational device? In that case the whole organism can be considered an ensemble of a large number of interacting computational devices?
If this is the case, biology can be studied using methods of graph theory, network theory, computation theory and complex systems theory.

The answer is YES, if you can do this, But you can't (at least currently) because your devices are not powerful.

If you abstract enough, anything cam be considered as a computational device. The issue with doing this with cells is the sheer number of variables.
For any given cell, the following internal variables exist:

Internal ion concentrations for dozens of ions of importance importance
Internal concentrations of hundreds or thousands of various simple organic molecules, including "raw" internalised molecules, various steps in dozens or even hundreds of metabolic processes, and metabolic end-products and by-products.
Internal concentrations of hundreds or thousands of different proteins and other complex biological "mechanical parts", as well as the states of these "parts".
The physical state of the cell - stretched, contracted, relaxed, hot, cold, etc.

This list is not exhaustive.
It's also worth noting that the above variables may also exist for multiple separate "compartments" within the cell; vesicles, the endoplasmic reticulum and the golgi apparatus being three which come to mind immediately.
The other issue is that cells do not exist in a vacuum; the external environment plays an important role in their functioning. The human body is at any one moment existing in direct contact and interaction with the following extracellular environments:

The atmosphere (Mainly, but not only, temperature exchange)
The air within the respiratory system, including nose and mouth
Stomach contents
Small intestine contents (which would need to be considered in several segements, since the nature of the interaction changes along the path of the small intestine.
Large intestine contents
Blood
Cerebrospinal fluid (Fluid found "inside" the brain)
Extracellular fluid, or "tissue fluid" (A separate compartment for each small swatch of tissue in the body)
Lymph
Pleural fluid (Fluid surrounding the lungs; a separate compartment for each lung)
Pericardial fluid (A small amount of fluid surrounding the heart)
Joint capsule contents (A separate compartment for each joint)

...and the list goes on. Each of these compartments requires tracking of the same variables as individual cells.
This is yet further complicated by the fact that some of these compartments can't easily be considered as one big compartment, because of the importance of spatial relations. For example, the oxygen and carbon dioxide concentrations of blood (as well as the concentrations of other substances like alcohol) change centimeter-to-centimeter. Yet another issue is the fact that cells are not static in terms of their relations to each other; red blood cells move with blood flow, and experience turbulence and other effects, and other cells (like macrophages) are capable of "deliberate" movement in the blood and in tissue.
You would also have to account for physical disturbances - things like a stab wound or even a pinprick are ludicrously complex at a cellular level.
Of course, human beings are very complex organisms, and there exist much simpler organisms. You might be interested in OpenWorm, which is an attempt to computationally simulate Caenorhabditis elegans, a species of roundworm, at a cellular level. Doing so even for an organism as simple as C. elegans is a massive undertaking, as evidenced by the fact that even with the contributions of dozens of experts in their fields the project has been ongoing for some time and is yet to reach stage one.
The short version: Is it possible? Perhaps. Is it easy? Definitely not.

As a mathematician interested in biology I am very curious about informed answers, here I add mine, with the understanding that it is in no way complete and it might be very biased or ignorant as concerns biology.
We may understand a cell as a chemical and physics based program which runs itself. The cell is a computational device in the sense that the outcomes of its activity are computable functions of its inputs (a reasonable hypothesis), but more than that: at the cell level there is no distinction between the computer, the program which runs on the computer, input and output data AND the execution of the program. All is at the same level, i.e. every abstraction is embodied in a concrete chemical or physical thing.
This concreteness part adds, I believe to the difficulty, because the usual thinking in computer science is all about structuring abstractions, while in biology everything is ultimately at only one level: real, physics and chemistry embodied.
This is a claim which needs strong supporting evidence. Being a matter of principle, it cannot be proved rigorously, but it might be given a rigorous support by constructing simple proofs of principle models.
There are many computing models which are inspired by chemistry, therefore in return they can be seen as such proof of principles.
There are Chemical Reaction Networks and Petri Nets models which are more like structuring tools than real embodied models of computation, because they don't consider the structure of molecules (they are just nodes in a graph), nor the way chemical reactions happen (they are edges in a graph). They are very useful tools though and the description given here is very much simplified.
There is the CHAM (chemical abstract machine), G. Berry and G. Boudol. The chemical abstract machine. Theoretical Computer Science, 96(1):217–248, 1992. In this model states of the machine (imagine: a cell) "are chemical solutions where floating molecules can interact according to reaction rules" (cite from the abstract). In this model "solution" means a multiset of molecules, reaction rules are between molecules and they do not apply inside molecules. This is a limitation of the model because the structure of the molecule is not as important as the number of molecules in a species.
Another very interesting model is the Algorithmic Chemistry of Fontana and Buss. The main idea is that chemistry and computation are basically the same. The reasoning goes as following. There are two pillars of the rigorous notion of computation: the Turing Machine (well known) and Church's lambda calculus. Lambda calculus is less known outside computer science, but is a formalism which may be more helpful to chemists, or biologists even, than the Turing machine.  Fontana and Buss propose that lambda calculus is a kind of chemistry, in the sense that the its basic operations, namely abstraction and application, can be given chemical analogies. Molecules are like mathematical functions, abstractions are like reaction sites and applications are like chemical reactions.
The Algorithmic Chemistry is almost as closer as possible to be (proof of principle) answer to the question.
Finally I mention chemlambda, or the Chemical concrete machine, which is like Algorithmic Chemistry, but it is far more concrete. Molecules are graphs, applications and abstractions are molecules, chemical reactions are graph rewrites.
What is very interesting in all these models, in my opinion, is that they suggest that answering to the question "Can we understand a cell as an organic computational device?" is somehow relevant to the Computer Science question "How to design an asynchronous, decentralized Internet?".


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Biology Analogy
In my book are given several paired analogies with me being asked to give reason for them. I could solve all of them except this:

liver = thrifty house-keeper

I mean, I do not understand why the liver is being called so. The functions of liver haven't been taught yet (so this is kind of out-of-course), but still, I thought I should ask it as the functions are not given anywhere in the entire book.

The liver does quite a lot of "housekeeping". It is responsible for a lot of energy metabolism: Gluconeogenesis (the synthesis of glucose), Glycogenolysis (the breakdown of glycogen into glucose), Glycogenesis (the synthesis of glycogen from glucose).
It is important for protein degradation as well as for amino acid synthesis, as well as in the lipid metabolism. This includes synthesis of cholesterols, lipoproteins and fatty acids. The liver produces a number of factors important for coagulation including prothrombin and a number of hormones.
It is very important for the breakdown of Bilirubin and insulin, and it detoxifies the body via the cytochrome P450 system. It is storing some substances as vitamin A, B12, D and K as well as iron and important for their regulation. For more details read the corresponding Wikipedia article on the liver.
So easy speaking does the liver a lot of maintenance in the human body which is important for a lot of different processes.


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Can human change its morphology or anatomy due to ecological changes?
According to Charles Darwin, as the surrounding environment changes, so changes the anatomy or morphology of a specific organism.
But nowadays, humans have become very advanced in the technology and when the surrounding temperature changes, humans in turn change the surrounding temperature (e.g. the use of ACs), and maintain the surrounding as they like.
What I want to emphasize is can human being evolve with these scopes in mind?

related question: http://biology.stackexchange.com/questions/8401/has-medical-progress-stopped-human-evolution Incidentally, Darwin was not awarded a knighthood.

I went ahead and changed it, as other people are going to come in trying to correct it as well.

i think we have bigger bellies now :P

It's important to note that populations evolve; individual organisms do not.

@p.s.w.g very good concept to be focused so can the population evolve now

@agharehanabbas Yes, human populates can and do evolve now

@ p.s.w.g That's Berkeley opinion. Which is wrong :)


text:
Can I compare Shannon-Wiener diversity indices between plots of different sizes (area)?
Can I compare the Shannon-Wiener (a.k.a. Shannon-Weaver) Index of diversity ($H'$) of plots (communities) with varying sizes (areas)?
If not, what steps do I need to take and/or which tests should I use to compare the diversity of different-sized plots?
I also wonder if this is possible for Simpson's Index of diversity?
Shannon-Wiener Index:
$$H' = -\sum \limits_{i=1}^S p_i \ln p_i$$
Simpson Index:
$$D = 1 -\sum \limits_{i=1}^S {p_i}^2$$
Where $p_i$ is the proportion of species $i$, and $S$ is the number of species.

Welcome to Biology.SE. I am not an ecologist and I don't know the Shannon-Wiener index (and don't remember by heart the definition of the Simpson's index). However, if you were to include the definitions of those indices, I (and others) might be able to answer without having to search the literature for those definitions. When you say different-sized plot, do you mean different total number of individuals (total abundance) per plot?

Different sized plots strictly in terms of each plot having inconsistent physical AREA. For example, 1 plot might be 500m2, while another might be 1100m2.

Oh Shannon-wiener index is just what I would call the Shannon Index. This is why I did not recognize it at first place. Thanks for the edit +1

No problem. I think the science community needs to make up their minds about what to call it ha!

Theoretically the index for two habitats of different areas are not directly comparable. Consider the species area relationship. You see more species when you look over a larger area. So you will potentially see a different index just from considering a larger area, and not necessarily because there is something different about the habitats.
Borda-de-Agua et al tackle this head on. They use fractals to account for differences in area when comparing diversity indexes. It's complicated and I won't try to put the methods here because I don't understand them. Definietly worth looking at yourself though.
I would also consider using species abundance distribution (SAD) curves for comparison. They give information about diversity but don't sum it up in one nice number like indexes. I feel they are area invariant too. Since if you keep increasing the area of your sample, the total species will only increase from relatively few rare species, while abundances will increase mostly with the abundant species. This will not change the slope of the curve but just the intercept (My hypothesis, not sure if it's actually true). Checkout a good comparison of SAD's and diversity indexes in the intro to McGill et al.

References
Borda‐de‐Água, L., Hubbell, S. P., & McAllister, M. (2002). Species‐area curves, diversity indices, and species abundance distributions: a multifractal analysis. The American Naturalist, 159(2), 138-155. Link
McGill, B. J., Etienne, R. S., Gray, J. S., Alonso, D., Anderson, M. J., Benecha, H. K., Dornelas, M., Enquist, B. J., Green, J. L., He, F., Hurlbert, A. H., Magurran, A. E., Marquet, P. A., Maurer, B. A., Ostling, A., Soykan, C. U., Ugland, K. I. and White, E. P. (2007), Species abundance distributions: moving beyond single prediction theories to integration within an ecological framework. Ecology Letters, 10: 995–1015. Link


text:
What is the surface area of the human heart?
I heard that the human heart had a surface area of 1000 square feet, and I thought that that cannot be true. So what is the surface area of the human heart and what are the different ways it can be measured?

The number you are looking for might be quite large depending on the level of detail you demand for the measurement.  There is no single number for the area of most objects in fact.
The importance of fractals is much related to the question of what is the perimeter or surface area of something.  The classic example is trying to determine the length of Britain's coastline.  If you took a surveyors sight and set a point every 500 ft you would get a certain number, if you paced it out in strides you would end up taking more curves and turns and you would get a longer number.  If you took out a ruler and measured down to the inch you would get a still larger number.  In these two wikipedia pictures you would get a perimeter of 2400 km and 3400 km for points set every 200 and 50 km respectively:

As you can see that makes a big difference.  So in the same thought organs also need to be measured using fractal sorts of measurements- depending on the level of detail desired. For a heart, if you were to cover the organ with a tight stretch of Saran wrap, you'd have maybe 1-2 square feet, but if you estimate the surface area for not only the inner chambers, but the blood vessels and capillaries, it would be much larger.  The latter is probably relevant if you are a physiologist and want to know how much oxygen the heart is taking in as it beats.
I can't find a reference for a human heart, but fractal calculations for the human lungs tell me that 1000 sq ft seems reasonable.  If you take the oxygen accessible area of lungs, including every bronchial passage and aveoli, the answer is 50-100 m^2. This is about 538- 1,076 sq feet.
The heart does not need to have as much surface area as the lung, but the capillaries and arteries that feed the heart need to be spaced a few millimeters apart to keep the tissue oxygen saturated.  1000 sq feet seems a possible range for the heart compared to the lung's surface area, maybe on the high end...

pardon changing the area numbers for lung- just caught my error of 100x.  I think the conclusion still holds water though.


text:
Mitotic chromosome condensation screen
If I want to screen for mutant yeast (S. cerevisiae) colonies that have defects in mitotic chromosome condensation, can I screen for colonies arrested in Mid-M phase? Would that work?

It is going to need to be a temperature sensitive mutation, so that you can get them to grow at the permissive temperature and arrest during mitosis at the restrictive temperature, because otherwise your cells would not grow.

You probably would also want to do a thorough research review of Leland Hartwell and Paul Nurse's work as they worked out the cell cycle using yeast.

The ts mutation would be like a "primary screen" from there one can do a more sensitive secondary screen? Thank you!

Right. So you find the ts mutant, and then you isolate mRNA from population grown at permissive temp and population grown at restrictive temp. Then you make cDNA and run that out on a microarray (They probably have plenty of whole genome chips available for yeast). You can then see the genes that are down (or up) regulated from a comparison of the two arrays, and that should tell you where gene expression has changed. You will then need to make probes for those genes and do FISH to try and determine where they are localized in the nucleus.


text:
Help Identifying Tree
I live in the upper southeastern region of Arizona in U.S. There's a type of tree growing in my back yard that I can't seem to identify. Its growing in an arrangement very similar to an ocotillo plant.  It has single spiny stems coming up out of the ground.  They don't branch out but have large sharp spines with leafs growing out of them.  It doesn't look anything at all like any of the native desert plants in the area.  There's mesquite and sage and various types of cactus.
At the moment the stems are about five feet tall.  I took clippings about two feet in length and photographed them.  It seems I'm only able to post two links so I've chosen the clearest images that I have.  I'm very curious as to what this is and any help would be greatly appreciated.

Have you ever seen flowers or berries? although I am not familiar with the flora over there I would suggest it could be a Pyracantha (Rosaceae)

I have seen that up in the mountains in this area but only above a certain elevation and mostly among oak trees.  This plant's spines have claws like a rose bush.  My sister said it appeared about four years ago and she tries to uproot it every spring but it keeps growing back.  As far as she can tell she's never seen it bloom any flowers or produce berries.  She thought it was a type of mesquite known in the area as "cats claw" but it's leaves do not look like any kind of mesquite leaf I've ever seen.  It has a lush green appearance that contrasts it from the other desert plants in the area.

Can you take a picture of the whole tree and a picture up-close of the leaf?

Also, you mention also seeing this in a montane oak forest. Could you comment on the elevation, the aspect (side of the mountain), species of oak, possible presence of conifers, how dense the understory is, or anything else notable about the habitat you've seen it in?

@theforestecologist  I removed the plant in Oct.  This pic is nearest to how it looked but not as dense or as high.
The elevation where I spotted a cluster of the red orange berries similar to the Pyracantha was above 2,600 ft.  The azfirescape website is a close description to the area.  I can’t say where exactly I saw it only that I know I have seen a red cluster of berries like it  before.
link
link

It looks like this could be Lotebush, Ziziphus obtusifolia. The thorny branchlets and blue-green color (at least, as it appears in the photos) suggest Ziziphus to me, although you could compare it with the photos or description here. If it is in the buckthorn family, it does seem to key out to Ziziphus using the Christie et al. key.
If you wanted to be sure, you could follow up with the ASU herbarium (see citation).

Christie, K., M. Currie, L.S. Davis, M.-E. Hill, S. Neal and T. Ayers (2006). Vascular Plants of Arizona: Rhamnaceae. Canotia 2(1): 23-46. Open access

The leaves aren't a perfect match for any of the photos I've seen, but the description does note that the leaves are quite variable, especially in young shoots.


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Is the discovery of dominant and recessive genes the only reason Mendel matters?
We've known that offspring inherit various traits from their parents since (at least) Aristotle. In The Elements of Plant Hybridization, Gregor Mendel treats that fact as common knowledge. Clearly, we don't credit Mendel with discovering it. Accordingly, it seems to me that Mendel's only notable discovery was the discovery of the existence of dominant and recessive genes. However, that discovery doesn't seem to justify the title 'founder of modern genetics', which Wikipedia, and other sources, use to refer to him.
Why is Mendel the big deal that he is?

I think he did more than discover dominant/recessive, he discovered ratios of traits in offspring, like the 3/4 dominant 1/4 recessive phenotype, and that organisms could carry a gene for a trait without showing it, then pass that trait to it's offspring. The whole thing suggested that there were rules governing inheritance which could be deciphered and used to breed plants/animals more effectively. Darwin suggested that traits were selected for by environmental pressures, but Mendel showed how traits were passed down.

Aristotelian pre-science wasn't concerned with experimentation at all - it was just people throwing hypotheses around, basically. Contrast with Mendel, who developed a strong theoretical framework, coupled with precise experiments, tons of data and actually increased understanding of the subject matter. In other words, his was the first book on the subject that actually presented not just ideas, but also hard data anyone could verify for themselves. Not to mention that he also did deliberate genetical engineering on a level never done before.

http://mac122.icu.ac.jp/gen-ed/mendel-gifs/18-mendel-cartoon.JPG

@Luaan there's also the suggestion that he may have "doctored" some of his data...

Independent assortment. Mendel showed that his genetic markers for different traits, or phenotypes are transmitted randomly to the F1 generation. This was before the concept of linkage was discovered, so fortunately he selected unlinked genes.
Segregation of alleles. The dominant and recessive alleles segregate away from each other when the germ cells are created, therefore each parent has two copies of every Gene.
Distinguishing phenotype from genotype in a predictable and testable framework.
The test cross. It was only careful record keeping and back crosses that revealed the recessive copies of mutant alleles in heterozygotes.

One description of his contributions is available on Wikipedia.  Other sites include MendelWeb, Learn Genetics,

great answer +1. A reference would be nice to allow people to look up background info to your answer.


text:
What happens when we re-start a PCR reaction?
Recently when my PCR reaction was running there was power fluctuation and the entire lab was blacked out for a few minutes and unfortunately PCR that I was running got switched off. So, would it be okay to restart the PCR? What would happen if the same PCR program was run again?

How many cycles had elapsed? For how long was the power down?

about 12 cyces..

then you can run it for another 18 cycles. How long was the power down? Did the power come back immediately?

The power came back in half an hour

But what happens if the number of cycles is increased too much? how would that affect the reaction?

Theoretically, you can amplify your target sequences. Just run the number of cycles you planed in total. But no one tells the results. Loss of temp control may increase opportunities of none specific annealing and amplification. If it is qPCR, it could be very tricky... or I really don't know. If you just want to get PCR fragments, you could/might get bands. Then, just it is your decision. Remember you can not complain after you clone the PCR fragments into plasmids and the sequences turn out to be wrong.

The polymerase used in PCR is extremely stable at room temperature. I would expect you to be able to continue your PCR reaction from the cycle it was stopped at without too much trouble. However, it is important to not over cycle your product. This will produce non-specific products. If a clean result is imperative, take a 1-5ul sample from your original reaction to use as a template in a new reaction.

In this case you can run your PCR for another 18 cycles (if your total number of cycles was 30). However, do the initial denaturation for 1-2min. You may run the same program again (full 30 cycles) but you'll just end up wasting time because after a point all the dNTPs and primers would be exhausted and further cycles will have no effect on the concentration of the amplicon.