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Do squirrels and blue jays play a role in oak tree distribution?
White oak (Quercas alba) acorns have lower tannin levels than red oak (Quercas rubra) acorns, therefore animals tend to eat the white oak acorns before red oak acorns.  Animals such as squirrels and blue jays will often catch red oak acorns for later consumption when the tannin levels have lessened or when food sources are scarce.  Since red oak acorns are more likely to be hauled off, cached, and forgotten about wouldn't this cause red oaks to be more widely dispersed than white oaks?  By this I mean that white oak trees would be spaced closer together than red oaks.
Source 1: https://www.allianceforthebay.org/2017/09/the-complicated-relationship-between-acorns-and-animals/
Source 2: https://link.springer.com/chapter/10.1007/978-1-4419-0378-5_6?no-access=true

I just checked recovery rates from articles, they cited losses of 75, 40, 80 percent. Squirrels and many species of birds that cache foods. any loss rate higher than 3 percent would mean that every squirrel grows at least 3-10 trees far away from the parent tree every year.

I remember hearing a loss rate in the 70 percent range years ago.  I'm not having much luck finding squirrel population data, but the best I could find is ~50/acre in an urban setting from this site.  There is also a q&a site with an answer of 3 squirrels for every human world wide - no reference cited though.  Terms like widespread and abundant are used often.

In case anybody is curious this paper seems to answer this question.

The obvious conclusion to follow from these summaries is that acorns
  of RO have a significant dispersal advantage. RO acorns are dispersed
  greater distances from their sources, cached more often in a wide
  variety of environments, and even show the ability, under some
  circumstances, to escape partial predation. Acorns of WO, in contrast,
  should show short dispersal distances and may be in fact adapted for
  rapid germination near or under parent trees.


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Should corn be considered an invasive species in the Midwest?
Per the United States Department of Agriculture (USDA) an invasive species is defined as:

non-native (or alien) to the ecosystem under consideration

whose introduction causes or is likely to cause economic or
  environmental harm or harm to human health

Corn in the Midwest, USA (often referred to as the Corn Belt) would seem to satisfy the first requirement as an invasive species as it is not native to this area.  Regarding the second requirement, it could be argued that corn in the Midwest causes environmental harm because it is in place of many indigenous plants that many other animals rely on to survive.  For example, habitat loss is considered a cause in the decline of the regal fritillary (Speyeria idalia) butterfly.
A Google search brought me to this Q&A site where many argued that corn is not an invasive species because it cannot survive or spread by itself without human intervention.  I tend to agree with this logic but it does not seem to be within the scope of the USDA definition.
Should corn be considered an invasive species in the Midwest?

I'm voting to close as opinion-based, because there isn't really any biology in this question.

A q for sustainability?

You answered your own question. It does not survive in the wild. Corn IS native to the ecosystem in which it exists, which is an agricultural corn monoculture.

@Karl Kjer.  What seemed to be confusing me is that the agricultural corn monoculture ecosystem is not the native, predominately tall grass prairie, ecosystem for this area.  After reviewing the first part of the definition I do see it says non-native to the ecosystem under consideration (not the native ecosystem) which would mean it's not an invasive species to the Midwest.  Thank you for the explanation.

This list does not exist to consider USDA directives or semantics. Please someone else vote to close this.

OMG i never realized that humans are an invasive species.

Having observed several invasive plants in my yard , I would certainly not consider corn ( or soybeans ) to be invasive.

I’m voting to close this question because it is fundamentally opinion-based and falls outside the remit of this site. That this is opinion is reinforced by the links to a regulatory definition and a non-scientific Q&A.

Should corn be considered an invasive species in the Midwest?

I agree with commenter Bryan Krause in that this question requires opinion -- but I think it only requires opinion as to the definition of what we consider "invasive".
The concept of an "invasive" species is highly contested among biologists. It is often used interchangeably with the terms non-native, non-indigenous, and alien.
Some people think we should consider a species as 'invasive' even if it is native to the region but is causing "economic or environmental harm or harm to human health". For example, the USDA considers Juniperus virginia a native species, despite its spread from plantings and its economic and ecological impacts in 'invaded' regions.

Species are only considered invasive if they become widely established in sustaining, wild populations. If the species is widely cultivated, but rarely or never escapes cultivation, it is not invasive. Even if it widely escapes cultivation, it may not necessarily be invasive because it might not be vigorous enough in the wild.
Corn has escaped and formed wild sustaining populations in North America, including in the Midwest. Here is BONAP's range map:
http://bonap.net/MapGallery/County/Zea%20mays.png
It shows that it is established in all lower 48 states as well as many of the Canadian provinces that border the US. However, if you look at the county-level distribution, you will see that it is spotty.
Given how widely it is cultivated in many of those states (it covers much of Iowa and Illinois, for instance) yet how sparsely it is established there (it only shows up as established in the wild in isolated counties in both states, this provides pretty strong evidence that it's not really that vigorous in the wild.
I have also observed corn plants growing in the wild in the US. They aren't particularly vigorous: there will be one plant here or there, and it never dominates or forms large monocultures. Those highlighted counties are where corn has formed some sustaining population. Not necessarily where it is vigorous, common, or abundant.
Want to see what a map of an invasive species looks like? Here is BONAP's map on garlic mustard, Alliaria petiolata, widely agreed to be invasive:
http://bonap.net/MapGallery/County/Alliaria%20petiolata.png
In spite of the fact that it is not cultivated, it is found in nearly all counties of broad regions from Wisconsin/Illinois east through New England. Furthermore, if you examine it in the wild, you find it forming huge monocultures, shutting out all sorts of other plants.
But back to corn:
The ecological damage caused by corn in North America is not caused by wild corn, i.e. not caused by corn as an invasive species. Rather, it is caused by the agriculture itself, specifically, by vast monocultures of corn and other crops, and various other aspects (fertilizer and other chemical applications) of yield-intensive agriculture.
So I think the answer here, even accounting for the high level of subjectivity in the definitions of "invasive", is definitively no.

Welcome to Biology.SE. First, while this looks like a good answer, it is to a question that is off-topic for this site (because it is asking for opinions) and it would be better to leave such questions unanswered. Second, for future posts where possible please provide references (with full citations) since links can (and do) break. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [ask] and [Answer] effectively on this site.

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What benefits do sloths and manatees gain from algae growth on their fur/skin?
Slow moving sloths and manatees have green algae growing on their fur/skin.  Are there any other animals that have algae growth on them, and does the algae benefit the fitness of these animals?

Source: Canadian Museum of Nature

Source: wildlife.org

Is there anything to suggest there is a benefit to manatees? My boat has a layer of algae on it.

@kmm 1: I seem to remember reading that the algae on manatees acted like a sunblock, but there were no references to this claim.  Unfortunately, I cannot remember anymore where I read it either.

I don't know about manatees, but sloths have a symbiotic relationship with the moths living in their fur because the moths supplement the sloth's diet with additional nutrients via algae. Sloth moths grow and die in a sloth's fur, decomposing to provide nutrients for the algae. The sloth then eats the algae. What the moth gets out of this is that its larvae can feed on the sloth's poop, and when they grow up, they make a home in the sloth's fur again.
Here's an infograph summarizing the relationship: http://www.pbs.org/wnet/nature/sloth-named-velcro-sloth-moths-mutually-beneficial-relationship/11159/

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Online phylogenetic tree of human lineages
I am looking for a source of information about the diversity of human lineages and their relationships.
With a quick google search it is easy to find this type of tree

A perfect online resource would...

Contain a lot of lineages going to the most detailed lineages
Contain links to wikipedia or other source of information that could help someone to:

identify a group
have an overview of their culture

Contain visualization of their current (or past) geographic range.
Contain visualization of migration patterns
As mtDNA and Y chromosome may typically show different story, it'd be great if the resource would differentiate these and highlights specific cases where the two tree differ.

Can you recommend some online resources?
A review paper with nice graphs would also be welcome.

Related:

The post The best free and most up to date phylogenetic tree on the internet? recommend resources for visualizing the tree of life.
This webite offers a pretty amazing tree of religions.

Note that the structure of the human evolutionary tree depends on the kind of markers that are considered, male and female lineages don't necessarily have the same history, so SNPs from the mtDNA and Y chromosome will tell a different history, at least when looking into the details.

@bli Good point! I forgot about it. Following your comment, I added a bullet point in my list of descriptions for a perfect ressource. Thank you

Great link about the Tree of Religions!

Such a "tree" actually also has gene flow across branches. Related: Human migration by haplogroups, World map of Y-DNA haplogroups, Early human migrations, Simplified interactive map, Other

Trees for haplogroups
See

https://www.eupedia.com/genetics/phylogenetic_trees_Y-DNA_haplogroups.shtml
https://www.eupedia.com/genetics/
focus on Europe: https://www.eupedia.com/europe/origins_haplogroups_europe.shtml

and many pages linked therein such as https://www.eupedia.com/europe/Haplogroup_J2_Y-DNA.shtml#subclades

and so on.

More detailed for mtDNA (female lineage):

https://en.wikipedia.org/wiki/Human_mitochondrial_DNA_haplogroup

and many links therein

More detailed for the Y chromosome (male lineage):

https://en.wikipedia.org/wiki/Human_Y-chromosome_DNA_haplogroup

and many links therein

https://en.wikipedia.org/wiki/List_of_Y-chromosome_haplogroups_in_populations_of_the_world and links therein
https://isogg.org/tree/index.html
and the Google Sheets linked therein
https://www.yfull.com/tree/

"Trees" for populations
Note that the trees are for genes/haplogroups, whereas such a "tree" for populations actually also has gene flow across branches. Imagine overlaying the tree for mtDNA (female lineage) with the slightly different tree for Y-DNA (male lineage).
Geography of migration
Migration and geographical distance played a key role in the emergence of distinct populations. See

maps of migration by haplogroups: Human migration by haplogroups, World map of Y-DNA haplogroups, Early human migrations, Simplified interactive map, And so on.
maps of distribution of haplogroups: mtDNA in Europe, Y-DNA in Europe, many of the links listed here, and so on

Also check out how theories about migration are changing. For example about mutation M174: theory around the year 2010 vs. theory since at least 2016.

There are a lot of very good resources in your answer. Thank you!

I have used this online tool it has many of the features you are looking for.
http://itol.embl.de/shared/ivica
You can see some example in this page.

How to use this website, where exactly are human lineages?

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Geographic regions as subpopulations/demes
I am developing a computational simulation for DNA barcoding. One of the parameters in my simulation is the number of subpopulation/demes, which I label as $K$. Most studies that use DNA barcodes tend to focus on a single geographic region.
My question is: is it valid to presume that a single geographic region is equivalent to a single subpopulation/deme?
For example, if the focus was on cichlids of Lake Malawi, would it be a safe assumption that Lake Malawi comprises a single subpopulation/deme?
Eventually, I would also like to incorporate migration rates into my simulation, but these are very difficult to estimate without accurate data on $F_{ST}$.
Any insight would be most helpful and is warmly welcomed.

For simulating DNA barcoding, it is valid to presume that a single geographic region is equivalent to a single subpopulation. Although there do occur cases where one or two nucleotides differ at the same location, that is rare, and these few differences would still cluster together in any analysis of barcode data.

In terms of developing a simulation (simulations need not be perfect), over 50,000 specimens that I personally barcoded, I virtually never saw differences at the same location, and most data in BOLD are from single locations. "Region" in BOLD most often = single site. http://rstb.royalsocietypublishing.org/content/371/1702/20160025

Thank Karl! Based on your advice then, I am thinking that a user of my finished simulation could simply set the number of demes (K) to be equal to the number of sampling sites. Other more-involved options include using the software program STRUCTURE (Pritchard et al., 2000) to determine K using a Bayesian framework.

Yes, I agree. Sampling in BOLD is supposed to be geographically diverse. But it is common to have a single individual barcoded. Sometimes however, hundreds were sampled at the same site, and these were almost always identical. When the sampling was designed for barcoding, sites are usually at the extremes of species distributions, and these almost always differ. In this case, sites are not regions like "Virginia", but places where a collector stoped the car and collected. I have heard of "STRUCTURE", but have not used it. It sounds good though.

It is impossible to answer your question in the general sense. Yes, detailed population structure may matter. It very much depends upon what your question is and what parameter space you are willing to answer but it is possible that assuming panmixis would be unrealistic.
Note that accurate data on $F_{ST}$ won't suffice to estimate migration rate $m$.
Note also that many simulation platform already exist and you might not have to reinvent the wheel (see Sequence evolution simulation tool).

Thanks! I am not aware of any DNA barcoding studies that estimate migration rate; however an isolation-by-distance assumption would be required given population subdivision into demes.


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Did you know that the fact of evolution is as well established as the fact that evolution is impotent?
We all know that evolution is a fact. Fact is a truth known by actual experience or observation. Evolution is defined by mutations, gene migration, natural selection and genetic drift. The first two create variation while the latter two sort variation, and this is something that we know by actual experience or observation.
But, we also know by actual experience or observation, that evolution can't create new genes. The biggest observation of evolution in action is Lenski's E.coli experiment. After more than 67.000 generations, which translated into human generations is equivalent to around one million years, this experiment resulted in 0 - zero new genes. Most of the changes in this experiment involved streamlining the genome, deleting genes no longer needed, or reducing protein expression. One of the changes involved something that proponents of evolution refers to as evidence for bacteria evolving a "key innovation" But, nothing structurally new evolved. After about 31,000 generations there was a mutational transfer of one pre-existing gene(citT) from one location to another which resulted in the ability of E.coli to grow on citrate under the oxygen-rich conditions.
How can we explain this fact of impotence of evolution? Well, quite simple. The total number of mutations in the history of life is estimated at 10^43, while the average E. coli gene size is 1000 bp which gives a library of 10^602 DNA seqeunces. Meaning, even with all evolutionary mutations spent, and with a functional landscape of size 10^100, still there is a 459 orders of magnitude lack of mutational resources to explore this library and find new functional landscapes.
So evolution is indeed a fact, but the fact is also that evolution can't create anything new that is useful.

I'm voting to close this question as off-topic because this is a polemic, not a question.

Is evolution a fact?
Let's start with a little bit of semantic.
In lay terms, it is easy and pleasant to just say it is a fact but the reality is that there is no fact in science discoveries. Hence, evolution is not a fact. Evolution is a theory in the scientific sense. In other words, evolution is a set of hypotheses that are extremely strongly supported by evidence.
Have a look at Is evolution a fact? for more info about this semantic.
Do gene duplication occur?
Your question is based on the false claim that gene duplication do not occur. This is simply wrong. There are thousands of evidence of gene duplication.
Evidence of gene duplication with neofunctionalization (that is the duplicated gene take a new function) are rarer but still very common. Consider for example

Qian and Zhang (2014) review evidences of gene duplication with neofunctionalization in the the Saccharomyces (yeast) genus only.
Beisswanger and Stephan (2007) as well as Calvo-Martin et al. (2017) review evidences of gene duplication with neofunctionalization in the the Drosophila (fly) genus only.

In fact, tandem duplications also occurred in the Lenski experiments (Blount et al. 2012)
Gene creation
There is a simple logical fallacy in your argument. When you say

After about 31,000 generations there was a mutational transfer of one pre-existing gene(citT) from one location to another which resulted in the ability of E.coli to grow on citrate under the oxygen-rich conditions.

The claim refers to a tandem duplication. Therefore, this claim seems to suggest that "gene creation" and "gene duplication" are different things. In fact, we never use the term "gene creation" in evolutionary biology. We talk about gene duplication and neofunctionalization. Neofunctionalization is the process by which a gene takes a new function, different from the ancestral gene before the duplication. But it is essentially the same thing. Gene rarely (if ever) come to existence all of sudden out of nothing with a single mutation. In general, gene duplicate and then slowly diverge, one gene taking a new function. This is how the number of genes (and the number of functional genes) can increase eventually through time.


text:
What percent am I?
*If my Great Great Great Great Grandma was one hundred percent Hispanic what percent am I? I'm unsure of what percentage in this ethnicity I would be.

You need to include information about all 64 of them before one can answer. If for example the other 63 are each 0%, it needs to be included in your question.

That depends on which genes are passed on with each generation, all we can assess from the given information is most likely average estimated percentage of your ancestors DNA you carry assuming no other sources, which would be 0.5 raised to the 6th power. however these assumptions are rarely true.

Interpretation of the question
How do you define "being xth percent hispanic"? In a simple conversation, when people say that they are 25% hispanic (or any other etnic group of course), they just mean that they have one grand parent that was born in a clearly hispanic community/country and that all the others were born from completely unrelated etnical background.
Answer
You would be $\frac{1}{2^6} = \frac{1}{64}$ hispanic.

OP did not mention anything about the other 63, could be a trick question! :-)

@uhoh I think I made clear that I was making this assumption in my answer.

25% could be one grandparent... or two great-grandparents, or four great-great-grandparents...

one percent as the OP indicated


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How is Na concentration re-established after action potential
I understand that the repolarization is because some K+ chanels are opened with the action potential. But whats happens with the sodium chemical gradient that is needed for a new action potential? Are there further Na-K pumps in the axon membrane?

Na+/K+ pumps are extremely ubiquitous. I recall reading that 1/3rd of an average cell's energy budget goes to maintaining that gradient, with neurons bringing this up to 2/3rds.

Yes, there are Na-K pumps all over.
However, it is important to recognize that ion concentrations change very little during action potentials. The change in membrane potential is due to changes in ion conductances, very few ions actually flow. It is still necessary to maintain concentration gradients over many many action potentials, but the change in concentrations during the course of a single action potential is negligible.

Probably too late to ask but I'd love an explanation for the downvote.

No not too late. Just a lack of sources. Also the fact it's a four liner makes it a bit of a content less answer. Ping me once updated. Happy to upvote.

Heck, the question is quite poor too. Poor question, mediocre answer. I'll remove the downvote.

@AliceD If you want to merge it with https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne that could be done, I like my answer better there anyways. Might need to make a new canonical answer and question to fit all those types of questions though, because there are a variety of questions people ask that deserve basically exactly the same response.


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Feeding behavior of organisms that prey on microorganisms
Is there a specific term for organisms that feed on micro-organisms?


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Identify Bronze Coloured Beetle
Spotted this beetle on Morfa Nefyn, a beach in North Wales, UK. The beach is a mixture of sand and stone, with large sandy cliff faces and rocky outcrops.

The beetle was about 3 to 5 mm or so long, running around on the rocks at the edge of a rock pool (not in the water though!), on a warm sunny day. It was moving are quickly, but not really fast, maybe around 1cm per second.
I've seen them on the beach before and sure I know what they were called but can't for the life of me remember.

I'm reasonably sure you have a Ground Beetle (family Carabidae) here, but I don't know the British complement of that group, so going deeper isn't an option for me.

Amara aenea (Common Sun Beetle)

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Cutting dna using restriction endonuclease
Genomic dna is digested with alu 1 which is a four base pair cutter. What is the frequency with wich it will cut the dna assuming a normal distribution of bases.
(this is not a homework)

I guess it is the probability of getting the 4 specific base pair in a row which is 1/4 1/41/4*1/4.

You can teach yourself to answer this type of question using this resource which I wrote some time ago: https://www.mvls.gla.ac.uk/Teaching/SLS-FTB/ren.html

Welcome to Biology.SE. I think this question would be better on-topic on math.SE.
Assuming the chromosome is either 4 bases long or infinitely long, then the answer is simply $\left(\frac{1}{4}\right)^4$. However, chromosomes are not infinitely long so the result should be (negligibly) lower than $\left(\frac{1}{4}\right)^4$. If chromosomes are only 3 nucleotide long, then of course, the probability will be $0$. If it is 4 bases long the probability is $\left(\frac{1}{4}\right)^4$. If it is 5 bases long the probability is $\frac{2}{4^5} = \frac{1}{2}\left(\frac{1}{4}\right)^4$.
Consider this numerical approximation, to ensure the result is correct with this simple one liner in R
n = 1e7
length(gregexpr('abcd', paste(letters[sample(1:4,n,replace=TRUE)], collapse=""), perl=TRUE)[[1]])/n
[1] 0.0039041

which is really close to $\left(\frac{1}{4}\right)^4 ≈ 0.00390625$.
So, in a genome of 3 giga bases, that represents an expected $\frac{3\cdot 10^9}{4^4} = 11,718,750$ (or ~11 millions) such locations where Alu 1 can cut.

Remi.b what is the boundary effect.  Btw thank you

@user7635691 I edited the answer to add some info on that.


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Can you use a cell in meiosis to create a karyotype?
Why might it be problematic to use a cell undergoing meiosis to create a karyotype?

Yes, you can, but it's way more difficult.
First of all, in order to see meiotic chromosomes, you need to colect young floral bud in the right stage of development (not too young, since you don't want microspore mother cell, and not too old, since you don't want polen), and that's not that easy.
Then, once you found the right stage and made a slide, you need good knowledge on all the phases of meiosis to understand what you are looking at. Bivalents and translocation rings can make it very difficult to really understand the chromosomes set you have in the cell, so you need a good sized sample and a lot of observation and analysis. If the species you are analyzing has small chromosomes, it's even more difficult to understand what you are looking at.


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I'm trying to unserstand Yamanaka's iPS cells paper
Can someone please explain to me what is the beta-geo cassette and why is it used? I understand that it was inserted in the Fbx15 gene, and this gene is present in ES cells, and I believe this cassette is used as a marker of the Fbx15 locus, but why does it have resistance genes (beta-galactosidase and neomycin), what are they resistant for? What is their role? Thanks!

This question is incomprehensible as it stands. If you ask a question relating to a specific paper, not only should you give a citation but describe the system the system you do not understand. Please take the guided tour and read how to write a good question for SE Biology.

Suppose you want to insert a cassette in a gene.  How will you know it is there?  What if only a small percentage of cells are successfully transfected?  What if your reagents were bad.  You do not want to waste time on cels that did not take up your cassette.
Those resistance genes are for detection of the presence of the cassette in a cell (or colony derived from a single cell).  You can have other things ride along with your cassette that will let you detect its presence.  Neomycin resistance: if you grow the cells that you have engineered in the presence of neomycin, only the ones that successfully got your cassette will live because the cassette gave them resistance.  All the ones that did not take up the cassette, or took it up wrong will die.
An active beta-galactosidase gene can work on a substrate to make a blue color.

An active enzyme may be detected using X-gal, which forms an intense
  blue product after cleavage by β-galactosidase, and is easy to
  identify and quantify.

Again this lets you detect cells (or colonies of cells) which have successfully taken up your cassette.


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Dyes that won’t bind to dna
I am looking for a dye that won’t bind to DNA. I want to add dye to proteinase K to make is visible when adding to clear buffer liquid samples. I need it to not bind to the DNA so it will be removed during the purification process. Or a dye that will not show up later under fluorescence during processing.
Thank you!

You may try Crystal violet. This dye is also intercalating with DNA, though it is not fluorescent as far as I know. Disadvantage is that the dye has a low sensitivity.


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How do the bacteria producing bacteriocins protect themselves from it?
Whenever there is Col plasmid in a bacteria it will produce bacteriocins which will kill other bacteria around it. Why will the bacteriocin not kill the bacteria which has produced it? How does the Col plasmid also help protect the bacteria from its own bacteriocin?


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Why ions created in our body doesn't give any sensation of electric shock?
We know almost every cell in human body uses ions specially nerve cells , still why we are not getting shocked by those ions ?

Curiosity is an excellent thing, if you want to know more about nerve transmission and the general functioning of the nervous system, you're going to need to do some research on your own. By all means ask questions here, but once you've done some research yourself and understand a bit more about what it is you're asking. The Wikipedia article on the subject has lots of background and many links to follow, I'm sure you'll find it very interesting.

Quite apart from the fact that those ionic potentials are what we feel WITH, they're on the order of 70-80 millivolts.  Would you expect to be shocked by say a common 1.5 volt battery?  Or even the 12 volts of an ordinary car battery? Even the ordinary sort of static electricity shock, such as you might feel from stroking a cat on a dry day, can be thousands of volts.

Hi , I also want to know how this ionic small electrical signals transforms into a something sensible , like light, sound, touch etc . We don't feel any current , we feel colors , cry of a baby etc . Why is that?

@Koushik Pal: The only real answer is that nobody really knows.  We know a good bit about how stimuli - light, sound, pressure, &c - get transformed into nerve impulses (which BTW aren't really electrical signals, they're waves of membrane depolarization along nerve fibers), but almost nothing (AFAIK, anyway) about how the brain converts them into the various qualia that we experience.  It's a queston that exists in the terra incognita between neurobiology and philosophy.  As for feeling current, ask how the 1.1-1.5 volt currents of your CPU got transformed to this text :-)


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Why we can't feel the different parts of ear during hearing which is mentioned in all biology books?
We can't feel our outer ear, middle ear and inner ear during hearing something. Why is that such a complex phenomenon is happening all the time but still we don't have any clue regarding that in our practical life?  We just get the sensation of hearing something and get no sensation/feeling how  different parts of our ear work all together .why all these happening within our ear and we never conscious about them ? In fact , we can know them only after studying biology.

Can you think of a benefit we would gain? I can see only drawbacks, like "investment" in additional sensors and extra processing.

Going to be productive instead of posting unhelpful snarky comments and downvoting.
You can only perceive what you have nerves for. Considering humans are unaware of all the rattling going on between the eardrum and inner ear, the only logical explanation is that there are no nerves in the region made to perceive said rattling.

That's not quite true actually, the brain is really good at filtering out / ignoring unnecessary (mostly constant) sensory input. For example there are blood vessels above the retina, which you normally can't see (I think with a quickly moving light source or something like that you can make the shadows visible)

Your comment isn't quite true actually, tell that to the many people living with chronic pain. I'm sure their brain is doing an excellent job at filtering out or ignoring it. /sarcasm

I didn't want to say that the brain filters out all constant (sensory) input (pain is different than normal sensory input anyway), just that it can do it - therefore the 'logical conclusion' that any area we don't actively notice doesn't have nerves is wrong.


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Why we can't feel our internal organs?
We have lungs,kidneys, stomach etc.But why we can not feel them consciously?

We do feel some sensations in the internal organs; it depends on the distribution of the sensory receptors in them.
TOUCH
Receptors for touch are in the skin, outer ear canal and eardrum, cornea, nasal cavity, mouth, throat and upper third of the esophagus, trachea and bronchi, vagina and anal canal, but not in other internal organs. For example, you can feel the inhaled foreign object in the bronchi (cough reflex), but you do not usually feel the movement of the food through the gut.
On the other hand, you can feel the distension of the urinary bladder or rectum. Distension of other hollow organs may be perceived as pain rather than just distension.
TEMPERATURE
Temperature receptors are in the skin, cornea, tongue and urinary bladder (Wikipedia), liver and skeletal muscles (ScienceDirect).
PAIN
Pain receptors (nociceptors) are in the skin, surfaces of the joints, joint capsules, synovial membranes and ligaments, tendons, blood vessels, periosteum, endosteum; other organs, such as the gut and muscles, have fewer pain receptors (Health24.com, McGill University).
Within the skull, pain receptors are in the pia and dura matter and their feeding vessels, and small cerebral vessels but not in the brain parenchyma (PubMed, McGill University). This explains why brain tumors cause pain only when they invade blood vessels or other pain-sensitive structures or when they result in increased intracranial pressure (Hopkins Medicine).
In the hollow organs (esophagus, stomach, intestine, gallbladder and bile ducts, bladder, ureter, urethra, uterus) pain can be due to their distension (ScienceDirect). This is why a stone in an ureter can cause pain
 (Clinical Methods, NCBI).
In the muscular organs (the skeletal muscles, heart, stomach, uterus, intestine) pain can be due to ischemia (WebMD).
In the parenchimal organs (liver, spleen, lungs, pancreas, kidneys), the pain does not arise from the parenchyma, but from the blood vessels in them or from the distension, inflammation or injury of their capsules or membranes (Scielo.br). This is why cirrhosis with a shrunk liver usually doesn't hurt, but hepatitis with swollen liver (and hence distended capsule) does (MedicineNet).

note much of our digestive system has some of those, temprature and pressure mostly.

@John, in most of gastrointestinal part (except in the mouth, throat, upper esophageus, rectum and anus), you do not feel food or hot water or normal (physiological) distension.  You can feel pain from excessive distension, as I mentioned.

I updated the answer.


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Can Neurons be connected in Series and will that pattern create huge voltage in human body?
We have learned in Physics that when multiple voltage sources are connected in Series , the resultant voltage becomes the summation of all voltages .
Now, my question is - Can Neurons be connected in same pattern and if it's possible , can let's say billions of neurons connected in Series , create a huge voltage in the body?
also , can the resultant voltage thus created become harmful for human body as an electrical shock?

In a typical nervous system, no, that's not how neurons are connected at all. Neurons have a voltage across their membrane, a potential difference inside versus outside of the cell. A "connection" between neurons either involves a chemical synapse where there is a gap of "outside" between the two neurons that neurotransmitters are released into (so relative to outside the potential is zero between the neurons) or electrical synapse where the insides of the neurons are directly connected (so relative to each other there is no potential difference). Think also of all the other surface area of two connected neurons: to have an accumulating voltage these surfaces would also need to maintain that full voltage across the membrane. I would recommend trying to draw out a circuit diagram along the whole membrane of two connected diagrammatic neurons and I think you'll discover the problems quickly.
However, the configuration you describe is roughly how an electric eel operates to generate voltage (particularly for a strongly electric fish that is capable of damaging shocks), not with neurons exactly but with a special electric organ.


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What is the neural coding of rod and cone cells?
In Rushton's paper on the Principle of Univariance, he states:

Thus, though the rod input has two variables, wave-length and energy, the output differs only in one respect, namely 'brightness'.

However, as far as I understand, a photon can only vary according to one dimension, namely wavelength (vibrational energy), because the wavelength and energy of a photon are interdependent.
This suggests then that the input to a cone cell, for brightness to be perceived (i.e. the intensity of light), must be a beam of photons, so that the input can vary in wavelength and amplitude (does this equate to the number of quanta being absorbed by the photopigment per unit of time?).
My question, then, is how can a discrete event (the changing of shape of a photopigment) encode a continuous value (i.e. intensity)?

Indeed, brightness is a matter of photon count.
In any given rod, there are numerous photopigment molecules. There are about 1 billion rhodopsin molecules in any given rod, so although a change in conformation of any single rhodopsin molecule is a discrete event, you can consider the fraction of 11-cis- versus all-trans retinal (a photoreceptor's initial readout of brightness) to be effectively continuous, even more so because there is a <1 probability of a photon of light being absorbed by any rhodopsin molecule, so the discrete measure itself is an approximation of the 'actual' brightness/photon count.
Although it isn't perfectly analogous, because here we are talking about proportions rather than actual bitwise encoding, consider that computers are also able to represent fairly continuous values, but they are still always discrete approximations to those continuous values. A 24-bit computer monitor, for example, can actually only display 256 different intensities for each R, G, and B color stream (8 bits each).
The principle being discussed in the paper you describe is that once a rod (or cone) absorbs a photon, it loses any information about what the wavelength was, only that it was sufficient energy to activate the rhodopsin in that photoreceptor. There are several other questions and answers here on Biology.SE that discuss how wavelength (i.e. color) information can be extracted by differential activation of different cone types, for example:
Why can cones detect color but rods can't?
How do our eyes detect light at different frequencies?


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Can one conduct “novel” research without an advanced laboratory? Has it been done by school pupils?
I want to conduct an experiment but as a secondary school pupil I will be using my school’s laboratory and to make novel or interesting discoveries, wouldn’t one need advanced equipment, a prospect which is not feasible for one of my station in life? I want to know if anybody has done a simple experiment and discovered anything new? Thanks.

Do you mean a groundbreaking discovery? That would be hard. But smaller ones that built upon others works are really feasible.

@Charles It is about science but since I wanted to experiment in Biology I posted it here.

I would advise to conduct a field experiment. Field work typically requires many eyes (school pupils) and not necessarily a lab.

I can point to two published papers in which students performed useful experiments.

The present study (on the vision of bumble-bees) goes even further, since it was not only performed outside my laboratory (in a Norman church in the southwest of England), but the ‘games’ were themselves devised in collaboration with 25 8- to 10-year-old children. ... They also drew the figures (in coloured pencil) and wrote the paper.
Principal finding ‘We discovered that bumble-bees can use a combination of colour and spatial relationships in deciding which colour of flower to forage from. We also discovered that science is cool and fun because you get to do stuff that no one has ever done before. (Children from Blackawton)’.

--Blackawton bees

As part of a high school class project, influenza sequences with possible errors were identified in the public databases based on the size of the gene being longer than expected, with the hypothesis that these sequences would have an error. Students contacted sequence submitters alerting them of the possible sequence issue(s) and requested they the suspect sequence(s) be correct as appropriate.

--Sequencing artifacts in the type A influenza databases and attempts to correct them
You'll notice that both of these projects were guided by "professional" scientists. The biggest problem with doing your own experiments is that you're very likely to simply repeat something that's already done, or else do something that's not useful or is trivial. It's very difficult even for professional scientists to have a reasonable grasp of even a very focused field of science, and for someone outside the field to try to understand what has and hasn't been done, and what is and isn't considered interesting, is nearly impossible.

Thanks. I am not sure I will be allowed to do a data-based project for the science fair though.

All kinds of interesting stuff you can do.  How novel it is depends largely on your approach.
While it didn't lead to a paper, I heard the following story from a microbiologist an New Mexico State. I think it was second hand then.
School loses it's science teacher.   It's a small college town, and it was only a part time position. One section of biology is for "kids who are good with their hands" a euphemism for ones not on the college track, the dummies.  They take a lot of shop, industrial arts etc.
They hire a grad student from the local college to fill in.  The principle tells him that if can just keep the dummies quiet that's sufficient.
Grad student goes away and thinks about this.
Comes in first day of class with a mouse trap.  Doesn't say a word.  Sets the trap, then with a pencil nuzzles the trigger until SNAP.  Makes choking sound.  "Dead Pencil"
"As you can see, this is a trap for getting rid of mice.  But it makes the mouse hard to reuse.  I want a live trap.  I want a trap that will catch a mouse without hurting it. How do we do that?"
The rest of that class was spent brainstorming ideas.  At the end of the period he gave each kid a trap.  "Make a live trap."
Most of them came with traps the next day.
They went into the rough country behind the school and set the traps.
Next day some of the traps were gone.  Trap and all.  Coyotes thought they were box lunches.  The ones that were alive  were anesthetized, banded, sexed, weighed, and released.
The quality of the traps got better.  Fewer mice died.  Less bait used with no mouse to show.  Some of the kids had a half dozen traps.
He made them pool their data and make a map of every trap, and the distances to other things.  Trees, grassy areas, bushes.
After a couple weeks he taught them how to determine their age.
As they accumulated data they started catching some mice that had already been banded.
By asking questions he got the idea of sampling to them.  Based on the number of banded ones to unbanded ones, they could figure out how many mice there were out there.
He had them plot where the 2 and 3 time mice were caught.  From this they figured out how big a world a mouse lives in -- what was their territory.
They kept a few in the lab, and the kids watched them.  Watched them mate, and later deliver litters of pups.   They weighed pups.  Weighed mom.  Measured the food they ate.  Figured out how much food it would take in the wild.
Some of htem asked if wild mice would behave the same, eat the same.  "Good Question.  How would you find out?"
Often when they caught a mouse, it had been in there long enough to crap.  He taught them how to analyze the crap for parasite eggs.  He showed them lice, and fleas.
By mid winter they were doing all kinds of stats.  Since they were 'good with their hands' their math was chequebook and carpenter math.  He had them calculating variance, and correlations.
This is solid science.  Papers?  Probably not.  You'd have to find something different from the literature.  But as a teaching or learning exercise it's first rate.
There are lots of critters out there that we don't know a lot about.
Google "Citizen Science" for more ideas.  Locally we have a prof that crowd sources climate change indicators over western Canada.  She has a web site where you report when wild flowers bloom, when you hear the first boreal or chorus frog, when the first flight of geese with more than 12 birds goes overhead.  First tiger swallowtail.
Turns out that some of them don't correlate well with temperature.  Some do.  Then someone realized that this same dataset can be used to measure biodiversity, and see if the ranges are changing.  People near a sighting of X last year were asked to watch for it this year.  People were given a protocol for walking a known strip of land, and counting this and that.  If they couldn't id it they took a pciture with their phone, and said "30 of these thingies"  Prof had a grad student to turn 'thingy' into blazing meadow star.  Grad student asks people to stop in the middle of the strip and take 4 shots with their phone with the bottom edge of the image about 10 feet away.  From this and looking at grass seed head shapes, he gets an idea of what the relative population of different classes of grass are.
Citizen science.

The class of dummies doesn't have a happy ending.  Two weeks before the end of the year, the school inspector comes in, and sits in on the class.  The class is excited.  A lot of their mice got through the winter and they are seeing small mice -- mouse teenagers -- appearing in their traps.  The grad student is talking about reproductive success and population dynamics.
The superintendent goes to the principal.  "He's not teaching the state bio
curriculum."  Principal explains that no one has ever had this kind of success with the dummies.  "Doesn't matter.  He's not teaching the curriculum.  Fire him."


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What does 'per capita births and deaths' mean?
My book says,

If in a pond there are 20 lotus plants last year and through reproduction 8 new plants are added, taking the current population to 28, we calculate the birth rate as 8/20 = 0.4 offspring per lotus per year.

..

If 4 individuals in a laboratory population of 40 fruitflies died during a specified time interval, say a week, the death rate in the population during that period is 4/40 = 0.1 individuals per fruitfly per week.

What does per lotus per year, and, per fruitfly per week imply?

Please rewrite the quote. Images are not searcheable and can pose problems to visually impaired people

0.4 offspring per lotus per year means that each lotus produces on average 0.4 offspring every year.

Thanks! +1 You might want to comment on my answer if something is still unclear to you.

1 per 1000 capita is 0.001 per capita.


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Which organs in the body are responsible for measuring temperature?
As an instrumentation engineer, I have designed temperature control systems
capable of measuring and controlling temperature with a precision of 0.001K over a
wide temperature range.  I have always wondered how the human body maintains its
temperature within a fraction of a degree; specifically, where and how is the
temperature measurement done?

https://en.wikipedia.org/wiki/Thermoregulation#In_humans

http://en.wikipedia.org/wiki/Thermoreceptor

As @inf3rno said there are thermoreceptors (TRPV ion channels) that are responsive to temperature. They are involved in temperature sensation of the environment as well as the body itself. I am not fully sure if they are the sole temperature sensors of the body. Have a look at these articles: [1], [2] and [3]

Human thermo detection comes from a protein, expressed in high levels in the nervous system.
As per comments, there are a group of transmembrane proteins called transient receptor potential cation channel subfamily V (TRPV) ion channels that can detect temperature changes. Although the exact mechanism of the protein remains unclear, a study published in Nature 2010 showed that a protein called TRPV1 opens and closes to allow increased or decreased sensitivity to temperature change.
There is no specific organ that is responsible for temperature detection, however TRPV1 is expressed in high levels in the nervous system.


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Are added yogurt cultures harmful to the gut?
I have read somewhere that the live culture added to yogurt acting as "healthy" gut bacteria are actually synthetic and harmful.
Any truth to this? If so, what are some alternatives to getting good gut bacteria?

What do you mean with "synthetic bacteria"?

I have no idea what you mean by synthetic bacteria but please don't equate synthetic with harmful and natural with healthy. The most dangerous substances we know are 100% natural. Consider, for example, rattlesnake venom, hydrochloric acid and plutonium.

I'm not sure what you mean by 'synthetic' gut bacteria, so I can't address that. is yogurt harmful to the gut? I believe the answer is no.
Women (and their doctors) have long known that taking antibiotics can result in Candidia (a yeast infection). Physicians have been advising women taking antibiotics to eat yogurt with live cultures, including lactobacillus spp. and bifidus spp. In keeping with today's movement towards evidence based medicine, Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale: Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, Ineffective, and Insufficient Evidence to Rate.
The effectiveness ratings for (just) LACTOBACILLUS are as follows:
Likely effective for:

Diarrhea in children caused by a certain virus (rotavirus). Children with rotaviral diarrhea who are being treated with lactobacillus seem to get over their diarrhea about a half day earlier than they would without this treatment. Larger doses of lactobacillus are more effective than smaller ones. At least 10 billion colony-forming units during the first 48 hours should be used.

Possibly effective for...

Preventing diarrhea in children caused by antibiotics.
Preventing diarrhea in hospitalized adults. Drinking a specific beverage containing Lactobacillus casei, Lactobacillus bulgaricus, and Streptococcus thermophilus (Actimel, Danone) twice daily during antibiotic treatment and for a week afterwards significantly decreases the risk of developing diarrhea.
  -Preventing diarrhea due to traveling. Taking a specific strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle) seems to help prevent diarrhea in travelers.
Preventing diarrhea due to cancer treatment (chemotherapy). There is some evidence that patients with cancer of the colon or rectum have less severe diarrhea, less stomach discomfort, shorter hospital care, and require fewer chemotherapy dose reductions due to GI side effects when they take a particular strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle).
Colic in babies. Taking a specific Lactobacillus reuteri product seems to be more effective than using the drug simethicone.
Lung infections. Children ages 1 to 6 years who attend daycare centers seem to get fewer and less severe lung infections when given milk containing lactobacillus GG or a specific combination product containing both Lactobacillus acidophilus and Bifidobacterium (HOWARU Protect).
Treating a bowel condition called ulcerative colitis. Some research suggests that taking a specific combination product containing lactobacillus, bifidobacteria, and streptococcus might improve symptoms.
Treating irritable bowel syndrome (IBS). There is some research showing that certain strains of lactobacillus, but not others, can improve symptoms of IBS such as bloating, and stomach pain.
Treating vaginal infections caused by bacteria (bacterial vaginosis).
Treating and preventing eczema (atopic dermatitis) in infants and children who are allergic to cow’s milk.
Helping prescription medications treat Helicobacter pylori (H pylori) infection, which causes stomach ulcers.
Treating diarrhea caused by the bacterium Clostridium difficile.

Though some of the recommendations are for specific probiotic formulations, one can achieve similar results by reading yogurt packages and mixing types to assure coverage with the proper bacterial spp.
National Institutes of Health


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Earliest and latest onset of Huntington's Disease(Chorea)?
Huntington's disease can hit at any age, although it tends to hit middleaged people most often. What is the youngest and oldest person that has exhibited Huntington's?
Clarification: By oldest I mean with no prior symptoms until the age.

Huntington's disease may become symptomatic starting from as low as 2 years old [1] and rarely after 55 years old [2] (yet there is evidence of onset at 65 years old [3] and even more according to newer studies).

Figure: Copyright © 2004, The American Society for Experimental NeuroTherapeutics, Inc.
Richard H. Myers. Huntington’s Disease Genetics. NeuroRx. Apr 2004; 1(2): 255–262. doi:  10.1602/neurorx.1.2.255. PMCID: PMC534940
Factors [4]:

CAG number (65%-71% of the variance in age of onset)
siblingship (11%-19%)

[...] paternal age is negatively associated with age at onset of HD (Huntington's disease), particularly among subjects who inherit the mutant gene from grandfathers [5].

References:

Huntington's Disease Society Of America. What is Huntington's Disease (HD)? Available from http://www.hdsa.org/about/our-mission/what-is-hd.html (accessed 26.10.2014)
National Institute of Neurological Disorders and Stroke. Huntington's Disease: Hope Through Research Available from http://www.ninds.nih.gov/disorders/huntington/detail_huntington.htm (accessed 26.10.2014)
Myers RH, Madden JJ, Teague JL, Falek A. Factors related to onset age of Huntington disease. Am J Hum Genet. 1982 May;34(3):481-8. PMID: 6211092. Full text available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685335/
Rosenblatt A, Brinkman RR, Liang KY, Almqvist EW, Margolis RL, Huang CY, Sherr M, Franz ML, Abbott MH, Hayden MR, Ross CA. Familial influence on age of onset among siblings with Huntington disease. Am J Med Genet. 2001 Jul 8;105(5):399-403. PMID: 11449389. Available from http://www.ncbi.nlm.nih.gov/pubmed/11449389
Farrer LA, Cupples LA, Kiely DK, Conneally PM, Myers RH. Inverse relationship between age at onset of Huntington disease and paternal age suggests involvement of genetic imprinting. Am J Hum Genet. 1992 Mar;50(3):528-35. PMID: 1531729. Full text available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684271/

Any exact dates? Like a child of 612 days exhibiting it? Or a woman of 72 years?

I first experienced Huntington's Chorea at 7-1/2 years of age. My father took me to Vanderbilt Hospital in Nashville, TN where it was confirmed by testing. I am now 71-1/2 years old, and have suffered Rheumatic Fever, a stroke, 4 heart attacks, and atrial fibrillation, along with many other less serious diseaes. I still have occasional bouts of Chorea, but am leading a mostly normal life.  During my earlier life at age 60, I completed a Bachelor of Science and an M.B.A. degree, so my reasoning faculties and ability to organize and study successfully are still intact. I may be on borrowed time, but don't worry about it.


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DNA linking number, twist and writhe
The image below is taken from a molecular biology textbook.
It is not clear to me that what is happening at the two writhe crossings matches up with the numbers provided.
Is there  a problem with this example? And if not, is anyone able to explain (without using Calugareanu's Theorem, i.e. $\text{Lk}=\text{Tw}+\text{Wr}$) why the linking number is $23$? When I give the two strands orientations and half the sums of signs of crossings, I do not get $23$.

Does this answer help?

@canadianer I understand how to compute Lk, Tw and Wr, but I think the linking number in this particular example is not as clear as any of those in your answer, and I am seeking to verify whether or not this example is correct. I am having trouble around the two places where there is writhe. I am also using a different (but equivalent) definition of Lk - the one which gives  orientations to the strands and signs to the crossings, as seen on the wikipedia page here: https://en.wikipedia.org/wiki/Linking_number

Oh I see. Actually that picture is awful since it shows all four strands intertwined at the sites of duplex crossover (which is not what happens).


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How do alcohols and aldehydes destroy the plasma membranes of bacteria?
I am interested in knowing why a 60-80% solution of alcohol (usually ethanol or 2-propanol) can effectively kill vegetative bacteria and fungi. I know that it can coagulate essential proteins like enzymes but the process has never been explained to me.
I'm also interested in knowing how aldehydes like the polymerized form of glutaraldehyde inactivates proteins and nucleic acids. Could someone with any insight / knowledge share what they know?

Alcohols are dehydrating - they remove water from the cell. And since cells need water to survive, this is lethal to bacteria. However, in order to work effectively, an alcohol needs the proper amount of time to penetrate the cell membrane of the bacterium. If the percentage of alcohol is too high, it will evaporate before entering the cell. Too low, and it will enter the cell but not be lethal. 70% alcohol turns out to be the most effective concentration for use as a surface disinfectant with many different types bacteria.


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Proteins in different organisms
I know that DNA is universal meaning that all organisms have the same 4 base pairs and also that the same codons code for the same amino acid in all organisms. What I am wondering is that say humans and bacteria and rats all have the same gene which codes for the same metabolic enzyme. Will the amino acid sequence of that protein enzyme also be the same in all three of those organisms? And that specific gene segment will also have the exact same base pair sequence in all three organisms too correct?

Welcome to Biology.SE. What do you mean by "same gene", if not "same base pair sequence"?

Before I go into answering your question, I just want to correct some mistake you have. Although DNA nucleotides (bases) are (almost) universal, the genetic code is not - there are organisms that use a slightly different genetic code. See here for example. Moreover, even the mitochondria in humans (and vertebrates in general) uses a slightly different code.
Now, to answer your question, it all comes down to evolution. Humans, rats and bacteria all have a common ancestor somewhere in our evolutionary past. Let's assume that this ancestor had some crucial and universally-useful gene. Since then, human+rat diversified from bacteria and then from each other, but all 3 species kept this gene, since its function was absolutely necessary. However, mutations were acquired along the way in each lineage. These mutations can be random and may not even have an effect on the amino acid results (synonymous), or they can be a result of natural selection and have an effect on the amino acid sequence (non-synonymous). In many cases, the different life styles and selective pressures acting on each species lead to rather different nucleotide and amino acid sequences. So to sum up, you can expect DNA, RNA and protein sequences to be different, although more similar between human and rat than bacteria.
In fact, the concept of the "same gene in different organisms" is somewhat wrong. As I explained, this is not the same gene, but you may say that it is homologous between the species, and more specifically orthologous.

Alright, but say that 2 organisms do have the exact same gene for some protein enzyme. I know there can be mutations and all and this is unlikely, but say that happens. Will those two widely different organisms have the same DNA sequence for that gene and hence the same amino acid sequence, resulting in the same protein? Or can the exact same protein enzyme be coded from different DNA sequences in different organisms? I'm thinking that in order to be the exact same protein, the gene sequence MUST be the exact same as well but I'm not sure.

Just to make sure I understand: you're asking something like "Suppose I see that two organisms produce the exact same protein (same AA sequence), does that mean that the respective DNA sequence is the same?" Is that correct? If so, then the answer is of course not! Take a look at the genetic code table. How many ways are there to code Proline? Glycine? There are numerous way to code the same protein. On top of that, there is splicing, RNA editing, protein processing etc that could be going on and different between the organisms.


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Does this procedure for extracting DNA from strawberries work?
I wanted to try out this experiment for extracting DNA from strawberries that can be done at home:
https://www.stevespanglerscience.com/lab/experiments/strawberry-dna/
However, while doing a bit of reading, I came across this article:
http://www.ncbe.reading.ac.uk/PRACTICALS/PDF/DNA_isolation.pdf
It states that, "Although these fruits [kiwi fruit, bananas and strawberries] seem to yield copious amounts of DNA, the substance produced is in fact little more than pectin."
Are they right? How could you tell that what you've extracted is actually DNA?

I have taught that experiment using strawberries as a TA. If I remember right, we used SYBR Gold to detect DNA, though that could have been a different experiment.

The extraction protocol described in the first article is a standard DNA extraction protocol. I've used variations on this method in the lab (with some refinements) on other types of cells at least hundreds, if not thousands, of times. The "strawberry" experiment is very popular for classroom demonstrations, especially at the middle-school and high-school levels, because it's visually interesting and uses commonly available reagents. While these reagents aren't laboratory-grade, they're more than sufficient for a basic extraction of DNA.
I can't think of a scientific basis for why the author in the second article would claim that the extracted substance is "little more than pectin". Since he didn't provide data, or a reference to any data, it's hard to know what he's basing his conclusion on.
It's definitely possible that the DNA is pulling down a certain amount of cellular proteins during the alcohol precipitation step (the final step). This is why in a lab setting you typically perform a few more steps to "clean up" the DNA and remove any co-precipitating proteins. This would be essential if you plan to do further analysis of the DNA, because protein contaminants can interfere with subsequent analyses, making the data unreliable. One exception would be if you're studying protein-DNA interactions, but that's a separate type of experiment.
I'm assuming this experiment will be done for/by beginner level students, as opposed to a college or graduate level class? If so, then for the purposes of a classroom demonstration, those extra purification steps aren't warranted. It's time-consuming, and it would be very boring to watch... As is the case with most labwork. :-) Even if you perform those additional steps, the purified DNA is often precipitated with alcohol again, and it's visually similar to what you saw in the first alcohol precipitation, just a bit less opaque. Probably not something most students would notice or find interesting.
Either way, it's entirely acurate to say that the strawberry experiment is extracting DNA. You could always explain that the DNA might have cellular proteins binding (or "sticking") to it, and that a few other steps would have to be performed if you wanted to analyze the DNA in a lab setting, because the proteins would interfere with DNA analysis. This would also give beginner-level students an introduction to the fact that DNA and proteins interact with each other.
Hope that helps!

Thanks for the info! I was interested in doing the experiment at home for fun, but if it were indeed "little more than pectin", that would have been a bit disappointing.

No problem! Glad you're interested in this! Btw, you can isolate your own DNA (from cheek cells, aka "buccal cells") using a similar method. Here are two protocols. Either one should work fine: https://www.livescience.com/37252-dna-science-experiment.html https://scienceaces.wordpress.com/2015/06/18/biotechies-bucket-biology-on-the-cheap-gatorade-dna-extraction/   I've done this with students before and they seemed to enjoy it. One student was a bit freaked out to see her own DNA in a tube. I told her to just be sure the feds don't get a hold of it or she'll end up in a secret database. ;-)


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Bistability vs bimodelity
In a systematic viewpoint, bistability refers to the existence of two stable equilibriums for a biological system. But, I don't understand the difference between bistability and bimodality. In both cases, the system should have two different behaviors, so I guess bistability is a specific case of bimodality, in which either of the system's behaviors might not be stable. Is this a valid distinction between these terms?

I am not a big system biologist, so I am not really used to the terms used in this discippline. In statistics bimodality simply refers to the existence of two peaks in the frequency distribution of a variable. Do you think you could add a quote just so that we have a context in which those terms are being used?

Bistability referrers to two coexisting stable conditions (if you disrupt they will tend to restore to one of those two areas) and has a slightly broader application it can also involve chemical stability for instance. Bistability includes the element of stability (obvious in the name) if disrupted bistable condition tend to return to one of two stable configurations. Enzyme stable configurations could be another. Galapagos finch beak shape during wet years is the one I think of but that could also be argued as tri-stable. to go really simple you can even think of a clicky pen, fully clicked is stable and unclicked is stable but anything else immediately moves to one of the other states.
Bimodal just means the distribution has two peaks, they may or may not be stable, many are only temporary. It is a much simpler concept.
Another way to consider it is bimodal is purely descriptive while bistability has a predictive quality.

It is a little unclear to me the distribution of what has two peaks. That's why I think we would need a specific quote to discuss. Also, talking about bi-stability and sex. The variable to the system could be sex-ratio typically, in which, such systems typically have a single stable equilibrium at 0.5.

For the sex thing sure it all in how you describe it, as a variable in a population it is bistable but it can of course also be described as a ratio, or in a number of other ways. I t will just add confusion so I will delete it.  As I said bistability is Not a purely a statistical term unike bimodal. biochemical stability can be a good example as many enzymes will have two stable configurations with all the inbetween configurations being unstable.

To expand on what you said, bistability in the dynamics of a system can result in bimodality of the distribution of whatever the system does or makes.


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What is a 1-flowered raceme?
PlantNET describes the inflorescences of Daviesia acicularis as:

Racemes reduced to 1 flower

How is a 1-flowered raceme different from a single flower?


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Animal reproduction when resources are scarce
(This question is aimed at animals that take care of their young, e.g. dolphins.)
As I understand it, most animals reproduce if possible. The only way they don't is because they run out of resources. I'm wondering how this shows up in practice:

Do they simply not have sex? If so, does this mean they don't have sex drive?
Do they conceive and then let their children starve to death?
Do they fail to conceive (that is, are there biological changes to a mother who's not getting enough food such that she is no longer fertile)?

Option #2 seems the least likely to me because presumably pregnancy involves a cost to the parent, and with resources already scarce this would be a waste; however the plot of White Fang does indeed involve this situation (I have no idea how scientifically accurate that book is however).

Rabbits reproduce when resources are scarce. They then eat their young. There are many more options than the three you present. Consider, for example, that nutritionally challenged females might not have an estrus cycle, which would prevent pregnancy. Humans reproduce when resources are scarce as well, and it does indeed take a great toll on mothers and children. But it happens anyway.

@anongoodnurse by the second law of thermodynamics, wouldn't it be more resource-intensive to produce children and then eat them? Not having an estrus cycle would be similar to option #3. As for humans ... I'd say that's out of the scope of the question.

Humans are animals, too, and where sex is concerned, dolphins are like us. So, not outside of scope imo.

Different animals use different strategies and all the three mechanisms are valid and there possibly are even more. Moreover, the laws of thermodynamics are applicable to particles and not organismal behaviour. Organisms need to choose the "theoretically most optimal" strategy for different reasons.

I think this is probably too broad to be answerable, for the reasons pointed out in the comments. From a selection standpoint, you have to consider that resource scarcity can fluctuate, and an organism that fails to mate today does not have an opportunity to take advantage of an increase in resources in some future months. There are also a limited number of opportunities to ever reproduce: for some animals, even those that raise their young to some extent, there is only one chance ever. Consider that, on average, a given individual will produce ~2 offspring that grow up to successfully breed.

@BryanKrause I'm not thinking about that though - in this question I'm flat out assuming scarce resources, and wondering how that translates to lack of population growth.

This is actually a comment, but was not allowed to comment.
I think what you're interested is more in population dynamics and I think what you're really asking about is more in line with what system of  differential equations explains a network of animals and how their populations grow and decrease with the amount of resources and the species population.
I think the problem is that, there's actually no good model, because there are so many factors which seem to contribute to shifts.
@ MIT this year, they had a visiting prof from Tufts give a talk on this, and they're working on models, to try and describe this, and even HE- the prof said, yeah, it gets complicated even for two species.
I would recommend, that if you have time to read up on this?
https://sites.tufts.edu/hening/publications/ <--- a link to his publications
https://arxiv.org/abs/1710.01220
Also, this is probably more a question for the mathematics stack.

I'm not more interested in population dynamics unfortunately. This is a biology question, not one about differential equations.

@Allure - It's kinda sad that you don't recognize a good and helpful answer when given one. You think the user who answered isn't giving you a "biology" answer?

ThermoRestart, thank you for this insightful and helpful answer. I hope we get more answers from you.

@anongoodnurse considering I asked the question you'd think I'd know what kind of answers I'm looking for. They are of the kind that "so-and-so species adopts strategy #1, this one does #3, nobody does #2, and there's #4 which you haven't considered". This answer is inapplicable to what I had in mind. I'm not going to downvote it, but I'm not going to accept it either.


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Why does the colossal squid range over only the Southern Ocean?
Wikipedia's article on the colossal squid gives the distribution as in the Southern Ocean only.
It makes sense for many animals found in the Antarctic to not also be found in the Artic even if the environments are similar, simply because there's no way for the species to get from the Antarctic to the Artic. However if colossal squids can range more than a kilometer under sea level, then by that depth, the ocean should look the same in every direction: it would be so dark and cold that there's no easy way to tell if one is on the equator or under the North Pole. In other words the squid should be found in every ocean, not just the Southern Ocean.
What is wrong with this reasoning?

Possible reason might be ocean currents. They impact migration and availability of food. Also, (mainly indirect) observation seems to be rare. Can we really say they don't occur elsewhere (maybe in smaller numbers, which makes observation less likely)?


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If sexuality is genetic, how did asexuality evolve?
If sexuality is genetic, then it stands to reason that evolution would strongly favor people who have children. In other words, heterosexuality & bisexuality should be favored, while homosexuality and asexuality should be disfavored and in fact eliminated by evolution. Why hasn't that happened?
I can find plenty of resources via Google for the evolution of homosexuality, such as this one, but not for the evolution of asexuality. Asexuality seems to pose a bigger challenge as well, since the lack of sexual attraction entirely should make it even less likely for asexual people to have children. Some of the explanations for the evolution of homosexuality can conceivably apply to asexuality too (such as "the genes for asexuality do other things"); still, I would like an authoritative paper/reference if there is one.

can you point to a reference that suggests that sexuality is in fact substantially genetic? i'm not disputing that you can find some signature of heritability, but for this variation to be selected upon, there should likely be a fairly strong genetic signal. furthermore, can you demonstrate that asexual/homosexual people have fewer children? this is less obvious than you seem to think it is, and it is also a necessary prerequisite

@MaximilianPress there's this that addresses both points for homosexual people. I have no sources for asexual people - it just seems natural, given what applies for homosexuals.

If 1% of a population is asexual, but can have children when they want to, or when a well positioned male wants to, perhaps that has a negligible or a positive effect on group success and evolution. https://external-preview.redd.it/Y28QUOGsV7qbq2YCfjF7u10-4BpujEdAXTetnKoR0xs.png?auto=webp&s=111feab8fe6d218ab006b83740a23744ce7ff259 For some reason, I think that Freddy Mercury was on the far right of that graph.

@aliential I don't understand - homosexual people can also have children if/when they want to, but they still have fewer children than the rest of the population. Presumably the same would also apply for asexual people.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Update:
See @Bryan Krause comment. Just because something exists (or equally, doesn't exist) does not mean that it was selected for or has any evolutionary relevance. Imputing selection to any particular state of affairs is usually bad reasoning without a lot of evidence.
I didn't do a good job of coming out and saying this in my answer.
My answer is best understood as answering the question: how could asexuality evolve under selection?
It does not at all address the question: DID asexuality evolve under selection (in humans)?
This second question is one for which the answer is probably "no". Without more evidence, we cannot say whether asexuality has any evolutionary/selective relevance at all.
Original answer:
I would suggest looking more into the evolution of social animals for which large proportions of the population is non-reproductive (or sterile). There are many such examples, with insects as the obvious case:

Contrary to widespread belief based on heuristic arguments of genetic relatedness, non-reproductive workers can easily evolve in polyandrous species. The crucial quantity is the functional relationship between a colony’s reproductive rate and the fraction of non-reproductive workers present in that colony.

I would suggest looking more into that paper and citations therein. The question to answer is whether an individual's labor can be more important than their gonads to the continuation of their genes.
As suggested in the wikipedia article on homosexuality that you link to in your own comment, there is a positive effect on female fertility from having homosexual family members ("kin selection"). Granted, what causal mechanism is behind this is likely difficult to sort out.
It's quite plausible that asexuality behaves similarly to homosexuality in this regard. Those authors want it to be a genetic factor driving both sexuality and fertility. But to me it seems a bit more parsimonious to posit that it's good to have more warm adult bodies around to care for/support children.
From a practical perspective, if grandparents with non-functional gonads can help raise kids (i.e. increase effective fertility of kin), why not asexual relatives too?

There is also https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont Not to say there is anything wrong about asexuality, but to say that the existence of a trait does not mean that the trait was selected for, and similarly, just because a trait does not exist does not mean that the trait was selected against, even if the trait is entirely genetic.

@BryanKrause that is an excellent point that I did not explicitly address. I'll edit.


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Are there limits to drug resistance?
It's well-known that indiscriminate use of a drug leads to resistance. My question is what the limits on resistance are. It seems obvious that there must be limits: for example I can hardly imagine a tiger evolving "resistance to bullets", and similarly I can hardly imagine a microorganism evolving resistance to heat treatment @ 1000 degrees celsius (surely its proteins must long denature before then).
Are there methods of killing microbes that cannot be resisted? If so, can we make similar cannot-be-resisted drugs?

You mean drugs that eliminate bacteria without killing the host, right? Otherwise every strong enough poison is a candidate drug :D

There are physical limits to the existance of life forms, wether temperature, pressure, osmolarity, etc. But these are usually physicochemical fields acting over a wide spatial structure. In the case of drugs, they are physically localized molecular entities. They are usually very tiny, even compared to the smallest microbes. Even though the genome of any microbe is finite and they could not, in theory, recognize the infinitely many drugs we can synthesize (assuming the simple case they need one gene per drug resisted), they can just evolve very generic mechanisms like preventing these molecules to get into the microbe, pumping them out of the cell, or other generic mechanism; with the same overall effect: preventing the drug from acting in the desired way.
The question you ask is very interesting, and it is the focus of some recent efforts and discussions among academics. Here you can find a recent article discussing the possibility of "evolution-proof" drugs. As you can see, the subject is not trivial.
Cheers,
Pedro

The article you link to discusses a very important and basic principle that you might include in your answer. In the absence of selecting pressure, the frequency of resistance shouldn't increase. Theoretically.

The link's dead ... any idea what the title was so I can try to find it?

I just updated the link. Depending on your situation, you might need to access it through SciHub (using its DOI).

In case I need it again, the paper title is "Targeting virulence: can we make evolution-proof drugs?" by Richard C. Allen, Roman Popat, Stephen P. Diggle & Sam P. Brown.


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Why do fat people and thin people get hungry at the same time?
Say a fat person and a thin person take breakfast at the same time. Around lunchtime, they'll both be hungry. Why? After all, the fat person theoretically has lots of body fat the body can consume instead, so the fat person does not have to feel hungry.

Consider that part of it is simply social conditioning.  People in western cultures are generally trained to expect meals at certain times.

I am not sure your statement is true, fat and thin people may not always get hungry at the same time. You cannot simply compare these two categories as they contain subcategories including people "feeling hungry" because of disorders related to their mental health, physiology, diseases,...
The term you are looking for is "appetite regulation" and reading the wikipedia page will give you an overview of this subject and why your question is too broad to be answered. https://en.wikipedia.org/wiki/Appetite#Regulation

I accepted your answer because it tells me that my question is poorly formed: instead of asking "which body needs energy", I should be asking "what governs appetite".


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Given a vaccine, can you deduce that a disease exists?
For example, if a scientist from 2018 found one of today's Covid vaccines, can they tell that it is a vaccine to a hitherto unknown disease, and therefore infer that Covid exists?
I'm guessing that the answer depends on the type of vaccine, in which case I'm interested in all of them.

@JiminyCricket. that sounds like the answer I'm looking for. (Although how can you tell it appears to be an inoculation of some kind?)

I'll write an answer.

The main giveaway that it's designed to produce an immune response would be the presence of an immunological-adjuvant:

a substance that increases or modulates the immune response to a vaccine.

Now, of course, adjuvants are used in cancer treatment, but the difference with inoculations for pathogens is that there'd be an additional molecule or set of them which triggers a specific immune response.
There are nearly a dozen types of "vaccine" for COVID and variants, the majority are focusing on making use of the spike protein of the virus to create a response, but there are some which are designed to create a response to the capsid proteins, i.e. the viral-shell. Neither the spike protein nor the capsid would be expected to be found natively existing in the human body.
This doesn't mean they all contain the spike protein (or any other target protein), the mRNA version for example is designed to induce the body's own systems to produce the spike.
Some contain an adenovirus - a familiar companion found usually in the mucus membranes of human populations causing a number of familiar respiratory diseases. This being also designed to induce the body to produce the spike protein and only that. They would be otherwise reproductively inert.
Some contain artificially produced virus-like particles which have some characteristic in common with the target virus.
The one producing arguably the broadest response would be the virus particles themselves, artificially cultured then inactivated before administration. This would be straight-up identify the virus that the vaccine is designed to combat. At the time of writing, these seem to have been primarily developed and deployed in China.

Thanks for answer. I take it the short version is yes - it's possible to tell that the unknown substance is an artificially produced vaccine. Do you know if it's obvious or if it's only obvious in hindsight?

I guess I didn't explicitly say, but yes. If the mRNA vaccine, we should have been able to identify that from about 1990 onwards as its development began in the 1980s. The rest is older and would be recognised. An exception might be the virus-like particles which resemble other things found in nature - like the substances found in the sting of some parasitic wasps - it might be suspected that we're trying to mind-control caterpillars if not for other clues like the adjuvant ;) @Allure


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Can you splice out the first and last exon from pre-mRNA?
I think the answer is no because there are no introns before the first exon or after the last exon, although I am not sure if this assumption is correct. Thanks!


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Can one type of bacteria cause several diseases?
If yes.
Does it change its shape in every disease, or does it remain in the same shape and cause several diseases?

If you are describing a taxon of bacterium, then it is definite that a bacterial taxon is capable of this, depending on your definition of disease. A pathogenic bacterium could infect two different host species (Mycobacterium sp. in fish and humans). Additionally, a particular pathogenesis may be determined by the site of the bacterial infection. For example, Staphylococcus aureus is often associated with cutaneous diseases (Staph infection) like dermatitis. It may also induce pneumonia and endocarditis, still retaining the same shape - a coccoid-type - and still cause several diseases.

Yes, one type of bacteria can cause multiple diseases.  For example:
"Rheumatic fever is caused by group A Streptococcus. This bacterium causes strep throat or, in a small percentage of people, scarlet fever. It’s an inflammatory disorder." [https://www.healthline.com/health/rheumatic-fever#causes].
The difference is in how the individual's immune system responds to the infection (and how the infection is treated).  Everyone responds a bit differently to the same infection.

"The difference is in how the individual's immune system responds to the infection (and how the infection is treated). Everyone responds a bit differently to the same infection." Can you support this with a reliable source?

I can give you some good examples:

Valley fever (a fungus disease that affects the lungs) is no more serious than a minor cold to some people, but kills some people.  Although malaria is a multicellular parasite, the fact that people with sickle-cell anemia (which is due to a particular genetic variation) are more resistant than other people shows that a victim's genetics can affect how a disease affects the victim.  Flu often affects certain age groups more severely than other age groups.

And, a classical example is the results of Europeans' introduction of measles to the native Americans: a disease that was a minor discomfort to the Europeans was deadly to the native Americans.

The example of group A Streptococcus causing strep throat sometimes, rheumatic fever sometimes, and scarlet fever sometimes is really perfect: the same bacterium affects different people differently.

Your opinions aren't what I mean by a reliable source, unless you can link to research articles you've written and which have been accepted by peer-reviewed journals. Or if you wrote a chapter on immunology in a textbook, etc.

Do you need research articles, or would you accept, e.g., a statement by the Mayo Clinic? [https://www.mayoclinic.org/diseases-conditions/rheumatic-fever/symptoms-causes/syc-20354588]

Or perhaps The Merck Manual: [https://www.merckmanuals.com/professional/infectious-diseases/gram-positive-cocci/streptococcal-infections].  A good counter-argument would be to assert that scarlet fever, rheumatic fever, strep throat, etc., are all the same disease because they are caused by the same Streptococcus pyogenes bacterium; but per [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299105/] which points out the vagueness of the definition of "disease", that would just be an opinion. The Merck Manual calls them different diseases.


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Why is it called Nematocyst "Battery"?
I was reading an article on Hydra where they mentioned Nematocyst Battery. I know that Hydra and other Cnidarians have nematocyst but why are they called Nematocyst 'Battery'?

Welcome to Bio. Can you add that reference?

sorry I cannot give you the reference right now. But i googled it and found this where the writer also called it the "Battery of Nematocyst" http://www.iaszoology.com/nematocysts/

Since cnidae are "single use" cells, and this costs a lot of energy, in order to regulate discharge, cnidocytes are connected as "batteries", containing several types of cnidocytes connected to supporting cells and neurons (from Wikipedia)

A battery generally refers to a series. E.g., a test battery is a (generally quite large) set of (related) tests. In this case you can replace "test" by "nematocyst" I guess. But I haven't looked at the link yet.

So it just means series and not related to energy source?


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Why only human have noticeable difference in face?
Our facial appearance is pretty much different from each other unless we are talking about twin. Credit goes to crossing over of chromosome. But why can't we distinguish between other animals of same species? Yes there are some very little differences but not that much clear and obvious difference like we have. Why is that?

So it's because we are human. Therefore  we can distinguish between two human easily?


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Why plants and animals are so different even though they come from the same ancestors?
All the documentaries I have watched, books I have read so far on the starting of life on earth only talk about animals. The very first life form on earth was bacteria. Then evolution took us this far. But what about the trees? They must also come from that single cellular bacteria. Since when they got separated from animals? What made them to be so much different than animals? Besides, apparently their evolution is very slow, isn't it? Why are they lagging behind in the race of living organism?

because the last common ancestor was a long long looooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooong time ago. (a quick google search shows estimates are around 1,600,000,000 years ago).

I strongly suggest reading through Understanding Evolution from the University of California, Berkeley. It will correct a lot of the misconceptions you have.

This question shows so much misunderstanding in evolutionary biology (no offense) that it is hard to fully answer. As @MattDMo suggested, you will benefit from having a look to an introductory course to evolutionary biology such as Understanding Evolution.

But what about the trees? They must also come from that single cellular bacteria

The Most Recent Common Ancestor (MRCA) of animals and plants was not a bacteria but single-celled eukaryote.
Once you'd have a look at the course Understanding Evolution, you might want to have a look at the tree of life on tolweb.org for example

Since when they got separated from animals?

The MRCA of animals and plants lived about 1.6 billion years ago.

What made them to be so much different than animals?

Time has passed and with time different lineages diverse through a number of different processes. By increasing your understanding of evolutionary biology (Understanding Evolution again), you will be able to understand these processes much better.
Note that while with time (1.6 billion years) genetic differences have accumulated between animals and plants, there are still a large number of similitudes. Some of these similitudes are also shared with other organisms such as bacteria for example and some are not shared with bacteria. Here is a short, non-exhaustive list of similitudes:

Both use DNA to store genetic information
Both use Adenosine Triphosphate (ATP) for transferring energy within cells
Both use lots of water.
Both have a cell membrane
Both undergo cellular respiration
Both undergo mitosis
Both undergo meiosis
Both have their DNA contained in a nucleus
Both have endoplasmic reticulum
Both have DNA organized in chromosomes
Both contain mitochondria
Both have histones

Note by the way, that I focused exclusively on similitudes that are caused by shared ancestry and not by convergent evolution.

Besides, apparently their evolution is very slow, isn't it?

The terms slow and fast are obviously relative. To discuss really how fast is evolution, you would need to know what evolution is and you would need to know a little more about the processes that drive evolution.
In very short and largely simplified: Evolution is a change in allele frequency (at a given locus) trough time. Such change occurs every second in a big population. However, the evolution of a large phenotypic trait that was previously completely inexistant may take much more time depending on how much genetic variance, you have to start with, depending on the mutation rate, depending on the number of mutations required, depending on the selection coefficient for each of these steps and depending on a number of different things.
So the answer to "How much time does it takes for evolution to occur" varies between a fraction of a second and infinity depending on what you mean exactly.

Why are they lagging behind in the race of living organism?

I don't understand this question. I don't know who is "they", I don't know what you mean by "behind" and I don't know what you mean by "the race of living organism".


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Why do some trees hold their leaves through fall and winter?
Why do some species of oak (Quercus spp.) retain their leaves through fall and winter?  I've found that these leaves are called marcescent leaves. There must be some benefit that the tree gains from this because it seems like it would increase the possibility of limb damage due to snow accumulation on the leaves.

Some trees only grow in places where there is no snow.

The trait might not necessarily allow for an advantage, but a few possibilities have been proposed:

Nutrient return to the soil when needed in the spring
Less palatability to grazing animals

Source:
 http://northernwoodlands.org/articles/article/why-do-some-leaves-persist-on-beech-and-oak-trees-well-into-winter


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Are there animal species in which the females expend more energy attracting males than in their offspring?
In general, males of a species expend a lot of energy attracting females.  There are many instances where males utilize much of their nutrient intake to produce antlers, tusks, horns, etc. to either attract females or compete with other males for potential mates.  Are their any instances in animals in which the females do this to attract males or to compete with other females?  If so, what features have the females evolved to win over potential mates and fight off competitors and what advantage is there for the species?
I'm aware of a few animals, such as the seahorse and jacana where the males invest more energy in the offspring, but I'm not sure that the females of these species expend some of the energy saved in the offpring and put it into attracting males or competition with other females.

On the risk of being hilarious? Humans.

One thing to consider here is the definition of female. Females are not defined by their genitalia, but rather, the size of their gametes. The animal with the larger gametes is the female. As such, her gametes are more valuable as a resource. Sperm are cheap and expendable. Eggs are precious resources. So this explains the difference. I kind of agree with skymningen's comment about humans. Human females DO spend more effort to attract mates. But they are more selective than their suitors, while men spend more time "seeking"

The reason why, in most species, males are competing to access females and females are choosy is due to Bateman's principle.

Bateman suggested that, since males are capable of producing millions of sperm cells with little effort, while females invest much higher levels of energy in order to nurture a relatively small number of eggs, the female plays a significantly larger role in their offspring's reproductive success. Bateman’s paradigm thus views females as the limiting factor of parental investment, over which males will compete in order to copulate successfully.

But there are exceptions to this general rule.
Fish
In many fish species (e.g. pipefish, scissortail sergeant and seahorses), males are choosy and females are competing. In these species, females deposit their eggs in a special brooding pouch that the male possesses. The male then has the energy cost of raising the offspring, while the female does not provide any parental care. As a result, males in these species must choose among competiting females for mates( Vincent et al., 1992)
Birds
In many bird species, there is bi-parental care, leading to competition among mates in both species. See the interesting case of Jacana jacana (Emlen and Wrege, 2004).
Frogs
In poison-arrow frogs (Dendrobates auratus), the male spend more energy for raising the offspring than the females and the males are therefore choosy (Wells, 1978).

Related: Why are female not competitive for reproduction like males?

I'm looking at this as a total energy used by both sexes and am interested in how the female utilizes the saved energy when the male is using more of the total on the offspring.  So, if I'm reading the article correctly for the Jacana jacana, it appears that the females have greater development of fleshy facial ornamentation (attraction) and wing spurs (for competition) in exchange for the energy saved from raising offspring?