text:
Why is the DNA codon table "equal" to the RNA codon table
Before anything else please pay attention of the double quotes on the "equal" in the title - I know they are not equal, but you will understand in a bit.
If I look at the DNA codon table here or in wikipedia, and at the RNA codon table here or in wikipedia, their only difference is that the former has thymine (T) whereas the latter has uridine (U). But I am not understanding how all other nucleotides are the same. Bear in mind that transcription reads DNA from 3'->5' and translation reads mRNA from 5'->3'.
Look at this example, focusing on the 3'-TAC-5' of the antisense strand.

The 3'-TAC-5' codes for Tyrosine according to the DNA codon table. However, it transcribes and translates  3'-TAC-5' -> 5'-AUG-3' -> Methionine.
Now focus on the corresponding codon in the sense strand, 5'-ATG-3', which codes for Valine according to the DNA table (it is read from 3' to 5'). This codon transcribes and translates 3'-GTA-5' -> 5'-CAU-3' -> Histidine, not Valine and not Methionine.
So my questions are:

Why do DNA codon tables show the correspondence between codons and amino acids in the sense strands (5'-ATG-3'), if the only way to go from ATG to Met as in the figure is to consider the antisense strand?
I can see that the AUG codon translates to Methionine, and it is translated by reading the 3'-TAC-5' codon in antisense strand, whose corresponding codon in sense strand is 5'-ATG-3'. But this last one is read from 3'->5', so it reads 3'-GTA-5' -> 5'-CAU-3' -> His.

I am guessing I'm getting many things wrongly in this... Maybe on the way that I'm reading  the tables: I always take into account that transcription is read 3'->5' and this is the order I take to read DNA tables.
Thank you and sorry if I was confusing.

Translation is done on the mRNA, not on the antisense strand, and it is done from 5' -> 3'. The first codon is AUG. This is a start code, and codes for methionine. Check this illustrated explanation out, too.

Yes, I understand why AUG translates to Methionine. My question is on why do people refer to the ATG codon coding for Methionine if ATG -> UAC -> His. But I think the main message was that I was reading the tables as polimerase would, and this is not the right thing to do :)

eh, now I understand that :) I was reading 5'-ATG-3' -> 3'-UAC-5' -> His because I was looking for the nucleotide order according to the transcription/translation order

I can understand your confusion but it all makes sense. The basic idea is that what we call the "antisense" strand is actually the one being transcribed. However, since that is in effect a mirror image, it is much simpler to think in terms of the sense strand.
To take a very simple example:
5' ATG 3' <-- sense strand
3' TAC 5' <-- antisense strand

The antisense strand will be read in a 3' to 5' direction:
3' TAC 5' <-- antisense strand
5' AUG 3' <-- mRNA

Since the mRNA is a mirror image, it has the sequence of the sense strand. It is this mRNA that is then translated and this is read in a 5' to 3' direction. So, AUG is translated as Met. To illustrate, have a look at this image from Wikipedia (click on it for a larger version),

In the image above you can see the growing polypeptide (protein) chain snaking its way through the ribosome. The flying blue things are tRNA molecules and the black chain at the bottom is the mRNA being translated. You can't really see it very well in this image but if you look at the original you can clearly see it is moving from the right towards the left. The right hand side is the 5' end and the left is the 3'. Or, in a more static version (adapted from here):

So, the antisense strand is read, transcribed to RNA (which has the sequence of the sense strand but with T converted to U) and it is this mRNA which is read (in a 5' to 3' direction) to produce the protein.

Thank you! But this raises another question in my mind. It seems kind of a "waste" to have the sense strand there if only the antisense is transcribed. Is the sense strand doing nothing more than stabilizing the DNA and wouldn't the same be achieved by having mRNA alone instead of DNA?

@Sosi no, the double strands are essential for many things including i) DNA replication ii) error repair (the "right" sequence can be inferred from the opposite strand iii) most importantly, genes can be found on both strands. The sense/antisense is only with respect to a given gene. What is the sense strand for geneX can be the antisense for geneY.

Thank you! I see, I was misinterpreting and thinking that the sense strand was always the sense strand :)

Genetic code and codons are always used with reference to RNA. When talking about DNA, the the sense strand of a gene is considered its sequence. The anti-sense strand though is the template for mRNA synthesis, does not represent the gene.
DNA-codon table has simply U replaced by T. Apart from a wikipedia article, I don't find the term being popularly (not colloquially) used elsewhere.

Maybe you'd like to add something about the reading of those tables not having to do with the reading direction of the polymerase? This seemed to have been my problem

@Sosi The reading of those tables is directly related to the direction of the polymerase. The polymerase reads 5' to 3', translation happens in that direction too, and that is the direction the tables are read.

@Sosi as I mentioned The anti-sense strand though is the template for mRNA synthesis, does not represent the gene. The direction of RNA polymerase movement is not a factor here.

@JasonC: Just for clarification — RNA polymerase reads 3'→ 5' but produces 5'→ 3'.

@WYSIWYG that is exactly my source of confusion: if it is reading a 5'-ATG-3' strand from 3'->5', it would be reading GTA. But despite "walking" the DNA strand in the 3'->5', it still reads it ATG that's it?

@Sosi.. No RNAP reads a 3'→ 5' strand (with 3'-…-TAC-…-5') and produces a 5'…-AUG-…-3' mRNA. And note that RNA synthesis does not start at ATG (it is the protein synthesis).


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Was Raymond Gosling supervised by Rosalind Franklin?
The story of how the structure of DNA was deduced is fairly complicated and controversial, but most parties agree that a key pieces of data was "Photo 51", an X-ray diffraction image of DNA taken by Raymond Gosling in May 1952 (or possibly other similar images taken at the time as part of the same study).
Ray Gosling, who took the photo, was a doctoral student at the time. The Wikipedia page for the photo indicates that he was supervised by Rosalind Franklin, at least for a while:

James Watson was shown the photo by Maurice Wilkins without Rosalind
Franklin's approval or knowledge (although by this time Gosling had
returned to the supervision of Wilkins).

One controversy in the story is that the photo was shown to Watson and Crick without Franklin's knowledge or permission, which should have been sought first as she was his supervisor.
However, this article discussing a 2015 play about the issue (called Photo 51) includes an explanation by Professor Tony North, who was also supervised by Wilkins and shared equipment with Wilkins and Franklin, that:

Wilkins had to know what Gosling was doing, as he rather than Franklin
was his PhD supervisor. Franklin was ineligible for the role because
she did not have a formal university position, but a personal research
fellowship, Professor North said.
“The result is that Maurice had every right to know what Raymond had
been doing and what results he had achieved, so that he had a right to
see photo 51 without seeking Rosalind’s permission,” he said.

A quote from a primary source seems more credible. I also know from experience that other lab members often play a substantial role in training or supervising doctoral students without necessarily having a formal role in their supervision (i.e. being registered as a supervisor).
Was Rosalind Franklin, at any point, formally supervising Raymond Gosling's doctorate?

I'm voting to close this question because it would be more appropriate on the History of Science & Math Stack Exchange site.

@tomd yes, my mistake - I thought it was an Oxbridge thing. Now removed.

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Why do pink rain lilies flower only after rains, and not from being watered?
We have pink rain lilies (Zephyranthes carinata) in the garden. In my personal experience, I've found that they always flower, without exception, shortly after rains. However, there are roughly ten totally dry months each year. During this time, even though I water them regularly with well-water, they never flower. I've tried copious amounts of water, and frequent watering, but to no avail. They seem to depend on rain.
The rains here come at different times each year. We just had a totally unexpected rainstorm in May, causing them to flower. We are inland in southern India. It's very hot here, and the climate is quite dry in the periods when it's not raining.
How can this be? What's going on inside the plant, biologically speaking? How can it "know" whether it's getting rain water or well water? I'm looking for a description of the biological processes inside the plant which cause these different responses to rains versus watering.
Also, (minor, secondary point) is there any evolutionary reason why a plant would develop this trait?
I prefer answers that cite their sources for the information.
Edit: A user added some quite relevant personal observations in the form of an answer. I'm adding it here, as the observations are quite relevant to the question.

I live in central India which is marked by a heavy rainy season from mid June to September and almost dry rest of the year. This behavior of rain lilies has been a mystery to all of us for generations.
No matter what season, what temperature, the lily bush will give you
  at least one bloom even if rains for a mere few minutes. Rest of the
  time, any amount of watering does not help. I've seen the plant bloom
  with just a bit of drizzling in summers when temps cross 40 degrees
  celsius.
Whereas, a friend is growing them in a pot in a water lily pond.
  Basically, in shallow water where the rain lilies are just dipping
  their feet in water all the time. So basically, for a large portion of
  the year, the plant is meeting the low temperature, high water criterion.
  It doesn't work. The plants bloom only and only when it showers.
By the way, the behavior is not limited to pink rain lilies. It's the same with yellow and white lilies.

These are seasonal rains? Does any rain cause the plant to flower? Plants do have flowering cycles.

@WYSIWYG The rains can come at any time during the year. It depends on a complex set of conditions in the Indian Ocean and Bay of Bengal. It's pretty random. There are some months when it's more likely to rain, though. Yes, it seems the rain causes the flowering. I've seen it flower every single time after rains, but never without rains, even though I water it a lot with water from a well. It should be noted that rain generally tends to be pretty heavy here when it does come.

Perhaps they bloom just after it rains because many bees come out of their hive at this time, which would allow the flower to reproduce more effectively and thus get the evolutionary advantage. I don't have any information to back this theory up (couldn't find any), and I don't know much about biology. Can somebody confirm or deny this hypothesis?

@DivideByZero We could test this hypothesis by having several plants, and surrounding some of them with insect netting.

@Fiksdal - I don't think that's what DBZ meant. I think what they meant is that perhaps the plant flowers because they are expecting (because of past experiences) more bees to come around, not in response to more bees coming around at a particular time.

@KevinFegan Ah, I see. Interesting.

It looks like sustained or consistent moisture might be (at least part of) the phenological cue for flowering:
The wikipedia article mentions that consistent humidity will induce flowering in at least some species and cites Fernández-Alonso & Groenendijk (2004), which says:

It generally flowers after the rainy periods, but in humid pastures and under cultivation conditions, colonies show staggered flowering during the whole year.

There's a reference in Lange et al. 2013 to Zephyranthes flowering after "watering of at least 10 h[ours]", but I'm not able to find the original citation in the google books preview (which is given at "Nitsch 1965").

Edit: I tracked down Nitsch 1965, who cites 2 sources on the topic. He reports Kerling 1949 as showing that Zephyranthes rosea after a certain period of development goes into dormancy, which is broken when two conditions are met: low temperature and high water, which must be extended over at least 10 hrs. He adds that Holdsworth (1961) presents evidence showing that Zephyranthes citrina and Z. tubispatha are primarily triggered by soil moisture.

Fernández-Alonso, J. L. & J. P. Groenendijk (2004). A new species of Zephyranthes Herb. s. l. (Amaryllidaceae, Hippeastreae), with notes on the genus in Colombia. Rev. Acad. Colomb. Cienc. 28: 177-186
Holdsworth, M. (1961) The flowering of rain flowers. Journal of the West African Science Association 7︰28-36.
Kerling, L.C.P (1949) The gregarious flowering of Zephyranthes rosea Lindl. Annals of the Botanic. Gardens. Buitenzorg 51: 1-41
Nitsch, J. P. (1965). Physiology of flower and fruit development. pp 1537-1647 in Encyclopedia of Plant Physiology Vol XV Part 1, W. Ruhland (ed.)
O. L. Lange, P. S. Nobel, C. B. Osmond, H. Ziegler (2013). Physiological Plant Ecology III: Responses to the Chemical and Biological Environment. Springer.

Thanks for this answer! Does this suggest that it's the mere duration of the watering that's the key here? This would make sense, rains are typically heavy here and last for a long time. Maybe I could test this hypothesis by setting up some sort of automatic sprinkler that watered it constantly for a few days?

@Fiksdal sounds like a great experiment to me! For +1, have a control patch that you don't water / water normally! :)

There's a new answer (which isn't really an answer, but includes very relevant observations). I have added it to OP in case it gets deleted (as not an answer.) After considering this information, I have concluded that we still need to look for different hypotheses here.

It's a nice question, I've tried looking for research papers to no avail. But I will add a few things that I hope will help:

Firstly, tap water's composition is quite different from rain water- two criteria for distinction that  come to mind would be pH and TDS, details follow:

Tap water has a higher TDS (total dissolved solids)than rain water, making it harder(1). Additionally it has a higher pH(2). Rain water has virtually no dissolved solutes in it that affect it's hardness and it's pH is acidic(3)(4). Thus while tap water may have a TDS in the hundreds, rain water has a TDS in the tens- a stark difference.

Have you considered that 'Photoperiodism' may be at play? Having grown up in India, I can attest to the over-cast sky after heavy shower, sometimes for hours. This plant may be a short-day plant i.e. it flowers only when the duration of daylight has fallen below a certain threshold(5).

References:

http://www.water-research.net/index.php/water-treatment/tools/total-dissolved-solids
https://www.watersystemscouncil.org/download/wellcare_information_sheets/potential_groundwater_contaminant_information_sheets/9709284pH_Update_September_2007.pdf
http://www3.epa.gov/acidrain/education/site_students/phscale.html
http://ei.lehigh.edu/envirosci/watershed/wq/wqbackground/tdsbg.html
http://extension.oregonstate.edu/gardening/what-are-short-day-and-long-day-plants

Some of the resources aren't as reliable as I would want them to be, but it's the best I could find. Number 4 has a great run-down of TDS for different water sources.

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Could potatoes that have been refrigerated for 142 days still sprout?
I know that potatoes can still sprout even after being refrigerated, but could you refrigerate them for 142 days still use them as seeds to grow more plants after that?
As for the temperature of the fridge, look at this.
 Considering that, what would be likely?
What about frozen or hermetic potatoes?
If anyone's wondering why I'm asking such a strange question, here's why.

This question is probably better suited to [gardening.se].

It would also be better if you can specify what range of temperature you are talking about. By fridged, you mean ~4⁰C?

@WYSIWYG I updated the question.


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Previously frozen papaya seeds sprouted. How will it affect the plants?
I thought about asking this on Gardening SE, but it seems to me as a technical subject which requires biological expertise to answer. This is not something that usually occurs for gardeners, so I don't think anyone there would have experience with it.
A bunch of seeds from a papaya fruit were put in the refrigerator. They were taken straight out of the fruit, along with pieces of pulp, sarcotesta and all.
The seeds ended up below zero. Probably only by a few degrees, at worst. They would have been in that state only for a few hours, at most. However, ice crystals had formed on them, and the pouch had hardened a little bit. I then thawed them. All that happened on May 19.
Well, I decided to plant them, as an experiment. And a few days ago, they started sprouting.

I actually have more seeds from the same fruit, which have not been exposed to below zero temperatures.
Now my question is: If I let these plants become large trees, will they in any way be different from the normal seeds? (Assuming they get equal treatment.)
I thought the seeds would die, so I was surprised when they sprouted. But since this is a tropical plant, could the negative temperatures have damaged their DNA in any way? Or had some other detrimental effect on them? Or can I expect these plants to be exactly like the other group? (Except for individual variations unrelated to the freezing, of course.)

Seeds are generally made in order to stand dry/cold conditions.
I don't see any reason to believe that the DNA got damaged during freezing (that could cause mutation and phenotypic changes). So, if they have germinated, the plants should not be any different from the controls.

How does the "made to withstand cold" part differ between seeds from tropical plants vs those native to colder climates?

The strategy to stand extreme environments is roughly the same, the seeds tend to have very little water inside them. This is an advantage in many situations including low temperature so that ice crystals will not be able to form and destroy the cells. For sure there are differences in the strategies used by tropical plants and alpine plants, but overall they reach the same goal, to make a strong and long lasting seed.

Have a look at this Wikipedia's article to get some more info about it. https://en.wikipedia.org/wiki/Seed_dormancy


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Relationship between genetic diversity within and between species
Here is a quote from Wagner (2008)

A second line of evidence [against neutralism] comes from the relationship between the mean number of polymorphic differences between alleles within a species, $\pi$, and the number of fixed differences between genes in two species, $d$. For neutral mutations, a positive association between $\pi$ and $d$ should exist, because the neutral theory predicts that both quantities are linearly proportional to the rate at which neutral mutations arise. Recent genome-scale data shows instead that this association is in fact negative.

What do "the mean number of polymorphic differences between alleles within a species" and "the number of fixed differences between genes in two species" have to do with each other?  Why should there be any relationship at all?  And by "two species", are they talking about Eastern Yellowback Whooping Finches versus Western Yellowback Whooping Finches, or any arbitrary two species, like E. Coli versus Muskrats?
I found this related question, but it doesn't say anything about different species.

Good question +1. I edited your post to get rid of what I thought was unnecessary information. Feel free to roll back if you don't like the edit.

Assuming everyone else here has the necessary background, it's fine.  I'm not a biologist, so the neutralism/selectionism theories were news to me.

Metrics of interest
The two metrics you are interested in are

$\pi$ - the mean number of differences between two randomly sampled (with replacement) alleles in a population
$d$ - the mean number of differences between two randomly sampled (with replacement) alleles coming from two different species

Consider two sequences

ATCGTCAAT
ATAGTTAAT

There are 2 pairwise differences between these two sequences (positions 3 and 6).
The whole point here is to understand that two individuals in the same population coalesce at a given time in the past just like two individuals coming from two different species. The number of pairwise differences is just equal to the rate at which mutations accumulate multiplied by the coalescence time. Let me develop this idea with a few equations below.
Neutral Expectations
Let's do the math! We will do two important assumptions below.

Every mutation makes a new allele (it is an infinite allele model)
All mutations are substitutions (no indels, no gene duplication, etc...)

Intro to Coalescence Theory
Let's first make sure you understand the concept of coalescence. Imagine you were to look at an evolving population backward in time. A coalescent event, is an event by which two lineages become one (looking backward in time). For simplicity consider a case of an asexual population (but future calculations don't do this assumption). In an asexual population, two siblings coalesced the previous generation, as in the previous generation the genes they are carrying were in a single individual (their parent).
We will see below how to calculate coalescence time between two randomly drawn individual from a population and how we can make inference about genetic diversity from this coalescent time.
Rate of accumulation of neutral mutations
The rate of accumulation of neutral mutation is also called the fixation rate of neutral mutations. Let $fix$ be this fixation rate. Consider a panmictic diploid population of constant size $N$. At a given locus of interest, the mutation rate is $\mu$. The number of mutations occurring every generation in this population is $2N\mu$ (The $2$ comes from the fact that in a diploid population, there are two homologous copies of every gene in each cell). If the mutation is neutral, then every single individual in the population has the same probability to end up being the parent of the whole population in a long time in the future. In other words, starting to look at this problem from the future and looking backward in time, any individual in a distance far enough in the future descends from a single individual in the present. As a consequence, the probability of a new mutation to reach fixation is $\frac{1}{2N}$. Multiplying the probability of fixation by the rate at which mutations occur in the whole population we obtain $\frac{1}{2N} 2N\mu = \mu$. In other words the rate of fixation of new neutral mutations is simply equal to the rate at which mutation occur.
Key equation:
$$fix=\frac{1}{2N} 2N\mu = \mu$$
$d$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from different species
Consider two species which common ancestor lived $T$ generations ago. Each lineage accumulated mutations at rate $\mu$ (and explained above) and therefore the expected (average) total number of pairwise differences is $\bar d=2\mu T$. The probability of having exactly $d$ pairwise differences comes from a Poisson distribution with rate $2\mu T$ ($P(D=d) = Poisson(2\mu T)$).
Key equation: $$\bar d=2\mu T$$
$\pi$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from the same population
Here the calculations follows the same logic as above $\pi = 2 \mu T$. The whole issue is that $T$ (the coalescence time) is unknown for the moment and we need to calculate it.
Let $P(T)$ be the probability that two randomly sampled (with replacement) individuals from a diploid panmictic population coalesce exactly $T$ generations ago. The probability of coalescing in a given generation is simply the probability for drawing the same individual, that is $\frac{1}{2N}$ and the probability of not coalescing in any subsequent generation is $1-\frac{1}{2N}$. Iterating over the generations we obtain
$$P(T) = \frac{1}{2N} \left( 1-\frac{1}{2N} \right)^T \approx \frac{1}{2N}e^{-\frac{T}{2N}}$$
, where $e \approx 2.7$ is Euler's number. The above approximation is accurate for large $N$ (say larger than 100). In case you are interest, you will find on this Math.SE post, an explanation for this approximation.
The expected value (average) $\bar T$ of this distribution is $\bar T=2N$ (and the variance is $var(T) = 4N^2$). As a consequence the expected number of pairwise differences between these two individuals is $\pi = 2 \mu 2 N = 4N\mu$
Quickly speaking, these calculations can be extended to calculate the coalescent time between $k$ randomly sampled alleles. The expected coalescent time is then $\bar T = \frac{4N}{k(k-1)}$ and therefore some algebra shows that the total expected time (along all branches) is $4 N \sum_{i=1}^{k-1}\frac{1}{i}$ and the expected number of segregating sites is $4 N \mu \sum_{i=1}^{k-1}\frac{1}{i}$.
Key equation: $$\pi = 4N\mu$$
Conclusion
It is clear from the above that $\pi = 4N\mu$ and $d=2\mu T$ are correlated as they are both linearly related to the mutation rate. As it is said in your quote

For neutral mutations, a positive association between $\pi$ and $d$ should exist, because the neutral theory predicts that both quantities are linearly proportional to the rate at which neutral mutations arise

The quote goes one saying

Recent genome-scale data shows instead that this association is in fact negative.

Such negative relationship between $d$ and $\pi$ cannot be caused by neutral processes. Therefore selection must be involved somehow.
Imagine for example that two species are both selected at different optima (opposite selection pressures). In such case, you would see purifying selection within species reducing the probability of a new mutation to reach fixation to a value lower than $\frac{1}{2N}$ and therefore reducing the rate of fixation $fix$ so that $fix<\mu$. However, such opposite selection pressure among species will yield the species to diverge more than expected by random processes that is $\pi > 4N\mu$. Such selective pattern could explain the observed negative relationship.
More information
This post offers book recommendation on the subject (population genetics).

when you say "mean number of differences", how is this quantified?  Number of differing base pairs?

Yes exactly. There are two assumptions (I forgot about in my answer but I will add them) 1. All mutations are substitutions (no indel, no whole chromosome duplication etc..) and 2. every mutation makes a new allele (infinite-allele model)

Are those assumptions specific to neutral theory?  I guess this is supposed to be a proof by contradiction, so I want to see which specific premises are leading us to the contradiction.

Those are very common assumptions found in the neutral theory literature and more globally in the literature on genetic drift. The concept of proof by contradiction applies to math but not to empirical sciences (isn't it?). We just have a null prediction (model without selection) and if the data don't match these then something else must be going on. (Thanks for the edit)


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A strange insect
I saw this ant-like insect in Brazil, close to Rio de Janeiro. It was around 2 cm long. I tried to  use google's search by image, but no luck. Does any one know the name of the species?

I would have though a Polyrhachis is you had found it in Australia but they don't seem to exist in Brazil. Here is the list of ant species living in Brazil.

Its not an ant.

Possibly Mutillidae or a related family? (but beyond that I have no clue).

Insects like this are commonly called "velvet ants", but they are wasps, not ants. This insect is in the family Mutillidae, and it's called Hopolocrates cephalotes.
(https://www.inaturalist.org/taxa/629302-Hoplocrates-cephalotes/browse_photos)


text:
Pyura DNA extraction
I'm am struggling with genomic DNA extraction from different samples of Pyura chilensis; the DNA is degraded as can be seen on the gel.
We've always used GeneJET Genomic DNA purification Kit (by ThermoFisher), and it works fine for samples from other species; so the kit isn't the problem.
We've always used tissue samples stored in 95% Ethanol (which are washed with water prior to DNA extraction), but the problem persists irrespective of whether the samples are one day old or a few years old.
The storage method seems to work fine for gDNA extraction from other species.
Then, my guess is that the problem is with Pyura itself. So I have to figure out if either the extraction or the storage isn't appropriate for Pyura. I read that Pyura has a lot of copper in it. We planned to use a new buffer for storing it: salt Saturated DMSO, containing EDTA.
I would like to ask if any of you have ever worked with this organism (and if you have, then how did you manage to extract DNA from it). Do you have any suggestions on any DNA purification protocols?

1st lane is the ladder (1kb) and last 3 lanes with long blurred thing instead of bands are my DNA samples.

With reference to your gel photo, the genomic DNA (in the three Pyura sample lanes) does not look badly degraded.  If the size marker is 1 Kb ladder, then the majority of the DNA is of high molecular size. During extraction it is common for high molecular weight DNA to become "sheared" to some degree (mechanically broken into smaller fragments). This can appear as the faint downward smear. The lanes may be somewhat over loaded as well. You can try to use more gentle extraction technique and see if it helps to your satisfaction. Any of those you mention will work.
Badly degraded genomic DNA would appear as a more intense "smear" near the lower portion of the 1 Kb size standard.

This is from a published work by Segovia et al. 2017:

Mantle tissue (0.2 g) from each individual was used to extract DNA using the DNeasy Blood® & Tissue Kit (QIAGEN®, USA) according to the manufacturer’s instructions. Quantity/purity of DNA was measured in Nanodrop 2,000 (Thermo, USA).

They have done SNP identification from the genome. So I assume that their gDNA would have been of decent quality.


text:
A human lifespan
Recently, I read an article that said a human lifespan does not have any limit and when a man turns 105 he has a 50/50 chance to survive another year. Some scientists say that a man who will reach the age of 140 has already been born. Is it possible that the length of a human's life will be prolonged over time? I know that we don't know what the limit is and if it exists at all, but it is possible to one day expect it to be completely normal for a human being to live 300 years or so? I mean, without the intervention of any "elixirs of youth", development of technology, medicines etc.?
I ask because in 2016 there was an article published in "Nature" that says we know what the limit is (115 years) and they believe that Jeanne Calment (who died at age 122) was lucky to live that long. On the other hand, another article published in "Science" this year says that we don't know what the limit is.

Welcome to SE Biology. Adding links to the articles that you discuss will improve this question.

"Nature": https://www.nature.com/articles/nature19793, "Science": http://science.sciencemag.org/content/360/6396/1459

Looking at these lists of oldest people a 'limit' of 115 seems unfounded. Also, Calment's actual age seems to be a somewhat controversial topic.

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text:
Giga base or Giga byte

"we reported ~2.66- Gb genome sequence of"
"we generated 191.5 Gb high quality reads"

I am very confused with these two quoted lines and I am not sure about giga byte or giga base pair.
and an additional question: How to count base pairs from a FASTQ file?
I have read numbers and length.

This refers to base pairs.
File size has no particular meaning beyond practical considerations, given that it depends on the format. (For example, 2bit files use 2 bits per base, as the name indicates, compared to the 8 bits necessary for each letter in a plain text format like FASTA & derivatives.)
For your additional question, (number of reads * length of each read) gives the total length of sequence contained in the file. It is not really a property of the file format, but a parameter of the sequencing run.

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text:
Darwin's views on Lamarckian Heredity?
Currently I'm reading She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity, a fascinating book about heredity by the popular science author Carl Zimmer.
While reading this I came across this following passage, which bothers me.

It also meant that the inheritance of acquired traits - taken as a fact by Hippocrates, Lamarck, and Darwin alike - was impossible.
~ Chapter 2: Traveling Across the Face of Time

I've read Darwin's The Origin of Species, and a fair bit of other stuff on Evolutionary Biology, and as far as I know Darwin clearly opposed the idea of Lamarckian heredity. Which is why I was quite surprised to see this, from Zimmer, who's a very highly reputed author. How can he make such an obvious mistake, or is there something more to it than I know? Did Darwin ever agree with some form of Lamarckian heredity?
EDIT
Here's the passage of the book where it appears, for context.

It sounds like a weird claim to me too. Note that a book is not peer-reviewed, small mistakes are not so uncommon. Also Carl Zimmer is a reputed popular author. He is not a researcher (but I he likely has a very decent understanding of evolutionary processes).

@Remi.b yes, I considered the possibility of a small error slipping in, but I find that a little hard to buy. I've read many of his books, and he has a very good understanding of evolution, which means, this is a difficult mistake to make. There's such a fundamental difference between Darwinian and Lamarckian ideas. I've never had a formal education in biology, I'm completely self taught because I found it interesting, and even if I could find the mistake, how could a team of people dedicated to the subject, not.

From wikipedia (without reference): Weismann starts out believing, like many other 19th century scientists, among them Charles Darwin, that the observed variability of individuals of one species is due to the inheritance of sports (Darwin's term). He believed, as written in 1876, that transmutation of species is directly due to the influence of environment.. So the claim might be correct as a reference to Darwin's early thoughts.

According to Ghiselin (here): Darwin accepted the inheritance of acquired characteristics, just as Lamarck did, and Darwin even thought that there was some experimental evidence to support it

@Remi.b — this is really interesting, and should certainly be made into an answer that would be of value. It may explain something I was reading about Morgan recently to answer another question. The Wikipedia entry states Morgan "but rejected Darwin's proposed mechanism of natural selection acting on small, constantly produced variations." However I wonder if it was more that he favoured the idea of genetic mutations (as produced the first X-linked mutant, white, in 1910) being the driver of evolution, rather than aquired characteristics.

I finished reading Ghiselin's article. While some of it sounds legit, he too is guilty of the the same errors textbook authors he criticizes do; providing no or very minimal references. The only really possible way to settle this is reading both Origin and The Variation... by Darwin keeping this question in mind. I'm actually thinking of writing to Zimmer about this as well, hopefully he'll reply.

@Remi.b — Forgot to mention that I noticed and was puzzled by the word "sports" in Morgan's 1910 paper. The phrase "due to further sporting" occurs on the first (free) page. I see from Merriam-Webster that this can mean "tending to mutate freely"

This is sign of good research work :)

I wrote to Carl Zimmer, and he replied within two hours. That's pretty cool!
So I thought I'd put everything I learned about this here as an answer with all the links, and if you guys have more to add, feel free to post more answers.
My Original Email:
Currently I'm reading She Has Her Mother's Laugh, which is a fascinating book, and I'm thoroughly hooked. However, while reading it, I came across this passage that troubled me. The bit in question is in Chapter 2: Traveling Across the Face of Time.

"It also meant that the inheritance of acquired traits - taken as a
  fact by Hippocrates, Lamarck, and Darwin alike - was impossible."

From what I've read on the subject over the years, almost unanimously people agree that Darwin opposed the idea of Lamarckian heredity. I thought that Darwin's idea is that small modifications arising from random mutations (although he didn't know about DNA and genes at the time), if beneficial, were retained and accumulated over the generations resulting in new species. But is it not the case? Did actually Darwin subscribe to the idea of Lamarckian heredity?
I did a little bit of research on this, and found some conflicting and confusing information.
To start with, I've read Darwin's Origin of Species and though I remembered him opposing the idea, so I searched through the book again and found the following para.

Thus, as I believe, the wonderful fact of two distinctly defined
  castes of sterile workers existing in the same nest, both widely
  different from each other and from their parents, has originated. We
  can see how useful their production may have been to a social
  community of insects, on the same principle that the division of
  labour is useful to civilised man. As ants work by inherited instincts
  and by inherited tools or weapons, and not by acquired knowledge and
  manufactured instruments, a perfect division of labour could be
  effected with them only by the workers being sterile; for had they
  been fertile, they would have intercrossed, and their instincts and
  structure would have become blended. And nature has, as I believe,
  effected this admirable division of labour in the communities of ants,
  by the means of natural selection. But I am bound to confess, that,
  with all my faith in this principle, I should never have anticipated
  that natural selection could have been efficient in so high a degree,
  had not the case of these neuter insects convinced me of the fact. I
  have, therefore, discussed this case, at some little but wholly
  insufficient length, in order to show the power of natural selection,
  and likewise because this is by far the most serious special
  difficulty, which my theory has encountered. The case, also, is very
  interesting, as it proves that with animals, as with plants, any
  amount of modification in structure can be effected by the
  accumulation of numerous, slight, and as we must call them accidental,
  variations, which are in any manner profitable, without exercise or
  habit having come into play. For no amount of exercise, or habit, or
  volition, in the utterly sterile members of a community could possibly
  have affected the structure or instincts of the fertile members, which
  alone leave descendants. I am surprised that no one has advanced this
  demonstrative case of neuter insects, against the well-known doctrine
  of Lamarck.

If you read the last few sentences, Darwin says "accumulation of numerous, slight, and as we must call them accidental, variations,..." which to me indicates he's referring to random mutations in genes even though he didn't know what genes were. Furthermore, a little later, "For no amount of exercise, or habit, or volition, in the utterly sterile members of a community could possibly have affected the structure or instincts of the fertile members, which alone leave descendants." and "I am surprised that no one has advanced this demonstrative case of neuter insects, against the well-known doctrine of Lamarck."
To me this clearly indicates he was opposed to the idea of Lamarckian heredity. Could you please explain a little bit more about your stance? I'd love to hear the different viewpoint and the reason(s) behind it.
Since I was curious about this, I posted the same question on StackExchange biology forum.
One of the users pointed me to an article by Michael T. Ghiselin who seems to be in agreement with you regarding the matter.
While some of his points about textbook authors misunderstanding Lamarckian heredity sounds fair and valid, I can't quite see how he came to the conclusion that Darwin agreed with Lamarck. The passage he points to (Lamarck was the first man whose conclusions ...") doesn't say anything about Darwin agreeing with Lamarck about acquired traits being passed down the generations.
In Wiki page about Pangenesis, the following is mentioned just as you have in your book.

"Darwin thought that environmental effects that caused altered
  characteristics would lead to altered gemmules for the affected body
  part. The altered gemmules would then have a chance of being
  transferred to offspring, since they were assumed to be produced
  throughout an organisms life.2 Thus, pangenesis theory allowed for
  the Lamarckian idea of transmission of characteristics acquired
  through use and disuse. Accidental gemmule development in incorrect
  parts of the body could explain deformations and the 'monstrosities'
  Darwin cited in Variation."

Which indeed supports your viewpoint, but to me that seems like a direct contradiction to Darwin's own words in Origin of Species.
So which of it is true? Or, since Pangenesis theory came after he published Origin, did he change his mind later?

Carl Zimmer's reply:

Thanks for your email. I've also had to struggle to work out Darwin's
  views about Lamarck--they were complicated and changed over his
  career. Basically, the more Darwin thought about heredity, the more he
  warmed up to the possibility of the inheritance of acquired
  characters. I've attached a few good papers that may be of interest.
Best wishes, Carl Zimmer

Papers Referred by Carl Zimmer:
Gemmules and Elements: On Darwin’s and Mendel’s Concepts and Methods in Heredity.
Lamarck, Evolution, and the Inheritance of Acquired Characters.
orgThe Early History of the Idea of the Inheritance of Acquired Characters and of Pangenesis.

I haven't read those papers yet, will do so when I find time and hopefully it will shed some more light on it.
So, I'm still not quite sure about the issue, but I do think Carl Zimmer's point of view is fair enough, that it is possible Darwin's views evolved over time. Particularly, given that nobody knew what exactly even heredity means at the time, it's possible that Darwin thought it cannot just be ruled out. Besides doesn't seem like he was out campaigning for the idea, rather allowed for it with his Pangenesis hypothesis.
After all, Darwin's theory was about how small modifications accumulated over time leads to species change, not how those changes occurred in the first place. So, while it turned out to be untrue, if there was a mechanism in which experiences could be stored in the unit that transmitted heredity, you can probably incorporate that into Darwin's theory of evolution. That probably was a line of thought Darwin had.

Wow amazing. Thanks for sharing your email with C. Zimmer. If you happen to read the linked articles and wish to summarize them, it could be quite awesome to add you summary to your answer.

@Remi.b yeah I plan to read those three papers as soon as I can, and will try to summarize them here afterwards.

I realize I'm several years late to this post but thought I'd still share for anyone else who comes across this post. I have the 150th Anniversary Edition of Origin by Signet Classics and found this passage about inheritance of acquired characters (which he also refers to as use and disuse). In Chapter 1, the opening paragraph of the subsection "Effects of Habit and of the Use and Disuse of Parts; Correlated Variation; Inheritance" reads:
"Changed habits produce an inherited effect, as in the period of the flowering of plants when transported from one climate to another With animals the increased use or disuse of parts has had a more marked influence; thus I find in the domestic duck that the bones of the wing weigh less and the bones of the leg more, in proportion to the whole skeleton, than do the same bones in the wild-duck; and this change may be safely attributed to the domestic duck flying much less, and walking more, than its wild parents. The great and inherited development of the udders in cows and goats in countries where they are habitually milked, in comparison with these organs in other countries, is probably another instance of the effects of use. Not one of our domestic animals can be named which has not in some country drooping ears; and the view which has been suggested that the drooping is due to disuse of the muscles of the ear, from the animals being seldom much alarmed, seems probable."
So, in fact, Darwin does appear to give credence to the idea of inheritence of acquired characters. A quick Google search shows several other sources that provide additional citations that confirm this. So interesting!

Interesting in so far as it shows once again that you should judge an idea on its scientific merits rather than on the reputation of the person who propounded it.

For sure. I've always been irked by the phrase "Darwinian" evolution, which almost suggests evolutionary theory is a belief that simply follows Darwin's every word.


text:
What does (G+) (G++) in terms of male mutation rate and male-heterogametic XY-system?

What's the expression for $\alpha_m$ in case of male-heterogametic XY systems (G+)?

Derive the corresponding $\alpha_m$ expression of for (sic) male-heterogametic XY systems (G++)

I have absolutely no idea what they mean with G+ and G++ in the exercises. I have searched the whole Internet and the lecture slides for this but I think I am going crazy. Has it something to do with the gametes? Anyone who knows?
Thanks in advance!

I don't know what G+ and G++ mean. I don't know what $\alpha_m$ mean either. Can you provide some context that could help?

Please do not post text as images as images are not searchable and can pose problem to visually impaired users.

I think you need to provide more context.  When I saw G++, my first thought was the C++ compiler of that name.  I am unaware of any universal use for the term in biology.  It could very well be context specific.  It is common to use that sort of notation when describing alleles in a population, with the pluses following whatever variable name you gave to the allele.  So if we had an allele that we called G, and an individual had two copies of that allele, it would be common to see that individual referred to as G++, with G+ being used to refer to someone with only one copy.  I think it is quite possible that this is what the term means in your context but it is impossible to say for sure without more information on what the question you are being asked is in reference to.  Maybe it would help if you posted questions 1-4 or the blurb that precedes the problem set so we could see what you are actually being asked.


text:
What is the meaning of 'state of nature' in On the Origin of species by Charles Darwin?
I have started reading "On the origin of species" by Charles Darwin.
The beginning paragraph is:

When we look to the individuals of the same variety or sub-variety of our older cultivated plants and animals, one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.

What does he mean by state of nature here?
Note:
The term state of nature is very often used in this book, so for anyone reading this book my question would be helpful for greater understanding.
Edit: One user has requested for more context for better understanding...I would like to provide the next paragraph and also a related paragraph.

When we look to the individuals of the same variety or sub-variety of our older cultivated plants and animals, one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.
When we reflect on the vast diversity of the plants and animals which have been cultivated, and which have varied during all ages under the most different climates and treatment, I think we are driven to conclude that this greater variability is simply due to our domestic productions having been raised under conditions of life not so uniform as, and somewhat different from, those to which the parent-species have been exposed under nature. "

Another paragraph in which State of nature has been used:

Sterility has been said to be the bane of horticulture; but on this view we owe variability to the same cause which produces sterility; and variability is the source of all the choicest productions of the garden. I may add, that as some organisms will breed most freely under the most unnatural conditions (for instance, the rabbit and ferret kept in hutches), showing that their reproductive system has not been thus affected; so will some animals and plants withstand domestication or cultivation, and vary very slightly—perhaps hardly more than in a state of nature.

Doesn't the second paragraph explain exactly what Darwin means?  "State of nature" = things that are not cultivated.

I would think that by "state of nature", he probably referred to any non-cultivated species. As @David suggested in the comments, the expression "in the wild" could also be a good replacement for "in a state of nature".
I think that the first paragraph you quote could be rephrased in the short sentence

There is more phenotypic variation in cultivated species than in non-cultivated species.

My sentence is more concise but of course, is quite a bit less pleasant to read. Darwin was a very good writer after all.

I have provided some more details.Please have a look at them!

I concur with this interpretation. It's his way of saying "wild-type".

@ayc Your edits comforted me in my interpretation. Thanks

This seems correct. @vkehayas — "Wild type" has a specific genetic connotation and even today would not be comprehensible by the layman. The English expression that is applicable and would be understood is "in the wild" (although this does bring up an image of Victorian explorers in pith helmets shooting tigers, rather than Victorian vicars sketching primroses on the Downs).

... one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.

Can be easily re-written as

...in their natural state.

Which is the most minimalistic change to the original text, that still makes the sentence more easily accessible, as its less formal and less old-fashioned language use.


text:
What are the advantages of forgetting?
How  forgetting things is helpful for the brain or the human body  biologically? This web page

After some moment of being rude, selfish, or weak, either we are able to put it behind us, or the person who suffered at the result of our imperfection moves on. The reason for this is our ability to forget about it. We forget not because we have an imperfect hippocampus (our brain’s memory organ); it's actually an evolved solution. The ability to lose information allows new information to come in that is more relevant, more pertinent to an ongoing reality. Forgetting allows us to update.

and this Huffington post article

According to a study in Nature, our awareness is limited to only three or four objects at any given time. To be able to think at your highest level, you therefore must be very efficient at filtering out all of the background noise: Your racing thoughts, the ringing phone, your neighbor’s barking dog, and the list goes on.
The Nature study found that when participants were asked to “hold in mind” certain objects while ignoring others, there are significant variations in how well each of us can keep irrelevant objects out of our awareness.
The researchers concluded that our memory capacity is therefore not simply about storage space, but rather “how efficiently irrelevant information is excluded from using up vital storage capacity.”

provide some backgrounds.

That link is to a psychology article titled "Why Forgetting the Past Can Be a Good Thing, in other words, remembering the time you were drunk and did something incredibly embarrassing to you is better fot your self esteem to forget. This is not a biology question. Maybe Cognitive Science.SE

I'm voting to close this question as off-topic because cogsci.se is a better place for it.

But I don't want to know the psychological answer . Psychological answers are plenty available on the net

I think that link was the culprit :-)

This is more of an idea I have than actual research and the other answers are better, but it occurs to me that we think of as "memory" as being a record of past events for its own sake, but there is zero reason for us to evolve a record of past events for its own sake. Memory certainly evolved as part of our general cognition because it allows to better model, predict and function in the world, but it would evolve only insofar as it does help with those things. So maybe the assumption that remembering is the default and forgetting needs to be explained is wrong.

Because not every association the brain makes is correct. Imagine never being able to learn to spell cat (cat) if the first time you tried you spelled it (kat).

Darn, the answer is on the tip of my tongue!

What if your body never "forgot" that it was injured?

I used to know the answer to this one...

@John: But I can readily remember getting things wrong the first time around (or indeed, the first few dozen times), yet still know the right way once I've learned it.

you remember more recent error or particularly egregious ones but you don not remember the vast number of corrections your brain has made. you don't remember all the times you flailed around trying to learn your limbs or the first time you wrote letters.

Because the human skull has a finite volume and new memories consume some of that volume e.g. memories require matter. So if we remembered every single thing we ever experienced, we'd all be far less attractive. Think 1950s alien movies. Big blue heads. This is just one of the many purposes of sleep btw - optimising how useful info from the day is sorted and stored and then throwing away the rest, one by product of that process of knitting in the new pages of memory is of course "dreams".

I voted to re-open as I do not see any benefit in closing a well upvoted question that received an accepted, well received answer 5 days ago. See the corresponding meta question

"I'm voting to close this question as off-topic because cogsci.se is a better place for it.".. This is no valid reason. This question is on-topic. If it is a better fit elsewhere then a mod attention flag could have been raised for a suitable migration. @Mesentery It would be great if you can summarize the linked pages so that the question is somewhat complete by itself.

Short answer
It has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.
Background
First off all, there are many types of memories, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental.

Beneficial effects of loosing memories
Long-term memory is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that detect (anterior cingulate cortex) and resolve (dorsolateral and ventrolateral prefrontal cortex) mnemonic competition (Kuhl et al., 2007). The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones (Shea & Right, 1991).
Inherently volatile memory
Short-term working memory is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (which objects depicted here match the colors you just saw?). If all these memories would be retained, tasks dependent on working memory would not be possible. Sensory memory an ultra-short term memory that is kept only for very short amounts of time, allowing people to, e.g., track a light and make a symbol or letter out of it before the information is funneled to the short term-memory.
Neutral effects of loss of neural function: a side track off memory lane
However, forgetting may be simply another example of the use it or lose it principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the plasticity of the cortex. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated (Stronks et al, 2015). In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available per se. Hence, 'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever, barred a minority of studies that showed a slight benefit of being blind in auditory tasks (Stronks et al., 2015).
Pathological memory loss - not so good:
However, forgetting of memories may also be pathological; think of the impaired short-term memory of Alzheimer's patients, or amnesia due to stroke. Forgetting is not always beneficial.

References
- Kuhl et al., Nature Neurosci (2007); 10: 908-14
- Shea & Right, Res Quarterly Exercise Sport (1991); 62(3)
- Stronks et al., Brain Res (2015); 1624: 140–52

Wow, so much research :D

@ABcDexter - Thanks mate! No half-baked answers here ;-)

! second @ABcDexter's comment. And I learned an exciting new word, too: *deafferented". Clearly I haven't been reading enough neuroscience. :)

@anongoodnurse - thanks for the compliments and I'm glad I was able to add a word to your dictionary ^__^

Re: "Short-term working memory is explicitly designed to be volatile and non-lasting": Can you maybe find a more scientific way to express this idea? (By the way, you mean "lose" rather than "loose", though in context it's clear. :-) )

Interesting answer !!! I didn't expect this question to be answered by the previous comments.Extremely thankful for answering the question.+3 @AliceD

Interesting recent paper on exactly the subject of benefits of forgetting (creatively rebranded as "transience" of memory): http://www.cell.com/neuron/fulltext/S0896-6273(17)30365-3

Memory is formed by building connections between nerve cells (i.e. neurons). These connections are called synapses. The synapses form a network between several (or tens or hundreds) of neurons, therefore giving us the ability to retrieve something we had memorized before.
Learning something new requires building new connections, but the older connections might interfere with the new ones and thereby interrupt our memory or what we have learnt. So sometimes older connections must be broken in favor to new connections and new abilities. For instance, you might remember crawling on both hands and knees as a child, but slowly you practiced walking and at one point you stood up and never crawled again. Children crawl like it's no big deal, but grown-ups have to think and struggle and in the end it's not gonna be very good. That's because older connections regarding crawling have been broken in favor to new connections for walking.
Check out: Izquierdo, Ivan. "The art of forgetting." Springer International Publishing, 2015.

I really think you need to cite some sources. You're very short on evidence here. For example, "older connections must be broken." What does that actually mean? Is it loss of facilitation, loss of synapse, or something else? It sounds good, but it sounds like a lot of opinion as well.

@anongoodnurse I agree, especially with regard to adults having difficulty crawling. I can think of many reasons why an adult might struggle to crawl, none of which is at all related to missing memories.

I agree with the above, and @Dan's comment in particular: Conversely it does not seem clear to me that "children crawl like it's no big deal". (Also fwiw I don't find crawling difficult at all.)

@anongoodnurse (and everyone else) Thank you very much. That's a fair comment. I wrote this on the go and couldn't look up my sources, but my main source is the book I introduced. (thumps up)

I think this is the article about babies forgetting things: http://dx.doi.org/10.1126/science.1248903.  I had read it when it came out. @hossein Please check and incorporate if necessary.

One famous person, Solomon Shereshevsky, had an unusual ability to remember everything he encountered: sights, numbers, words in foreign languages, events from infancy, and more.

Unfortunately, S’s gift was a serious handicap. He was unable to block unwanted memories. Also, he had a terrible memory for faces because he memorized them so exactly. People’s faces change with time, lighting, mood, and expression. S had difficulty recognizing faces because they looked so different to him from the ones he had completely memorized in the past.

Extrapolating from that, one could conclude that the inability to block unwanted memories could easily lead to the development of PTSD — especially if, as in Shereshevsky's case, the total recall is combined with synaesthesia.

Who says it has to be good?
We cannot assume that every trait that evolves is beneficial to the species. A lot of people assume that the species of an ecosystem will evolve optimally; that is, they assume each species evolves to have the best possible genes for its environment. My understanding is this is not the case. Species have to adapt or face extinction, but they only have to adapt to be good enough. Perhaps it's not that forgetting is good, but rather it just doesn't impede survival or reproduction. (Well, except when you forget your spouse's anniversary!) Which leads us to the next point...
It's a side effect of how human memory works.
First off, storing a memory in the brain is not like running a tape recorder or camera. The brain actually stores very little of the information coming into it, just enough so that it can later fill in the blanks and make a decent reproduction. In computer terms, the data is filtered through a very lossy compression algorithm before being stored. It's just good enough that we usually don't notice, but sometimes things go wrong and we get phenomena like confabulation.
Now about how that data is stored. As you know, the data is stored by the synapses in the neurons. But here's the thing: those synapses aren't dedicated to that specific memory! Storing a new memory affects synapses that are part of other memories. One synapse might be storing a piece of information for any number of memories, because those memories all have some tiny thing in common. I wish I could explain this better and in more detail, but this became pretty obvious to me when I read up on artificial neural networks, which are crude models of brains.
Sometimes, neurons just die. Obviously this is going to affect the brain's ability to recall the information the dead synapses contained. There's enough redundancy built into the brain that this is rarely a problem, except in cases like Alzheimer's, where the brain just suffers too much damage.
To me, the question isn't why we forget. The question is how we can remember stuff at all!

You're right that forgetting doesn't have to be "good" but I think @AliceD's answer has some well-cited research for why indeed forgetting is beneficial in some cases because of the evolved environment and how memory works.

True. But the OP seemed to be making assumptions before verifying that they actually hold; a big part of my aim was to make counterpoints to those assumptions. A bit of a gentle Zen slap, if you will. I figured the existing answers were sufficient to address the idea that forgetting is indeed beneficial, so I wanted to take a different approach.

What are the advantages of forgetting?

Perhaps the question asked should be what is the disadvantage of remembering every little detail?
The answer is cost. It cost energy/neuron to remember everything. Neural tissue are expensive to maintain and feed. At rest, the human brain consume 20% of all calories. And that is alot of energy when the human brain is only 1% of all tissue in the body.(http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html)
It is also inefficient. If you remember everything, it will take time to reach the appropriate memory. When time is life, it is inefficient to have a large store of unimportant memories to search through for the one important memory.
Also, this being biology... is there a selective drive for perfect memory? Without a section pressure for perfect memory, it won't evolve. Memory that is good enough to survive is what we will get. We do not get cheetahs which are as fast as biologically possible. We get the cheetah that can catch the slowest gazelle.

Please provide sources supporting the claims you suggest in your final two paragraphs. Also, please avoid simply copying links, but instead provide them some context (e.g., what part of your answer they actually support, etc.). This can be done through tagging links with some statement using "" or through endnotes, parenthetic citations, etc.


text:
If a mother had a child with her own son, could a paternity test yield positive result for the son's father?
Let's imagine a family composed of Mr A and Mrs B, who have a son named John.
Now, if for whatever twisted reason, John had a child with Mrs B, could a paternity test yield positive result for Mr A?
Since John's genes all come from Mr A and Mrs B, the child's genes would all come originally from Mr A and Mrs B as well. Thus it seems to me like the test could suggest Mr A is the father of the child.
Or would there definitely be some "red flags" that suggest something wrong happened?
For example, if the child is a girl, that would mean both of her X chromosomes originally came from Mrs A (since John's X chromosome comes from his mother, as for all males), possibly even the same chromosome twice.
Let's consider that only Mr. A is tested, and not John. Would the child be considered genetically close enough to Mr. A that a test could attest that he is probably the child's father, granting there is no other test showing someone else as a much more likely candidate?

Let's approach some different methods of distinguishing parents:
1: The Y chromosome. These are passed down from father to son. Therefore, if the baby is male, its Y chromosome will be the same as John's and his father's - it will be indistinguishable who it's from.
2: The X chromosome. A male baby always has one of the mother's X chromosomes. A female baby always has its father's X and one of the mother's X. A male baby of John and Mrs B would always end up with one of Mrs B's X chromosomes, meaning that this can't distinguish the father. A female baby would have two X chromosomes from Mrs B (because John's own X came from her), proving that it is the product of incest.
3: Mitochondrial DNA. mtDNA is passed on from mothers to their children, never from the father. Therefore regardless of whether John or Mr A is the father, the baby would have Mrs B's mtDNA - not useful.
4: DNA fingerprint. This is primarily based on stretches of the human genome that contain repeats of short DNA sequences (so-called STR/short tandem repeats, or VNTR/variable number tandem repeats). In both cases, the sequence is the same in individuals, but the number of repeats is extremely variable and each human therefore has a (possibly) unique combination across the different repeat locations in the genome. Because children inherit 50% of their DNA sequences from the father and 50% from the mother, John himself will have his mother's characteristic lengths in 50% of repeat locations and his father's in the remaining 50% of locations (roughly). A child of John and Mrs B would have MrA's repeat lengths in 25% of locations and Mrs B's in 75%. The fractions "100% Mr A" vs. "50% Mr A" vs. "25% Mr A" can be distinguished by this method.

Sorry to answer a really old question but I've been researching this exact topic and this post often appears near the top of search engine results, and I think it could use some more info; the top answer does a great job outlining the technical factors at play, but it neglects to consider a couple of practical factors that will affect the outcome of paternity testing in the real world. I am going to assume we are using commercial paternity testing services widely available to the general public, and not a service that is specifically more precise.

Because only Mr. A is being tested and not John, there is a significant possibility that commercial paternity testing services will return a "false positive" for Mr. A being the father. These testing services have articles specifically mentioning scenarios just like this one, sans mention of incest. According to these articles, it is not unthinkably uncommon for two potential fathers to be closely related, i.e. brothers or father and son. Quote: "When the two potential fathers share a father and son relationship, it must be mentioned to the testing facility beforehand, as failing to mention this might result in a high false-positive result." The ubiquity of this kind of disclaimer across articles from multiple different paternity testing services suggests that false positives in scenarios like this one are not only possible, but especially likely if the testing service is not made aware of any of the broader context.

What are the chances that Mrs. B participates in the test? This reduces the likelihood of a false-positive scenario. Quote: "[...] your best chance of receiving an accurate result lies in both parties agreeing to take the test. But in this case, the likelihood of success further increases if the mother agrees to undergo a test as well, which will help isolate the genetics of the offspring to an easier degree." So even if John does not participate at all, if Mrs. B participates, it will reduce the chances of a false-positive scenario. For most commercial paternity testing services, the participation of the mother is an optional feature offered at additional cost for greater certainty. Greater certainty would only be required if there was reason to doubt the results of a standard paternity test, so in a scenario that makes the fewest assumptions, Mrs. B does not participate, leaving increased probability of a false-positive.

This is probably the biggest factor overall — will the paternity testers be specifically told anything that might indicate the situation is non-standard? Or will it just be a blind test of "Is Mr. A likely the father of Mrs. B's latest child?" Even if the testing service is not advised of specific details like the possibility of incest, if any questions of the test's potential validity are raised, they are highly likely to ask for additional samples, if for no other reason than to upsell you — these are commercial services after all.

In summary, for a real world commercial paternity testing scenario, it appears to be a numbers game that's difficult to predict; if the test really is just a DNA sample of Mr. A and the child with no additional context, then yes, there is a strong possibility that a testing service will determine it's "close enough" and send back a "positive" result. They quite literally admit this. The likelihood of that outcome depends on the policies of the testing service and the personal standards of the personnel doing the testing (and, lets be honest, whether their lunch break is about to start!) whether a "close" result like this one would be considered "close enough" to send back positive, or whether it warranted a closer look and/or request for additional samples.
Sources:

Home DNA Direct
DNA Center
Easy-DNA


text:
Where can I find a list of medical conditions and their incidence rates?
Where can I find a list of diseases and their incidence rates? I'm giving a presentation on Long QT Syndrome, which affects 1 in 2000 people, or 50 per 100,000. I'm trying to find other, more well-known diseases with a similar incidence to give my audience a frame of reference.
(Note: This is not a duplicate of this question. That question is asking about very rare diseases, and the answers to that question reflect that)

Welcome to Biology.SE. The question would be a better fit on Health.SE.

The WHO probably have this kind of data. Consider this document for example.

Thanks. Didn't realize there was a Health.SE, I'll ask there if I can't find it from the WHO


text:
What are the effects of oxygen toxicity in human blood?
I was reading some text on deep sea Physiology, and for to know that diving to do could cause oxygen toxicity in the blood. This was the exact text from the book Textbook of Medical Physiology by Arthur Guyton and John E. Hall:

A  column  of seawater  33  feet  (10.1  meters)  deep  exerts  the  same  pressure  at  its  bottom  as  the  pressure  of  the  atmosphere  above the  sea.  Therefore,  a  person  33  feet  beneath  the  ocean surface  is  exposed  to  2  atmospheres  pressure,  with  1  atmosphere  of  pressure  caused  by  the  weight  of  the  air  above the  water  and  the  second  atmosphere caused by the weight of  the  water.
When  the  PO2  in  the  blood  rises  above  100  mm  Hg, the  amount  of  O2  dissolved  in  the  water  of  the  blood increases  markedly. Note  that in  the  normal  range  of  alveolar  PO2  (below  120  mm  Hg), almost  none  of  the  total  O2  in  the  blood  is  accounted  for by  dissolved  O2,  but  as  the  O2  pressure  rises  into  the thousands  of  millimeters  of  mercury,  a  large  portion  of the  total  O2  is  then  dissolved  in  the  water  of  the  blood,  in addition  to  that  bound  with  hemoglobin.

I understand that high pressure causes more oxygen to dissolve in blood, but cannot figure out how excess dissolved oxygen in the blood disturbs the normal physiological balance of the body.
I'd be grateful if someone knowing the answer can help me.

This is from a Wikipedia article:
Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness.
Oxygen toxicity - Wikipedia
https://en.wikipedia.org/wiki/Oxygen_toxicity
It says there's hemolysis of red blood cells - i.e., they lyse = break open.


text:
Bacterial cells disappearing from culture with time
While growing my bacterial culture in liquid media for protein expression, I have been observing that the bacterial cells (E. coli) grow well for some till OD600 reaches ~0.4-0.6, then suddenly disappears. The turbid culture having grown cells turned clear, and I could not see significant cell debris precipitated. But I do see some particles that make the media look hazy. Seems like the cells are getting lysed. I have tried changing the media components, resources, temperature, cell lines, genes of interest, etc. BUt nothing seems to work. The pH of the media seems to be the same before and after inoculation and lysis as well. The behavior is quite random and doesn't follow any pattern. Any suggestions on possible causes or similar experiences would be really helpful. Thanks.

That sounds like phage. The pattern of initial growth followed by catastrophic death with some cell debris is classic for induction and lysis.
Have you observed anything strange on plates? You could just do a simple plaque assay using some of your liquid culture to confirm.

I thought of that possibility as well. The transformed colonies on plates with antibiotic looks normal. A few times I have observed wierd colony morphology (not quite circular, but distorted). I did try plaque assay, but couldn't notice any area of clearance on LB-agar plate with bacterial lawn. We fumigated (formaldehyde-permanganate) the lab and all equipment, washed all glassware with bleach, and alcohol followed by autoclaving before preparing fresh media. Still the problem persists. Do you know of any other method to detect/ get rid of phage contamination?

That's tough. I was in a lab that struggled with recurrent phage contamination before, and there isn't a great solution. Fumigation sounds like a good idea - we weren't able to do that. We found a few things seemed to work well enough to keep things under control: this might not work for your combination of phage and cells.
-Virkon is better than bleach. Wash all flasks and regularly wipe down counters,  pipettes, and common instruments and spaces.
-High temperature is better than autoclaving. See if there's an oven you can use to sterilize flasks.

(cont)
-Filter pipet tips may prevent transferring aerosolized phage.
-Try to prevent aerosols in general. Be gentle with your cells and don't leave plates open.
-You mentioned trying alternative strains, but you might look into this a bit more. Some common phage receptors differ between B and K strains, for instance.
-You could try low temperature or cold inductions to potentially reduce induction.
-Regular maintenance: once phage has established itself, you probably want to have regularly-scheduled deep cleaning (especially surfaces where it can linger) to keep it down.

(end)
-Vigilance: you will never remove all the phage, you'll just keep them under control. Make sure everyone watches for signs of lysis and communicates them.

Is it possible that your E. coli strain is a lysogen? Prophage induction at high cell density could explain why your culture is crashing

This might be an unrelated question, but may I know what protein you are expressing ?


text:
Sex chromosome of transgender people
I have always wondered what the sex chromosomes of transgender people are. I mean, sure, the sex chromosomes of males are XY and that of females are XX, and those define those sexes.
But what's the sex chromosome of transgenders?
I have searched in Google, but found no satisfactory answers. They somehow define transgender people as a male who identifies as woman or whatsoever. But I did not get much help regarding the biology behind it.

Welcome FKcos theta. (I've no idea how to produce the character!) Please take our [tour] and refer to the [ask] section of the [help] for guidance as to our ways. You'll note that we require evidence of prior research when posting. Please edit your post to include the foundation for your implicit assertion that there is a biological basis for transgenderism, and your other findings.

@JiminyCricket. Copy/paste seems to work well for symbols/characters in answers/questions, but I've not tried it in comments.

θ - Oh, yeah. Kind of a pain on mobile, but I don't use one here ;) Thanks. @bob1

Your question contains a misconception that should be cleared up first:
XX and XY do not define either gender or biological sex
The biological basis for the assignment of individuals, or parts of individuals, to male or female is anisogamy - that is, the production of microgametes (e.g. sperm) or macrogametes (e.g. eggs). It is this generalised conception of male and female that allows us to talk about sex across from the whole spread of life from birds and ants, through flowers, trees, and algae. Were we to define XX as being female, we'd be surprised to discover that male birds are in fact female (birds use ZW sex-determination), be baffled by the nature of male ants, and completely unable to assign sexes to the flowering parts of flowers, or understand how angler fish can change sex during their lifetimes.
However, this general grounding for a biological meaning of sex is not necessarily a good fit for our more general notions of what sex means. We do not generally exclude pre-pubescent boys or the infertile from having being male or female, for example.
Social gender is grounded in chromosomal and biological sex not defined by it
That said, in humans, the distinction between male and female is usually associated with these two chromosomal pairings: males are normally XY and females are normally XX with this system forming the basis of the random assignment of sexes to offspring during reproduction. However, neither this nor anisogamy are actually used to assign people to either gender; instead we use the external features of their body. Those with external genitalia are assigned as male, whilst those who do not are assigned as female; leaving a few people with intersex features who are assigned to one or the other in a variety of ways.
But whilst that assignment is very likely to match the expected XX or XY chromosomal pairing, it is not always the case. There are a wide variety of conditions, referred to as disorders of sex development (DSDs), that can mean that someone with XX chromosomes can present as male or someone with XY chromosomes can present as female (or a variety of intermediate states). The discovery that someone has a chromosomal abnormality does not cause us to redefine that person as being of a different sex as the one they have always adopted.
Transgender is with respect to the assigned social gender
Someone is, definitionally, transgender if they have changed their gender from the one they were assigned at birth (and thus carried into later life). It is not based on whether or not their current gender matches the expected biological sex based on their chromosomes. Note however, that some people with DSDs who change their gender do not identify as transgender.
Most transwomen are XY, and most transmen are XX
Although gender dysphoria is much more common in people with DSDs than in the general population, the rates of DSDs (0.1-0.2% of the population) are substantially lower than the rates of transgenderism, which are currently as high as 2% and thus most transgender people do not have DSDs. Instead, the majority of transgender people have the expected chromosomes for the gender they were assigned at birth: that being XY for transwomen and XX for transmen.
But there is evidence of biological differences in transgender people
There are many studies showing differences in brain structure (reviewed here) in transgender people, and some reporting genetic and epigenetic associations. This suggests that there is a biological basis for transgenderism although the research does not currently provide any clear explanation of what that might be. This is not surprising as, to date, there are precious few examples of well grounded biological explanations of any complex psychological or behavioural traits in humans.

One supported idea to explain transgenderism is the homones/hormone receptors that control the sexualization of the body and the sexualization of the brain are not identical so its makes haveing a mismatch between the two very possible.


text:
Can two populations of the same species pollinate during different times?
My question comes from the Barron's SAT Subject Test Practice Test #1 question 2
It states:

Two populations of rhododendron, R. ferrugineum, grow in the same region of Connecticut. Although rhododendrons are able to cross-pollinate, these two population never hybridize. Which of the following is the most likely reason for this phenomenon?
A) Genetic drift has caused one populatoin to be betteer adapted than the other.
B) Self pollination is more advantageous because it increases variation in the gene pool.
C) One population produces pollen in early June when the pistils of the other population are not ready to receive pollen.
D)The two populations demonstrate convergence of two separate species over time.
E) The two populations fill different niches

The Barron's book says that the correct answer is C. Why? If the it's the same species, shouldn't they produce pollen at the same time?

Yes, they can.  Consider an original population that produces pollen over a fairly long time, and then something happens to select earlier & later times for different populations.  This is actually quite common for domestic plants such as fruit trees, where different varieties are selected (by humans) to produce fruit at different times.
As far as the question itself goes, it's more a case of the other answers being either obviously wrong, or not supported by the information in the question.

You are obviously right (+1). I do however find the answer peculiar, because I doubt how often this occurs in the wild. A much more logical explanation would be that the two populations are seperated by a mountain range or a desert (and afterwards the pollen time started to grow apart).

@RHA: I don't know how often it would happen naturally, though logically it could be caused by a random mutation, and like anything that produces reproductive isolation, would be the start of the two populations eventually evolving into different species.

given the number of imported or specially bred rhododendrons have two populations end up with different seasonal triggers is not unbelievable. Nowhere does it say they are native species.

@John: Good point!  You got me curious.  I don't recall rhododendrons as being native to the northeast, though apparently there are some.  However, the R. ferrugineum of the question is native to Europe, so ones in Connecticut would almost certainly be garden varieties: https://en.wikipedia.org/wiki/Rhododendron_ferrugineum  So now we can pretty well assume that the populations were selected for different bloom times by humans :-)

There are species native to the US appalachia https://en.wikipedia.org/wiki/Rhododendron_maximum but yes R. ferrugineum is invasive. Because of that the two populations could have two different origin events.


text:
Why are there no multicellular prokaryotes
Why don't complex multicellular prokaryotes exist and also what makes eukaryotes multicellular?

Prokaryotes are called so because they are unicellular. If they were multicellular, they would be called eukaryotes. Similarly, if unicellular, it would be a prokaryote. That is just how these cells have been named.

@TheLastWord "If they were multicellular they would be called eukaryotes" - this is false. The more specific definition of prokaryote vs eukaryote has to do with the presence of membrane-bound organelles in eukaryotes. There are many many single-celled eukaryotes.

@BryanKrause Yes, I got that from the answer. I did not think about single celled eukaryotes.

@TheLastWord True, just don't want a misleading comment to confuse future users that come here, there is no way to downvote a comment, and someone already upvoted yours.

@BryanKrause Yes, I noticed the error much earlier but let it stay so that someone  else does not make the same error.

If you consider mitochondria and chloroplasts, in a way they have.

Why are there no multicellular prokaryotes?

From a Molecular Cell Biology introduction course web resource from the University of Illinios, which explains the general sentiment in microbiology over this question:
There are lots of unicellular eukaryotes, including amoebas, paramecium, yeast, and so on. As to whether there are multicellular prokaryotes, the standard answer is No, but there is a lot of evidence that some bacterial species can aggregate together and divide labor so that the "colony" is working more efficiently. This is characteristic of any traditional multicellular organism, but there's still a lot of resistance to the idea of calling these prokaryotes "multicellular."
Here's a Scientific American article on the subject, which is good for the layman and will add to your understanding. Note that the most complex 'multicellular prokaryotes' known do not form comparably large or complicated structures when contrasted with eukaryotes. Even though prokaryotes have more biochemical tools available to them, their largest multicellular specimen pales in comparison to our small multicellular eukaryotes, let alone out large eukaryotes like the Armillaria ostoyae fungus in Oregon (nicknamed "the largest organism on Earth"), giant sequoia trees, the dinosaurs, or blue whales. But I digress! Total organism size is not a requisite for multicellularity, which is why some bacteria can be termed so.
Here is a paper I found in the literature on the first reported 'true' multicellular prokaryote, from 2004. Similar organisms have been observed since. See Pubmed link.
The same question has also been answered extensively by specialists on Quora and on ResearchGate.

What made eukaryotes to become multicellular?

Your question implies external influence. Biological evolution does not proceed teleologically, with an end goal in mind. Instead, traits gradually accumulate if they are not detrimental to the replication of the genes. The evolution of multicellularity is a complex and active field of research but there is no reason behind this major switch in cellularity other than that it works as a strategy for the replicating organism and its genes. Multicellular organisms survive. That's all.

Why don't multicellular prokaryotes survive?


text:
Is it correct to use the terms multinucleate and syncitia interchangeably?
If you see the skeletal muscle,it is having several nuclei and is said to be "multinucleate".Similarly the cardiac muscle is also having several nuclei yet it is specifically termed"syncitial".So my question is: Is there any reason behind this or are the terms interchangeable?
I am listing the sources from which the question came up in my mind:
[Source1]

Individual muscle fibers are formed during development from the fusion of several undifferentiated immature cells known as myoblasts into long, cylindrical, multi-nucleated cells. Differentiation into this state is primarily completed before birth.[Source2]
The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium.[Source3]

No, the terms multinucleate and syncytium are not synonymous in this context.  Most cardiomyocytes are not multinuclear. To be clear, syncytium is used to refer to multinuclear cells that originate from fusion of uninuclear cells, including the skeletal muscle, but that isn't what is referred to in the context of cardiac muscle.
The Wikipedia page on syncytium summarizes this nicely:

Cardiac tissue is therefore described as a functional syncytium, as opposed to the true syncytium of skeletal muscle.

The "intercalated disks" of cardiac muscle are filled with gap junctions and desmosomes. The desmosomes hold the cells together physically, while gap junctions allow ions (and small molecules) to pass directly between cells, forming "electrical synapses". This allows electrical signals to propagate between the myocytes to coordinate contraction.
Gap junctions are formed by proteins, rather than fusions of the plasma membrane, so they are relatively small. This means that not everything in the cytoplasm can pass through them, mostly just ions and some small molecules. Proteins, for example, would not pass through gap junctions. Therefore, cells that are connected via gap junctions, like cardiomyocytes, are still somewhat independent, unlike fully multinuclear cells.
There are also types of neurons, including some in the CNS, that also form gap junctions and act at least somewhat in concert in this way.


text:
Are all phenotypes normally distributed
Reposting from the stats stackexchange.
John Cook, in his blog https://www.johndcook.com/blog/2015/03/09/why-isnt-everything-normally-distributed/, writes that many aren't:

Adult heights follow a Gaussian, a.k.a. normal, distribution [1]. The usual explanation is that many factors go into determining one’s height, and the net effect of many separate causes is approximately normal because of the central limit theorem.
If that’s the case, why aren’t more phenomena normally distributed? Someone asked me this morning specifically about phenotypes with many genetic inputs.
The central limit theorem says that the sum of many independent, additive effects is approximately normally distributed [2]. Genes are more digital than analog, and do not produce independent, additive effects. For example, the effects of dominant and recessive genes act more like max and min than addition. Genes do not appear independently—if you have some genes, you’re more likely to have certain other genes—nor do they act independently—some genes determine how other genes are expressed.
Height is influenced by environmental effects as well as genetic effects, such as nutrition, and these environmental effects may be more additive or independent than genetic effects.

I have two questions regarding this. First, I can't come up with any obvious example of phenotypes that don't follow a normal distribution. Could anyone help me? And second, his claims seem to contradict this other paper: https://www.uvm.edu/~dstratto/bcor102/readings/4_Evol_of_Phenotypes.pdf

To understand the genetic basis of quantitative traits, it is important
to think about the effect of a particular allele, not simply its
presence or absence. A single locus can produce three discrete
phenotypes, but as more and more loci contribute to a trait the
phenotypic distribution comes closer and closer to a normal (bell
shaped) distribution

Who is right here? Does the fact that genes are digital rather than analog really make a difference? And what about the second argument that they aren't independent. Is that really necessary (second paper seems to indicate otherwise if I am understanding properly).

What about the most obvious Mendelian traits? Those would be phenotypes that follow a bimodal distribution, because they are caused by a single gene with just two alleles. Many other phenotypes also follow a bimodal distribution for the same reason. As you add in more modulatory or regulatory genetic variation you will smear the distribution and it will become more normally distributed. That is exactly what your references are telling you.

Many phenotypes might be normally distributed assuming a large enough population size and many QTL (Quantitative Trait Loci) as the normal distribution is a simple result of the CTL (Central Limit Theorem). If it is unclear to you, you should definitely have a look at the central limit theorem.
Typically, if the number of loci is too low, the phenotype may for example follow some kind of continuous approximation to a Poisson distribution. Of course, if the allelic effects are correlated among loci or if there is some linkage disequilibrium or if the phenotype is bounded or discrete, or nominal, you may not end up with a normal distribution of phenotypes but all of that is a discussion for another time.

I can't come up with any obvious example of phenotypes that don't follow a normal distribution

As, the second quote says, think of any phenotype that is discrete. Here are a few examples

sex
right / left handed
eye color

Now if you want a quantitative phenotype that is not normally distributed, then height (which is the bad example of your first quote) is very slightly bimodal due to an average height difference between male and females (look at Are males taller than females in humans?). You can also think of any phenotypes that are bounded. For example running speed. Athletes will cause a very long right tail, while people in wheel chairs will make a big stack of probability mass in 0 km/h.
There is a lot of things to consider when trying to guess whether a is normally distributed or not in a population. It will take some good knowledge of statistics and good knowledge of the genetics of the population.

Thanks for this clear answer! I've never been convinced by the "height can't be normally distributed because it can't be negative" argument, since it can still be approximated reasonably well by a normal. Running speed seems like something you can't approximate with a normal then, but I didn't know it's considered a phenotype! Any explicit example for something that follows a poisson distribution?

Pretty much anything can be a considered a phenotype. A phenotype is whatever effect the genotype has on the world around it which mainly include all the characteristic (behaviour, anatomy, physiology, ...) of the body. I should have said "some kind of 'continuous approximation' to a Poisson distribution'" (now edited). It is just some theoretical reality of a model where there are few loci all biallelic with allelic effect 0 or 1, then you would see Poisson distributed trait. I can't give a specific example.