text:
What does the empty space in the bamboo stem do?
Is the empty space inside a bamboo stem a xylem? And why is the space so large?

No, its not xylem. Bamboo is a grass, and the stem (culm) of many grasses are hollow in the middle (see e.g. Grass Structures from Oregon state for some more info).
The exact reason for why Bamboo have hollow stems is most likely due to evolutionary contingencies. However, from a mechanical stability point of view, a hollow stem is much more rigid and stable than a solid (but much thinner) stem composed of the same amount of biomass (Niklas & Spatz, 2012, p. 191ff). So from the perspective of efficiency, the hollow stems of grasses are very useful. The solid node discs found in grass stems (and in other plants with hollow stems) are however really important for increasing overall stability and ability of stems to resist deformations, while only contributing to a very small amount of the total biomass.

Interesting. But why is it hollow?

@ChrisStronks Because that is the growth pattern of the ancestor of grasses along with current grasses. Why do oaks lack a hollow core? Why do you have 2 ears and not 4? Why do octopus have 8 arms and not 10? Most explanations for these kind of evolutionary contingencies do not have a clear explanation, and most possible explanations will be rather speculative and tentative.

I'd also suggest that having a hollow stem allows for height to be obtained much more quickly (and therefore access to sunlight in a forest/jungle). A solid stem at the same rate of biomass addition would be about 1/3rd the height of the hollow stem.


text:
Resilience to the neurotoxins of Indian King Cobra
I read on Wikipedia about this:
King Cobra - Wikipedia
In Thailand, a concoction of alcohol and the ground root of turmeric is ingested, which has been clinically shown to create a strong resilience against the venom of the king cobra, and other snakes with neurotoxic venom.
Though, I have been in the village parts of India where King Cobra is frequently encountered, I have never heard of this knowledge.
Can somebody please explain the scientific basis of this statement and possible reasons for this?
[PS]: Can somebody also please create a tag for "Snakes"?

Well, turmerin, the compound in turmeric has been medically proven to help neutralize venom from King Cobras in snakes (reference1, reference2). It has also been used in ayurveda for snake bite treatment (reference) The alcohol I guess is just used to help ingest the turmeric and act as a pain reliever, though it strangely seems counter-productive since most snakebite help guides advice against the consumption of alcohol after getting bitten (reference1, reference2) due to its blood thinning properties.
Having said that, I guess personally, I would go for anti-venom rather than ingest turmeric. As a quick remedy until you get the anti-venom you should be able to depend on turmeric.

I think the alcohol is used to extract the turmerin from the roots.

@Chris Yes it is one way of doing so apparently.

Turmerin is water soluble. Perhaps they extract curcumin with alcohol.

As The Last Word said turmeric is a suggested medicine for cobra bites in India,also Bromelain found in Pineapple and Papain in Papaya fruit are also suggested medicines by folks. Although they are unaware of these chemicals they do use these fruits for venom treatment.
Also oral administration of garlic is said as a prophylactic tool against cobra venom.
Azadirachta indica(Neem) is also a prescribed medicine for Indian Cobra bites.
http://www.google.co.in/url?sa=t&rct=j&q=&esrc=s&source=web&cd=9&ved=0CE8QFjAI&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F51064057_Herbs_and_herbal_constituents_active_against_snake_bite%2Flinks%2F0912f50a48bd135b2c000000&ei=AlF0VImNFoaNuASv8YCICw&usg=AFQjCNE9BJ_rGjd3eG2TH-rSJh4-bIaq6w&sig2=1iP7DTk7Z34YZ4vWiQnvbg&bvm=bv.80185997,d.c2E&cad=rja

Cipadessa baccifera leaves have powerful anti venom properties, especially for the treatment of cobra poison.
  http://indiabiodiversity.org/species/show/31204

Aristolochia taxa have also been used as reptile repellents. Aristolochia  serpentaria (Virginia snakeroot) is thus named because the root was used to treat snakebite, as "so offensive to these reptiles, that they not only avoid the places where it grows, but even flee from the traveler who carries a piece of it in his hand".
I couldn't find if there is any remedy for snake bites exist in Thailand as you said but i found this,

A hospital in Thailand hooked up with Mahasarakham University and brewed up a remedy. It’s a mix of betel nut, lime juice and the root of Trigonstemon reidiodes. "
  https://hughpaxton.wordpress.com/tag/kap-choeng-hospital-develops-herbal-cure-for-cobra-snake-bite/

Without references I would suggest a traditional snake bite remedy used in my place called "Vishakallu"[Venom Stone] with ingredients
Ocimum sanctum (Tulsi leaves),
Anisomeles malabarica(Perumthumba),
Sandal wood
these medicines are treated with a stone and this stone is used for healing and it is then placed in cow milk and stored in cow dung ash and can be reused 15+ times.

what it means is that a warm clear extract of turmeric powder given as oral drink and  washing of the snake bite wound will save the person from death till the antibody injection is given. the above is due to stoppage of a toxic enzyme called PLA2 which universally present in all snake venoms
if one thinks that it is like an ad it  shows the in ability to understand and i feel such irresponsible statements are best avoided
 leela srinivas

Welcome to Bio and thanks for the great answer. Do you happen to have a reference at hand?

Thank you for the query, I would have search would have shown that, we are the pioneers to first use Turmeric against snake venom.  Be it, Cobra, Krait or Viper. It is the universal truth that, all the snake venom is 90% protein and out of that, 60% is the lethal inflammatory toxic enzyme called Phospholipase A2 (PLA2).  PLA2 is an enzyme that breaks down the cellular plasma membrane containing phospholipid and allows the entry of toxic enzyme.  The toxic enzyme let loose a cascade of events that goes through cyclo-oxygenase and lipoxygenase pathway with release of arachidonic acid - 20 carbon fatty acid which forms the precursor of pain causing inflammatory by-products.  Since, Turmeric can destroy the activity of phospholipase A2,the inflammation and accompanying inflammation reduced considerably and the life of the patient extended by two to three hours giving time for the anti-venom antibody treatment. The attractive feature of the above "On the spot" treatment by Turmeric is that, the snake can be any species because PLA2 is the key toxic enzyme in all the venoms. The way to administer Turmeric on the field is to take two to three fist full of Turmeric powder and dissolve it in warm water, then it is filtered through a clean cloth and the clear extract without any residue about a glass is given to drink by the patient when it is warm.  The rest of the water is used to continuously washed the bitten spot so that, the local inflammation is subsidized. You may refer the to the following publications where it is shown that Turmerin, a water soluble antioxidant protein from Turmeric binds to PLA2 distal to the active site and changes the conformation of Phospholipase A2 in such a way that, it is no more hypertoxic.  Thus extending the life of the patient and reducing pain and inflammation.
Reference:
New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.

As of current, it's unclear what you are trying to convey with this answer. Could you clean up this post?

It reads more like an advertisement to me. I vote for deletion.

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text:
How big should the human population be, as predicted by body mass?
I would guess there is a theory in biology which states that the population size for a given species is inversely proportional to the body mass of individuals in that species.  In other words, there are zillions of ants, billions of mice, millions of deer, and just a few elephants.
If humans existed in a "state of nature" (i.e., were not able to manipulate their environment more than any other mammal), what population size would be predicted by their ~70 kg body mass?
(Assume that the human population has spread globally.)
I imagine we would fall somewhere between the wolf and bear populations.

The question is interesting. Yes, there is probably such negative correlation. However, in order to make predictions from such regression, one has to make some arbitrary decision about what species to include in the regression. Do you want to include only mammals, all vertebrates or all living things (assuming this is well defined) on earth? I am hoping someone can come up with a good answer of what the regression look like depending on what clades we include in the regression.

Note also, that in general large species suffer from the presence of human and therefore, such regression is likely to be very different today to what it was a 1000 years ago.

It is certainly possible to use general relationships to predict human population density or abundance. The relationship between population density/abundance and body size is an old topic in ecology that falls within the field of allometrics (how different features of organisms scale with body size). A closely related allometric relationship is Kleiber's law, which deals with the relationship between body size and metabolic rate.
Your assumption of a generally negative relationship between body size and abundance is correct, and the relationship is approximately linear on a log-log scale. As mentioned in the comments, the exact shape of the regression will depend on what organism groups are included, since the scaling relationship is known to differ between taxa. However, to get a reasonable ballpark figure we can look at a the classic paper by Damuth (1981), which include 307 mammal herbivores. The scaling relationship found there is:
$$D = 10^{4.23}*W^{-0.75}$$
where density (D) is in individuals per km2 and body weight is adult body mass in grams. Using your example of 70kg for humans would result in a predicted density of 3.9 individuals/km2. The scaling coefficient -0.75 (or -3/4) is often labelled "Damuth's rule", and is usually also found when pooling both ectotherms and endotherms.
However, remember that this regression was based on primary consumers, i.e. mainly herbivore grazers. Alternative data for groups of mammals can be found in Peters & Raelson (1984). That paper presents regressions for both carnivores+omnivores as well as for all groups of mammals (herbivores, carnivores, omnivores). The relationship for carnivores + omnivores (CO) is:
$$D = 15.7*W^{-1.15}$$
and the regression with all groups is (HCO):
$$D = 40.7*W^{-0.859}$$
In both of these regressions body weight is expressed in kg. Using the CO regression results in a predicted human density of 0.1 individuals/km2, and the HCO regression gives a human density of 1.1 individuals/km2.
Looking at these values, it is reasonable to assume that the predicted "natural" population density of humans lies in the range 0.1 - 4 individuals/km2, but certainly biased towards the lower part of the range. I suspect that a regression looking only at primates would predict an even lower value, so I would not rule out values below 0.1 individuals/km2.
To get a grasp of what this means in actual population numbers, we can extrapolate the densities to the entire earth. If we use the predicted density from the carnivore+omnivore model in Peters & Raelson (1984) and the entire land area of the earth, which is ~150 million km2 (Wikipedia: Earth), the predicted human population would be about 18 million. Using the high estimate from Damuth (1981) would correspond to about 600 million people. However, remember that this is using the entire land area, including deserts, mountain ranges and arctic areas.
Another point of reference is the estimated historical human population density during the Paleolithic, when we lived as hunter-gatherers. I have often seen population densities in the area of 1 per mile2, i.e. 2.6 individuals per km2. These estimates are naturally very uncertain, but shows that the allometric scaling relationships seem to provide at least reasonable order-of-magnitude estimates of "natural" human population density.
It is also somewhat enlightening to consider that our current human population size of 7 billion corresponds to the predicted population size of a 380 gram carnivorous mammal (using the CO relationship from Peters & Raelson (1984)), making the unrealistic assumption that this mammal has managed to colonize all land areas on earth. This shows pretty clearly what an outlier modern humans represent.
The generality of these types of relationships for predicting densities of individual species can however be questioned. For instance, the regression relationships also differ between climatic regions (see Peters & Raelson (1984) for more), and, as indicated in the comment by @remi.b, it is also unclear what population states that should be included. For instance, should only population densities in "ideal" habitats be used, when we know that population densities of the same species can differ by orders of magnitude in different habitats? It is also unclear if/how to consider the effects of modern humans. Silva & Downing (1995) also argue that the scaling relationship is nonlinear on the log scale, with a more shallow slope for larger species, and also find essentially no relationship between body size and density within some groups of species. More recent papers have also highlighted that studies on global relationships between density and body size often mix-up several different processes and relationships, see White et al (2007) for an overview on this.

dang thats 2 billion people tops.

@shigeta but that is using the entire surface of the earth, right (including water)?

I think I googled the land area of the earth, but it would include antarctica.  I think it would be great if we could get to 2b human beings though.  with good technology we could be sustainable I think.

Thank you, @fileunderwater.  This is a very thorough answer.  I especially appreciate the equations!

@SlowMagic You're welcome. I enjoyed revisiting some of the litterature and writing it.

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text:
Large scale reverse transcription?
I need to make RNA:DNA duplexes. I can make 100 to 200 ug of mRNA through in vitro transcription, and I know how to use reverse transcription to make a cDNA library, but I have questions with this.
The mRNA I make with IVT is all poly A RNA, and the reverse transcription kit I have says to use 5ug of total RNA or 500ng of poly A RNA. I need to make at least 10ug of RNA:DNA, which is 20 times the suggested limit for poly A RNA, so a direct scale up probably isn't practical.
I can't find a literature precedent for making such large amounts of DNA through reverse transcription, everything I have found that uses RNA:DNA duplexes used short strands that were chemically synthesized and combined, my mRNA is 1800 bases long, so I can't just order an oligo, I have to make it.
EDIT : I can't comment on my own question.
The duplexes will be about 1800 bases long, it's for firefly luciferase.
Trying to make the DNA for the duplex from the original DNA template presents other issues. While it would be easy to cut it out from the plasmid, it would be double stranded, and I would have to mix with the RNA and heat it up to dissociate everything and hope that the RNA bound before the DNA strands reassociated. I also think it would complicate my controls, because it would be harder to say that any expression I see after delivering these duplexes came from the RNA and not the DNA. Of course synthesizing the DNA from the RNA could also introduce that problem.
Some crude calculations suggests that the dNTPs are the limiting reagent for a transcript this size, and that even with 5ug of mRNA I should have enough oligo dT primer for the reaction. I right now I am running reactions from 0.5 to 5ug of mRNA, 1uL of primer, and 4uL of dNTPs, to make sure I have enough. Hopefully the gel will turn out ok.
EDIT: I got the results. So far it looks like 3.0ug of mRNA works the best. It has the darkest band, and looks like the right length. Less mRNA gives fainter bands that appear too short, and more mRNA gives slightly fainter bands that appear slightly too short. Also, I ran the reaction for 2 hours instead of 1.

Can't you use the template you used to synthetize the RNA? You'd need two restriction sites to remove the parts you don't want, but using DNA to synthesize RNA and then using that RNA to synthesize DNA again seems a bit cumbersome.

how big should your RNA-DNA duplexes be ?

The best way for scaling up these kinds of reactions is to set up many reactions. Prepare a mastermix for lets say 20 reactions. You can pool them together, precipitate the RNA and dissolve to appropriate concentration in nuclease free water. Also, use gene specific primer instead of oligo-dT and don't add poly-A tails (poly-A does not affect the in-vitro stability of RNA).
As Mad Scientist already indicated, you would not need to make DNA again from RNA. Simply take 1:2 molar ratio of your IVT template dsDNA (restriction digested) and the RNA (post IVT). Heat and anneal slowly. DNA-RNA hybrids are stronger then DNA-DNA hybrids and the former is more likely to form after annealing. You can digest the unpaired strands using enzymes like mung bean nuclease.

I had almost forgotten about this question. I think we've all but abandoned this idea, RNase H seems to be a problem with RNA DNA hybrids, we paired a PolyA tailed mRNA with a 25 base oligo(dT) and dosed it to mice, completely stopped protein expression. If we used an oligo(rU) the signal was not affected, so we suspect it's RNase H cutting the polyA tail off and starting the mRNA degrdation process.


text:
List of dinosaurs synonyms
Is there a comprehensive list of dinosaurs synonyms with indications of which name is now considered correct? Something like "there's no brontosaurus, there's only Apatosaurus", "there's no Anatotitan, there's only Edmontosaurus" and so on.

Here is one list that includes synonyms, but I don't know how credible it is and it seems to lack references. Encyklopedia of Life also includes information on synonyms (see link for Apatosaurus)- not a list but searchable.

Just for fun: This TED talk might be slightly related to your question.

Thank you Remi, this TED talk that i saw a few days ago is exactly what made me ask the question. I am creating a board game about dinosaurs and i need several names but i don't want to have two dinosaurs with different names that are actually the same dinosaurs and this is why i am here. I need a list, not a directory, just for convenience, because it would be so much more easier to scroll a list instead of looking for 120 different names (this is the current size of my dinosaur "pool"). thank you anyways!

@JohannesWentu For that use, the second list in my answer should be sufficient. It seems like several professional paleontologists are included in the project.

Actually, a paper in 2015 resurrected Brontosaurus as a valid genus. What is surprising is that the "thunder lizard" was smaller than the dully-named Apatosaurus.

Encyclopedia of Life includes information on synonyms (see link for Apatosaurus) - not a list but searchable and often with references and background info. After a quick google search I also found this list from dinosaurcentral.com, but I don't know how credible and updated it is and it seems to lack references.


text:
What species of Cerapoda lived during the Jurassic?
So far, I've found eleven species of Cerapoda that lived during the Jurassic period. Are there any other known species that I've missed?
The eleven that I've found out about are:

Agilisaurus
Albalophosaurus
Camptosaurus
Chaoyangsaurus
Dryosaurus
Heterodontosaurus
Othnielosaurus
Uteodon
Xuanhuaceratops
Yandusaurus
Yinlong

I am a game board designer working on a game related to dinosaurs. The "only" research i did is Wikipedia + the DK book "Prehistoric" + Dino Directory web site + several more lesser sites. I would appreciate any information on other species if my list isn't exhaustive, or literature suggestions that might help me.

I made your list look better, please look over the edit to ensure I didn't mess up your species names, because I couldn't understand your original list.

VTC because this looks like a homework question without evidence of any research. If it in fact is not, please provide evidence otherwise.

I am a game board designer working on a game related to dinosaurs. The "only" research i did is Wikipedia + the DK book "Prehistoric" + Dino Directory web site + several more lesser sites. If finding already 11 Jurassic Cerapoda seems "no evidence of any reasearch" I am sorry, I found it quite hard even to find these eleven names as Cerapoda had their "explosion" in the late Cretaceous. I was hoping to find some more help in finding another example of an early Cerapod. Thank you

@JohannesWentu I added the info from you comment to the question. Please clarify further if you have more information.

I can't understand why this question is being voted on for being closed... And how is this a homework question? Please be more diligent when voting to close.

I'm a little confused by your question. You ask specifically about Cerapoda, but your list includes several non-cerapod genera (Heterodontosaurus and Agilisaurus). Do you want only Cerapoda, or Ornithischia more broadly?

@kmm. I am only looking for Cerapoda and unfortunately, from my extremely little experience in this world, i already saw that not everyone agrees with classifications. For instance Agilisaurus is not a Cerapod in WP and is a Cerapod in NHM: http://www.nhm.ac.uk/nature-online/life/dinosaurs-other-extinct-creatures/dino-directory/agilisaurus.html . Same thing with Heterodontosaurus: http://www.nhm.ac.uk/nature-online/life/dinosaurs-other-extinct-creatures/dino-directory/heterodontosaurus.html  How a layman like me should choose who is correct?

Try starting here, http://www.gavinrymill.com/dinosaurs/Cladogram/CladogramOrnithischia.jpg it will at least give you a list of names you can check individually for the time. It is not perfect but it is among the most complete. This site will help in checking them. https://en.wikipedia.org/wiki/List_of_dinosaur_genera

Here is a cladogram from "The phylogeny of the ornithischian dinosaurs", Butler, Upchurch, & Norman, Journal of Systematic Palaeontology (2008):

Of these, :

Ferganocephale (Pachycephalosauridae)
Chaoyangsaurus
Camptosaurus (Ankylopollexia)
Uteodon (Ankylopollexia)
Callovosaurus (Dryosauridae)
Dryosaurus (Dryosauridae)
Dysalotosaurus (Dryosauridae)

lived during the Jurassic.

The synopsis explains well why this classification is subject to adjustment, and why you may have seen contradictory models in your research:

SYNOPSIS Ornithischia is a familiar and diverse clade of dinosaurs whose global phylogeny has
  remained largely unaltered since early cladistic analyses in the mid 1980s. Current understanding of
  ornithischian evolution is hampered by a paucity of explicitly numerical phylogenetic analyses that
  consider the entire clade. As a result, it is difficult to assess the robustness of current phylogenetic
  hypotheses for Ornithischia and the effect that the addition of new taxa or characters is likely to have
  on the overall topology of the clade.
The new phylogenetic analysis presented here incorporates a range of new basal taxa and characters
  in an attempt to rigorously test global ornithischian phylogeny. Parsimony analysis is carried out
  with 46 taxa and 221 characters. Although the strict component consensus tree shows poor resolution
  in a number of areas, application of reduced consensus methods provides a well-resolved picture
  of ornithischian interrelationships. Surprisingly, Heterodontosauridae is placed as the most basal
  group of all well-known ornithischians, phylogenetically distant from a stem-defined Ornithopoda,
  creating a topology that is more congruent with the known ornithischian stratigraphical record. There
  is no evidence for a monophyletic ‘Fabrosauridae’, and Lesothosaurus (the best-known ‘fabrosaur’)
  occupies an unusual position as the most basal member of Thyreophora. Other relationships within
  Thyreophora remain largely stable. The primitive thyreophoran Scelidosaurus is the sister taxon of
  Eurypoda (stegosaurs and ankylosaurs), rather than a basal ankylosaur as implied by some previous
  studies.
The taxonomic content of Ornithopoda differs significantly from previous analyses and basal
  relationships within the clade are weakly supported, requiring further investigation. ‘Hypsilophodontidae’
  is paraphyletic, with some taxa (Agilisaurus, Hexinlusaurus, Othnielia) placed outside
  of Ornithopoda as non-cerapodans. Ceratopsia and Pachycephalosauria are monophyletic and are
  united as Marginocephalia; however, the stability of these clades is reduced by a number of poorly
  preserved basal taxa.
This analysis reaffirms much of the currently accepted ornithischian topology. Nevertheless, instability
  in the position and content of several clades (notably Heterodontosauridae and Ornithopoda)
  indicates that considerable future work on ornithischian phylogeny is required and causes problems
  for several current phylogenetic definitions.


text:
Citing species in a biology article
My question concern the abbreviation of the genus of a species.
I talk about two species: Amphiprion clarkii and Amphiprion perideraion.
Question 1
Let's assume I haven't said a word about these species in my article yet. Should I say:

Amphiprion perideraion is a small fish and Amphiprion clarkii is a big fish

or

Amphiprion perideraion is a small fish and A. clarkii is a big fish

Question 2
If I talk about these two species in the abstract, should I use the abreviation the first time I cite them in the introduction or not?

I would use the long form for the first citation in the main text end after that the short form. You also wouldn't put references into an abstract, so this is repeated later (even if its part of an abstract) and then correctly referenced.

To avoid confusion all species names should be written in full at first, and can then be abbreviated. In this particular example it would probably not be a problem to use the second, shorter version. But what if you had four species divided into three genera with all names starting with 'A'? As for question 2, the full name usually only needs to be used in the title (if relevant) and once in the body text (which includes the abstract), so you can abbreviate after the abstract. However, this is really only a space issue, and you can use the full name at all instances (you may abbreviate, but don't have to), unless of course journal style prohibits this. I find it useful to write the name in full both in the abstract and once in the main text.
See The International Code of Zoological Nomenclature (Appendix B: General Recommendations) for a reference. To be picky, technically, authorship and year of species names should also be included at least once in each paper (e.g. Amphiprion clarkii Bennett, 1830), to clarify exactly what definition of a name you are using. However, this is often not done in practice (in fields outside taxonomy/systematics). What you often see is that people refer to a authoritative source, e.g. "... all species names used in the study follow Doe et al. (2008)."


text:
Can Escherichia coli survive on glucose and water alone?
I am novice to biochemistry and biology in general. I am reading Lehninger Principles of Biochemistry, and I found the following sentence at the beginning of the chapter on glycolysis:

A bacterium such as Escherichia coli can obtain from glucose the carbon
  skeletons for every amino acid, nucleotide, coenzyme, fatty acid, or
  other metabolic intermediate it needs for growth.

Does this mean that E.coli can survive in a medium containing H₂O and glucose alone? E.coli can synthesize any other nutrient it needs?

This quote is not really true.  Nitrogen is necessary for all the co-enzymes and proteins to sustain life.  In order to get energy, if E coli. needs to metabolize nitogen at all as opposed to recycling it, I'd think that the bacteria would eventually all die out.

@shigeta And where can E coli find Nitrogen, in normal conditions? I assume E coli can't synthesize Nitrogen from other atoms, since that would involve nuclear reactions!

i expanded into an answer... normally E coli live in the gut and the food we eat supplies their nitrogen (and carbohydrate) needs. Its pretty hard to find an environment on earth with no nitrogen available.

The answer and comments about N and P are correct, but the quote is literally true - since it is restricted to a statement about carbon skeletons, not entire molecules.

The minimum requirement for E. coli and other bacteria to grow and survive is called minimal medium.  It's even defined at Merriam-Webster:

a medium that contains only inorganic salts, a simple carbon source (as carbon dioxide or glucose), and water

Water and glucose are pretty easy, but the source of salts may often change; regardless, you really need some potassium, phosphate, and nitrogen for amino acid synthesis.  This page has a bunch of information on bacterial growth, including some "recipes" for a few bacterial strains.  For E. coli, the classic media is M9, which over at Sigma is made of:

33.9g Na₂HPO₄.7H₂O
15g KH₂PO₄
5g NH₄Cl
2.5g NaCl

per litre of solution.

Here are some other recipes.

Yes, but no. In other words, this quote is not probably not true in the ways you'd think.  Bacteria can survive on practically nothing for long periods of time, but whether you call that life is subjective.
Nitrogen is necessary for all the co-enzymes and proteins to sustain life. In order to get energy, if E coli. needs to metabolize nitrogen to waste at all, all the bacteria would eventually all die out.  The same feat for human beings would be to add a little sugar into sewage and surviving on it.  Nobody would die right away, but its hard to call that living maybe.
Unless a medium is exchanged, E coli in a laboratory culture will start a massive die off.  When the E coli culture becomes terminal in this way, a portion of the bacteria go into stationary phases where the bacteria can survive for very long times - for months or possibly years.  So some of the bacteria would survive, but they would be dormant. You might not call this survival, but tens of thousands of bacteria are still alive and can generate colonies if transferred to fresh media.
Laboratory cultures and media are of course artificial conditions which don't reflect the environment which bacteria are adapted.  In their life cycle, they typically have other sorts of behavior and experience low nutrient conditions often enough.  Bacteria are also different in that a 99.99% die off can be considered a typical event in some cases.

It should also need some $P$ and I would guess other things like $Cl$ and $K$ too right?


text:
What makes the amide bond the lowest energy pathway?
I've reading about proteomics and how it can be used with mass spectrometry to sequence digested peptides.
Reading this paper the author states (in box 2):

peptide fragmentation induced by collisions with residual gas, and
  bond breakage mainly occurs through the lowest energy pathways - that
  is, cleavage of the amide bonds

Why is cleavage predominately at the amide bond? What makes the amide bond the lowest energy pathway?

This question is probably better suited to Chemistry.SE

@MattDMo While this is a chemistry question, it is also about biologically important molecules, so it is still on-topic here.

@MadScientist Even though it is about a biological relevant molecule the principle behind this question is chemistry. Note that this is not about peptide formation and degradation in-vivo; it is about collision induced decay (nothing biological here).


text:
How to identify the genes that distal enhancers pair?
I am writing a project proposal and I have to talk about this problem: how to identify the genes that distal enhancers pair?
I am really new to this topic and I don't know what it is all about. I have been searching the literature but I did not find anything useful. Can someone explain to me what it is all about?
Maybe suggest some papers to me.

To make sure I understand your question right: You want to know how distal enhancers of genes are identified?

@Chris Yes, and how enhancers regulate distal genes. Thanks.

Check this technique called Chromosome Conformation Capture (3C). Its variants exist such as 4C, Hi-C etc.
Basically, the principle of this technique is based on the physical interaction between the enhancer and promoter that is bridged by a transcriptional modulator(protein).

The chromatin is crosslinked
DNA is sheared
The protein is pulled down (Optional)
The fragments of the promoter and enhancer are ligated together and then sequencing/qRTPCR is done.

Sequencing (low throughput- sanger) can be used to identify enhancers of a given promoter. qRTPCR can be used to quantify the strength of the association.
What I just said is not a high throughput technique. Hi-C is high throughput variant of 3C. See the protocol here.


text:
What's the longest transcript known?
What's the longest functional transcript known?  I'm wondering about RNA length post splicing, so not including introns.

You are looking for the longest, processed mRNA transcript. In which species? Human?

I was wondering if anyone knew of any beyond the human set.  We might have found one today in the Databases....

Top 10 long processed transcripts in humans (with multiple isoforms), from gencode 19 annotations:
Transcript    Length(bases)
------------------------
TTN-018        108861     <-- Titin
TTN-019        103988
TTN-002        101206
KCNQ1OT1-001    91666
TTN-201         82413
TTN-202         82212
TTN-003         81838
MUC16-001       43732
TSIX-001        37026
MCC-009         29616

Ignoring isoforms (only longest isoforms shown)
Transcript    Length(bases)
------------------------
TTN-018         108861
KCNQ1OT1-001     91666
MUC16-001        43732
TSIX-001         37026
MCC-009          29616
TRAPPC9-015      29514
SYNE1-001        27602
GRIN2B-001       27204
OBSCN-011        26811
NEB-204          26020

Titin clearly is the longest transcript in humans
However this is the list of longest genes:
Gene           Length(Kb)
-------------------------
CNTNAP2        2304.64
LSAMP          2186.93
DLG2           2169.35
DMD            2092.29
PTPRD          2084.57
MACROD2        2057.83
CSMD1          2056.87
EYS            1987.24
LRP1B          1900.28
PCDH15         1806.76
CTNNA3         1783.65
ROBO2          1740.82
RBFOX1         1691.87
NRXN3          1619.64
DAB1           1548.83
RP11-420N3.2   1536.21
PDE4D          1513.42
FHIT           1502.09
AGBL4          1491.06
CCSER1         1474.33

Top 5 in Zebrafish (Zv9.75); longest isoforms:
ttna-203             93727   <-- Titin
ttnb-202             82632
si:dkey-16p6.1-001   67263
syne2b-201           31867
si:dkey-30j22.1-001  29269

Top 5 in Drosophila (FlyBase r6.02); longest isoforms:
dp-RQ           71300   <-- Dumpy
sls-RP          56448   <-- Titin
Muc14A-RA       48719
Msp300-RG       43105
Ank2-RU         42107

Top 5 in C.elegans (WormBase WS220); longest isoforms:
W06H8.8g        55623   <-- Titin
K07E12.1a.2     39257   <-- dig-1
ZK973.6         25608
C09D1.1b        24198
C41A3.1         23457

Top 5 in Arabidopsis (TAIR 10.23):
AT1G67120.1     16272   <-- Midasin homolog
AT3G02260.1     15451   <-- Calossin-like protein
AT5G28263.1     15194
AT1G43060.1     14622
AT5G30269.1     14590

Top 5 in yeast (SGD):
YLR106C         14733   <-- Midasin
Q0045           12884   <-- Subunit I of cytochrome c oxidase
YKR054C         12279
YHR099W         11235
YDR457W          9807

It seems that Titin is on the top of the list in many species. Interesting.

I think a good candidate is the human titin gene. The gene itself has 363 exons, depending on the isoform it has between 27.000 and 34.000 residues. This makes up a processed mRNA length of up to 100kb for the full length isoform. See either the Wikipedia article or the one linked below for more details:

The complete gene sequence of titin, expression of an unusual
approximately 700-kDa titin isoform, and its interaction with
obscurin identify a novel Z-line to I-band linking system

If you are looking for the longest primary transcript, then the human dystrophin gene should be your favorite. It has a length of about 2.4 Megabases for the primary transcript, the processed transcript has only a length of about 14kb. It takes about 16 hours to transcribe and co-transcriptionally splice the sequence. See here for more details:

The human dystrophin gene requires 16 hours to be transcribed and is
cotranscriptionally spliced.

why does it transcribe 2.4 million bases and cut it down to 14,000? Seems like a waste of time and energy, not to mention the potential for mutations, which if muscular dystrophy is any clue, would be deadly.

alternative splicing is a wierd thing to be sure. biology is not rational but then human science has not yet produced a living cell from first principles...

Cases like this make me wonder why alternative splicing would be worth it. If you divide 2.4 million bases by 14000 bases you get 171.4. Seems like you could just make multiple copies of dystrophin to cover all the isoforms and still save space, and only need to transcribe the copy you want. Evolution should have gotten an engineering degree.

I don't have a reference for this, but I was told by a professor once that a long developmental gene is Drosophila takes longer to transcribe than the length of the cell cycle during initial development so that is not actually expressed until the cell cycle lengthens later in development. That's perhaps one answer (if uncommon) to the question of why some genes are so long.


text:
How do the variable portions of antibody genes look in cells which don't produce antibodies?
There are several families of antibodies found in mammals.  They may have two or more antibody domains which contain heavy and light chains.  The variable regions of the light and heavy chains genes in the chromosome are spliced in antibody producing cells so that each cell produces a different antibody, with a unique sequence of amino acids in the variable regions.
Here's a cartoon:

The variable regions are disproportionately large here, but it gives some idea...
What I'm having trouble finding is how the DNA regions of these genes look in cells which don't produce antibodies.  Are they the same as that in the germline?  Do they undergo recombination but are not expressed?
Any help would be appreciated.

I can't find a definitive reference, but I'm pretty sure that Ig gene rearrangement is a phenomenon that is restricted to lymphoid cells. See WP http://en.wikipedia.org/wiki/Recombination_activating_gene for an assertion that expression of the specific recombinases is limited to lymphocytes.

If "cells that don't produce antibodies" means generally all other kinds of cells (e. g. skin cells or so), then the answer is: yes, the DNA regions are the same as the germline. The VDJ recombination bharat_iyengar mentioned is a controlled procedure that has to be initiated and doesn't occur randomly.
If you refer to lymphoid cells that do not yet express antibodies, the answer is: that depends. It depends on the state the cell is in, because it is done in distinct steps (pre-B cells are different from pro-B cells).

Perhaps you want to ask how VDJ recombination is regulated in non lymphoid cells..
Well even in immature lymphoid cells VDJ recombination is regulated. And also Ig genes are suppressed in T-cell and TCR genes are suppressed in B-cells..
Also, the recombination of Ig is suppressed in T-cell and vice-versa.
RAG-1,2(Recombination activating gene) downregulation partly does the job, but not fully.
Earlier reports say that transcription in the locus is essential and epigenetic regulation of transcription in turn regulates recombination.
But what it exactly means is that accessibility to the RSS (Recombination signal sequences) is limited in a repressed chromatin and recent reports say that nucleosomes are appropriately positioned over the RSS to control recombination.
Have a look at these:
http://www.cell.com/abstract/S0092-8674%2802%2900675-X
http://www.sciencedirect.com/science/article/pii/S0952791506000057
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC204470/

Thanks for pointing out how many varieties of cells have VDJ recombination.  It sounds like getting a germline Ig sequence would be the typical result.

There are the IgG sequences in the germline along with several pseudogenes. They are kept repressed..
Have a look at this. Perhaps this is what you are looking for: http://www.ncbi.nlm.nih.gov/igblast/showGermline.cgi

Also, check this out.

This is why I normally try to avoid immunology - the cell differentiation and function leads to as many new questions as answers... thanks!

immunology always full of anomalies :P


text:
Metapopulation structure - book recommendations
What book would you recommend me to study:

the dynamics of metapopulations,
the structure of metapopulations,
the evolution in structured metapopulations?

I am not looking for an introduction but for a book that offers good and extensive mathematical formulations.

Probably the best source to start would be Ilkka Hanksi's work, you can find a full list here: http://www.helsinki.fi/science/metapop/People/IlkkaPub2.htm.  The seminal work would be "Ecology, Genetics and Evolution of Metapopulations"  It gives a strong mathematical treatment

I was indeed thinking about "Ecology, Genetics and Evolution of Metapopulations". Thank you!


text:
Can diploidy evolve in absence of sexual reproduction?
Theoretical question

Can diploidy (or polyploidy) evolve from a haploid lineage in the absence of sexual reproduction ?
For what theoretical reason? How can such evolution take place?

Empirical evidence
Beside theoretical answers I'd like to also ask for empirical examples:

Are there any examples of diploid (or polyploid) species that reproduce exclusively asexually, and for which sexual reproduction never occurred in the evolutionary lineage of this species?

Or in other words,

Does diploidy (or polyploidy) exist in lineages that has never underwent sexual reproduction?

Is my assumption correct?
I am assuming that in eukaryotes haploidy appeared before diploidy. Is this assumption correct?

By sexual reproduction I mean that the genome of the offspring is a combination (with or without recombination/crossover) of two parent individuals. I don't mean reproduction with sexes (or with mating types). I welcome the discussion of self-fertilization if needed.

I can only offer a partial answer on the theoretical aspects. I don't know if you are familiar with the mid-90s papers by Otto et al. (Otto & Goldstein,1992, Otto & Marks, 1996), but these are definitely relevant to your question. They deal with the "masking hypothesis" of diploidy, i.e. that deleterious mutations can be masked by "healthy" alleles, and the trade-offs between diploidy (ploidy level), recombination rate, and purging of deleterious alleles. Otto & Goldstein (1992) shows that recombination is essential for the evolution of diploidy, and without recombination, haploids will "win" over diploids.
Otto & Marks (1996) is a fairly comprehensive paper that builds on the previous one, and looks at how different mating systems interact with recombination and purging to influence the evolution of ploidy levels. As a general result, they predict a correlation between mating system and ploidy level, with sexual reproduction favoring diploidy, while asexual reproduction favors haploidy. However, from what I can see after a quick re-read, there is nothing that prohibits asexually reproducing species to be diploid (and vice versa) - see e.g. page 206 - and the paper includes a condition that must hold for diploids to invade in asexually reproducing or selfing populations. I have not followed this literature closely, though, and I imagine that tracing recent papers that cite Otto & Marks (1996) can be useful to find further relevant studies.
You should also consider that ploidy levels can differ between sexes (e.g. bees), which can lead to antagonistic selection, which can influence ploidy evolution (see e.g. Immler & Otto, 2014).
As for the empirical evidence part, I do not have any good examples. However, I imagine that it can be extremely difficult to prove that a lineage has only reproduced asexually (or never asexually), since these things are hard to track in fossils. Also consider that it is common to have both sexual and asexual stages, and many species can have a long asexual diploid stage followed by a shorter sexual haploid stage. From what I know, this is the norm in e.g. algae (arguably a group of fairly "basal" taxa). However, I don't know what the ancestral state of algae was (i.e. if they became diploid before having a sexual stage).
As for the ancestral state of eukaryotes, there seems to be evidence that the ancestral state was in fact facultatively sexual (Dacks & Roger, 1999), which would invalidate your assumption. However, this is only based on a couple of quick literature searches on my part, and I am in no way an expert in this area. There are probably more recent studies on this topic as well. However, it is clear that you cannot blindly assume that eukaryotic haploid is ancestral.

Thanks a lot for this literature. It is very interesting indeed. And thanks for the Dacks and Roger's article too!

This is not on theoretical grounds, but here is an existence proof: a number of bacteria, which reproduce asexually, are polyploid. Here is a blog I really like informally discussing the concept of ploidy in bacteria. The example I am familiar with is cyanobacteria, which can have 3-4 all the way up to 142 copies of its genome, according to this paper (1). There are other examples as well, such as Epulopisculum, a sturgeonfish symbiont (2). This paper even reports a diploid bacteria (3). Searching in Pubmed should reveal other interesting cases of this.
A more borderline example would be even the most typical bug E. coli. When E. coli grows rapidly, it is well known that it has more than one copy of its genome per cell; this allows the organism to be creating the genome for the granddaughters of the current cell, allowing the time between divisions to be shorter than the time it takes to replicate DNA (4). Here is an intuitive explanation of this. Depending on your definition of polyploidy this might not count, but the bacteria presumably are able to make use of this copy number effect.
(1) Greise M et al. (2011). Ploidy in cyanobacteria. FEMS Microbiol. Lett. 323(2):124-31
(2) Mendell JE et al (2008). Extreme polyploidy in a large bacterium. PNAS 105(18): 6730-34
(3) Michelsen O et al (2010). J. Bacteriol. 192(4): 1058-65
(4) Helmstetter CE (1968). DNA synthesis during the division cycle of rapidly growing Escherichia coli B/r. J. Mol. Biol. 31(3) 507-518 ---non-free, unfortunately, but see also Nielsen HJ et al (2007). J. Bacteriol. 189(23):8660-6

Nice examples, but I suspect that the original poster is looking for eukaryotic examples (based on the Is my assuption correct? part)

From a theoretical viewpoint, why should it matter? If you are looking only at whether an asexually reproducing species can evolve polyploidy, then I feel that asexual eukaryotes and asexual prokaryotes are reproducing the same way, and so will provide viable models for this process. Furthermore, are there any uniformly haploid eukaryotes? If not current, do we have evidence of any in the fossil record?

All the mechanisms that I know influencing heredity (and thus evolution) that differ between eukaryotes and prokaryotes (e.g. homologous recombination) have to do with sexual reproduction or are intrinsically features of a polyploid organism. They couldn't factor into the evolution of polyploidy in a haploid organism, prokaryote or eukaryote. The only difference would be if there is an effect of having multiple, different chromosomes; most bacteria only have one type of chromosome, and I'm not sure how polyploid the few examples of bacteria with multiple chromosomes are.

I mostly agree, and just pointed out what the Q seemed to ask for. However, I guess horizontal transfer could make a difference in bacteria, but I cannot really say if this should be important specifically for the evolution of diploidy. Overall, I agree that they should face the same problems going from haploid->diploid. Does "masking" of deleterious alleles work the same way in diploid bacteria as in eukaryotes?

+1 Thanks for these empirical observations. They are meaningful to my question and impressive.


text:
Is our genome decaying (see "Genetic Entropy"), and, if so, is this evidence for our genome being "young"?
In the book Genetic Entropy & the Mystery of the Genome the author says that the genome cannot be old because the genome is "decaying". Decay is a very subjective term, but in this case he means that the fitness of humans is going down not up. Is it true that our genome is decaying over time, and that the fitness of humans is decreasing? Here is a quote from the book, that might explain his argument:

Kondrashov, an evolutionist who is an expert on this subject, has advised me that virtually all the human geneticists he knows agree that man is degenerating genetically. The most definitive findings were published in 2010 in the Proceedings of the National Academy of Science by Lynch.4 That paper indicates human fitness is declining at 3–5% per generation.There is really no debate on current human genetic degeneration.

Perhaps this more shines more enlightenment in my question. This idea of human fitness going "down" is my main concern. Essentially, in his book he claims that because we are going "down" (meaning fitness is declining) not "up" (whatever that means) our genome must therefore be young. If I understand the issue correctly, mutations "create new information" by creating different proteins or leading to an abnormal protein products. However, I thought that the force of natural selection should be strong enough to get a rid of those genes that are so and so responsible for our fitness declining.
Sanford, John C., and John R. Baumgardner. Genetic Entropy & the Mystery of the Genome. Waterloo, NY: FMS Publications, 2008. Print.
Feel free to point me to similar questions that may been helpful or are similar to this one.

You need to be more specific with what you are referring to with the "the genome is decaying" statement. "Decay" is also a very subjective/value-laden description of a genetic process, and you should specify exactly what process you are interested in. Is it just "random mutations" -> "genetic dissimilarity over time" (~genetic distance), or something else?  At the moment, it is really hard to understand exactly what you are asking about, and therefore hard to formulate a relevant answer.

@Lucian - I suggest you edit this as much as needed to make it acceptable as a clear question, or let someone else do this for you. You won't get your question answered if you get it closed first. Avoid personal claims like, "I have read extensively on evolutionary biology." You may well have read a few books, but if the books are written from a Creationist point of view, you have not read extensively. That's a bit like claiming you've read a lot about astrophysics because you've read every one of Ken Ham's books. A good answer follows from a good question. Help us to help you.

I think this question has been completely changed, to the point that neither of the answers to it make any sense.

@MarchHo I still think the core aspects of your answer is relevant though, to the last part of the question (you might need to reframe it a bit though).

The question makes more sense now, I removed my down vote. Good job for improving over your original post!

The book you quote is not peer-reviewed; assertions like these are not scientific, they are just the author's opinions: "Kondrashov, an evolutionist who is an expert on this subject, has advised me that virtually all the human geneticists he knows agree that man is degenerating genetically." I would encourage you to distinguish between replicable observations ("facts") vs. rumors, anecdotes, and hearsay.

@mdperry As the OP mentioned, they are not familiar with the discipline of evolutionary biology. Therefore it is not justified on out part to expect them to discern between a bad reference and good ones. We should point the right references to them. The question is clear now and is on-topic.

@WYSIWYG Did you ever consider that this OP could be trolling? Cutting and pasting excerpts from a creationist for one's Biology SE posts could be considered inflammatory.  If the OP is genuinely curious then helping them to evaluate the literature in a field, and pointing out weak vs. strong arguments is demonstrating the epistemology of the scientific approach. If we just spoon feed them I fear we will end up with a generation of scientists who rely on others instead of reasoning answers for themselves.

@mdperry I apologize if that was ever the image I projected. I was advised to not use personal statements like "Ive read about evo bio", I am no evolutionary biologist. I am a double major in geology and chemistry with interest in planetary science. I am very interested in knowing the mechanism by which the non living chemicals formed the first living thing. I am not an evolutionary biology, in my original question i've stated the reason why I wanted to know, but I removed it. I felt that I was being lied to when this was brought up from creationist all the time.

This question is also addressed in this post. You can have a look there, too.

@WYSIWYG yes someone earlier pointed out to a very similar question. I managed to get answers to questions that I did not even know how to ask yet.

If I understand the question correctly, you are asking why random mutations (most of the non-silent ones are deleterious) cannot create information and improve the overall fitness of the organism.
This is a common creationist statement, and has been shown to be incorrect in many different ways. The best way this can be shown to be false is by simply applying natural selection.
E. coli has a beneficial mutation rate of $10^{-5}$ per genome-generation (source) and a detrimental mutation rate of $2×10^{-4}$ per genome-generation (source).
Therefore, at first glance, the claim that the "genome is deteriorating" appears plausible. However, natural selection quickly acts on these mutants with deleterious mutations due to their low fitness. Therefore, the deleterious mutations are removed from the gene pool and are replaced with their beneficial counterparts instead.
If we define "information" as beneficial adaptations to the environment, random mutations themselves do not directly create the information. It is the application of natural selection that allows the fitness of the organism to increase despite the presence of random mutations.

I have two concerns with this answer: 1) How did you do to infer that the OP was interested in the ratio of beneficial over deleterious mutations? 2) you said random mutations themselves do not directly create the information. I can see you are trying to use the OP's words (which is great in general) but it end up sounding quite weird. Definitely, mutations create genetic variance (and therefore increase information or decrease Shannon entropy) while directional selection reduces genetic variance (decrease information).

Of course, it is the combined effect of those two things that allow for adaptation. It is also wrong to say atural selection that allows the fitness of the organism to increase despite the presence of random mutations as it seems like mutations are bad and NS is good which is wrong.

@Remi.b - Selective pressure is shown to select out the beneficial mutations. That's how evolution works.

I am well aware of the basics of evolutionary biology. Mutations increase genetic variance (and therefore shannon's definition of information) by introducing new variants in the population. Natural selection decreases genetic variance (by selecting out deleterious variants) and it therefore decreases information. This is the very basics of evolutionary biology. The term "information" seems to be slightly loaded as being "a good thing" but under the standard mathematical definition the above answer is partially wrong

I agree with @Remi.b Information content is basically a log likelihood function of the entropy. MarchHo, I think you mean information in the sense of functional repertoire of genes, but such a terminology may be misleading. You should clarify it.

The book in question is more of an informational pamphlet than a scholarly monograph. The sort of thing that you might find someone handing out on a street corner. The sophistication of composition is at about the second year UG level. The problem I have with this post is that the term "Genetic Entropy" has no clear sense, and may mean different things to different people. The notion seems to approximate: "The Shannon-entropy of the human genomic sequence". Shannon-entropy measures information content in bits, in contrast to thermodynamic entropy which uses energy units to measure disorder.

@Remi.b should I delete this question?, I thought it was silly to ask the question we are having discussion about this and I had no way of defending natural selection, as like I stated I am only familiar with genomic research. In the book a lot of analogies are used to make the reader understand. the author is a 25+ year Cornell University professor, so he is not just some guy. The argument he poses is used very commonly from creationist I come around ( I am heavily surrounded by creationist views) and really it is an eye opener to me how passionate creationist are about "debunking evolution"

Well, the question is unclear (I hope I managed to make clear why this is the case in my now deleted answer/comment). The question ended up being closed as unclear. You can delete if you want but you don't need to as it is closed anyway. However, as you checked @MarchHo's answer, it seems like he managed to give you a helpful answer (and so other might see something helpful in MarchHo's answer). So maybe just keep it like this. I am just hoping that the error/misleading information in the last paragraph will be corrected by March Ho. Thank you Lucian09474

@Remi.b You make a good point on defining information in terms of Shannon entropy, I think I have a misconception here, will update the question once I figure out what is wrong.

@Lucian09474 You cannot delete posts with upvoted answers. The question is okay if you clarify it. It is fine if you do not know a certain concept and ask a question about it. However, your question should be specific and should have a clear statement.

@Remi.b I think the answer makes sense if "information" is not defined in the sense of Shannon entropy, since the "information" as defined by the question clearly has nothing to do with it.

To my knowledge there is no other commonly accepted definition of information than the one suggested by Shannon. I don't mind using another definition but the definition should then be written down (which is currently not the case neither in the question nor in your answer).

Kolmogorov information is also commonly used - most kinds of mutations other than substitutions (such as duplications, be they internal tandem or whole-gene or genome) automatically increase the Kolmogorov information content because the strings that represent genome sequences have to be made of more bits to describe them.
Any mutation also increases the Kolmogorov information content of the gene pool.

The book makes the argument that the human population with access to modern medicines is at a point where natural selection is less fierce and allows carrying more of the deleterious genes into the next generation than ever before. This argument cannot be countered by referencing E.coli, since we are in a different evolutionary situation. I completely disagree with the findings of the book, but this answer does not provide a satisfying retort for me.

Regarding the reference to Lynch, actually reading this paper is illuminating (http://www.pnas.org/content/107/3/961.full). What Lynch is saying with regards to degeneration is that he and others feel that modern technological advances may relax selection pressures, thus allowing the survival and reproduction of many who would otherwise be selected against, increasing the rate of mildly deleterious mutations in the human population.
Sandford willfully misreads this in order to inject his creationist/intelligent design mythology (Man's creation by god, the fall, no evolution, but rather decay from god's perfection, etc). However, this is definitively NOT what Lynch and other biologists are suggesting. Decay is a loaded word. The genome is constantly changing from generation to generation on an individual basis. Selection simply eliminates overtly deleterious mutations.
Lynch is suggesting a sort-of technological doomsday, where human success at subverting selection ultimately lead to an unsustainable mutational burden and the collapse/extinct of humanity. Differences in selection pressure affect what genomes are propagated onward. Previously deleterious mutations that can be survived in our current environment are seen some malign decay, but this is how selection works. As the environment changes (including technological changes), selection pressures changes. If selection pressures revert, such persons will once again be selected against. An overly dramatic shift in selection pressure (such as collapse of society, or other forms of massive environmental change) could indeed kill us off, but this is true of any species and is in no way unique to humans.

Are you suggesting that Prof. Sandford's assertion, quoted above "There is really no debate on current human genetic degeneration." is not actually supported by the reference that he cites?

Well, I think he's being intentionally misleading, especially in his word choice. This is probably related to a typical (sometimes intentional) creationist misunderstanding of evolutionary processes. If there were some ideal human genome, then most mutations, increasing our divergence from this ideal, could reasonably be seen as degeneration.
Evolutionarily speaking, there is no ideal genome, only those that are more or less well-suited to their current environment. He's postulating a non-existent absolute where there are only relative differences.

A small addition to what March Ho has mentioned in their answer.

Fitness is not absolute; it is dependent on the present environment. Fitness has no meaning when the selection factor is not defined.
You can consider a commonplace example: Can you, by just looking at an individual say how fit they are (of course I am not talking about those who are clearly ill, obese or malnutritioned)? Unless you assess their performance in a task you cannot really say how fit they are. Same goes with evolution.
Now consider another hypothetical example. You would be aware of the fact that the sickle cell trait (mutant haemoglobin) provides immunity against malaria. If your task is some kind of physical exercise then obviously the sickle cell trait is deleterious. However, if there is a malaria pandemic then the sickle cell trait would provide a great survival advantage and therefore these individuals would be deemed fit under these conditions.
It is to be understood that evolution does not work towards "improvisation" of species. Just because we assume that a certain trait is advantageous for an organism, it is not necessary that it would evolve. Have a look at this post.

Also, as a deleterious allele spreads through the population, it can eliminate carriers from the population at an increased rate, meaning that non-carriers have an advantage and the mean fitness of the population consequently goes up. Sanford's main flaw is the treatment of relative fitness as absolute.
Also, the whole mutational meltdown from decay stuff is only a problem in small populations, where deleterious alleles can be fixed that much more rapidly. To extrapolate this to organisms with large population sizes or to hold it as a general truth of evolution is iffy.

Well, you've already mentioned Alexei Kondrashov. Here's his talk  (in russian unfortunately): http://www.youtube.com/watch?v=YsgO8JTN7KE
To summarize it:
Yes, that decay is happening and at a pretty catastrophic rate. As of 2012, he estimated the rate of IQ decay (and fitness decay is somewhere close) to be within the range of 1% and 10% per generation. The former is ok according to him, cause "in 100 generations we'll surely be swept away by a nuclear war between big-endians and little-endians". The latter will be unfortunate, cause in 10 generations we'll "fall prey to our own stupidity". He speaks of stupidity because our brain is the most transcriptionally complex structure in our organism, thus it suffers from genetic damage sooner than anything else.
(It's worth noting here that AFAIK, one of Kondrashov's children has Down syndrome; another one, Fedor, is a remarkable geneticist as well, focused on epistasis.)
Those estimations are supported by the following molecular data: no matter the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations per each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1 out of 70 leads to a change in aminoacid sequence of some protein, usually harmful.
Here are 2 papers: decay of cognitive indicators of children with parent's age: http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040
Another link from Kondrashov: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation: http://www.ncbi.nlm.nih.gov/pubmed/9371795.
Kondrashov says that after several generations you can hear the difference between MCN drosophila and wild-type - wild-type is much more noisy and active.
He also mentions that frequency of autism, diagnosed in the US has increased 5-fold since 1950.

It appears to me you are using a nonstandard definition of fitness. Fitness is simply the expected number of offspring, given a genotype, for a carrier with that genotype. Cognitive indicators et cetera don't necessarily correlate with the ability to reproduce, and unless they did there are no real implications for fitness.

@AnkurChakravarthy True. In fact, I'm mixing here the data about IQ and about fitness. They say that average non-silent aminoacid substitution in a protein decreases fitness (expected # of children) of organism by 1%, so 2-3% per generation, when fathers are ~30 year old on average seems to be a correct estimation.


text:
Can Bacteria Repair Dephosphorylated Plasmids?
I have been trying to insert a short sequence of DNA into a plasmid. I wanted to make two different versions, with the insert at different locations. I chose HinDIII and SalI sites approximately opposite each other on the plasmid and designed oligos with HinDIII or SalI sites, and of course extra bases on the ends to allow proper cutting.
I cut the plasmids and oligos and dephosphorylated the vector to help prevent empty vector ligations. I mixed the plasmid and oligos and ligated, then transformed into bacteria, all standard stuff.
The HinDIII version worked the first time, with few colonies on the empty vector control plate, and more colonies on the plates that received oligos during the ligation. I confirmed insertion by using the BpmI cut site the oligos just happened to carry.
However, the SalI version has failed every time I tried it. The empty vector control and all other plates are a just a carpet of cells. There are very few individual colonies, and the ones that exist don't look right, too small. I haven't even tried a miniprep, too likely to get an empty vector back. I did do a nontransformed control, where the cells were not given any DNA and were just directly plated. Those cells died, indicating it's not an issue with my ampicillin.
My hypothesis is that unligated empty vector outnumbers the correctly ligated plasmids, and that cells that pick up a copy of the unligated DNA somehow repair the cut, even though it's dephosphorylated. This is made more likely because I only used a single digest, so the plasmid has matching sticky ends, however the HinDIII version used the same strategy. I have been including a 1 hour 37 C SOC media incubation, which could allow the bacteria more time to carry out this repair. If I skip the incubation, maybe that would prevent unwanted repair.
I am testing this hypothesis with some additional controls, including transforming bacteria with empty vector that hasn't been treated with ligase to make sure the ligation reaction isn't the problem, as well as using the previously ligated DNA without the SOC incubation. I will report that data as it becomes available. I am short on competent cells, so I can't do much else right now.
Also, what do you think about treating the ligated DNA with klenow to blunt any remaining sticky ends before transformation?
EDIT: I have the data for the transformations that skipped the ligation and SOC media incubation. Skipping the incubation did not change anything, neither did skipping the ligation. All plates continue to show a carpet of cells.

So your insert has same sites on both ends— a non-directional cloning? Plus, do you see the linearized plasmid on the gel? Do you use gel purification? Also, how much plasmid did you use for digestion and ligation?

It is indeed nondirectional. I'm just inserting a zinc finger binding site, I don't care about direction, just need to make a zinc finger protein we already have bind to this plasmid. I have confirmed that SalI cuts the plasmid, but have not used gel purification. Since it's a single cut site there would not be extra DNA to remove. I have not run a confirmation gel every time I have tried the experiment either, so hypothetically the enzyme could have stopped working. The oligos I am adding are short, 56 bases, but I suppose a high density polyacrylamide gel might work to see cuts there.

But you can see the linearized plasmid when you do a gel purification. No need to look for the drop-out. How do you clean up your digestion reaction? Just simple column-purification? There is a likelihood that your enzyme did not cut properly. Bacteria can repair nicks but I am not sure if they preferentially phosphorylate one enzyme site. You can try blunting and see if the problem persists.

I do phenol chloroform purification and isopropanol precipitation after digestion and dephosphorylation for both vector and oligos. (I don't dephosphorylate the oligos obviously) And when I say I have confirmed the digestion, I mean I did the SalI digest and ran a gel, and it was cut. There was a section of the plasmid where we weren't sure of the sequence and I needed to make sure it didn't contain any SalI sites. I do not run the gel every time I attempt the cloning.

@WYSIWYG I think you were right. I finally got around to trying this again, using gel purification as recommended. The gel revealed that the SalI enzyme was not cutting the plasmid very well, with most of the DNA still in the supercoiled form, and a lot as nicked circles. I carefully cut out the linear DNA in the middle and the control plate had only 1 colony. The problem is that the experimental plates have 2 - 5 colonies each, I'll have to see what I get on miniprep. Also, my gel extractions have been poor. When starting with 4 ug of DNA, I get less than 100 ng of DNA after extraction.

You can summarise all of these, post it as an answer and accept it.

As per WYSIWYG's suggestion, I tried the digest and dephosphorylation again with SalI and ran a gel. The gel showed that SalI was less than ideal at cutting this plasmid.

As you can see, the most intense band is the bottom band, which is most likely supercoiled DNA, with the linear DNA I want appearing in the middle, and open circle DNA coming in third. I very carefully cut the middle band out and did a gel extraction. When I ligated this the control plate had 1 colony. Unfortunately, the experimental plates had between 2 and 6 colonies each. I am running minipreps on those now, will just have to see what I get.
This explains why the previous attempts produced so many colonies on the control plates, most of the DNA was uncut, so no amount of dephosphorylation would help it.
One thing that does bother me, is that my gel extractions seem like they have had really poor yields. I typically start a digest with 4 ug of plasmid. After phenol:chloroform extraction and isopropanol precipitation, I'll usually recover 2 - 3 or more ug of DNA. After gel extraction, I'm lucky to get 300 ng of DNA. To make things weirder, the liquid that comes off the spin column in the final elution step will gel up, like a low density agarose gel. The only explanation I can come up with is that residual agarose in the spin column is somehow forcing its way through the membrane and into the elution buffer. The goo clogs pipette tips and makes life difficult.

SalI is a fussy  cutter; I avoid it for routine cloning where possible.  Since it's cutting poorly you'll need to gel purify, as you found.  Be sure you're getting anything cut at all, I'm not convinced by your gel that you are. Use an alternate enzyme if possible.  If you're doubting your gel purification, use a commercial product e.g. one of Qiagen's columns (or competitors, I have no particular attachment to Qiagen); they are more expensive but are pretty reliable.  Don't waste your time with transformations until you know you have clean linear DNA. Good luck.

This is why I often recommend running a negative control of uncut plasmid in parallel to verify that your identification of the supercoiled band is accurate.

@iayork I just got my sequencing results back last week, and my "Successful" plasmids have absolutely no difference from the original plasmid. Now that I can order oligos again, I think I'll try a PCR based cloning without using any restriction sites. If it works, I can avoid the SalI issues and I'll have a method to insert the binding site sequence anywhere I want. I couldn't do it earlier due to weird rules with the budget, we couldn't spend any money during the last month of the fiscal year. Now it's a new fiscal year and I can order as many oligos as I want.

Budget issues are exasperating. Can't spend $50 on a primer, but it's OK to waste a week of your time ...


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Closing a Plasmid by Ligation
I have been having trouble with what should be a fairly simple ligation. I had a plasmid that I needed to cut part out of, so I designed a couple PCR primers to do that. The plasmid already had a BamHI site on 1 side of the region I wanted to remove, so I made the other PCR primer with a BamHI site on its 5' end with 3 extra Cs so the restriction enzyme would bind better. Here is a crude diagram of what I tried to do:

So I did the PCR and BamHI digest, it looked good on gel, so I purified it from the gel, got the concentration on the Nanodrop, and set up a ligation.
However, I keep getting zero colonies. I have tried a 24 hour reaction at 4 degrees, and 10 minute reaction at room temp. I am currently trying a reaction where I supplement the buffer with fresh ATP, because the buffers are a little old. If that works, problem solved, if not, I am asking how to troubleshoot this.
This seems like it should be relatively simple, because I have no insert, just trying to close an empty vector, which seems to happen on its own when I don't want it to and dephosphorylate the vector.
UPDATE:
The reaction with extra ATP did not produce colonies. I will keep trying. One idea I had was to do the PCR and then try blunt end ligation, since the Pfu polymerase should make blunt ends. Also got a new sample of ligase.

Can you heat inhibit your restriction enzyme and go straight to ligation without the purification step? I am asking because gel purification (or column purification) sometimes trim a bit the end and interfere with the ligation. This is quite rare but might have happen to you.

@cagliari2005 According the NEB poster on my wall, BamHI probably can't be heat denatured.

How do you know the BamHI enzyme is working? 2. How do you know the ligase is working? 3. How do you know the cells are actually competent? 4. What is the selectable marker--is that the same drug in your plates?

@mdperry The removed sections are too small to tell if the digest worked, but the same BamHI batch works for other plasmids with visible fragments. The same batches of cells produced colonies when transformed with intact plasmid. The plasmid has an ampicillin resistance gene, and ampicillin is in the plates, the plates are less than a week old and have been stored in the fridge. Only thing I'm not sure about is the ligase or its buffer.

How far from the end of your PCR product are the restriction sites located?

@Chris The short end is only three nucleotides, which concerns me a little because other sources I've read suggest I should use 6, but I've gotten away with 3 before, but those used other restriction enzymes, maybe BamHI is a little more sensitive.

Hmm. According to NEB this should be ok.

Could it be due to low transformation efficiency? Have you tried higher competency cells?

@MarchHo No, just standard subcloning DH5 Alpha E. coli so far. Might see if I can borrow a tube of better cells from another lab, our on campus store makes me buy a whole box of the better cells, but I can get the subcloning cells 1 tube at a time for less money.

One more question, have you checked your primer's BamHI site directionality? If the sticky ends produced are in the wrong orientation, it can explain the poor ligation.

@MarchHo That might be it, I just looked at the primer sequences and tried to draw what the overhangs would look like and I think I got one of the sites flipped. Primer 1 is 5' GGATCC 3' and primer 2 is also 5' GGATCC 3'. I think if I get another primer with the CCTAGG orientation this might work better. Alternatively I could trim the overhangs down with klenow and try blunt end ligation.

@MarchHo After thinking about it a little more and writing the sequences on strips of paper, cutting the ends and wrapping them in a circle, I'm not so sure I was wrong the first time. Either way, I already ordered the new primer, will give it a try.

The recognition sequences of type II restriction enzymes are palindromic, so if you always read the sequence of each strand from 5' to 3' prime it will always be the same sequence. If, reading from 5' to 3' you specified the sequence CCTAGG then after PCR there would be absolutely no overhanging sticky ends on that end of the fragment. It would be completely blunt. BamHI cannot recognize or cut CCTAGG.


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Which types of hydrogen bonds are known to exist in RNA secondary structures?
I'm programming an implementation of an algorithm for pattern matching in RNA structures.
The algorithm assumes the following types of base pairs:

Plain: No base pairs (just the primary structure of the RNA)
Single: Each base can be connected to at most one other base
Multiple: Each base can be maximally connected to a number of other bases (where 'number' can be constant or infinite)

Although there is no problem with the implementation of the above types of base pairs (apart from the probable high computation complexity), I wonder if all of them were observed in real RNAs?
In particular, I'm interested in the following cases:

A base pair between two adjacent bases i,j.
One base (i) which connected to two different bases (j,k) (i is not adjacent to j or/and k).
One base (i) which connected to more than two different bases, all of them not adjacent to i.

Can these exist? Some of them?
If they can, how common is their existence?

A base pair between two adjacent bases i,j.

It is not possible. To form an intramolecular hydrogen bond, the RNA has to bend. The persistence length i.e. the minimum length of the chain required for bending, is around 4 bases for ssRNA (I am not very sure about this number. At this moment I am not able to locate the exact reference. I remember this number from the back of my head which I heard somewhere).

One base (i) which connected to two different bases (j,k) (i is not adjacent to j or/and k).

It is definitely possible for one pair after considering the persistence length. If a single base is bound to more than two bases then atleast one interaction should have to form a non Watson-Crick type bonding, as indicated by Mad Scientist.

One base (i) which connected to more than two different bases, all of
  them not adjacent to i

Very less likely. There are no known reports. Even if it happens, the bond will be weak because of limitation in the number of H-bond donor/acceptor sites in the bases.

By far the most common type of base pair is the Watson-Crick base pair in an RNA helix. Those are comparably easy to predict, e.g. Mfold and the Vienna RNA package can do this.
Base triples, three nucleobases that form hydrogen bonds to each other are not uncommon in RNAs with a complex tertiary structure. There is even a database of RNA triples, though this one also contains triples where not all three bases make contact with each other.
There are also quadruplexes, but there each base only makes contact with two other bases. I don't know if there are any structures where one base makes contact with more than two other ones.


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Vaccination and population dynamics of an epidemic
I'm trying to figure out how should a vaccination model be built to correlate with population density, and I'm having problems to understand meanings of the results I receive when I apply theory on specific data I'm provided with.
Theory(i):
The initial phase of an outburst of a disease can be described by an exponential growth
model. The relevant equation is:
$(1)\frac{dI}{dt}=\beta n(1-q)I-\mu I$ where:
$n$ = the population density. Let us measure it in units of $km^{-2}$.
$I$ = the density of already infected individuals in the population; measured in the
same units as $n$.
$q$ = the fraction of the population that is immune to the disease, either naturally of
due to vaccination. Consequently, $1-q$ is the fraction of the population that is
susceptible, i.e., at risk of getting infected. $q$ is a pure number between $0$ and $1$,
and has no units.
$\beta$ = is the transmission rate of the disease. It measures how easily and quickly
the disease can be transmitted from an infected individual to an non-infected
susceptible individual. $\beta$ includes within it both the rate at which encounter
between infected and non-infected individuals occur, and the probability that
such an encounter would result in actual transmission of the disease. $\beta$ has
dimensions of $\frac{1}{time\times density^{2}}$, so let us measure it in units of $week^{-1}km^{4}$.
$\mu$ = the rate at which infected individuals are eliminated from the group of
infected individual, either because they recover, or because they die. $\frac{1}{\mu}$ is the average duration of the infection, i.e., the average time that an individual remains
infected before it either recovers or dies. Let us measure $\mu$ in units of $week^{-1}$.
This equation derives from the differential equation $(2) \frac{dN}{dt}=rN$ where $r$ is called instantaneous rate of increase. It is easy to see that $I$ from equation $(1)$ is equivalent to $N$ from equation $(2)$ and therefore, $r$ for equation $(1)$ will be $(3) r=\beta n(1-q)-\mu$. When we look at equation $(3)$, we see two factors:
$\beta n(1-q)$ - A positive factor(ii)
$\mu$ - A negative factor
Minding the above, when $r=0$, there is no increase in population(iii). From this, we can compute $q_{0}$ which is the minimum fraction of vaccinated/immune individuals in the population that is required in order to prevent the disease from spreading. From equation $(3)$ we can figure out that $q_{0}=1-\frac{\mu}{\beta n}$. Just as $q$, $q_{0}$ is a pure number between $0$ and $1$.
Welcome to the desert of the real (my question):
Suppose we compare two countries with the following data:

Israel: $n=347km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$
Finland: $n=16km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$

When we look for $q_{0}$ for Israel we see that $q_{0}(Israel)=1-\frac{0.25}{0.0015\times347}=0.52=52$% while for Finland we see that $q_{0}(Finland)=1-\frac{0.25}{0.0015\times16}=-9.42=-942$%. Assuming that we've got correct data in the first place, $q_{0}$ is a negative pure numbers which is not between $0$ and $1$.

Do such, and similar results make any sense at all? Especially when they are not between the defined boundaries of the variable.
If they do make sense, what does it mean getting a negative results? How should it affect my vaccination policy?

Footnotes:
(i) Taken from my Populations Ecology lecture slides
(ii) Positive when looking at it from the epidemic point of view
(iii) Of infected individuals

You should ensure that the basic reproductive number for your Finland model is capable of sustaining an epidemic without vaccination.

@EpiGrad In other words, I need to make sure that the epidemic will keep on being at least stable without vaccination?

Yes, that's correct.

According to this we increase μ when we quarantine infected ppl.

I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate.
The number of people who have this disease will be fewer each week.  I think this makes sense because at 16 / km^2, you can expect that practically nobody will ever see each other.
This is a flawed model though because it assumes that the mean density is uniform.  In a city like Helsinki (2,800 / km^2) you would expect the disease to get caught by nearly everyone in just a week.
Helsinki: n = 94.5%
In Lapland (which has a population density of less than 2/km^2) , the transmission rate (beta) of 0.0015 translates to 0.003 incidents per week.  This is not a terribly catchy disease, you probably have to kiss someone, wear their clothes, or eat off their plate to get it. With only 2 people per km^2 the chances of this happening appear to be poor, though even here families tend to get the disease and the model breaks down.
So to sum up, the model is consistent within itself, BUT it is a baby model and makes some broad assumptions that do not help it describe the dynamics of the disease in a national scope or in a highly detailed scope.  It probably describes the chances balls will collide in a box as well as disease spreading.

So basicly, I shouldn't be strictly bound by 0<q0<1 in this case and use this only when the epidemic is self-sustained even without vaccination (as pointed by @EpiGrad in comment to the original question)?

Yes - this is an important point - if we include the social an economic costs of immunization sometimes we don't do it.  This was the case with tuberculosis.  In Europe, which has more borders and denser population (at the time) they used a vaccine which is effective 60-80% of the time (BCG).  In the US we decided to pass on that and use the skin test for prevention and detection (the vaccine makes you a false positive).  The difference is primarily in the number of patients and the density of the population at the time.

Reading through wikipedia, this looks like a standard deterministic model, but there is a description of multi-compartment models which would account for different populations or different subregions in a model...  http://en.wikipedia.org/wiki/Epidemic_model#Models_with_More_Compartments

"I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate. " - This is not necessary accurate, it depends on population density, social habits, level of technology, etc... how often ppl meet...

I don't think this model is valid by STDs like HIV.

" It probably describes the chances balls will collide in a box as well as disease spreading. " +1, I agree with that. Btw. do you know of better models?

I can imagine a model that explicitly tracks individuals and disease transmission events would work better.  Its not my field though, I'm just reading what you have here.


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Do the eyes play any role in producing the visual experiences you have during dreaming?
Sometimes, you remember a vivid picture of a dream that you saw. What is the role of your eye in this experience? Please provide me with the answer that is as simple as possible since I am in Class 10(Grade 10).

Your eye doesn't play a part in your dream aside from giving you the basic images which your brain later used to form the dream. The visual image in your dream comes from your brain itself.

While this may answer the question, it's best to add references, or list the literature you've cited. This is a scientific site. Please format accordingly.

The cerebrum is the centre of any unconsious activities that take place in our body. So there is hardly any part played by the eyes in visualising a dream. The brain does the visualising part

Welcome to Biology SE! While this may answer the question it lacks support from references in the scientific literature. Un-referenced answers may be challenged or deleted.


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Simple Mendelian Genetics Question
here is my question:
In certain plants, tall is dominant to short. If a heterozygous plant is crossed with a homozygous tall plant, what is the probability that the offspring will be short?
My Solution:
Let T be the allele for the tall phenotype and t be the allele for the short phenotype.
Then the parental cross would be Tt x TT = 100% tall phenotype (1/2 Tt, 1/2 TT).
Hence the probability of having short offspring should be $\fbox{0}$.
However, the answer key for this question says the answer is $\fbox{$\frac{1}{2}$}$. How can this be??? It really bothers me when the answer key is potentially incorrect because it makes me very unsure, and I end up wasting time trying to figure out if the key is wrong or if I am. Can somebody please let me know if what I did was correct/incorrect??
Thanks

What's the source? I'd suggest it is an incorrect answer key... or does the question say anything about dominance (if t is dominant to T then the answer would be 1/2). Edit: re-reading your question T is dominant to t thus the answer should be 0.

Agree with @GriffinEvo. If you have restated the question accurately, the given answer must be wrong.

Assuming you have stated the question correctly, the answer key is incorrect for exactly the reasons you have given and your reasoning and consequent answer are correct.
I would double-check you have read the question correctly and then conclude the answer key is incorrect. It happens.

This is a test cross - a cross with a recessive pair of alleles and either a heterozygous or homozygous pair of dominant alleles( eg- Tt X tt or TT x tt respectively). These crosses are carried out to check the if genes are homozygous or not. In this the ratio is always 1:1.
So don't worry. :)
Be confident about your answer, because it is obvious that the answer cannot be half if you work it out using the Punnett square.