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Do animals exhibit handedness (paw-ness?) preference?
I have been observing my cat and found that when confronted with an unknown item, she will always use her front left paw to touch it.
This has me wondering if animals exhibit handedness like humans do? (and do I have a left handed cat?)
One note of importance is that with an unknown item, her approach is always identical, so possibly using the left paw means allowing a fast possible exit based on how she positions her body.
This question is related to Are there dextral/sinistral higher animals?. However, I question the "paw-ness" as a consequence of how the cat is approaching new items (to be ready to flee), whereas the other question remarks about the high number of "right-pawed" dogs and questions the influence of people for this preference.

 Short Answer
Yes. handedness (or Behavioral Lateralization) has been documented in numerous vertebrates (mammals, reptiles and birds) as well as invertebrates.

This includes domestic cats (see Wells & Millsopp 2009).

 Long Answer
There have been numerous studies that have documented behavioral lateralization in many groups of animals including lower vertebrates (fish and amphibians), reptiles (even snakes!), birds and mammals. More recent work (e.g., Frasnelli 2013) has also shown that lateralization can also occur in invertebrates. In other words, "handedness" (or pawedness, footedness, eyedness, earedness, nostriledness,
toothedness, breastedness, gonadedness, etc.) occurs rather extensively across the animal kingdom.

These studies suggest that the evolution of brain lateralization, often linked to lateralized behaviors, may have occurred early in evolutionary history and may not have been the result of multiple independent evolutionary events as once thought.

Although this view of brain lateralization as a highly conserved trait throughout evolutionary history has gained popularity, it's still contested (reviewed by Bisazza et al. 1998; Vallortigara et al. 1999).

Note: Laterality of function may manifest in terms of preference (frequency) or performance (proficiency), with the former being far more often investigated.
And no, right-handedness is not always dominant.
But Why?

One hypothesis is that brain lateralization was the evolutionary result of the need to break up complex tasks and perform them with highly specialized neuronal units to avoid functional overlap (i.e., to account for "functional incompatibility").

In humans, many hypotheses have been developed including: division of labor, genetics, epigenetic factors, prenatal hormone exposure, prenatal vestibular asymmetry, and even ultrasound exposure in the womb.

Snake studies (see below) have suggested lateralization behavior can be dictated by environmental conditions (specifically, temperature).

Other work (Hoso et al. 2007) suggest that lateralization could be the result of convergent evolution. In this case, snakes developed feeding aparati that allow them to better consume more-common dextral species of snails.

Note: dextral (meaning "clockwise") is a type of chirality -- another form of "handedness"

Reviews:

Lateralization in non-human primates: McGrew & Marchant 1997.

Lateralized behaviors in mammals and birds:
Bradshaw & Rogers 1993; Rogers & Andrew 2002.

Lateralized behaviors in lower vertebrates: Bisazza et al. 1998; Vallortigara et al. 1999.

Some Examples:
Invertebrates

Some spiders appear to favor certain appendages for prey handling and protection (Ades & Novaes Ramires 2002).

Octopi (or octopodes) preferably use one eye over the other (Byrne et al. 2002; with seemingly no preference for right/left at the population level: Byrne et al. 2004) and also apparently have a preferred arm (Byrne et al. 2006).

Fish

Preferential ventral fin use in the gourami (Trichogaster trichopterus). [Bisazza et al. 2001].

Preferential eye use in a variety of fish species [Sovrano et al. 1999, 2001].

Amphibians

Lateralization of neural control for vocalization in frogs (Rana pipiens). [Bauer 1993].

Preferential use of hindlimbs (Robins et al. 1998), forelimbs (Bisazza et al. 1996) and eyes (Vallortigara et al. 1998) in adult anurans.

Snakes

Preferential use of right hemipenis over left under warm conditions. [Shine et al. 2000].

Coiling asymmetries were found at both the individual and population levels. [Roth 2003].

Birds

Tendency for parrots to use left-feet when feeding. [Friedmann & Davis 1938].

Mammals

Pawdness in mice. [Collins 1975].

left forelimb bias in a species of bat when using hands for climbing/grasping. [Zucca et al. 2010]

Behavior experiments show domesticated cats show strong preference to consistently use either left or right paw and that the lateralized behavior was strongly sex related (in their population: ♂ = left / ♀ = right). [Wells & Millsopp 2009].

Non-human Primates

Posture, reaching preference, tool use, gathering food, carrying, and many other tasks. See McGrew & Marchant (1997) for review.

Citations

Ades, C., and Novaes Ramires, E. (2002). Asymmetry of leg use during prey handling in the spider Scytodes globula (Scytodidae). Journal of Insect Behavior 15: 563–570.

Bauer, R. H. (1993). Lateralization of neural control for vocalization by the frog (Rana pipiens). Psychobiology, 21, 243–248.

Bisazza, A., Cantalupo, C., Robins, A., Rogers, L. J. & Vallortigara, G. (1996). Right-pawedness in toads. Nature, 379, 408.

Bisazza, A., Rogers, L. J. & Vallortigara, G. (1998). The origins of cerebral asymmetry: a review of evidence of behavioural and brain lateralization in fishes, reptiles and amphibians. Neuroscience and Biobehavioral Reviews, 22, 411–426.

Bisazza, A., Lippolis, G. & Vallortigara, G. (2001). Lateralization of ventral fins use during object exploration in the blue gourami (Trichogaster trichopterus). Physiology & Behavior, 72, 575–578.

Bradshaw, J. L. & Rogers, L. J. (1993). The Evolution of Lateral Asymmetries, Language, Tool Use and Intellect. San Diego: Academic Press.

Byrne, R.A., Kuba, M. and Griebel, U. (2002). Lateral asymmetry of eye use in Octopus vulgaris. Animal Behaviour, 64(3):461-468.

Byrne, R.A., Kuba, M.J. and Meisel, D.V. (2004). Lateralized eye use in Octopus vulgaris shows antisymmetrical distribution. Animal Behaviour, 68(5):1107-1114.

Byrne, R.A., Kuba, M.J., Meisel, D.V., Griebel, U. and Mather, J.A. (2006). Does Octopus vulgaris have preferred arms?. Journal of Comparative Psychology 120(3):198.

Collins RL (1975) When left-handed mice live in righthanded worlds. Science 187:181–184.

Friedmann, H., & Davis, M. (1938). " Left-Handedness" in Parrots. The Auk, 55(3), 478-480.

Hoso, M., Asami, T., & Hori, M. (2007). Right-handed snakes: convergent evolution of asymmetry for functional specialization. Biology Letters, 3(2), 169-173.

McGrew, W. C., & Marchant, L. F. (1997). On the other hand: current issues in and meta‐analysis of the behavioral laterality of hand function in nonhuman primates. American Journal of Physical Anthropology, 104(S25), 201-232.

Robins, A., Lippolis, G., Bisazza, A., Vallortigara, G. & Rogers, L. J. (1998). Lateralized agonistic responses and hindlimb use in toads. Animal Behaviour, 56, 875–881.

Rogers, L. J. & Andrew, R. J. (Eds) (2002). Comparative Vertebrate Lateralization. Cambridge: Cambridge University Press.

Roth, E. D. (2003). ‘Handedness’ in snakes? Lateralization of coiling behaviour in a cottonmouth, Agkistrodon piscivorus leucostoma, population. Animal behaviour, 66(2), 337-341.

Shine, R., Olsson, M. M., LeMaster, M. P., Moore, I. T., & Mason, R. T. (2000). Are snakes right-handed? Asymmetry in hemipenis size and usage in gartersnakes (Thamnophis sirtalis). Behavioral Ecology, 11(4), 411-415.

Sovrano, V. A., Rainoldi, C., Bisazza, A. & Vallortigara, G. (1999). Roots of brain specializations: preferential left-eye use during mirror-image inspection in six species of teleost fish. Behavioural Brain Research, 106, 175–180.

Sovrano, V. A., Bisazza, A. & Vallortigara, G. (2001). Lateralization of response to social stimuli in fishes: a comparison between different methods and species. Physiology & Behavior, 74, 237– 244.

Vallortigara, G., Rogers, L. J., Bisazza, A., Lippolis, G. & Robins, A. (1998). Complementary right and left hemifield use for predatory and agonistic behaviour in toads. NeuroReport, 9, 3341–3344.

Vallortigara, G., Rogers, L. J. & Bisazza, A. (1999). Possible evolutionary origins of cognitive brain lateralization. Brain Research Reviews, 30, 164–175.

Wells, D. L., & Millsopp, S. (2009). Lateralized behaviour in the domestic cat, Felis silvestris catus. Animal Behaviour, 78(2), 537-541.

Zucca, P., Palladini, A., Baciadonna, L. and Scaravelli, D. (2010). Handedness in the echolocating Schreiber's long-fingered bat (Miniopterus schreibersii). Behavioural processes, 84(3): 693-695.

@JanDvorak if you can supply a reputable source, I will gladly add it to my answer :)

Quick search suggests an article at nature.com, but its external links don't work. #2 is a paper at PubMed that I haven't bought. #4 looks promising but I didn't check the site it's published on,  but it seems to be the same paper as #2 offers for purchase. ScienceDirect hosts a different paper as well as a video but they seem to be mostly about movement.

I was actually looking for references for handedness in elephants, that i remembered. Surprisingly I found this science blog, stating that handedness is actually rare in animals.

Lateralization has also been shown in mother-infant interactions (left side of mother bias) in diverse mammal species, purportedly due to right brain hemisphere social processing Lateralization of mother–infant interactions in a diverse range of mammal species

Horses also display handedness in their gaits: http://www.equine-rehab.com/handedness-in-horses/  Also, they show it in their manes, which naturally fall either to the left or right side of their neck.  No idea whether that correlates to their gait, though.

Another fun example of handedness/chirality: Portuguese man o' war have dimorphic populations with ~50% having their sail ("pneumatophore") pointing left and 50% leaning right. When winds blow these organisms, this dimorphism ensures that at least some will not be randomly blown ashore to die. (Source: Wikipedia).  Evolution is fun :)

Stanley Coren, The Lefthander Syndrome, says that humans are distinctive, not in having preferred handedness, but in having a high majority of individuals right-sided instead of odds approaching 50-50.
There is a lot of urban legend biology that might be answered. For instance, right-handedness is a human combat advantage, because a right-handed attack or defense puts the heart slightly further away from an opponent than an attack that's left-handed. And that one doesn't require a real knowledge of biology to answer: 48% of Olympic fencers are left-handed, and among people who've studied it left-handed people are far more likely to be excellent at combat sports than right-handed people.
(I'd love to see someone debunk the array of folk explanations for why a large majority of humans are right-handed.)

Maybe it also swayed that way because humans co-operate a lot: I am left handed and as an experiment, I decided for a couple weeks to do interactions, when buying items, etc, as a right handed; it was amazing how much smoother everything was, just hands meeting one another to exchange an item alone was noticeably more direct than me interacting as a lefty; with that, it is possible that babies start to go the more convenient path, reinforcing the right handed majority; I highly recommend that experiment, it’s simple, fun and interesting.

If by answer you mean 'debunk', then this is consistent. Otherwise, you'd be saying that right-handed people have a combat advantage and left-handed people are better at combat sports, which wouldn't follow. I'm not sure which one it is.

A small number of peer reviewed studies seem to show that cats generally do have a paw preference and exhibit handedness similar to humans. Cats often use their “dominant” paw to reach for food or when attacking prey.  Much like humans, they can show a preference for their left or right paw and can even be ambidextrous (Ocklenburg et al 2019). These limited studies even suggest that handedness may be associated with gender or certain behaviors, however the data is ambiguous and largely based on owner interpretation. For instance, the current data indicates most female cats seem to prefer their right paw (McDowell et al 2018). Cats that preferred their left paws were described as being more shy and reserved according to their owners as compared to their other cats that preferred their right paw.


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What method would you use to genotype SNPs in low quality samples?
What method would you use to genotype SNPs in low quality samples? I ideally want to genotype hundreds of SNPs in hundreds of scat samples (very low amount of target DNA, potentially degraded and highly contaminated by other DNA).

It would help to have a little more info.  Are you looking at a specific marker gene, or are you trying to assemble long contigs of the original animals' genomes from a metagenome?  What sort of sequencing technology?  The read length and error rate could be a big problem for some of them.

I agree with @gchadwick that more infor would help.
However, based on my understanding of what you are trying to do (SNP genotyping on several genes), I suggest.
1) Enrich your DNA with DNA from the organism you want
2) Enrich your DNA with DNA in the desired regions (if any).
Solution: Target enrichment. You are probably aware that companies such as agilent, nimblegen and illumina offer target enrichment kist for next generation sequencing.
However, if your DNA is soooo bad, I suggest performing target selection with PCR.

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Reason for seeing grid-like patterns when strobing a solid black-white image?
I was trying to do some stimulation for SSVEPs by strobing a solid black square and a solid white square. Weird thing was, I ended up seeing weird grid like patterns that looked like this, always of the inverted color.
  _        _
 / \      / \
 | |      | |
 \ / _--_ \ / _--_
  O |    | O |    |
 / \ ---- / \ ----
 | |      | |
 \_/ _--_ \_/ _--_
  O |    | O |    |
     ----     ----

And that sort of pattern repeats itself around the strobing area (where the convex areas are always of opposite color than the current color on the screen).
I'm inclined to think about light and dark adaptation, but it still seems weird that it'd be shaped like that in particular. So... What's going on?
EDIT: Additional info that I should've realized was necessary >_<:

Strobe area: ~14x10.5 cm
Strobe frequency: 2 frames/half-cycle @ Laptop Vsync (~60 Hz) ~ 15 Hz
Viewing distance: ~55-60 cm and shorter.

Screen is backlit. Not sure about brightness metrics.
The pattern isn't offset to one corner like I've drawn, it's more evenly spaced. Horizontal bars are more accentuated than vertical ones (and the dark-on-light phenomenon is more visible for me than the light-on-dark). Moving in closer increases the visibility of the effect (I guess that was to be expected), and changes the number of times the pattern repeats across the screen (but it's hard to count them). The larger the area in my visual field the more times the pattern repeats. I'd say that at about 60 cm it's just one box, but with my nose a handful of cm away from the screen (it's hard to measure by myself >_<), there are maybe three in the horizontal direction... Or at least tens of them (increasingly large as it gets toward the center in both dimensions), depending on how focused in on the screen I am.
It's really really hard to count them.
I haven't had the chance to check with other people yet, but I'll try some time (this is just something I saw while working on a personal project).

Do other people see the same pattern as well? How big was the square and how fast was it presented? What's the spatial scale of the pattern?

@Memming Info added. This is just a personal project, so all info I have is just from myself at the moment. -.-' It's really hard to count these things without getting a bit dizzy.

@Memming Other people see the patterns as well, although not necessarily the same patterns I'm seeing.

interesting. let me put a bounty on this question.

It just occurred to me that cogsci.SE might have more psychophysics people.

I have actually experienced something similar before.  What are you using to make the strobe?  You can run into interesting patterns when you start strobing near the frequencies of your monitor (flashing refresh down as it's drawing).  I'd also make sure it's not a programming effect.  What is the difference between what you see and what other's see?

Are you strobing LCD or with LCD?? I bet you could not see that while strobing solid material with strobe light. You might see wiring of your LCD...

@Atash Any update?  Again you are likely seeing the pattern because of the way monitor is strobing, not because of any artifacts in your eye.

@AtlLED Oh, sorry - I can assure you that the screen is solid black and solid white (no vsync issues), and can additionally reference you to the underlying low-level code (SDL2's vsync-waiting update and GTK's GdkFrameClock for two different programs). Others have reported seeing the phenomenon, albeit with different patterns (they aren't necessarily consistent between people looking at the same screen; I have a really small sample size, though).

Seeing in animals is at some level using Gabor wavelets (Marčelja 1980 and later authors). Your images reminds of a combination of two low frequency Gabor basis vectors. Apparently the nervous system does not have time to model the incoming image into Gabor components of other frequencies.
Here is a picture of two low frequency Gabor basis vectors added. (In this image rotated 45 degrees compared to your image.)
http://medicalxpress.com/news/2013-01-feature-combination-perceptual-identification.html
This is a signal processing or a linear algebra question as much as a biology question.
One could argue that even lower frequency Gabor vectors would model the original images even better.

Hi David. Your information is certainly useful. Would it be possible for you to link the original research. This site seems professional enough but I know of many science blogs that exaggerate a lot.

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How can omnivores be in more than one trophic level?
I'm learning about the ecosystem and its relation to organisms, So organisms in a food chain can be put from producers to tertiary organisms. I just don't get the part where an organism can be labeled into 2 trophic levels ? how is it placed in the pyramid if so ?

You just represent a species twice, once at each level of interest. In reality a food network is much more representative than the fake hierarchical food chain represented in pyramids (and you would not have to represent one species twice).

I am not sure I fully understand where is your misunderstanding. I think your whole misunderstanding boils down to the representation of food chain. Actually, let's talk about food web as the name gives an intuition of what is happening that is more correct than the term food chain.
The conceptual view of the food web in a pyramid is super misleading. This is not how ecosystem work. But anyway, if one might want to make some ugly approximations and represent food web into a pyramid, then this person is totally free to represent one species twice, at two different levels. It makes sense that a species can eat things at several level in the same time. Just like you. You probably eat vegetables, salads, fruits, rice, corn, bread, etc... but also eventually fish and meat. Note also as indicated by @fileunderwater in the comments, that some species have different relationship with their ecosystem (typically eat different things) at different life stages.
Here are few examples of more or less realistic food webs. As you can see, one can roughly make category of trophic level but it is not all that clear.

Also note that a species can use different resources at different life stages, so that e.g. juveniles in a species of fish might eat plankton while adults are piscivores - hence the species as a whole functions at two trophic levels.


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Death because of distilled water consumption
One of my friends said that I would die if I drank distilled water (we were using it in a chemistry experiment) I gave it a go and surprisingly did not die.
I did a bit of Googling and found this
It said that drinking only this kind of water could definitely cause death, as distilled water was highly hypotonic and it would make the blood cells expand and finally explode and ultimately cause death.
I wanted to know exactly how much of this water on an average was needed to be consumed to cause death.

He said it would kill me, so I drank it.  Love it!

@RoryM that is precisely what happens when kids are told about dangerous stuff.....

An empirical if not wise approach

For the opposite scenario, see: http://biology.stackexchange.com/questions/3909/why-cant-humans-drink-sea-water

"experimental" tag added - he did test the hypothesis of his friend!

On a related note, what if you stick your hand in distilled water, will it disintegrate slowly? Or will your hand quickly alter the water, rendering it harmless. What if you jump into a pool of distilled water, would you slowly explode cell by cell? If not, what if you had a machine very quickly replacing all the water with previously distilled water, would you then explode cell by cell? I guess I should make this into it's own question, but it just seems related to heart of the issue here.

P.S. From now on, I will be adding a tiny bit of high quality, full spectrum salt to my distilled water before drinking it so as to avoid self asplosion.

I think I just invented the shower of the future! You just feed previously distilled water to your shower head! The water takes off the outer layer of your skin and hair along with the dirt, germs, viruses, and other things living in your hair. No shampoo or soap required! You can be super lazy! Just stand in the water for a few minutes! In a hurry? No problem, just increase the rate of flow to have it spray lots of water at you at high speeds, and you can be clean in a matter of seconds!

Don't Inuit drink nothing but distilled water?

I'm extremely skeptical of @leonardo's answer.  I suspect that what would happen if you drank only distilled water is nothing perceptible.  The only place where concentrations of distilled water would ever be high enough to conceivably matter is in the tissues of the mouth and throat, and even there, the effect would be temporary.
Compare drinking 8 glasses of either distilled or tap water every day.  With tap water, you're looking at less than 200 ppm of Mg, Na, K, and Ca combined.  That's less than 400mg of total mineral content per day.  Given that the combined RDA of all of those minerals is on the order of 7g for an adult male, this is not nothing, but it's certainly small.  Your dietary intake of these minerals probably varies by more than this daily, and your intestines, kidneys, sweat glands and mineral storage organs (like your bones and muscles) are constantly maintaining the mineral blood levels within a very narrow range, despite handling a throughput of several pounds of water and food daily.  They might have to work slightly harder to manage this range if you drank nothing but distilled water, but in a healthy adult, normal intakes already vary by more than this amount without major problems.  For example, the average American consumes more than 3.4 grams of sodium daily, while a low-sodium diet is on the order of 2g.  Low-sodium diets have been widely studied in the medical literature, and are considered safe.
As for pH, the lowered pH is caused by increased carbon-dioxide absorption to form carbonic acid.  Just as carbon dioxide is more soluble in distilled water, it is less soluble in stomach acid, and may be burped out.  Would you die of acidosis from drinking seltzer water all the time?  If that were the case, I'm sure there would be big health warnings about drinking soda, while it seems relatively benign. Furthermore, your body produces and excretes (through the lungs) around 1kg of CO2 daily, dwarfing any extra CO2 you might get by drinking distilled water.  If the small amounts of CO2 found in distilled water were dangerous, jogging would be invariably fatal.
If you were to drink nothing but distilled water, and eat no food, you probably would die of hyponatremia within a few weeks.  But you would also die of hyponatremia if you were to drink nothing but tap water, though perhaps slightly more slowly.

+1. I'm with Recursivelyironic. Most of the ions in our diet come from the foods we eat, not the water we drink. Unless you're sucking down softened water in the shower, your salt and calcium should be coming from your big dietary sources - fruit, veggies, meat, seasonings, etc.

+1  Unless you drink to hyperhydration, which is not what the original question was about at all, distilled water will not cause problems at all, literally zero problems.  You can buy distilled water by the gallon at the grocery store for goodness sake, and people commonly have reverse osmosis filters for their drinking water in their sinks, producing almost exactly the same effect.

Well, there are big health warnings about drinking excessive amounts of soda. But not because of its acidity.

I'm not sure why no one mentions this, but any food you eat would negate this effect entirely.
Assuming then, that you had no food, the lack of minerals in this pure water would simply be another deprivation for your body. The intestinal track actively reabsorbs ions, countering this. However, in this water-only deprivation, those mechanisms might fail as some are glucose dependent.

In general, if you want to know "exactly how much of X on an average is needed to be consumed to cause death", then the magic search term for Google is "LD50", that is the dose that kills 50% of victims.
I've seen the LD50 for water quoted as 90ml/kg for rats (that is, 90 ml per kg of body mass), for example on this safety data sheet. I presume that figure comes not from theorising about salt intake, but from giving measured quantities of distilled water to rats and counting how many die.
It's likely of the same order of magnitude for humans. Unlike many "poisons" it's not about subtleties of liver chemistry that will vary by species. What killed the rats was the swelling by osmosis of cells and tissues that they didn't want swelled.
For a largeish human that dose is 7 litres, approx 14 pints, drunk at a sitting. Which is fairly unlikely in a school chemistry lesson. Besides, with effort you could drown in less than that!
The distilled water in your chemistry lab has a relatively much larger chance of killing you for some reason other than its inherent toxicity (although it's still fairly unlikely in absolute terms). For example if it's stored for a while there could be legionella in the tanks. Probably best not to drink it, just as it's best not to drink any water that may have been sitting around for weeks in an unsealed container.
Definitely don't drink other stuff from the labs that your friend tells you is poisonous, because some of it really is. In particular the one everybody thinks of (because, like the water, it's similar to something they know about): lab ethanol can have methanol as an impurity, and may well have had benzene intentionally added because that's an easy way to get the last 4.5% water out that otherwise cannot be removed by distillation. A mouthful of ethanol isn't normally lethal (although it might be illegal), whereas methanol and benzene are both "properly" toxic in the sense that a few grams will kill you.
By the way, I can confirm that in my school days I obtained the same experimental result you did.

Drinking 7 liters of water in one sitting (30 minutes?) is unlikely physically possible and if it is it will quite likely kill you. People have died from drinking as "small" amounts of water as 6 liters in few hours. You can't establish LD50 for water without knowing the time in which the water is drunk (you can safely drink 12+ liters of water per day when needed), the hydration status, sodium consumption, etc.

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How can eating bacon not make me fat?
This page says it won't.
This page says it's the carb again http://www.mindbodygreen.com/0-10454/in-defense-of-bacon-why-eating-fat-can-help-you-get-thin.html
I don't see how eating fat will not make me gain weight while eating carbohydrates will, since fat is made of, well, fat.
It says eating carbs will make us fat. How can this be? Is this true?

I changed your title and text so that your question is a bit clearer, hope that's okay.

Fat in your body and the fat you eat are two different things. All the fat in your body is synthesized--made by the body. Dietary fat is not absorbed by the body. In fact, fat that you eat cannot even pass through the intestinal walls. It has to be broken down into carboxylic acid and monoglyceride. Carbs make you fat because the liver turns them into triglycerides, which is white fat. The liver also turns carbs into cholesterol hardening your arteries.

I think this question can also be said to be - how can the Atkins diet work?
Atkins and other low carbohydrate diets sound counterintuitive.  They vary in details, but the basic theme is: cut back on carbohydrates - e.g. bread, sugar, fruit, pasta, milk etc etc.  But eat as much fat and protein as you like - e.g. steak, ham, bacon, eggs, cheese etc etc.
These diets really do work.  Our metabolism allows us to draw food from two sources.  Glucose or fat. (there is also something called glycogen, but that is only used short term and not relevant for diets long term).
It was known in the late 50s that our metabolism will to switch over consuming fat, allowing weight loss, only based on the amount of carbohydrates we consume. low carb diets initiate this change from glucose to fat metabolism because our bodies make the switch based only on the amount of glucose available in the blood.  Our bodies think we are starving even if we are gorging ourselves on food which is has little or no glycemic index.
Low carb diets are not a hoax or snake oil - they really work.  They can be a shock to the system and so one should discuss with your doctor before engaging them.
The first link you have is also true though.  Eating fat will usually just make you gain weight.  The low carb response has to be induced by basically removing all carbohydrates from the diet.  If you break the low carb regime and eat a large amount of carbs, the body will switch practically instantly out of starvation mode and also take in all the fats you're eating.  Lots of people on low carb diets can gain a lot of weight rapidly if they break the diet.

It is still unclear, why bodies in the "starvation mode" do not absorb the dietary fat.

yes it doesn't entirely make sense either.  it may be that when drawing on the fat metabolism that its rare to be consuming fat... so storing fat and metabolizing it at the same time may conflict somehow.


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Do Yeast Insertion constructs revert?
If I insert a new gene with a yeast integrating plasmid and select with a drop out culture once, can I assume that the newly integrated gene will stay in the strain without putting selective pressure on it?  (i.e. can i use normal liquid culture and plates after getting the yeast with the newly integrated strain?

Can you give a little more detail about what exactly you did - what is the structure of the YIp, and did you cut it before transformation?

Thanks @AlanBoyd - I will need to get a YIp - if there are some that are more persistant than others I would like to know about it. your answer is helpful here. I'm considering how to adapt a LEU2 based plasmid that currently have. Just getting into yeast though and I'm really naive.

It depends upon exactly what you have done.
The standard way of using a yeast intergrating plasmid (YIp) is for it to integrate into the genome by recombination between a piece of yeast DNA that the YIp carries and the same DNA in the genome. This is often, but not necessarily, the selectable marker. So for example a YIp carrying the URA3 gene as its only yeast DNA will integrate at the URA3 locus (probably mutant to allow selection for Ura+, so more correctly ura3).
If the YIp is linearised by cutting at a site within the URA3 marker this will direct insertion and will increase the transformation efficiency.
Once insertion has taken place, the configuration at the integration site is:
chromosome...URA3...other YIp sequences...ura3...chromosome
This is inherently unstable because a looping-out event can take place via recombination between the URA3/ura3 regions. So removing selection means that you run the risk of losing the insert. Furthermore, it is possible for looping out to occur leaving the URA3 allele behind instead of the ura3 allele. So you can lose the vector even when selection is maintained (but this will depend on the exact nature of the mutation).
More complex configurations are possible where the targetting sequence is separate from the selectable marker, and where digestion removes a whole chunk of the targetting sequence before transformation. So for example if the TRP1 gene was used for targetting a plasmid with the URA3 marker in a TRP1 ura3 strain you would get:
chromosome...TRP1 fragment A...URA3+other YIp sequences...TRP1 fragment B...chromosome
the resulting transformant is now Ura+ because of the integrated URA3 plasmid, but some TRP1 DNA is now missing (the DNA that was excised when the plasmid was digested) so the strain is trp1. The appearance of this Trp- phenotype indicates that the transformation has probably occurred by the pathway described.
In this case the inserted plasmid is much more stable because those two remaining fragments of TRP1 DNA are not identical, so there is no possibility of looping out.
In summary, if your transformant has the insert carrying the "new gene" flanked by a repeating sequence then it is unstable, otherwise it is ok to remove selection. In the first case, if the new gene is at all deleterious then there will be a strong selective pressure in favour of cells which have lost the insert.
Addendum
You can avoid using YIp plasmids altogether by integrating your new gene at any locus using long targetting primers, as shown in the Figure below.
Design primers to amplify your gene as usual, but synthesise them with 40 bp 5' extensions corresponding to two sequences at the extreme ends of the integration site (URA3 used here for illustration purposes). The resulting fragment can then be used in a transformation and will integrate at the URA3 site by homologous recombination, replacing the resident DNA. The advantage of using URA3 for this is that you can select for integrants as Ura- cells by resistance to fluoorotic acid (FOA). Although you can probably select directly for this, I have always co-transformed the fragment together with another selectable plasmid (LEU2, TRP1 etc., but not a CEN plasmid) Then your e.g. Leu+ transformants can be screened for those that have also become FOAR. This co-transformation happens at quite high frequency because the cells that do take up DNA take up a lot of it. Once you remove selection for the co-transforming plasmid it will soon get lost, leaving you with a clean non-reverting integrant.
It's been a while since I did this sort of thing - probably there are even smarter methods around now.

Thanks Alan - I think this is helpful - Sounds like I can keep the selected strain in cold storage and only replate it once in a while if I avoid the repeats in my construct.  If I use a Leu2 knockout sequence I have maybe I can avoid this problem I hope.

Yeast integrating plasmids are known to be stable, even in absence of a selective medium but can revert like most homologous recombination plasmids.
Quoting from the book Yeast Gene Analysis (pg476):

YIps are generally more stable than YRp or YEp plasmids. As a result
  it is safe to grow most YIp-bearing strains in rich media, although it
  is good practice to store them under selective conditions. The
  stability of YIp-bearing strains depends on the nature of the
  integration event. For example, if the YIp generates a tandem repeat
  upon integration into the genome, this can  revert to wild-type by an
  intramolecular homologous recombination event.

-> hence use markers regularly and frequently.
Sources:
Mick F. Tuite, Yeast Gene Analysis Vol 26 (Academic Press, 1998 ) p.476

Thanks @LoSauer This was helpful so I'm upvoting though Alan's response is a little more detailed for the 'official' answer.


text:
How well can humans detect vitamin-richness?
Humans do prefer fatty, sweet/starchy and salty. And fatty foods are rich in vitamins. How well can humans detect vitamin content apart from fattiness of food? Can humans choose the vitamin-richer of otherwise identical peanut butter, cheese or chicken leg?

Do you have a source for your claim that "fatty foods are rich in vitamins"? Have you looked at the nutrition information on a bag of potato chips recently?

Based on what I could search I guess that humans (and other organisms) usually do not have strong sensory mechanisms for micronutrients (Miyamoto et al, 2013).
There are some reports on sensing of metal ions, especially zinc and copper, by some organisms, including mammals (Bird, 2015; Ballou and Wilson, 2016). However, I haven't come across any study that talks about vitamin sensing.

From wikipedia

A vitamin is an organic compound and a vital nutrient that an organism requires in limited amounts. An organic chemical compound (or related set of compounds) is called a vitamin when the organism cannot synthesize the compound in sufficient quantities, and it must be obtained through the diet; thus, the term "vitamin" is conditional upon the circumstances and the particular organism

A vitamin is therefore not defined by its structure but by its availability. There is therefore no taste associated to vitamins in general. So, no we are not able to sense vitamins generally speaking just because there is no natural objective category of substances that one can call vitamin.

Note by the way, that the health effect of vitamins supplmentation (for most people) is debated. For example, you might want to have a look at the following two skeptics posts

Do vitamins improve memory abilities?
Do vitamin supplements have any health benefits?

One of the most important scientist of the 20th century, Linus Pauling advocated for the health benefits of vitamin C. Due to his strong influence, the reputation of vitamin C quickly grew but his work remained controversial and there are still very little evidence that supplement of vitamin C does any good.

That wikipedia article seems human-centric and lists 13 vitamins. If we limit our definition of vitamin to those, is your "no we are not able to sense vitamins" still true?

Yes, very likely. You can have a look at the diversity of food source in which those vitamins are found and imagine a single taste would be common to them all.

"Note by the way, that the health effect of vitamins is debated." That's just wrong. The health effect of vitamin supplementation - at least for people without deficiencies - is debated. If you do not provide enough vitamins in your diet you will most definitely have adverse health effects.

That was more a typo than a misunderstanding from me as this point was made clear in the last paragraph. Thanks for the comment, I edited the post accordingly.

This sounds wrong to me. There are certainly structures associated with the recognized human vitamins. There are no taste receptors for them, but humans also have hundreds of olfactory receptors, and for most of them the ligands are still unknown. Also, we might detect vitamins "by proxy", for example recognizing the smell of citrus fruits as "healthy", even if there is no direct receptor for ascorbate (vitamin C). I don't think we know enough about olfaction to be able to answer this question in the negative.


text:
protein-binding sRNAs
I am actually a computational biologist, pardon me if my question description is a bit off-note, my curiosity is driving me on
A bit of background and context:
In bacteria, a regulatory protein termed CsrA binds certain structures in the UTR regions of genes and prevents their translation. These structures are short hairpin-like and all have AGGA nucleotides in the exposed part. There are sRNAs that isolate the protein from its targets, a common feature of these sRNAs is that they have several repetitive hairpins that more or less display AGGA nucleotides in the exposed part. So basically, the sRNAs mimic the structures on the targets of the proteins and that makes them potent competitors for protein binding against the genes actually targeted by the protein. By relying on this mimickry the sRNAs bind CsrA, isolate it from its targets and remove its suppression on gene translation.
My question: Are there any other examples that illustrate similar mechanisms of analogy/mimickry of sRNAs to bind protein?
What I tried
I've skimmed through a lot of literature to identify other similar systems in bacteria where sRNAs have conserved repetitive structures but to no avail. I hope someone with deeper experience directs me to such examples in any living organism, preferably bacteria but I am open to suggestion.
I found CRISPRs but these are  DNA based, I have come across few other cis-acting sRNAs which target mRNAs and aren't protein-binding. So could it be the case that sRNA mimickers aren't very pervasive in bacteria after all ?!

The sRNA mediated regulation in bacteria operates via diverse mechanisms. This case of sRNA competing with a mRNA for a protein is a passive kind of regulation. This might be good for finetuning but may not be very efficient. It is much better to actively regulate a mRNA by direct binding. Also, it will work only if the concerned protein is in limiting concentrations.
I haven't come across any examples of what you are interested in. There may be one similar situation in case of a eukaryotic system. miRNAs can be titrated away by long RNAs that bear multiple binding sites for that miRNA, thus making the miRNAs unavailable for binding to the target mRNA. These long RNAs are called ceRNA (competing endogenous RNA) or miRNA-sponges (this term is mostly used if the RNA is exogenous). However this is not really a protein-RNA interaction even though RISC complex contains proteins.


text:
Why does dehydration lead to low blood pressure
I understand that the two leading causes of death from dehydration is imbalance in electrolytes and loss of blood pressure. I'm trying to understand what role water is playing in these cases and how the loss of it causes these imbalances, focusing for now on the blood pressure angle.
While I understand that blood is made up heavily of water, I'm still a little confused why dehydration so quickly leads to drop in blood pressure.  Why can't the body continue to pump the already existing blood through the body, where is it using the water to keep the blood pressure up and what vital function is no longer being performed that causes that pressure to drop?

Hmm.... So I can imagine, that because of a reduced water level in the blood, it becomes more sticky and is pumped harder through the vessels. This may decrease the blood pressure

May this article helps you, too :)
https://www.reddit.com/r/askscience/comments/31ini6/how_does_dehydration_cause_low_blood_pressure/

The blood pressure is the  exertion of force upon the blood vessels by the blood fluids. Thus having less fluids will results in decreased pressure.


text:
How does high-fidelity of DNA replication depend on the formation of hydrogen bonds?
Replication has an error rate of less than 1 in 100 million. DNA polymerase forms H-bond with the H-bond acceptor atoms in the minor groove. <-- enhance fidelity here?
Binding of the triphosphate group to the active site of DNA polymerase triggers a conformational change. Changing a conserved Tyr residue increases the error rate by 40 fold.
I don't quite understand the above two statements. Can anyone explain in detail to me? Thanks!

Where do these statements come from? Can you post a link to the source?

it comes from my lecture note. Maybe similar statements can be found from here. The lecture quotes this from this reference book link

There's a few probs with this question one is h-bond acceptor- what is that? Then w the tyr residue are you talking about the polymerase? I have a feeling your instructor is using this mediocre example to explain to you: the structure of dna, and the fact that aa sequence determines over protein structure which determines protein function. I'm gonna post some info on  high fidelity pol but it's not going to completely answer your question cause I believe, respectfully, there could be some errors in it.

DNA polymerase must catalyse the addition of 4 different nucleotides to the growing strand. This means that it cannot directly determine which base to incorporate at a specific point (how would it 'know' which base to incorporate and how it would it change its specificity for different bases). This means that the specificity for which base pair to incorporate is dependent on the template DNA strand.
Correct Watson-Crick base pairing (that is, hydrogen bonding) between the template strand and the nucleotide to be incorporated triggers the closing of the finger domain of DNAP around the primer-template junction and positions the latter in the optimal position for catalysis (with the $\ce{\alpha-PO_4}$ of the incoming nucleotide near the $\ce{3'-OH}$ of the primer for a nucleophilic attack catalysed by two $\ce{Mg^{2+}}$ ions). This is where the conserved tyrosine residue you mentioned comes into play. An incorrectly paired nucleotide will not trigger this conformational change and will not be positioned optimally, thus catalysis is less likely.
Furthermore, the DNA polymerase makes contacts with the minor groove of the primer-template junction through hydrogen bonds. This interaction is not base-specific (all Watson-Crick base pairs have he same pattern of hydrogen-bond acceptors in the minor groove) but only occurs when the correct nucleotide is incorporated, thus stabilising the complex.
Finally, discrimination between ribonucleotides and deoxyribonucleotides is done by steric exclusion of the $\ce{2'-OH}$ by amino acid residues in the binding pocket.
These factors can be thought of as kinetic proofreading as they simply slow down the reaction rate and provide time for an incorrectly paired nucleotide to dissociate. However, they can still be incorporated and many DNA polymerases have a $\ce{3'->5'}$ proofreading exonuclease that can remove incorrectly paired nucleotides. This proofreading is again mediated by interactions between the DNAP and the primer-template junction (ie hydrogen bonding with the minor groove). A weakened interaction due to an incorrectly paired base reduces the affinity between DNA and the catalytic site and increases the affinity between DNA and the proofreading site (because it has a preference for cleaving ssDNA from the 3' end).

This is really helpful and detail. Now I understand!

I would upvote this over my own , good info

High-fidelity DNA polymerases have several safeguards to protect against both making and propagating mistakes while copying DNA.
Such enzymes have a significant binding preference for the correct versus the incorrect nucleoside triphosphate during polymerization.
If an incorrect nucleotide does bind in the polymerase active site, incorporation is slowed due to the sub-optimal architecture of the active site complex. This lag time increases the opportunity for the incorrect nucleotide to dissociate before polymerase progression, thereby allowing the process to start again, with a correct nucleoside triphosphate (1,2).
If an incorrect nucleotide is inserted, proofreading DNA polymerases have an extra line of defense
The perturbation caused by the mispaired bases is detected, and the polymerase moves the 3´ end of the growing DNA chain into a proofreading 3´→5´ exonuclease domain. There, the incorrect nucleotide is removed by the 3´→5´ exonuclease activity, whereupon the chain is moved back into the polymerase domain, where polymerization can continue.
From: New England biolabs:
https://www.neb.com/tools-and-resources/feature-articles/polymerase-fidelity-what-is-it-and-what-does-it-mean-for-your-pcr

Both the sentence can be understood from the below explanation.
In a newly synthesizing DNA strand, the DNA polymerase forms extensive hydrogen bonds with the newly added base everytime a new nucleotide is added. (First sentence) Polymerase also forms bonds with the DNA backbone of phosphate and sugar. (Second sentence)
The first sentence talks of how polymerase will form bonds via the minor groove of the newly synthesized DNA. Second sentence talks about the changing of an amino acid from the DNA polymerase (which is important for forming bonds with DNA backbone). This changing of amino acid will cause error in the nucleotide added (as the Polymerase is not positioned properly which you will understand in the following explaination)
These bonds of polymerase and bases along with the bonds between the DNA backbone and polymerase position the DNA polymerase.
When a newly added nucleotide is correctly base paired, the structure of the paired bases will be such that the bonds formed between polymerase and base will allow DNA polymerase to be positioned for the addition of next new nucleotide.
If a incorrect nucleotide was added the DNA polymerase positions such that it's exonuclease site is at a position to catalyse exonuclease activity.
Thus, the hydrogen bonds between the base and Polymerase is needed for correct positioning of polymerase to either allow the next nucleotide to be added (if correct base was added) or allow exonuclease activity of Polymerase (if an incorrect base was added). This will help in proofreading and thus provide high fidelity.

authors: Михайло Олександрович Іванцов


text:
Why do stomata close in salt water?
Why do the guard cells of the stomata close when they come in contact with salt water?
I recognize it has something to do with osmosis and the fact that osmosis makes the water drain in some sort, following this distilled water has the opposite effect.. why?

INTRODUCTION:
The basic process by which opening of stomata takes place is by endosmosis.Endosmosis causes an increase in turgidity in the guard cells thereby causing its opening.
The closing of stomata is achieved by exosmosis which makes the guard cells flaccid.
HOW DO THE REGULATION TAKES PLACE IN PLANTS:
If you read the theory proposed by Levitt from the given [link]
,in which the theory is explained in simple steps with diagrams, you will understand that $K^+$-$H^+$ pumps is the main driving force which regulates whether endosmosis or exosmosis would take place.
When the concentration of $K^+$ increases in the guard cells there is osmotic influx of water from the surrounding epidermal cells  and thus 'endosmosis' occurs causing opening of stomata.
Similarly when concentration of $K^+$ decreases there is osmotic loss of water from the guard cells to cause 'exosmosis' and thus closing of stomata.
WHY THE STOMATA CLOSE IN SALT WATER:
When the guard cells of the stomata are open it means they are turgid due to endosmosis.However when such a turgid plant cell is placed is  in salt water(hypertonic solution) the latter having a higher concentration of salt ions than the guard cells causes the loss of water from the guard cells.
Thus the salt water is inducing exosmosis to take place in the guard cells due to which they become flaccid and close.
REFERENCE:
[link]

Osmosis. According to answers.com (and I know this is not a good site for research, but I couldn't find anything else), There are potassium ions in stomatal guard cells, and since salt water has a higher concentration of these ions than the cells, the stomata closes to retain moisture.

down voted because stomata donot close to retain moisture.They close because they loose moisture.

Yes, I feel that answers.com doesn't quite live up to it's reputation. It should not be used for research...


text:
Viruses selected by evolution
I had a conversation with a family member who is a bio-computer-scientist and he talked to me about what his colleagues (biologist) are doing and I feel confused about it.
They work in Chile and are studying plants that live in the desert.
If I understand correctly his team is trying to explore the idea that some viruses might actually be good for the plants they are infecting and might have been "selected" and are now "part" of the species.
The way I understand it is that they collect samples of plants and somehow by analyzing their DNA notice that these plants are all infected by some kind of virus and they tell themselves that maybe if all the plants have the virus it's because it's good for the plants.
My questions are:
1) Does any of this make sense?
2) If it does how would the selection process happen ? Combining my (old) high-school knowledge and Wikipedia I see a virus as a piece of DNA that goes into a cell and then uses the cell's tools for it's own purpose, but it is not part of DNA. So how can it be treated as part of the plant ?
3) Do you know any good references (preferably for an enthusiast layman) about this subject (i.e. the potential good of some viruses and maybe potential applications in bio-engineering) ? I find especially fascinating the idea that maybe evolution isn't just the result of mutations but also of "contamination".

Have a look at "symbiosis"...

Thanks for you answer. I don't really understand the link though. Obviously this just means i'm dumb not that your answer is wrong. Would you mind elaborating a little bit ?

I guess Remi has answered this extensively below now :)

Welcome to Biology.SE!
About your title
Let me first react to your title: Viruses selected by evolution.
Evolution is any process of genetic (and eventually phenotypic) change in a population through time. Selection (Natural Selection for example) is one of such process. Genetic drift is another such process. So, evolution doesn't select viruses unlike your title suggests. Viruses are selected and therefore evolution occurs. When saying "viruses are selected", it means some viruses have a higher fitness (fitness is a function of both survival and reproductive success) than others.
Species interactions
Generalities
Species interact. Species actually interact a lot. One can classify species interactions into categories. Here is a table of possible biological interactions (comes from wiki), where a + indicates "beneficial", a - indicates "detrimental" and a 0 indicates it has no effect on fitness.

Note about symbiosis - comes in reaction to @Gerhard's comment
Different authors use the word symbiosis differently. From wikipedia:

The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any type of persistent biological interaction (i.e. mutualistic, commensalistic, or parasitic).4 After 130+ years of debate,5 current biology and ecology textbooks now use the latter "de Bary" definition or an even broader definition (i.e. symbiosis = all species interactions), with the restrictive definition no longer used (i.e. symbiosis = mutualism)

Blurry limits
Generalities
It may seem pretty obvious that two species should have either one type or another type of interaction. However, the reality is often more complicated than that. An interaction might fall under one set of environmental conditions and fall under another category under another set of environmental conditions. In addition to that, it is not uncommon that due to selection on the host genes due to the presence of a parasite, the host evolve so to tolerate the presence of the parasite up to the point of actually having a lower fitness in the absence of the parasite.
Example
Parasites often have different life cycle of alternance of generation. That is a parasite sometimes need several hosts such as the parasite causing malaria for example that need both mosquitoes and a primate.
Consider for example a snail which is infected by a parasite. Let's assume (I think it is a real world example but I am too lazy to find out a reference) that the parasite need the snail to be eaten in order to reproduce in the body of the predator. In order to improve the chance of its host to be eaten the parasite is selected so to diminish the thickness of the snail's shell. In response to that, there is selection (which intensity depend also on the proportion of infected snails in the population) for having thicker shells. But now, snails that are not infected have shells that are so thick that the can't move as fast as they'd need to forage. So, by the end infected snails may have a higher fitness than non-infected snails. And therefore the interaction between the snail and its parasite is not a parasitic interaction anymore but a mutualistic interaction.
Can viruses have non-parasitic relationship with their host?
Well... why not? There is nothing so fundamental about viruses that would prevent them to have mutualistic relationship with their host. Actually I am aware of a few relationships. For example, female parasitoid wasps (parasitoids: parasite that kill their host). parasitoid wasps lay their egg in other insects larvea (host), the egg (and later the larvea I think) develop in the larvea (host), eat the larvea (host) and once the host is dead, the individual metamorphose to its adult form and fly away to find a mate a parasite the next larvea. Some lineage of those wasps have viruses in their ovary that infect the host to reduce the immune defence of the host to protect the growth of their egg (Flemming and Summers 1991). This is an example of mutualistic relationship between the wasp and the virus.
Sequencing to know if the plants are infected
You said

they collect samples of plants and somehow by analyzing their DNA notice that these plants are all infected by some kind of virus

Most likely, they make a PCR (amplification of DNA, that is increasing the number of copies of a given DNA sequence) on viral DNA and look for a signal. In other words they are not sequencing (=reading) the plant DNA but only seeking for viral DNA. If they find viral DNA, then the plant is infected if not, the plant is not infected.
What is unclear to me from your text
From your post, it is unclear to me yet how your "family member" plans to decide the type of interaction there are between viruses and plants. Knowing the frequency of infected plants won't tell you much about the interaction between the plant and the virus.
They will likely have to make growth experiment and try to measure the fitness of infected and non-infected plants.
EDIT - Following the first comment
Knowing that every plant individual is infected doesn't tell much of the virulence of the virus. The frequency of infected is not an information that can help understand the "type of biological interaction" (paratism, mutualism, etc..). One will need to actually make growth experiment and measure fitness (or measure phenotypic traits that are known to be good proxy for fitness).

One question about your answer is : can we really speak of a virus as a species and especially does your table really apply in this situation ?

The concept of species is not a natural category. It is a man-made, unclear, sometimes useful, category. Typically, it is hard to even talk of species for organisms that don't have sexual reproduction (which is the case of viruses). I wrote this other answer today about the concept of species, you may want to read it. Here is another post on the subject. Btw, talking about semantic issue, viruses are often not considered as alive. All those semantic issues don't have any impact on our understanding of biological processes.
But yes, the table applies to viruses as well. This table is indifferent to the concept of species. Consider just two genotypes (two individuals), one plant and one virus, the existence of the virus has (or has not) an impact on the fitness of the plant (and vice-verse) and therefore, you can classify the relationship between those two genotypes (individuals) into one category of the table. As a reminder, the nature of those relationship may depend on the environment. Typically, a photosynthetic endosymbiote might be very beneficial to the "host" if there is some sunlight but might be quite detrimental in the absence of sun light.

Wow, thanks for your great answer. I have no idea how they decide what kind of relation there is between the plant and the virus but what I understood was that every plant has the virus somehow, like now it is part of their DNA (which doesn't really make sense hence the question) and so that's why they think it must have a beneficial effect (in other word it has been "naturally selected"). One question about your answer is : can we really speak of a virus as a species and especially does your table really apply in this situation ?

One interesting thing I found on google was : http://news.sciencemag.org/2013/05/friendly-viruses-protect-us-against-bacteria

I guess in this example what I don't understand is the relationship between the virus in the mucus and the human-being itself. Do we produce this virus ourselves ? In this case is it really still a virus  since it doesn't seem like we are "contaminated" by it. I understand that the fact that I ask this questions probably reflects my lack of understanding of the subject so I apologize.

I don't understand why you talk about human. Are you talking about the parasitoid wasp example? I don't know in details how the virus come to exist in the ovary and I don't know if anybody knows the answer. Might be an interesting question for another post.

I was talking about the example given in the link I gave : http://news.sciencemag.org/2013/05/friendly-viruses-protect-us-against-bacteria

ah ok... hum...I don't really feel like reading the whole link. I think you may have better to open a new post for that.

Ah I believe I have a found the anwser to my question : http://en.wikipedia.org/wiki/Provirus. Basically the genome of a virus can be integrated in the host's genome allowing it to be "selected". Then the host can create the virus itself.

You may want to read about the lytic and lysogenic cycles. Viral DNA that is not integrated into a eukaryote genome is not free from selection. However, if integrated repeatedly into some eukaryote genome, its expression and changes between cycle can be under selection both in the eukaryotic genome and in the viral DNA (as it may gain through hitchhiking).

As a terminology note, "lysogenic" is a term used for viruses of bacteria, not eukaryotes, although there are analogous concepts for eukaryotes.

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


text:
Tests for object size discrimination in mammals?
Are there common testing protocols for establishing whether an animal (mammals especially) can distinguish the size of objects? In particular, are there procedures or is there good literature on ways to determine whether a given species can recognizes a given object as enlarged in specific settings, ideally in ways that can allow comparison across species (e.g., species A sees an object as enlarged while species B does not).


text:
Why is the gene regulation in eukaryotic cells needs multiple level of control than in prokaryotic cells?
That "eukaryotic cells are more complex" and "compartmentalized" are used to justify the need of more level of control of gene expression. I get the basic idea but can't convince myself why complexity or compartmentalization leads to more complex control (i.e. multiple levels) of gene regulation!
In control theory, we often use multiple level of control to minimize the variance (there are few other benefits as well from design perspective); probably that is what eukaryotic cell would also do. Moreover, simple combinatorics suggest that two level of control with $n_1$ and $n_2$ molecules involved at each level respectively would give me $n_1n_2$ possibilities of output which is higher than $n_1 + n_2$ distinct output I might get if I were to use these molecules with 1 level of control/regulation.
I was wondering if such simple reasoning are correct and can be used in the context of evolution? Are there other reasons as well?

There are additional levels of regulation in eukaryotes such as alternate splicing, miRNAs, long distance chromosomal interactions (enhancers/silencers), epigenetic regulation etc. Please add details as your question seems both a bit unclear and broad.

@WYSIWYG I rephrased the question to make is less broad. I may still be unclear since I am poor in Biological vocabulary/terms.

Some gene expressions need to response quickly by stimuli. In this case, cells may degrade mRNAs or proteins rather than inhibit gene promoters. Even if cells need proteins in some small areas of cells, cells could not turn down the promoter activity of the gene. Instead cells control translocation or degrade mis-localized  proteins. Space and time are also important. Multiple ways of regulations make cellular activities possible.

You don't want all genes expressed at all timepoints. Some need a tight control, while other shall react quick upon stimuli. This is only possible with a complex regulation.

I think you need to consider the overall amount of information that is needed to implement a proper control system in living organisms.
In prokaryotic cells, in most of the cases, you will find that one gene code for one enzyme, so if a simple organisms need 500 enzymes to stay alive you can expect 500 genes that code for that enzymes.
A more complex organism may need 100 times more enzymes to stay alive and so theoretically 100 times more genes. Now, evolution wise, to have a linear increase of DNA vs complexity is not a good option for very complex organisms. To keep everything compartmentalised in one single membrane is also not a good idea if you need to run millions of chemical reactions using thousands of enzymes that can cross react and need different optimal conditions to work properly, so multi-compartimentalization is a must.
Linked with it arises the problem of sending the right enzyme in the right place and this has been solved by adding tags, transporter enzymes, etc... in the pot... So, lots of more information is needed to make everything run smoothly.
It turned out that an efficient way to code for all that enzymes, tags, promoters and other regulators without increment the size of the DNA too much is by multi level control of the expression of a gene i.e. the same gene can be used to produce different enzymes (splicing etc...). The tradeoff to pay to have a more compact genome is to increase the complexity of its control system.
Lastly, consider that differently from normal electronic controllers, the biological one do affect each other. A biological controller system may produce an output molecule that interact with the system under control but also with other reactions going on all over... that is another burden that require an increase of complexity in the control system to make it work.


text:
Database of Geographic Range of Species
Is there a database of organisms which would contain their queriable geographic location?
I would need to perform a rather simple query, such as Animals of <Location>, where Location is some well defined geographic area such as Czech Republic or Europe.
So far I have found multiple lists on Wikipedia and other webpages, however they seem to be quite incomplete as their intersect is quite small. Moreover, I have found EOL (Encyclopedia of Life) collections but they appear to struggle the same way.

What taxa are you most interested in and for what purpose are going to use the data?

The data are supposed to be used for online tool for learning biology (in non-taxonomy matter). So for now I am mostly interested in vertebrates, but later some subselection of plants, fungus and other kingdoms will come to play.

This is to a large extent a question of how reliable the data in the database needs to be. Reliability (and spatial scale) will differ between datasets and between species groups within datasets, and it is difficult to give a general recommendation. I doubt that you will find a single database with good coverage over all taxonomic groups, even if it is in the form of country checklists. For the most reliable information, curated country checklists for specific taxonomic groups will probably be best, but these have to be searched for individually for each taxonomic group of interest.
As a starting point, you might want to look at the occurence data that can be found in gbif.org (The Global Biodiversity Facility). The data found there is certainly not complete, and it will be misleading for many species. However, for the current distribution of relatively well-known groups of species it will give you a good idea of their distribution. This has to be evaluated on a case-by-case basis though. You can access the data in gbif using external tools, for instance using R through rgbif (there is also tools for python or other languages). At the blog recology.info you can find a tutorial on how to get a species list for a particular country using rgbif (more specifically the function density_spplist).

The data completeness will always be problem, however with your suggestion of GBIF and triangulation from various sources mitigate this problem to much lower level. Thanks! :)

The GBIF database that was suggested can give you locations of occurrences given a specific animal. But you asked for lists of animals given some location. An excellent tool to give a list of animals given a location in the world is the Map of Life. Click on "Species by Location" which gives a map of the world, and click anywhere to get lists of species that could occur there.

Also seems very interesting and relevant, thanks for sharing!


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Survivorship Curves: Type II curve mortality rate is not constant?
In graphs of survivorship curves, I'm seeing that the Type II curves are straight lines, and the supplementary text says that the mortality rate is constant (i.e. the slope of the line is constant). However, it's also clearly stated that the y-axis is a logarithmic scale, which means that the original Type II curve is exponential:
$$\ln y=-rx+b$$
$$y=Ae^{-rx}$$
This implies that the real mortality rate is not constant, but changes as $$y'=-Ar(e^{-rx})$$
How are we defining the word rate, anyway?

Presumably $r$ (or $-r$) is the rate, which would appear to stay constant.

$r$ is the individual mortality rate per time step. Survivorship curves (plotted on a log scale) show the proportion of individuals surviving with time, and with a Type II curve a constant proportion is dying at each time step (constant mortality with age, $r$). When the model is expressed as $y$ you are looking at the number of individuals surviving to a time step, which is an negative exponential for Type II, since a smaller and smaller proportion of the population remains at each time step. Therefore $y'$ is the change (slope) in the number of individuals surviving over time. This can be seen as a rate, but it is not the mortality rate of individuals, and it is not accurate to describe it as the "..real mortality rate..".
For an introduction to survivorship curves you can also look at "Survivorship Curves" from Nature Education

For Discrete Time
There are two quantities you should be careful not to mix up.

One is the number of individuals who will die during a given interval: $d_x = N_x - N_{x+1}$.
One is the fraction, out of those alive at the beginning of a given interval, who will die during the interval: $q_x = \frac{d_x}{N_x}$

($N_x$ being the number of survivors at age $x$.)
On a regular plot, if $d_x$ is constant then survivorship will decrease linearly; if $q_x$ is constant then survivorship will decrease geometrically. On a semilog plot, when $q_x$ is constant then this geometric decrease will look like a straight line. This is, as far as I know, the main reason to even use semilog plots in the first place; it makes geometric decrease easy to recognize. $d_x$ is sometimes called the death rate and $q_x$ is sometimes called the mortality rate.
(In my opinion this usage is careless; they aren't rates, but just numbers. Compare: there is a distinction between travelling 10 miles in an hour, and travelling at 10 miles per hour.)
$q_x$ can also be thought of as estimating the probability that someone who is age $x$ will die before age $(x+1)$. It is therefore sometimes also called the "Age-Specific Probability of Death". Notice that it is bounded between 0 and 1.
(Probabilities can't be lower than 0 or higher than 1; and the fraction dying has to be somewhere in between "none of them" and "all of them"!)
Here's an example survivorship curve, on a regular plot, I made for constant $q_x = 0.1$.

This much should be enough to answer your question. But, for completeness...
For Continuous Time
I complained about calling $d_x$ the death rate. That's because rates have a unit of $time^{-1}$ ("...per second", "...per hour" etc.) Of course, dividing $d_x$ by the length of the interval, does give you the average death rate over the interval. And,

The slope of the survivorship curve (multiplied by -1; we want a positive rate of decrease, instead of a negative rate of increase) gives you the instantaneous death rate at age $x$: $-N^{'}_{x}$.

(For instantaneous rates to be useful, we have to "smooth-out" the survivorship curve instead of letting it be a stepped curve. If it was stepped, then the slope would just always be horizontal or vertical.)
This brings us to another quantity: the "Force of Mortality":

The instantaneous, age-specific, per-capita death rate; or, the death rate at age $x$, divided by the cohort size at age $x$: $\mu_x = -\frac{N^{'}_{x}}{N_x}$

To illustrate, if the death rate at age $x$ is "60 deaths per minute", and if at that instant there are 60 people, then the per-capita death rate is "1 death per person per minute". Because choice of time unit is arbitrary, this is the same as saying "60 deaths per person per hour" or "525600 deaths per person per year".
The Force of Mortality is unintuitive ("per-capita" death rate? - but everybody only dies once!) but the formula is coherent. The point of having a "per-capita rate" is to enable comparison between cohorts of different sizes, or the same cohort at different ages when it was bigger vs. smaller, and so on; in general the idea is that death rate has something to do with the number of members, but also something to do with the condition of each member, and $\mu_x$ is trying to get at the latter. It can be visualized as the slope of the survivorship curve (multiplied by -1 to make it positive), divided by the height of the survivorship curve.

There is a similarity between these two quantities, and the two which were defined for discrete time. If $-N^{'}_{x}$ is constant, then so is $d_x$; and if $\mu_x$ is constant, then so is $q_x$. And, again: on a regular plot, if $-N^{'}_{x}$ is constant then survivorship will decrease linearly; and if $\mu_x$ is constant then survivorship will decrease exponentially.
But they are distinct. It is the $time^{-1}$ dimension, and the fact that time units are interchangeable, which makes the difference.
If there are only 60 people, then it's obviously not possible for more than 60 people to die in the next year $(0 \le d_x \le 60)$; and it's not possible for the fraction dying to be higher than "all of them" $(0 \le q_x \le 1)$.
But suppose the rate of death at this instant is "60 deaths per hour". That's the same thing as saying it's "1 death per minute" or "525600 deaths per year". There's no implication that that many people will in fact die, because there's no implication that the rate will be kept up for the whole year. If this particular death rate were held constant as long as possible, then the cohort would all be dead in exactly an hour and then the rate would then hit 0. The instantaneous death rate can be as high as you like; it just can't stay high forever.
(If a death rate of "60 deaths per hour" is measured at an instant when there are 60 people, then the per-capita death rate is "1 death per person per hour" - or, equivalently, "$\frac{1}{60}^{th}$ of a death per person per hour", or "8760 deaths per person per year".)
Although the absolute death rate can't stay high forever, the per-capita death rate ($\mu_x$) can. That's what happens during constant $\mu_x$ (exponentially decreasing $N_x$), for example. The reason why this is not paradoxical is that the slope ($-N^{'}_{x}$; the numerator) is constantly decreasing; it's just that so is the height ($N_x$; the denominator).
The Force of Mortality $\mu_x$ has also sometimes been referred to as the "mortality rate". The equivocal use of language is unfortunate. It is also, especially in reliability engineering, known as the "hazard rate".
By the way
$q_x$ and $\mu_x$ have often been conflated, at least in gerontology (with which I am most familiar). But they are not the same. The first estimates a probability, and is bounded between 0 and 1. The second is not a probability, and has no upper bound.
One way they have been conflated is with the "Gompertz equation".
A Type II Survivorship Curve is one which is decreasing exponentially. When this is the case, both $q_x$ and $\mu_x$ are constant. We would call such a species "non-aging" or "non-senescing": your age makes no difference to your vulnerability.
But many species do age.
Benjamin Gompertz proposed that for many species including humans $\mu_x$ grows exponentially throughout adulthood:

Gompertz' Law of Mortality: $\mu_x = \mu_0 \cdot e^{Gx}$
Or, in its logarithmic form: $ln(\mu_x) = ln(\mu_0) + Gx$

(Where $\mu_0$ is the "initial mortality" and $G$ is the exponential "Gompertz parameter". In the logarithmic form, $ln(\mu_0)$ is the intercept, and $G$ is the slope.)
Whether or not $\mu_x$ follows such a law indefinitely is an empirical matter. (It's actually debated whether it decelerates in late life, and if so why.) But notice that $q_x$ couldn't possibly grow exponentially forever, since $q_x$ couldn't possibly ever exceed 1. And yet, due to the conflation, in recent times it has often been in terms of $q_x$ that the Gompertz equation has been presented and discussed.
Further Reading
Unfortunately, as far as I know the literature (both professional and pedagogical) is sorely lacking in treatments which are both intuitive and accurate!
Peter Medawar's "The Definition and Measurement of Senescence" (Chapter 1 in The CIBA Foundation Colloquia on Ageing, Vol. 1) is probably still the best introduction to the rationale behind why we care about survivorship curves and mortality, from the perspective of biogerontology. Medawar gives the correct definition and formula for $\mu_x$ (though he doesn't stress its distinction from $q_x$; indeed, he doesn't mention $q_x$ at all).
The distinction between $q_x$ and $\mu_x$ is discussed in Gavrilov and Gavrilova's The Biology of Life Span: A Quantitative Approach, as well as in some of their papers. They present the correct forumula for $\mu_x$, but do not really try to explain it.

This is a statistical property of the curve - in time to event analysis (which is what a survivorship curve is), a constant hazard (the instantaneous probability of an event occurring in time t given it has not occurred already) will yield an exponentially distributed survival function. When graphed on a log axis, this function looks like a straight line.


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Yellow/Orange Fungus on Oak Tree
What is the fungus pictured below? The photo was taken October 6, 2013 near San Antonio, TX.
I have Googled it and my results suggest Laetiporus root rot (Laetiporus sulfureus).
According to this website the presence of this fungus indicates the tree should be removed.
Is there any chance that this is something else? I would hate to remove such a beautiful oak tree.

Please mention when and where the picture was taken. Also ask around you neighborhood in case anyone is missing a brain, just in case ;).

Any chance we can get a closer shot of the section attached to the tree?  Regarding felling the tree, is it at risk of hitting a tree should it come down? From the photo it looks like it's pretty open.  You can also anchor trees with cables so that should they fall, it would be away from structures.

@losthorse please [edit] your question to add exra information rather than put it in the comments where it is easily overlooked.

@AtlLED - Unfortunately, I have already removed the fungus. It does not seem to be at risk of hitting another tree should it fall, but I would have to take a closer look to be sure.

@losthorse Well if it's not in danger of hitting anything, there is very little reason to fell it.  If nature wants to bring it down, it will.  More to the point, I question Laetiporus sulfureus id.  You normally see much clearer shelving with that, or at least all the ones I ate growing up did.  Do you live in the Rockies?

@AtlLED - thanks for the input and perspective... the tree is in south central Texas.

@losthorse If you took down the fungus, can you give us any more details on it?  Was it hard, slimy, smelly, or brittle?  Did it have gills/fins on the back towards the tree.  Does the tree show any of the other signs of heart rot?

I can't say for sure but it looks like a species of the Laetiporus mushrooms. Please refer to its wikipedia page for the full info.
edit: I did not read your question fully and now I see that you reached the same conclusion. Just ignore my answer. As to the second part of your question asking if it could be anything else, that is quite hard to visually determine as there are many look alikes in the mushroom kingdom. Read this for some imposters.

authors: حمدي عبد الباسط


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Anatomical differences between herbivores and omnivores
What are differences of herbivores vs omnivores? I do not mean dietary differences (obviously), but physical ones.
E.g., afaik herbivores have a much longer digestive tract than carnivores; then there is the difference in teeth, possession of carnivorous instincts or lack thereof, etc.
But where is the distinction between herbivores and omnivores? Is there a clear distinction at all, or is the border between the two groups somewhat fuzzy? Or are omnivores merely herbivores who are less picky?
EDIT
As pointed out in the comments, the last sentence seems to ask for dietary differences. It is not meant to; the only difference I am aware of is dietary, so it asks whether there are any anatomical distinctions, or the dietary is the only one. I.e. are they anatomically similar, and not distinguishable in the same way herbivores and carnivores are; hence are they herbivores that simply do not mind eating non-plant based food in a while?
I hope this serves to clarify.
EDIT 2
I realize that this question is quite broad, so while I am trying to get a good view of the bigger picture, partial answers will be more than welcome!

at first you're asking about anatomical differences, but your last paragraph seems more focused on the dietary behavior for which you said you were not asking about. If this is not the case, please clarify your question.

@theforestecologist I just did, I hope this clarifies!

This is a bit broad. Teeth, gastrointestinal differences (not alike in all herbivores), hooves/claws, eyes, etc, not to mention instincts... it's pretty broad.

@anongoodnurse I realize that it is. However, I lack the knowledge to narrow it down. Also, I am basically interested in the big picture, i.e. pretty much anything having an impact on how they feed.

@foaly Instead of making additional sections like EDIT1 or EDIT2 while retaining the original content, please actually edit the question so that it becomes short and precise.

@WYSIWYG For exactly that purpose I did not. The question is still correct and as precise as I can make it without wordy explanations. If anyone feels uncertain about it though, there is a clarification below in the edits. ;)


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How can I calculate Shannon-Wiener diversity index in caves with different kind of habitats and different sampling methods?
I would like to start a monitoring in different caves, compare caves of different age and length, and find out if there are any correlations between these factors and their diversity.
I was thinking to use the Shannon-Wiener diversity index and to use both pitfall traps and timed area search sampling methods. Can I get a single index value for each cave even if the methods are different?
And what about that caves which have stream or pools where the fauna can be very abundant? Even if I collect a sample of water, the abundance of certain species can be very high (e.g. copepoda).
Sorry for the banal questions but I have not experience with indices and statistics.

Clarification after comments:
I have about 20 caves to sample, I want to compare the fauna of these caves (richness and abundance). As I told they have differents lenghts, ages and others environmental features. Some of the caves have also streams or little pools (where I will take water samples to identify the fauna).
I have read some articles where the diversity indices were calculated using just one single methodology (traps or timed area search), and also for only one kind of fauna (acquatic or terrestrial).
The question is: Is there any methodology to get one single value of diversity index for each cave? (which considers both terrestrial and aquatic fauna). Or maybe in these conditions I can just get the number of species for each cave, without being able to compare their abundance?

So if I understand you have cave with only pitfall and cave with only timed area search sampling methods ?

Not sure if you can read the answer that I wrongly deleted. No, I was thinking to use both method in each cave. The question is, can I get a single index value for both aquatic and terrestrial fauna?

Why do you wanna do that ?

If I have two index values for caves which have both aquatic and terrestrial fauna, and just one value for others which have only terrestrial fauna, how can I compare them (in terms of abundance and richness)?

You could account for this in your statistical analysis. I'm assuming that  you will collect terrestrial fauna the same way in every cave, and if there is a stream in a cave aquatic fauna will be collected in some standardized way as well. I'll also assume you'll have some other explanatory variables that you think may explain diversity, richness, or abundance. These could include cave temperature, length, depth, etc.
Calculate the Shannon-Weiner index for each cave using all species and abundances, whether they came from an aquatic or terrestrial sample. Then for you statistical model include whether a stream was present in a cave or not using a binary variable along with your other explanatory variables.
index ~ f(temperature, length, depth, stream)
In this example temperature, length, and depth are all continuous variables. Stream will be a binary variable (either 0 or 1, 1 meaning a stream was present). This will give you a measure of how much a stream contributes to diversity.


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What are the evidence that all life today descended from a common ancestor (LUCA), and which organisms (if any) challenge the concept?
If I understand correctly, the concept of the LUCA (last universal common ancestor) is based on the hypothesis that archaea and bacteria share common ancestry.
In the realm of mathematics, the same discoveries have often been made more than once, in different places. Sometimes (like with calculus) these independent discoveries were made almost simultaneously. Sometimes the discoveries appear to  be totally unrelated (Hipparchus affirmative compound propositions before 100 BC, and David Hough's work on inserting parentheses in 1944).
If "life" started on Earth in some kind of primordial soup, it is conceivable that it started not once but many times, in different places and at different times.
How strong is the evidence that bacteria and archaea do not represent quite separate discoveries of "life", which (because of the nature of the chemical substances that they use) happen to share a number of features, such as DNA?

Multicellular, or metazoan, life may have evolved more than once, because sponges (Porifera) have a life-cycle and body plan unlike any other plants or animals (although this notion my be outdated).  Check out the evolution of the aminoacyl-tRNA synthetases. Some authors have argued that the fact that there are two discrete families, and that each family can charge tRNAs for the major classes of amino acids as evidence that this capacity, to prepare a limiting substrate for protein synthesis evolved at least twice.

It is quite likely (but impossible to study) that the first stages of life originated more than once. However, the evidence that all currently existing life originated from the same population is very strong.
On the most basic level, many of the basic building blocks of life, RNA, DNA, amino acids are chiral, which means they come in multiple forms, but for the basic processes in nature, always the same one is chosen. For example, the DNA double-helix is almost always right-handed in nature,
see also here. If there were multiple origins of archaea and bacteria, we would expect some to pick another form, if not other molecules. In addition, many crucial proteins such as DNA- and RNA- polymerases are very similar between all species, the probability that they would have originated independently is simply minuscule.

Isn't the right-handed nature of DNA the result of energy requirements ? Wouldn't any new life form tend to adopt the configuration that requires lower energy levels? Is there no evidence of genetic transfer between archaea and bacteria that could account for the sharing of proteins? Might not the choice of molecules have been dictated by what was available in the original "soup"?

(energy) you could build left-handed DNA with the same energy levels as right-handed DNA using L-Ribose (since the sugar is also chiral). 2. there is likely genetic transfer, but at this point you might want to think which parts of an organism you would consider ancestral, 3. at least for amino acids, the version not occuring in proteins is used for other things.

The universal nature of the genetic code strongly supports the hypothesis that unicellular life evolved once on  the planet (or that the organisms that used this genetic code won out).

If life did originate multiple times, it'd be quite a coincidence if it ended up with the same specific amino acids, nucleotides, sugars, genetic code and on top of that also the same chirality (for basic processes).

The genetic code of the tree of life is actively studied. So far, all the living beings have conformed to LUCA model. They are all RNA and DNA dependent, and no other life forms are known. All the RNA and DNA life forms share a tree like inheritance pattern with more simple organisms.
Sometimes there is doubt about wether mushrooms are more closely related to animals or plants.
Sometimes it is debated wether Prions are life forms or not. They are proteins that can reproduce by tricking human cells to making them and then transmit themselves, but they have not developed into anything else than a protein.
Some Virii have a special relationship with DNA, in that they just hyjack and eat DNA using RNA tricks, but their code is basically a lego block of other DNA they have hyjacked, they have fascinating evolution mechanism.
Here is the Tree Of Life, for the moment all genetic testing has found a tree structure shared by common acenstors, in all organsims, hence a LUCA:

here you can see it in detail, so far 50 000 species are on there, from the same philae and DNA -tested, and soon they will have more species, like 200k or something.
huge pdf poster:
http://www.timetree.org/public/data/poster/timetree24x32.pdf


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What makes animal to continually reproduce?
I was reading about Trypophobia and reached to Surinam Toad's reproduction methods. Then I had this doubt-
Why would animals want to reproduce so much?
In case of humans we mostly have the offsprings nearby for entire life, so some of them may take care of us. But in case of many other animals after birth they have no connection with their parents.
So why do they always try to reproduce in large quantities in entire life time?
What they achieve in this?

Life begets life. If organisms didn't reproduce, their species would die out. Simple as that.

I think the introduction on trypophobia is not necessary.

I don't get why people are voting to close this Q as "opinion-based". This is clearly answerable from the perspective of evolution of life histories.

@fileunderwater I agree that this question is not opinion-based, but it is rather unclear, and in any case it is rather broad. Organisms would be selected for optimal levels of reproduction, those that reproduce too little or too much would be selected against.

Why organisms reproduce
If they didn't reproduce, they would die out.
More concretely, suppose an animal is born with a mutation that removes the desire to reproduce.  That animal will not have any offspring, so its genes will not be passed on to the next generation.  When that animal dies, that mutation will die with it.
Why some organisms reproduce a lot
Different animals or other organisms have differing strategies for reproduction, based on their ecology.  Some animals, like the Surinam toad, try to have a lot of offspring with relatively little "investment" (of energy, time, effort, etc.) in each one.  Many of the offspring will die, but enough will survive that the organism's genes can persist.  Other animals, like elephants, only have a few offspring but spend a lot of effort in making sure those few offspring survive.
You can read more about this in the Wikipedia article on life history theory.


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How do climate and location affect the Pine Processionary moth?
I have statistics on the occurence of the Pine Processionary moth (Thaumetopoea pityocampa); we have the regions that are located in Algeria, infested area in percent, the defiliation degree (small, medium and high) and we have geographical location (longitude, lattitude).
The table is as follows:

Why is there a difference between infested areas, and is there a special pattern for the distribution of this insect? Is it known what the main drivers are for determining the distribution and abundance of this moth, and thereby why some areas are more infested than others?

I think you should merge this question with http://biology.stackexchange.com/questions/19103/classification-of-degree-of-infested-areas-by-pine-processionary-moth-on-regions, since they are very similar and clearly overlap.


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Classification of degree of infested areas by pine processionary moth on regions
I'm making a thesis about pine processionary moth distribution on the regions of algeria!
i'm making tests about if there are spatial autocorrelation of this insects on the regions.
and i'm doing also hierarchical clustering of (degree of infest, small defoliation, medium defoliation, and high defoliation, and lattitude and longitude coordinates ) on each region to see the regions that have the same caracteristics on the variables i muntioned above!
The problem is that i need some information about the effect of geographical location and climat on this specific insect ?
i have made some statistical tests, and i have found that each year have diffirent cluster caracteristics for this regions, so can anyone help me to know why it's diffirent each year ?
the final thing, if anyone could suggest to me some links, to previous some study on another country maybe , so i can take an idea of what do i have to include and do , and to compare also with my results ?