How does Genetic drift and selection affect fixation of an allele? I want to know how does genetic drift, and selection coefficient (s) together affect the fixation of an allele? For example, if there is a neutral allele (s=0), will only genetic drift cause the fixation or loss of an allele? Similarly, if an allele is beneficial which means that s > 0. In that case, how do genetic drift and selection coefficient together determine the fixation and loss of an allele? And what happens when s < 0 that is an allele is deleterious. Lastly, how do genetic drift and selection coefficient gets affected by the population size? I am reading about population genetics, and I am totally confused by this point. I would appreciate if someone can clear this to me.

It would take a lot of writing to fully answer your question. Below I give an answer without spending too much time on the underlying math assuming you are confortable with probability theory and Taylor series. If you really want to understand more of all of that you would just need to consider reading a book in population genetics (see end of the post for recommendation).
Probability of fixation under drift only
In absence of selection, mutation and migration, drift only may yield an allele to eventually reach fixation (or loss). The probability of an allele to get fixed is then just equal to its frequency $P_{fix}=p$. When the neutral mutation has just arisen, this probability is therefore $P_{fix}=p=\frac{1}{2N}$ for a diploid population of size $N$.
See this post for more information.
Drift and population size - Intuition
For some intuition about the effect of population size on drift you might want to have a look at Why is the strength of genetic drift inversely proportional to the population size?.
Drift and population size - Effective population size
To go a little further than the linked post, note that the the strength of genetic drift is defined by what we call the effective population size $Ne$. But before talking about that let's talk about the variance in possible allele frequencies in the next generation (which we'll call $var(p')$).
The number of alleles $A$ in the next generation follows a binomial distribution (if we follow Wright-Fisher model). The variance of this binomial distribution is $2 p N (1-p)$, where $p$ is the frequency of the allele $A$ in the previous generation. Dividing this variance by $(2N)^2$ (the square is caused by the fact that $var(k X) = k^2 var(X)$, where $X$ is a random variable), to get the variance in allele frequency in the next generation
$$var(p') = \frac{p(1-p)}{2N}$$
We define the strength of genetic drift as $var(p')$ and for intuition, we usually refers to it as the value of $N$ that corresponds and to avoid confusion with the actual population size we call this new measure $Ne$. Therefore,
$$var(p') = \frac{p(1-p)}{2Ne}$$
Solving for $Ne$ yields to
$$Ne = \frac{p(1-p)}{2var(p')}$$
and this effective population size $Ne$ is what we use to talk about strength of genetic drift.
Probability of not reproducing
As I will refer to this statistic later, I will introduce it here. What is the probability of a given individual to not reproduce? Let's call this quantity $P(k=0)$ as the probability that the number of offspring $k$ is $0$.
Imagine you sample $2N$ haplotypes (with replacement) to form the next generation and each of them has a probability $1-\frac{1}{2N}$ to be chosen, the the probability of not reproducing is $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N}$. Taking the Taylor series of this expression for large values of $N$ yield to the approximation $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N} ≈ e^{-1} ≈ 0.37$. So, any individual has a probability greater than a third to leave any offspring in the following generation.
Probability of fixation under both drift and selection
If an allele if beneficial, then its probability of fixation is greater than its frequency $p$ (and vice-versa if deleterious).
Approximation
There are a number of ways to derive such probability and they all end up with some complicated form. An easy approximation (which I am not going to make any demonstration) for this probability is
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4Nsp}}$$
Just to give you some intuition about the form of the above approximation (but without doing a full demonstration that would be quite long), consider that the number of offspring an individual have follows a Poisson distribution with fitness as the rate. The fitness of the mutant individual is $1+s$, and therefore the probability of this individual of having $k$ offspring is
$$P(k) = \frac{(1+s)^k e^{-1-s}}{k!}$$
Think of the generation where the mutation just arised and only one individual has this mutation. The probability of this mutation to disappear immediately is therefore
$$P(0) = e^{-1-s}$$
, which for reasonable values of $s$ is not very different from the probability of not reproducing when $s=0$ and the probability become $e^{-1}$ (as already shown above via an other mean).
A less accurate approximation (but with a very easy form) for the probability of fixation is
$$P_{fix} = 2Ns$$
Some more calculations about the interplay of drift and selection can be found in this post.
Source of information
The post Book recommendation on population/evolutionary genetics? will give you great sources of information to learn more on the subject. It will also re-explain what I just said with a lower pace. I particularly recommend Population Genetics: A Concise Guide


How do transport/carrier proteins rotate during facilitated diffusion? In my book, it is written that when a molecule binds to the carrier protein then the protein rotates and releases the molecule inside the cell. I want to know how is this possible. Wouldn't the surrounding phospholipid molecules or other proteins hinder its rotation?

EDIT

The rotation axis is in the plane of membrane

Source : http://ncert.nic.in/ncerts/l/kebo111.pdf (page 177, Third paragraph)

"How do transport/carrier proteins rotate during facilitated diffusion?"

They don't. The explanation in the PDF you linked...

  Figure 11.1 shows an extracellular molecule bound to the transport protein; the transport protein then rotates and releases the molecule inside the cell.

... is an oversimplification, to say the least (you could simply say that this is plain wrong). What really happens is way more complex.

We call it conformational change.

According to Alberts, Molecular Biology of the Cell (2002):

  Each type of carrier protein has one or more specific binding sites for its solute (substrate). It transfers the solute across the lipid bilayer by undergoing reversible conformational changes that alternately expose the solute-binding site first on one side of the membrane and then on the other. (emphasis mine)

This is an image that explains way better the process, from the same chapter in Alberts (the legend provides a detailed explanation):

Figure 11-11A model for the molecular mechanism of action of the bacterial lactose permease (A) A view from the cytosol of the proposed arrangement of the 12 predicted transmembrane helices in the membrane. The loops that connect the helices on either side of the membrane are omitted for clarity. A glutamic acid on helix X binds H+, and amino acids contributed by helices IV and V bind lactose. (B) During a transport cycle, the carrier flips between two conformational states: in one, the H+ -and lactose-binding sites are accessible to the extracellular space (1 and 2); in the other, they are exposed to the cytosol (3 and 4). Unloading of the solutes on the cytosolic face (3 → 4) is favored because the lactose-binding site is partly disrupted and a positive charge contributed by an arginine on helix IX displaces the H+ from the glutamic acid on helix X. (A, adapted from H.R. Kaback and J. Wu, Accts. Chem. Res. 32:805-813, 1999.)

Thus, as you can see, we have conformational states: one of them exposes the binding site to the extracellular space, while the other one exposes the binding site to the cytosol. Just like what happens when an enzyme changes conformation, the 3D changes in the protein structure are quite small, and it's hydrophobic regions keep in the same place in both states.

Source: Alberts, B., Johnson, A. and Lewis, J. (2002). Molecular biology of the cell. 1st ed. New York: Garland Science..


Do non-functional (‘junk’) protein sequences exist? For DNA one can distinguish between

protein-coding DNA sequences, i.e. nucleic acid sequences inside DNA (vs. non-coding sequences)
DNA sequences that do not code for proteins but are transcribed into functional RNA
non-transcribed DNA sequences that have other (e.g. regulatory or structural) functions
non-transcribed and non-functional DNA sequences (‘junk DNA’)

The relative proportions of these seem to depend heavily on the organism and are only roughly known.

  What I wonder is whether there are protein sequences (i.e. amino acid sequences inside a protein) that have no functional purpose.

A non-functional protein sequence might be a sequence that is neither effective to the outside (e.g. as a site for post-translational modification) nor to the inside (e.g. in folding). But even those parts of the protein might contribute structurally by their sheer presence and mass which is important when considering proteins not only as chemical but also as somehow mechanical devices. This might be called its structural purpose.

Assuming that each part of a protein has either a functional or only a structural purpose the question arises what the relative proportions of functional vs. only structural parts are.

This question is unanswerable as, if a protein exists as a physical entity in a cell it is possible to demonstrate it has a functional or structural role, but it is logically impossible to demonstrate it has no such role. The best one can say is that “it has no known function (role)”.

That said, in the course of evolution following gene duplication and divergence it is theoretically possible that on the way to acquiring a new functional role there is a stage at which a protein has no such role. One might be able to identify such proteins in a gene family like the globins by examining a range of species, as has been done for the globin genes. I am not aware of any such studies.


Why is there disagreement on the number of surfaces of the human heart? I am finding that some state that there are 5 and some that say that there are 3.

For example, "Cardiology: An Integrated Approach" that was published in 2018 states that

  There are 3 surfaces of the heart: anterior, inferior, and posterior

Radiopedia, Teach Me Anatomy, and others state that there are 5.

Why is there this difference? What exactly is a surface?

Heart surfaces are not clearly anatomically defined but arbitrary determined in the context of the heart orientation, that is the relation of the heart to other organs. Different sources mention 3 or 5 heart surfaces and there seems to be no "official" agreement about this.

Most sources (Dartmouth College, Gray's Anatomy for Students 2004...) agree about at least 3 surfaces:

Anterior (or sternocostal)
Inferior (or diaphragmatic)
Left pulmonary

Many sources (TeachMeAnatomy, KenHub...) mention additional 2 surfaces:

Posterior (or base)
Right pulmonary

The reasons for disagreement:

The heart base may not be considered a distinct surface (as in the picture).
The right pulmonary and anterior (sternocostal) surface are often considered one surface.

Picture: Heart surfaces (source: Echo Class 101)


Do nerves work as I think they work and what does that mean for our senses? Let me start off with a couple of metaphors.

In the third Lord of the Rings film, a signal for help is sent from Minas Tirith to Gondor, using a chain of beacons. When the keepers of one of these beacons sees that the one next to his lit, his orders are to light his own thus passing on the chain reaction. When the last one within sight of Gondor is lit, the message that Minas Tirith wants help is received.
There is nothing conveyed in the fire itself, no information within the flames, the beacons are either on or off. The only reason the beacons convey a message is that the citizens of Gondor know why that beacon would be lit.

Imagine a simple pressure sensor inside a building that is connected by a wire to an electric light on a control panel in a security room. When someone steps on the sensor it completes the circuit which sends electricity straight to the light turning it on. A label on the light says what it's connected to and where it is. So that when the light comes on, the person at the control panel knows someone is in that sector of the building.
But to be more precise, he knows someone has activated that particular pressure sensor, if it wasn't labelled he would have no idea what the message meant.

My understanding of the human nervous system is that it works in the same way. Based on information I learned from children's educational programs as a child and a few bits I picked up since.

Our ears have sensors designed to respond to sound. Each and every one has a direct connection to the brain via a chain of nerve cells. When one of the sensors is sufficiently stimulated, it zaps the neuron it's connected to, this in turn causes the neuron to zap the next one and so on all the way up to the brain.

The impulses/spikes themselves contain no actual information, they are just pure electricity, every spike contains the same amount of voltage. The only reason the brain is able to interpret them is because it knows exactly where each and every chain is connected to. When the impulse reaches the brain it knows it comes from a sensor in the ear that is responsible for a particular level of sound, the brain takes these signals and translates them into the sounds we hear. Nerve cells work something like binary, they are either on or off with nothing in between. The frequency of the spikes going along the chain indicates how intense the sound is. If the brain didn't know where that chain was connected to then the signal could mean absolutely anything.

This is supported by the condition known as synaesthesia where, because "wires are corssed" in the brain there are people who hear colour or taste music.

My questions are, is my reasoning correct? Is this exactly how nerves and perception work? Has this been scientifically proven beyond a doubt? Is there something within the impulses that contains additional information? Are the workings of the nervous system debated in scientific circles? I've been told we've never been able to plug an eyeball or any other kind of human sensory device into a computer so we've never been able to examine it as it's working, is this true?

But most of all, does this mean there are things our senses cannot detect?
I already know there are things beyond our range of vision and hearing and the brain blurrs then together. What I mean is this...

I know that we have different senses in our ears that are designed to respond to higher or lower sounds. Say we have a sensor that responds to a level 1 sound (I don't know the unit of measurement for sound) and next to it is a sensor that responds to a level 2 sound. What happens if we try to hear a 1.5 sound? Is it not detected by the ear because we don't have sensors in that range?

Can we only sense something if we have a sensor for it and are those sensors only built to sense one ultra specific thing?

I'll attempt an answer, but please know you don't have a clear nor defining question to address. This is more suited for conversation or open discussion, and I recommend starting a chat on the topic. Please be wary the question may be put on hold. I'll give it a go and respond from the top down. I absolutely don't think this is going to be fruitful for other people. Here goes:

  Our ears have sensors designed to respond to sound. Each and every one
  has a direct connection to the brain via a chain of nerve cells. When
  one of the sensors is sufficiently stimulated, it zaps the neuron it's
  connected to, this in turn causes the neuron to zap the next one and
  so on all the way up to the brain.

Take the example of the eye; the retina is composed of photosensitive neurons, a type of sensory neuron. The inner nose is innervated with olfactory sensory neurons. The cochlea is similarly innervated by neurons. Firstly, you haven't made it clear that the neurons are the sensors. But indeed, the sensory neuron is the first order neuron. The processing of sensory information proceeds through first, second, third and higher order neurons until the information is integrated functionally somewhere in the brain. There exist neurons that modulate the signal along the way (e.g. lateral inhibitory interneurons) that are not on the information highway but rather beside it, regulating the input and output of neurons. It's quite complex, but you have the general gist of the hierarchy of neurons from sensory input (e.g. odor) to output (behavior, response, perception).

  The impulses/spikes themselves contain no actual information [...]
  Nerve cells work something like binary, they are either on or off with
  nothing in between.

The exact temporal dynamics of this communication highway between neurons is very important. At some level, auditory volume may be coded by frequency, but this is restricted only to some level. Information is very quickly encoded and the 'raw' information sensory neurons provides becomes processed and transformed quite early in the chain. For instance, you may trigger circuits responsible for reflexes, which are (so-to-speak) dormant until a kind of neural activity activates them. Vision is well described in terms of encoding; at the first processing area of the brain for vision, things are simple, and are progressively more high-levels of encoding as the information is processed; there are regions responsible for motion, color, object recognition, even specialized regions for the recognition of faces, for instance.

  If the brain didn't know where that chain was connected to then the
  signal could mean absolutely anything.

Correct. Remember though that the brain is very plastic, and can learn. There are many curious cases in neuroscience where this is apparent. One well-known widely described example: you can wear glasses that invert the world, and this would feel strange. After some time though, your perception would switch the world the "right way up". The retina has been largely unaffected, but the perception and the integration of the information can drastically vary quite independently.

  Is there something within the impulses that contains additional
  information?

Remember that there are two kinds of connections between two neurons. Electrical and chemical synapses. A wave of depolarization does indeed travel through a neuronal axis, but in most cases, this does not occur across neurons. Instead, neurons (and related cells such as glia) release chemical messengers (neurotransmitters and neuromodulators) that act as inter-cell signals. These can inhibit or excite the post-synaptic neuron. Simply put, it's not a string of wires; it's a line of wires that interface with each other chemically; at each interface, chemicals must diffuse across the gaps and interact with the membrane-bound sensors found on the receiving neuron. This is not at all binary. And please know we are simplifying the system in order to describe it.

  Is this exactly how nerves and perception work?

This is a simplification of how neural circuits work. How perception works is a completely different thing you have not even begun to address. This is a completely different topic of discussion. Bonus link!

  But most of all, does this mean there are things our senses cannot detect?

A sensory system can only detect what it can detect. Your skin cannot detect radio waves. Your eyes cannot detect infra-red light. Your mobile phone, similarly equipped with sensors, cannot detect neutrinos.

  I don't know the unit of measurement for sound

Decibel (volume) or hertz (pitch or frequency).

  What happens if we try to hear a 1.5 sound? Is it not detected by the
  ear because we don't have sensors in that range?

You are describing the spectrum of volume as a graded, discontinuous thing. It's not! And more generally, yes. If your sensors cannot detect something, the organism is oblivious to it. Obvious.

  Can we only sense something if we have a sensor for it [...]?

Yes. But you underestimate the power of a sensor such as a photosensitive cell. It can transmit information about the amplitude of the light, and responds to a range of light. Moreover, each photosensor has a response spectrum and does not respond equally to different (although similar) wavelengths of light. More so, if you have a patch of photosensitive cells, you can infer motion, direction, speed, size, distance, and all the merry things we associate with vision. The wealth of information is easy to underestimate.

  ... are those sensors only built to sense one ultra specific thing?

It depends on how you define specific. The equipment of a neuron in the retina is usually specific (e.g. expression of proteins responsible for light sensitivity) but it's possible to have a neuron that is responsive to several things. Have you ever tried to rub your eyes, and you see phosphenes? Your retina is responding to the increased pressure. You could say these cells are sensitive to light and pressure. That's not ultra specific. You can similarly activate these neurons at short range electrically, or magnetically. That's starting to sound like a pretty unspecific sensor, depending on how you define it for yourself.

I absolutely don't mean to aggravate, I very much suggest you do some readings on the topic. It's one thing to have a pub-level confidence in vaguely worded funfacts about sensory circuits, and another to understand and appreciate the nuances and complexity and the many knowns and unknowns of neuroscience. It's not too difficult to grasp. I would instead ask you to ask about fundamentals before you ask to correct your outlook on biological sensory systems. Books are cheap and the internet comes in handy sometimes, and you may even spare someone else's time!


Why does the heart use lipids (and not glucose)? Fetal hearts use glucose as their primary metabolic substrate.  Adult hearts use free fatty acids, which are less efficient (require more $O_2$ to synthesize the same amount of ATP); however, during cardiac failure, the heart can switch to glucose utilization.  Why doesn't it just use glucose all the time?

Lipids require more oxygen to burn, but also they are cheaper to store (since they have great calorific power than carbohydrates and they're hydrophobic, thus not requiring water for their storage). The body can store so much lipids that it becomes an almost everlasting energy source (A normal adult have enough energy stored as fat to allow basal metabolism for weeks to months), which cannot apply to glucose. If fat is not present, glucose would have vanished from the body long time ago. Glucose levels must be maintained at a certain level, because it's the main energy source for the brain (which cannot use lipids ). The brain can use ketone bodies (product of fat oxidation) as a last resort.

For all the previous reasons, the heart (and many other organs, like the liver) uses fat while possible. If possible just means when not starving to death and with sufficient oxygen supply. This second condition doesn't apply to heart failure. In this case, oxygen supply fails and the tissue switch to glucose just because they can use it without oxygen (glycolysis and lactic fermentation).


Is this a Wolf Spider? I live in Illinois and this came running across my living room floor.  After I stopped freaking out, I threw a bowl over it and called someone to come get it.  It was about 5” across.  My son thought it was a wolf spider but I didn’t think they got that big.  I hope someone can help to identify it.  Just the thought of there being more around is making me want to book a hotel!

That's not a Wolf Spider, although it's often mistaken for one.  The long, jagged-edged-banded legs, splayed out in a characteristic flat posture, and the large, round carapace are pretty characteristic indicators of a Dolomedes fishing spider - one of the terrestrial ones that have moved into drier, upland areas and hunt more like Wolf Spiders do.
There are two species this could be, but the fact that you don't see a full white underline beneath the 'w's on its abdomen tells you it's not Dolomedes scriptus, but its common relative Dolomedes tenebrosus.
These spiders are actually pretty mild-mannered and can make good pets (as spiders go), but they will bite if bothered too much (how much "too much" is seems to be different from spider to spider).  The bite can be painful because of their size and large fangs, but the venom is not particularly effective against humans.  I'd rate it as a lot less painful than even a mild wasp sting, although of course every individual spider and every individual human is different.
Here's a link to the Bug Guide page, which has more information and lots of photos..
https://bugguide.net/node/view/2011

I should also add that these guys eat beetles and other relatively large insects and small animals that you might or might not want to share your home, if that makes any difference.  I can't see its pedipalps clearly, but the large cephalothorax and relatively small abdomen make me suspect it's an adult male, just wandering around looking for love.  It's unlikely that you have all that many individuals living with you - unless you have a dirt cellar, of course; they seem to like places that are a bit cave-like.

I also forgot I'm supposed to include an image:


Is there a database of pollen-seed distances across plant species? I was enjoying Richard Smith's excellent answer to this question, and wondered:

If you consider the pollen/seed distribution range to be plant locomotion, is there a database that compares these distances across plant taxa, or perhaps a paper that treats these distances as a trait (in a phylogenetic context, for example)? One might assume that in the transition from wind-pollination to animal pollination (or from wind seed dispersal to animal seed dispersal) there is a sacrifice of decreased distance for increased "accuracy", but maybe this isn't the case.

It seems like this information should be around somewhere – it has relevance to evolution, speciation, climate change adaptation, etc.

In my searching I didn't find a comprehensive database of this information. There are biologists interested in analyzing seed dispersal distance as a trait however.

Vittoz and Enger (2007) used plants with known seed dispersal along with characteristics about these species to predict dispersal distances for other species.

There is another study here that examines the relationship of plant height and seed dispersal. They provide interesting background information as well on the trade-offs associated with a particular dispersal mode. For example,

"It is often assumed that there is a trade-off between maternal provisioning and dispersal capacity, leading small-seeded species to disperse further than large-seeded species."

It is certainly an area of research actively being pursued but there doesn't seem to be a list or database of these dispersal traits by species. There is information on dispersal distance by mode in the appendix of the second link I've provided.


which signalling pathway is involved in cancer? Columnar epithelial cells from the colonic mucosa are studied to identify abnormalities in cell signaling pathways. Abnormal epithelial cells from colonic adenocarcinoma are shown to have a mutation that blocks hydrolysis of GTP-bound active RAS. Normal columnar cells have active RAS protein that undergoes hydrolysis to the inactive GDP-bound form. Which of the following signaling pathways is most likely abnormally stimulated in the carcinoma cells?

a. Jak-Stat Pathway
  b. MAP kinase pathway
  c. p53
  d. Both a & b

I think its MAP kinase pathway because RAS is part of MAP kinase pathway that ultimately leads to transcription and expression of genes but if GTP is not hydrolyzed then RAS will be constantly activated leading to continued gene expression that may lead to cancer but I am not completely sure about it because p53 is also a tumor suppressor gene.

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below:

If you are interested in more details, have a look at these papers:

RAS oncogenes: weaving a tumorigenic web
RAS mutations and oncogenesis: not all RAS mutations are created
equally


Role of epigenetics in evolution and transmission of defects caused by drugs In a documentary, they were saying that epigenetics changes caused by the environment in an individual can be transferred to the following generations. I have some questions on that:

How many generations are affected by an epigenetic change? can this be permanent?

Can drugs cause epigenetics changes in the current population that are visible in the following generations in the form of disease and birth defects?

Do epigenetic play any role in evolution? For example, is it possible that an epigenetic change becomes a permanent genetic change after a certain number of generations?

Generally speaking, epigenetic modifications are not inherited as they are reset during embryogenesis. However, subsequent epigenetic modifications can be acquired during the period of pregnancy, which as a mechanism depends on the epigenetic state before the reset and on the physiological conditions of the mother including nutrition, health, stress, etc.. Obviously drug-intake years before pregnancy can still affect the mothers health-state.
Answering your first question: Epigenetic modifications generally cannot be directly passed, but indirect effects could theoretically pass through multiple generations without hard limit.

A major barrier to transgenerational epigenetic inheritance is germline reprogramming, during which histone variants and their modifications, as well as small RNAs and DNA methylation, are all reset. In mammals reprogramming occurs both in the germline and in the zygote immediately after fertilization. (Source: Heard & Martienssen 2014 doi: 10.1016/j.cell.2014.02.045)

2: The great potato famine is said to still have epigenetic effects, generations later. 3.: Epigenetic changes cannot directly "become permanent" as genetic changes, although hypothetically speaking, epigenetic states can lead to viability of certain mutations that would otherwise be lethal and can therefore in theory influence evolution.


How to automatically obtain the "kingdom" of a species from its name? I'm looking for a simple way (such as a database) so that a program can get the kingdom of a species, knowing its name (such as "Prunus persica"). As a matter of fact the species I'm concerned with are the ones in the miRBase database.

You could try the Catalogue of Life

  The Catalogue of Life is the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species. This figure continues to rise as information is compiled from diverse sources around the world.

You can export the search results (in the above example indicating Kingdom Plantae for search term "Prunus persica") and analyze the exported table in your program of choice.


How does the telomere repeat sequence vary in Eukaryotes? Question:

How does the telomeric repeating sequence vary in non-vertebrate Eukaryotes? If you know the repeating sequence of a given species I would appreciate hearing it.

Background:

Telomerase is a ribonucleoprotein enzyme that adds DNA sequence repeats to the 3' end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes.

In vertebrates the conserved telomeric repeating sequence is "TTAGGG".

A database that answers the question, charting telomere repeat sequences for all known species, is: http://telomerase.asu.edu/sequences_telomere.html

For example in Yeast:


Is it possible to stop more/extra fat from being stored in the body? I don't mean simply by restricting eating or upping the activities, but a way to basically stop the body from adding more fat on itself down on the bio level. For example, I'm not too knowledgeable on this, but I believe fat is stored when the body can't make any extended use of extra energy put in to it.

Given such, could we simply direct the body to only use the energy needed and dispose of any "extra" while not storing it as fat/triglycerides? I know there are drugs that can speed up metabolism and etc., but this only heightens the body's ability to remove said fat -- not stop the process at which it is stored

This would be a great thing because then we could assure the body only uses the energy on what can be beneficial to us -- all the "rest" can be removed and not stored on us and being a con instead of a pro.

So in summary: Is there any feasible way this could be theoretically possible, given our biochemistry/physiology?

Fat storage comes from conversion of glycogen (a glucose polymer) to triglycerides (fats).  (source: https://en.wikipedia.org/wiki/Glycogen).

Intuitively, the simplest way to prevent fat storage is to block conversion of glycogen to fats. Unfortunately, this will cause a glut of glycogen which can cause an entirely different set of problems (see https://www.hopkinsmedicine.org/health/conditions-and-diseases/glycogen-storage-disease ), so you would want to couple this with a mechanism to eject excess glycogen.

Referencing what user1136 posted: uncoupling oxidation from phosphorylation is a really bad idea. That would basically "burn" fuel while blocking the expected ATP outlet. This will cause a dangerous energy buildup in the mitochondria which has to be unloaded somewhere - provable simply by conservation of energy. Energy can be converted to other forms of energy, but it is never destroyed. Physics is the ultimate anti-cheat tool.

Blocking expected energy outlets is almost always a bad idea in practice. Just to name some practical examples:

In archery class, instructors will warn you never to "dry-fire" a bow (draw the string back and release with no arrow). This can compromise the bow's structural integrity, causing it to splinter, snap, or explode later.
Microwave ovens should never be operated empty with no sink for the electromagnetic radiation they produce - this can damage them. See https://physics.stackexchange.com/questions/309154/what-happens-in-an-empty-microwave-oven for more info.
If you jam the pistons in a standard cylinder-based combustion engine (prevent them from moving), you end up with a lot of energy that needs to go somewhere, which will end up as massive vibration and extra heat - either of which could damage the engine as the design never expected this to happen.


How do nuclear receptors locate each other to form a DNA loop? Nuclear receptors can influence transcription far up- or downstream from their own binding sites by looping DNA (Rubina et al.; J Mol Bio 2004).

I am not sure how exactly the receptors first attach to the DNA (dimers on each site first or the whole complex on one site), but in any case they will need to attach to one response element, then loop the DNA and bind the other response element. It seems like something that should be obvious, but I cannot stop wondering: How do the receptors locate the other site?

Normally I would simply say: diffusion - it just randomly happens. But I imagine bending DNA in such a way would require a lot of energy; too much to just randomly waste it trying to find another site.

This probably isn't the complete answer as I don't know so much about eukaryotic transcription, but maybe I can start the answer.

First of all DNA bending can be sequence dependent - the double helix is not intrinsically straight.  DNA is also pretty easy to bend - it spends most of its time coiled pretty easily around histones, and eukaryotes, supercoiled into chromatin.

In transcription though, there are proteins that come along and effect bends in the DNA or even tight loops, so that the transcription initiation complex (TIC) can be activated by transcription factors (TFs) upstream as the DNA flops over.

see this happening in this video at about :40:
http://www.youtube.com/watch?v=5MfSYnItYvg&feature=related

I think in some cases there might be other proteins bound upstream of the TIC to make the influence of various TFs greater.   I know in highly regulated genes (such as developmental genes in animals) transcription regulation can be impossibly complicated with lots if internal logic.  The classic example is ENDO16 from sea urchin (see second image) which has scores of protein binding sites in front of it.

I was told that DNA binding proteins find their binding sites at a rate faster than diffusion.  The prof told me that she thought that there might be a tendency to diffuse along the length of the DNA because of its charge.  I have no reference for this, but it might help answer your question as to how the NRs pair up so quickly.


What is the role of potassium acetate in plasmid extraction? What is the role of potassium acetate in the alkaline lysis method of plasmid extraction?

Earlier I was thinking its role is to shield plasmid DNA (the same as sodium acetate in genomic DNA extraction). When 100% ethanol is added, it the DNA precipitates and then we remove potassium ions from the pellet using 70% ethanol.

However, I have read that potassium acetate does not have the same function as sodium acetate in genomic DNA isolation but, rather, is a neutralizing agent which helps small plasmid DNA to renature.

I am bit confused about the role of potassium acetate and why sodium acetate cannot be used instead.

The alkaline lysis method of plasmid purification involves the addition of sodium dodecyl sulfate to lyse the cells and sodium hydroxide (a strong base) to denture the DNA. Potassium acetate is then added for two reasons:

The acidic acetate buffer neutralizes the solution and allows catenated plasmids to renature.
Potassium dodecyl sulfate is poorly soluble in water. Adding potassium to solutions of dodecyl sulfate precipitates it, thus facilitating its removal.


How do circulating androgens contribute to higher rates of hirsuteness in some women? I was reading up on ethnic groups in which the women are naturally more hirsute (such as South Asian women) in the context of evolving standards of beauty. I came across this statement on a forum:

  Hirsutism is much more common in South Asian women (particularly North Indians such as Punjabi Sikhs) asymptomatically because they tend to have higher levels of circulating androgens than your typical [North or Western European ethnic group]. This is also true of Eastern European women to an extent.

Per Wikipedia, I learned:

  Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing sex differences.

So: do circulating androgens trigger higher testosterone production in some women? Is this what yields higher instances of "hirsutism" among certain populations? How are some women more prone to this than others? (That is, per the forum post, why are South Asian women more likely to have this than Western European women?)

This review may be of interest:

Sharma D, Shanker V, Tegta G, Gupta M, Verma GK. Clinico-investigative profile of patients of hirsutism in a tertiary level institution. Int J Trichol [serial online] 2012 [cited 2013 Feb 9];4:69-74. Available from: http://www.ijtrichology.com/text.asp?2012/4/2/69/96904

As for the genetic causes of hirsutism, researchers thought the number of CAG repeats in the androgen receptor gene might play a role, but there was no evidence to that effect, as of 2000.  I couldn't find any newer papers, but here you go: http://jcem.endojournals.org/content/85/4/1735.
This paper was cited by the previous review, but Sharma et al didn't read more than the title, because they cited Calvo et al as evidence for the role of CAG repeats in hirsutism.

tl;dr: read Sharma et al, and look up the references.


Darwin's first sketch of a phylogenetic tree Coming from Darwin's notebook this first sketch of a phylogenetic tree became one of the most emblematic image from Darwin's work.

I have a hard time to read what is written on it.

What is written on this page?

This is from Darwin's Notebook B: Transmutation of species from 1837–1838. From what I understand, the tree is a hypothetical depiction of descent used to discuss differences and relatedness between forms/species. This is the text that accompanies and follows the sketch (notebook pages 36-44):

  I think
   (sketch)

  Case must be that one generation then should be as many living as now. To do this & to have many species in same genus (as is) requires extinction.
  Thus between A & B immense gap of relation. C & B the finest gradation, B & D rather greater distinction. Thus genera would be formed. — bearing relation

  (page 37)

  to ancient types. — with several extinct forms
  for if each species an ancient (1) is capable of making 13 recent forms, twelve of the contemporarys must have left no offspring at all, so as to keep number of species constant. —
  With respect to extinction we can easy see that variety of ostrich, Petise may not be well adapted, and thus perish out, or on other hand like Orpheus being favourable

  (page 38)

  many might be produced. — This requires principle that the permanent varieties produced by inter confined breeding & changing circumstances are continued & produced according to the adaptation of such circumstances, & therefore that death of species is a consequence (contrary to what would appear from America)

  (page 39)

  of non-adaptation of circumstances. —
  Vide two, pages back.
  Diagram
  The largeness of present genera renders it probable that the many contemporary, would have left scarcely any types of their existence in the present world. — or we may suppose only each species in each generation only breeds; like individuals in a country not rapidly increasing. —

  (page 40)

  If we thus go very far back to look to the source of the Mammalian type of organization; it is extremely improbable that any of his relatives shall likewise the successors of his relations shall now exist — In same manner, if we take a man from any large family of 12 brothers & sisters in a state which does not increase

  (page 41)

  it will be chances against any one of them having progeny living ten thousand years hence; because at present day many are relatives, so that by tracing back the descen fathers would be reduced to small percentage. — & in therefore the chances are excessively great against any two of the 12. having progeny after that distant period. —

  (page 42)

  Hence if this is true, that the greater the groups the greater the gaps (or solutions of continuous structure) between them. — for instance, there would be great gap between birds and mammalia, Still greater between

  (page 43)

  Vertebrate and Articulata, still greater between animals & Plants.
  But yet, besides affinities from three elements, from the infinite variations, & all coming from one stock & obeying one law, they may approach, — some birds may approach animals, & some of the vertebrates invertebrates —
  Such a few on each side will yet present some anomaly & the g bearing

  (page 44)

  stamp of some great main type, & the gradation will be sudden.
  Heaven know whether this agrees with Nature: Cuidado.

The text together with actual pictures of the notebook pages can be seen at http://darwin-online.org.uk. Pages ~38-41 are often seen as key ideas for Darwin's formulation of natural selection. Also note that the presence/absence of a horizontal line at the tips are apparently used to denote extant vs extinct groups (see notes in link above).


Independence of Light independent reaction in photosynthesis? Inspired by a question asked to me by a classmate, I have the following question about Light-independent (dark phase) reactions in photosynthesis:-

  Let us suppose an algae sample was exposed to light for a considerable
  time so that maximum( if there is a limit) NADPH concentration was
  achieved. Now if the sample is placed in dark and radioactive
  ¹⁴CO₂ bubbled, will the cell be radiolabelled after some time of
  bubbling continuously?

I guess the answer depends on the active life of ATP and NADPH , the products of light reaction. If they are considerably stable, such that they are in sufficient concentration for executing Calvin cycle although their production (apart from respiratory ATP production) has ceased due to absence of light. If they are, then the ATP and NADPH produced during the initial exposure period will carry out carbon fixation with radioactive carbon and hence radio labelled sugars will be recoverable from the sample. If not, they will quickly degenerate (by hydrolysis, utilization or likewise) and they will be unable to carry out fixation after some fixed time after stopping the light.

What, under normal conditions, should be the time after which the light-reaction products are no longer capable of fixing CO₂ by Calvin cycle? And, ultimately, will the presence of radioactivity in sugars for the scenario above depend on the species of plant?

[I am ignoring all radioactivity due to dissolution of ¹⁴CO₂ in cytoplasm]

It turns out that the so-called light independent reactions are not light-independent at all: there are several regulatory mechanisms in place to prevent the turning of the Calvin Cycle when there is no light energy available to produce ATP/NADPH. The hypothetical situation you described in your question demonstrates the necessity of such regulation. The cell cannot allow levels of ATP and NADPH to drop too low because those two factors are required for everything. So if you let the Calvin Cycle run when there is no means of fueling it (ultimately) from light energy, then the Calvin Cycle will run until ATP/NADPH is too low to sustain it further, at which point the cell dies. So several key enzymes in the Calvin cycle are activated indirectly by light.

One of the most well-studied regulatory mechanisms is the ferrodoxin/thioredoxin regulatory system. The enzyme Ferredoxin-Thioredoxin reductase takes electrons from ferredoxin (which is reduced by light energy via the photosystems) and transfers it to thioredoxin, a disulfide-based redox protein. Then thioredoxin reduces several key enzymes in the Calvin Cycle, which activates them (through conformational changes induced by disulfide bonds). The upshot is that when light is around to facilitate reduction, the metabolic enzymes of the Calvin cycle can work, but in the dark the cell oxidizes and these enzymes are turned off, switching off the Calvin cycle and arresting CO$_2$ fixation.

An orthogonal direction of light regulation of the "light-independent" reactions is RuBisCO Activase, which is required to modify the RuBisCO active site to be active. This requires ATP hydrolysis, which amplifies the sensitivity of the Calvin Cycle to ATP availability.

The takeaway is the light-independent reactions may not directly require light as an input, but they are regulated by light availability. I tried to look up how much time in the dark would be required to shift the redox balance such that the Calvin Cycle enzymes would be inactivated, but I couldn't find that data. People in the literature, however, seem to believe it would be quick (1).

There is some description of this at Wikipedia. If you want to look further, Bob Buchanan at Berkeley made a lot of seminal advances in this area; a review of his you might want to check out is (2).

(1): Ruelland E, Miginiac-Maslow M. (1999). Trends in Plant Science. 4(4): 136-141

(2): Buchanan BB. (1980). Annual Review of Plant Physiology. 31:341-374.


Can anyone identify this chrysalis? (Identified) It's about 5 or 6 cm long. It's on the outside (north facing) wall of my garage about a metre above ground level.

Photo taken in Thailand near Hua Hin (about 12N 100E) in December 2014.

I've found it - it's a Common Rose Swallowtail (Pachliopta aristolochiae)

A few images on this page.
http://flickrhivemind.net/Tags/aristolochiae,butterfly/Interesting including these two

There is a picture also at http://en.wikipedia.org/wiki/Pachliopta_aristolochiae but this one is upside down compared to mine.

Mystery solved.


What effects does being cryogenically frozen have on a person's body? I'm wondering what effects are known to happen to a person's cells when a person is cryogenically frozen, especially those that need to be overcome in order to "bring them back to life."

From a cellular and maybe even molecular level, is the person exactly the same as before?

Short Answer
Death!
Longer Explanation
In terms of the cellular and molecular level, many of the relatively weak interactions holding a person together are disrupted by cold temperatures. As a cell freezes, most of its  proteins and lipid membrane content will denature and "fall apart", the same as if you boiled it.
As with many things in biology, the problem is water. At room temperature, the lipid bilayers and proteins of a cell are held together largely by way of a complex network of interactions with the surrounding water. If the cell gets too hot or too cold this network of interactions between biomolecules and water falls apart. This leads to a disruption of the cell's overall organization*, which in turn can cause problems up to and including complete cell rupture and death.
So in order to preserve a living creature under cryonic conditions you need to replace the water in and around its cells with a different molecule that will maintain most of the normal intermolecular interactions even under conditions of extreme cold. There are protocols for freezing cell cultures that use various different substances as replacements for water, such as glycerol or DMSO, and there's a frog that loads its own blood with carbohydrates at low temperatures in order to turn it into a better cryonic medium.
footnote
*The disruption of a cell's organization at extreme cold is likely to persist even if the cell is brought back to room temperature. See Gulevsky, et al for a complete review of the thermodynamics of cold denaturation.


If overcooked hard boiled eggs show these green sulfide rings, why do scrambled/fried eggs not show this? In the image above, the dark green rings are ferrous sulfide rings, caused when the sulfur from the egg white reacts with the iron in the egg yolk when the egg is overcooked.

I was wondering, given the same circumstances, why do we not see our scrambled/fried eggs coated with this layer of ferrous sulfide?

Scrambled eggs can change color, but you perhaps haven't run into a batch that shows discoloration. It is the same chemical reaction:

Why Scrambled Eggs Turn Green
When serving a large group, a buffet can provide enough food for everyone without the need to spend all of your time in the kitchen. Breakfast is a fairly simple buffet to set up, but there are special challenges when it comes to scrambled eggs. When scrambled eggs sit for a while, they tend to turn green or gray. This is a chemical reaction that happens as hydrogen sulfide in the egg white reacts with the iron in the yolk to form iron sulfide.

Via: https://living.thebump.com/lemon-juice-keep-raw-eggs-turning-green-cook-them-8383.html


How do bull semen companies get the semen out of the bulls? Prompted by this article, which discusses the low number of bulls who sire US dairy cows.

How do semen companies extract semen from bulls?

The procedure to extract semen from humans is simple enough, but I'm struggling to picture a lab operator masturbating a fully grown bull until it ejaculates to collect semen. Is there some kind of specialized equipment involved? What does the operating procedure look like?

Colorado State University has two helpful pages that explain the main procedures (h/t Tom). Semen Collection goes through the 3 ways that are used to collect semen from animals.

Semen Collection from Bulls helpfully expands on bulls specifically:

  Semen is most commonly collected from bulls in bull studs using an artificial vagina, as described below. Electroejaculation is an alternative method used with bulls that cannot mount or are too fractious for easy handling (e.g. range bulls). Finally, semen can be collected by message of the seminal vesicles and ampullae per rectum.

In a nutshell an Artificial Vagina (AV) uses thermal and mechanical stimulation to stimulate ejaculation. In the image below, the top item is an AV for use with rabbits and the bottom one is an AV for use with bulls. (The middle item is a director cone, which is used to collect semen from dogs.)

The procedure revolves around using a steer as a teaser to arouse and mount the bull, and then having an operator divert the penis the AV:

As one of the pages helpfully explains:

  Prerequisites to use of an AV are that the male be conscious, not significantly frightened of people, and more interested in ejaculating than in killing humans.

The main alternative for less docile bulls appears to be electroejaculation, which involves applying a series of short, low-voltage pulses of current to the pelvic nerves which are involved in the ejaculatory response. You then collect semen using a director cone much like the one in the image further up.


What are the differences between Trachinotus and Bramidae species? What are the differences between Trachinotus(Pompanos) and Bramidae(Pomfrets) ?

...like the difference between where they live/can be found, bone structure, etc.

Pomfrets comes from the order Perciformes (the largest order of fishes) and are part of the Bramidae family. They strictly live in marine environments, mainly the Atlantic, Indian, and Pacific Oceans. They have a dorsal fin extending over the length of the body in some and anterior dorsal fin spines unbranched.

http://www.fishbase.org/summary/FamilySummary.php?ID=319

Pompano comes also comes from the order Perciforme and are part of the Carangdide family which includes jacks, mackerels, scads, and runners. Most are fast-swimming predatory fish that hunt in the waters above reefs and in the open ocean. They also mainly live in marine environments such as the Atlantic, Indian, and Pacific Oceans, and are rarely found in brackish waters. Their body is generally compressed, although body shape extremely variable from very deep to fusiform.

Quote about Pompanos from Fishbase.org:

  Most species with only small cycloid scales. Scales along lateral line often modified into spiny scutes. Detached finlets, as many as nine, sometimes found behind dorsal and anal fins. Large juveniles and adults with 2 dorsal fins. Anterior dorsal fin with 3-9 spines; the second having 1 spine and usually 18-37 soft rays. Anal spines usually 3, the first 2 separate from the rest; soft rays usually 15-31. Widely forked caudal fin. Caudal peduncle slender. Pelvic fins lacking in Parona signata. Vertebrae 24-27 (modally 24).

Unfortunately, I can only post one link due to my rep, but it fairly easy to search fishbase.org for information on both species.


How to grow fibroblast colonies from single cells? I need to establish a cell line starting from single cells seeded on a 96 wells plate by a FACS sorter. The cells I am using are human fibroblasts RPE-1 cultured in F12 medium supplemented with 10% FBS and antibiotics. After having seeded 5x96 cells (one cell per well in 5 plates) I have obtained only 4 colonies. Does anyone know any good (preferably personally tested) protocol to efficiently grow fibroblast colonies from single cells?

This should be relatively straight forward. Sort the cells into single wells so all descendants are clones of the sorted cell and let them grow until they are dense enough to be transferred into a bigger plate (probably 48 or 24 well). Continue this process until you can go into big cell culture flasks or plates and make sure that you freeze away a number of aliquots as a backup if something goes wrong. Expand the cells further until you have enough cells to do an analysis.

Keratinocytes need some time to get highly proliferative (around a week or so) and if you don't grow them on a layer of feeder cells, usually also need a special conditioned medium. See the references below (if you have trouble accessing the papers, let me know).

What often also helps is the use of conditioned media. I know this from other cells in the skin which often don't like to grow (at least not as primary cells) unless you use conditioned media. For this, take of the media from the same sort of cells (here it would be keratinocytes) before it is completely used (typically yellow if the media contains pH indicators), centrifuge it to remove any cell debris and then mix it with fresh media to let your cells grow. You might need to experiment a bit with the mixing ratio between the "used" and the fresh media, but 50%:50% is usually a good starting point.

References:

Isolation and cultivation of human keratinocytes  from skin or
plucked hair for the generation of  induced pluripotent stem cells
Culture techniques for human keratinocytes
Improvement of human keratinocyte isolation and culture using
thermolysin


What's the advantage of autocrine signalling? In the antibody-mediated immune response, when the helper T cell gets activated by the costimulus (IL-2 and TNF-α secreted by the APC) which in turn produces IL-2, IL-2 acts in an autocrine manner. I'm just wondering why does IL-2 have to be secreted? Why doesn't it just exert an affect while it's already inside the helper T cell? What's the point of autocrine signalling?

I hope the answer isn't going to be, "Well, that's just the way it is..." because paracrine and endocrine make sense and have advantages, but autocrine just seems a bit extra.

Why doesn't it just exert an affect while it's already inside the helper T cell?

Because it interacts with membrane-bound receptors. Those are outside so there is no way IL-2 (or any autocrine factor) could signal while inside the cell. It has to exit.

Now, the next question is why the receptor is membrane-bound and outside. As far as I understand there are two parts to this answer:

Receptors are evolutionarily related so they follow similar synthesis pathways.
Membrane-bound receptors are (all?) transcribed while being secreted into the endoplasmic reticulum. This causes their agent-binding portion to reside inside the ER. From there, vesicles bud off, are transported towards the cell membrane, merge with it, and hence the formerly inside portion of the protein ends up on the outside.


Which functional annotations could be useful? Analyzing a genome, for a generic gene, which functional annotations (e.g from Gene Ontology) can help understanding its meaning/function or, at least, provide helpful informations?

Annotations of that gene
Annotations of orthologous genes (?)
Annotations of paralogous genes (?)
Co-expressed genes (given a biological condition) (?)
What else?

Thank you.

I'd add genetic effects of the gene and its orthologs in that own
host. Knockouts and overexpression are powerful in uncovering
function.
In terms of baseline or normal expression, I would add    tissue,
developmental or differentiation time points, and conditions which stimulate or repress expression.


Are boat-tailed grackles efficient flyers? The boat-tailed grackle's deep-V tail would seem to cause a great deal of drag or even downward deflection (like an airplane's elevators). How much does this actually affect the bird's flight?

I don't know of studies specifically of boat-tailed grackle flight, so I'll focus on elongated tails in general and come back to grackles at the end.

Long tails in birds are obviously interesting from the standpoint of sexual selection. Going all the way back to Darwin, one hypothesis has been that females prefer males with long tails. There seems to be evidence for this, although experimental reduction or elongation of tail feathers is perhaps of questionable success. See this back and forth in Behavioral Ecology.

Those interested in the study of flight have also studied elongate tail feathers to get at the questions you ask: are long tail feathers aerodynamically costly?

Balmford (1993) compared the aerodynamic properties of different tail shapes. He found that:

  A forked tail that has a triangular planform when spread to just over 120° gives the best aerodynamic performance and this may be close to a universal optimum, in terms of aerodynamic efficiency, for a means to control pitch and yaw.

But the results were more complicated. Forked tails are only used in extreme maneuvers, they are more unstable, and suffer from greater loss of performance when damaged. He leaves open the possibility that natural selection, rather than or in addition to sexual selection, has played a role in shaping bird tails, possibly for increased aerodynamic performance.

More relevant here, Balmford et al. (1993) studied pairs of species, one with a long tail and one without, to assess the aerodynamic cost of long tail feathers. They studied ~600 specimens and used aerodynamic modeling to predict cost. Their results are summarized in this figure:

Graduated (rounded) tails are costliest over all lengths. Forked tails are notably less costly over all lengths, and shallow forks more efficient than deep forks (but there the difference is not great).

They conclude:

  Our model suggests that as long forked tails deepen, it becomes more likely that they are aerodynamically costly..., and therefore increasingly probable that sexual rather than natural selection explains their evolution.

And of the species pairs:

  ... then among species with long forked tails, sexual dimorphism in tail length should increase with fork depth. Pairwise comparisons of closely related species support this prediction.

What of boat-tail grackles then?

From what images I could find, it looks like boat-tailed grackles appear to have graduated tails when spread. If so, then these tails would be very inefficient and males with longer tails would incur a proportionately higher cost of flight than males with shorter tails.

Balmford, A., A. L. R. Thomas, and I. Jones. 1993. Aerodynamics and the evolution of long tails in birds. Nature 361:628–631.

Thomas, A. L. R. 1993. On the Aerodynamics of Birds' Tails. Philosophical Transactions of the Royal Society of London B: Biological Sciences 340:361–380.


Does GFAJ-1 use Adenosine triarsenate as its energy currency? Regarding the bacteria found in Mono Lake, CA that scientists believe uses or can use arsenic in its DNA backbone where life as we know it uses phosphorus (according to their experiments depriving the microbes of phosphorus and providing much arsenic), have researchers conjectured and tested whether the energy currency molecule used is also arsenic-based instead of ATP?

I'd have to agree that it's highly improbably that the GFAJ-1 strain used nucleoside triarsenates as an energy source. There are three main lines of evidence pointed out in the Science reviews that were published after the initial publication of the paper.

The incorporation of arsenate ions into NTAs is not a plug-and-play process, per se. Arsenate does not simply replace phosphate ions from molecules. In order for an NTA to form, it must arsenylate (like phosphorylate) a ribose molecule, then have the purine/pyrmidine ring form (and be attached to the ribose), and then two more arsenates have to be linked via ester bond to the other first arsenate. Mind you, this all happens in water. Arsenate esters are notoriously unstable in water, so it's difficult to imagine an NTA forming stably.
The original team in Felisa Wolfe-Simon's lab didn't intentionally add phosphate ions to their growth media; instead, the approximate amount of phosphate impurity was measured and reported. The lab compared this level of phosphate with the minimal levels reported in E. coli from another paper and basically said, "There isn't enough phosphate in our growth media for our GFAJ-1 strain to grow solely on phosphorous." Well, that logic is a little non sequitur  because GFAJ-1 is a halomonad (they said so themselves) and there is literature pointing to a species within Halomonadaceae that can grow on phosphate levels lower than that of the impurities reported.
Although the Wolfe-Simon team added arsenate into their growth media, it's unlikely that any biologically-useful arsenic ended up in the cells at all. Under physiological electrochemical conditions, arsenate gets reduced to arsenite. Phosphate ions, on the other hand, are stable at physiological potentials.

All in all, there's a reason why life chose phosphorous instead of arsenic. Although both elements have ions with a propensity to make ester bonds, maybe arsenic just doesn't fit into our anthropocentric view of what life is.


What is the oldest example of DNA identified? What is the oldest sample of genetic material (presumably DNA) identified? What are the prospects of pushing back much further into the geologic record?

419 million year old DNA from halophilic bacteria.

http://news.discovery.com/earth/oldest-dna-bacteria-discovered.html


What is titratable acid? Why is ammonium not titratable acid? What exactly do we mean when we use term titratable acid in renal physiology? Why is ammonium not considered a titratable acid?

Titratable acidity is a total amount of acid in the solution as determined by the titration using a standard solution of sodium hydroxide (titrant). In other words, it is the maximal capacity of the solution to "neutralise" base solution.

H$^+$ produced from CO$_2$ and H$_2$O is actively transported into the distal tubular lumen.
Titratable acidity is the amount of the H+ which is buffered by bases present in the tubular lumen. Mostly by phosphate (the highest concentration).

When the urinary pH change other molecules can gain the ability to buffer H$^+$.  For example creatinine (pKa about 5.0) or ketoacids (pKa about 4.8)  may contribute to the titratable acidity.

Standard measurement of the titratable acidity with the standard solution of sodium hydroxide spans pH range up to 7.4. Therefore:

  Ammonium is not measured as part of the titratable acidity because the high pK of ammonium means no H$^+$ is removed from NH4$^+$ during titration to a pH of 7.4.

Source


How to identify whether something is in linkage disequilibrium? If the following loci indicated the presence of an SNP in flu strains, is Locus 2 and Locus 3, which are located 10 bp apart in linkage disequilibrium?

"When alleles and molecular
markers are associated with each other at a frequency that
is significantly higher than expected by random chance, they
are said to exhibit linkage disequilibrium" Brooker's Genetics

Both loci seem to be linked, but how do I determine if it is significant enough to be considered in disequilibrium or not.

As per the definition you gave, you check whether there is a statistical association between the two. If knowing when allele is present at a locus does not affect the probability of finding a given allele at the other locus, then they are independent (there is no association). Otherwise, there is an association and hence the two loci are in linkage disequilirium.

See wikipedia > Linakge disequilibrium for more info.


Which extinct creatures were most genetically distant from everything alive today? The more distant the common ancestor of two creatures the more genetically distinct the creatures will be. For example I am more genetically distinct from a mushroom than an ant. I am more genetically distinct from an ant than a fox. Etc.

Extinction in the deep past has cut off some evolutionary branches. Which extinct creatures (including all living organisms) were most genetically distinct (alien) from living creatures today?

The very first ones to go extinct would be the most genetically distant; at that distance, the issue becomes more "how do you define life?" or "how do you define a species?" to get the actual most distant. Overall, it sounds like an interesting question, but it really isn't: extinction isn't special, it's the norm. There are most certainly extinct organisms or pre-organisms of some level of development that never contributed to the existing life on earth and have no descendants or relatives.


Does double stranded RNA (dsRNA) exist in eukaryotic cells? I know it sounds like a stupid question. Obviously, tRNAs and rRNAs, for example, form loops and could therefore be considered as dsRNAs... but are they really considered as such?
Are there examples of RNAs, in eukaryotic cells, that could be considered exclusively as dsRNAs, or are dsRNAs considered as unique to certain viruses?
Thanks in advance for your help. I couldn't find a clear answer to that question in my textbooks and on the internet, so I hope you can help.

Yes, dsRNAs are present in eukaryotic cells and regulate various biological processes.
These nucleic acids are also present in the nucleus and regulate mitosis. Altering this nucleic acid could even lead to cell death.
(Reference: https://pubmed.ncbi.nlm.nih.gov/25504323/)


What is a deep exhalation/inhalation? I tried to find the academic definition of deep exhalation/inhalation but found nothing special.

I speculate that the correct definition is as follows:

  • Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "inhalation".

  • Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "exhalation".

The corresponding volumes of the air which is being moved inside respiratory tracts would be:

Vdeep exhalation = Tidal Volume + Expiratory reserve volume (ERV)

Vdeep inhalation = Tidal Volume + Inspiratory reserve volume (IRV)

But, in case we define them as below, the previous conclusion regarding the volumes turns wrong and consequently should be revised.

  • Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "exhalation".

  • Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "inhalation".

Vdeep exhalation = Expiratory reserve volume (ERV)

Vdeep inhalation = Inspiratory reserve volume (IRV)

I think it's impossible to assess without any subtle definition. I'm really confused.

Any help would be highly appreciated.

Deep inhalation and deep exhalation are informal terms and cannot be defined by lung volumes, because saying deep by itself does not tell how deep.

In the first part of the question deep refers to maximal:

Deep inhalation that means inhaling the air with effort as much as possible = maximal inhalation
Deep exhalation that means exhaling the air with effort as much as possible = maximal exhalation

According to Physiology, Residual Volume (StatPerls):

The volume of air in the lungs after maximal expiration is called residual volume (RV).

  Residual volume (RV) is the volume of air that remains in the lungs
  after maximum forceful expiration. In other words, it is the volume of
  air that cannot be expelled from the lungs. This volume remains
  unchanged regardless of the lung volume at which expiration was
  started.

The volume of air in the lungs after maximal inspiration is called total lung capacity (TLC).

  TLC is the total volume of the lungs at maximal inspiration.

According to Merriam-Webster dictionary:

Expiratory reserve volume = the additional amount of air that can be expired from the lungs by determined effort after normal expiration.

Inspiratory reserve volume = the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration.

Lung volumes:

Image source: Wikipedia, Creative Commons License


How to study the effect on tau protein isoforms on microtubule based transport? From what I read, A-beta plaques inhibit microtubule based transport of mitochondria when tau protein is present in the cell. How would I be able to do a test to see if one isoform of tau is more effective at conferring this A-beta sensitivity than another isofrom?

You can do a microscopy based assay to quantify the transport rate (both retrograde and anterograde). Mitochondria can be labeled with fluorescent proteins such as mito-dsRed, and its movement along the axon can be tracked by live cell imaging. You can check this paper; they have done this experiment. (Others have also done it but I remember this paper because someone told me about it recently).

How do you plan to see the effect of different isoforms? It may not be that easy. You will have to replace the common isoform with the others. It is not very easy to control splicing. So you may have to make lines that express only one variant (exon deletion). Though this study reports that alternative splicing can be controlled by using antisense oligonucleotides, the technology is not standardized yet; you can try it nonetheless, because making knockouts is difficult (you would have to make KO mice and then culture neurons from it).


Why haven't land animals evolved beyond urination? It occurred to me (while urinating) that this would seem to be selected against because water is a scarce resource.   Why are we constantly losing water we don't need to through urination?   What is it about the chemistry of urine and the waste products eliminated that make urination necessary as opposed to eliminating them through defecation and recovering the water on the way out?

It is probably true that toilets and other resting-ish area are always a great place to think about biology, I agree $\ddot \smile$.

Why do we urinate?

In short, urine contains the waste from our blood while defecation is just the stuff that we haven't digested. Kidneys are the organs responsible for draining wastes (mostly nitrogen-containing, or nitrogenous, wastes) from our blood.

Trade-off: energy cost vs. water loss

You're correct that the loss of water through urination is a considerable cost for an organism (especially those living in dry environments). But the amount of water used to excrete nitrogenous wastes is negatively correlated with the energy it costs to perform this excretion. In other words, there is a trade-off between water and energy loss during nitrogen excretion. Also, the question of toxicity is important.

Three ways to excrete nitrogenous wastes

Animals basically have three choices to excrete nitrogenous wastes:

Uric acid (excreted by uricotelic organisms)

Solid (crystal) with low water solubility
Low toxicity
Little water is needed
Lots of energy is needed

Ammonia (excreted by aminotelic organisms)

Highly soluble in water
High toxicity
Lots of water is needed to dilute it because of the toxicity
Not much energy is needed

Urea (excreted by ureotelic organisms)

Solid but highly soluble in water
"medium" amount of water is needed
"medium" toxicity
"medium" amount of energy is needed

What method is most beneficial for a given individual?

The amount of energy and the availability of water are very important aspects to understand whether a species is ureotelic, aminotelic or uricotelic. Another developmental constraint must be considered too. For example, birds are uricotelic (uric acid) probably because during the development of the embryo the wastes cannot be excreted outside the egg and therefore, excreting uric acid allows to greatly decrease the toxicity of the embryo's environment. In short, we must consider

Water availability
energy loss
developmental constraints

Note: This domain is not at all my field of study and I have no reference, typically for what concerns the toxicity, water amount and energy amount. One should not take my words for granted!


Test of antibiotic A for sensitivity as surrogate of antibiotic B I am reading the WHO Global Antimicrobial Resistance Surveillance System (GLASS) - Manual for Early Implementation. it mentioned some of the drug-bug combination that will be put under surveillance in page 8 of the following link, I have screen-captured the page below that I have some questions.

http://apps.who.int/iris/bitstream/10665/188783/1/9789241549400_eng.pdf

For S. aureus, Cefoxitin is selected for surveillance, but the remarks mentioned that Cefoxitin is a surrogate for testing susceptibility to oxacillin (methicillin, nafcillin). I know S. aureus showing resistance to methicillin is MRSA, but why test for Cefoxitin but not test methicillin directly?

The same question goes for S. pneumoniae for Oxacillin as a surrogate for testing reduced susceptibility or resistance to penicillin. Why not directly test for penicillin?

Sorry that I am not a microbiologist, just a data analyst recently working on microbiological data, hope that I won't be asking something too stupid.

Thanks!

This is not a proper answer as such and it's based on a bit of an 'educated guess' but it was too long for a comment.
I did however, find this article. Unsurprisingly, one of the big drivers of using surrogate antibiotics is down to availability and cost. Some antibiotics, while known about, may not be produced commercially at scale, or be widespread enough for testing facilties around the world to use. Consequently, the WHO can maintain a list of antibiotics with complementary 'cross-talking' modes of action, so that a resistance mechanism can be probed without needing the specific antibiotic.
Another reason for using a surrogate might be to avoid some of this cross-talk. I.e., if you wish to know the effectiveness of (say) imipenem, and you know imipenem and meropenem have the same mode of action, but perhaps the bacteria has a second resistance pathway that  is specific for imipenem - you could use meropenem as a surrogate, knowing that it won't be degraded/removed by pathway 2, and you can still probe the mode of action.*
*(This is a contrived example, I have no idea if you'd ever use those 2 antibiotics in this manner.)
It seems like, from reading online, the real drivers to use surrogate testing however, are purely as an interim measure due to the enormous lag phase between discovery of new drugs, testing, scale up, administrative approval, and then general market availability.


How to watch a Zebrafish embryo in detail? How much microscope zoom would I need to watch the development of a Zebrafish embryo in certain detail? Thanks guys!

From personal experience, it should be sufficient to observe zebrafish at 10-20x magnification for broad structural changes during development.  If your microscope has a 10x eyepiece, then that would be 1-2x zoom. If you are observing sub-cellular changes, you would benefit from higher magnification.


Is this a Tsetse fly? I found this on my back while looking in the mirror.It took me 10 minutes to kill it.I hit it well at least 5 times before it died.It kept flying to me every time i tried to hit it,trying to go under my shorts

Is this a TseTse fly?

what fly is this?

This is a species of Hippobosca, looks like H. equina. There aren't too many species of this genus, so the species may be this one, which is rather common in Europe, Africa and parts of Asia - see https://www.biodiversidadvirtual.org/insectarium/Hippobosca-equina-Linnaeus-1758-img485046.html. Since you suggested it could be a tsetse fly, I assume you are in Africa. Hippobosca equina occurs in Africa as well. Other hippoboscids are not as strong fliers as Hippobosca species, which would explain its flying back to you over and over.


How does promoter sequence affect initiation? I don't know if this might have been highlighted in recent research, but a textbook I have states that "the exact way in which promoter sequence affects [transcription] initiation is unclear"

I'm wondering if anyone can suggest sources for more information, or perhaps has seen recent research papers highlighting the properties that cause such variation between strong promoters and the weakest?

I've tried researching but the older research is descriptive rather than mechanistic and the search terms involved are quite ubiquitous so it's hard to actually find more on this specific point.

I agree that it is hard to search for papers but from graduate level classes this is some of the additional insight I have gained. Sequence context of promoters is important. Specific DNA sequences (motifs) can act as binding sites for specific transcription factors and combinations of these transcription factors help recruit RNA pol II to the promoter. These combinations of proteins are spatially and temporally regulated and will help decide if gene that is next to promoter will be activated. A luciferase reporter assay is often used to determine the strength of a promoter.

An example is as follows: A strong promoter might have certain histone marks that would recruit proteins to remodel the chromatin to be more accessible exposing binding sites of transcription factors that help recruit RNA Pol II. A weaker promoter might have less transcription factor binding sites or less chromatin accessibility and thus it is harder for RNA Pol II to be recruited. There are also some kinetics aspects you must keep in mind.


Trisomy 21 and Down syndrome Can Down syndrome occur without trisomy 21 in the karyotype of an individual? Or vice versa can a person have trisomy 21 while unaffected by Down syndrome?

First question: No, all Down Syndrome patients have a inappropriate duplication of part or all of chromosome 21.
Second Question: More complicated.  The phenotype can vary in severity depending how much much of chromosome is duplicated, whether it is duplicated and stuck onto the end of chromosome 14 (translocation vs. non-disjunction).  Lastly, a rare form of this event is defined by incomplete penetrance or mosaicism of cells that contain duplication.  Short Answer: No, In rare cases, a carrier can pass on trisomy 21 without being affected themselves but they themselves are a "balanced carrier" and don't have extra chromosome 21 material. See last paragraph below from the NIH and this quote from the Mayo Clinic:

When translocations are inherited, the mother or father has some rearranged genetic material, but no extra genetic material — this means he or she is a balanced carrier. A balanced carrier has no signs or symptoms of Down syndrome, but he or she can pass the translocation on to children, causing extra genetic material from chromosome 21

Types of Down Syndrome details from: NIH Down Syndrome Information Page

Research shows that three types of chromosomal changes can lead to Down syndrome.
Complete trisomy 21. In this case, an error during the formation of the egg or the sperm results in either one having an extra chromosome. So after the egg and sperm unite, the resulting cells will also have three copies of chromosome 21. The complete extra copy of chromosome 21 is in all of the person's cells—or a complete trisomy. Complete trisomy 21 is the cause of about 95% of Down syndrome cases.1,2,3
Mosaic trisomy 21. Not every cell in the body is exactly the same. In about 1% of Down syndrome cases, most of the cells in the body have the extra chromosome, but some of them don't. This is called "mosaicism." Mosaic trisomy 21 can occur when the error in cell division takes place early in development but after a normal egg and sperm unite. It can also occur early in development when some cells lose an extra chromosome 21 that was present at conception. The symptoms of someone with mosaic trisomy 21 may vary from those of someone with complete trisomy 21 or translocation trisomy 21, depending on how many cells have the extra chromosome.1,2
Translocation trisomy 21. In this type of chromosomal change, only part of an extra copy of chromosome 21 is in the cells. The extra part of the chromosome gets "stuck" to another chromosome and gets transmitted into other cells as the cells divide. This type of change causes about 4% of Down syndrome cases. There are no distinct cognitive or medical differences between people with translocation trisomy 21 and those with complete trisomy 21.
Sometimes, a parent who does not have Down syndrome may carry a translocation in chromosome 21 that can be passed on to children and cause Down syndrome. Studying the parents’ chromosomes can reveal whether this is the cause of the syndrome. A genetic counsellor can assist families affected by translocation trisomy 21 in understanding the risk of Down syndrome in future pregnancies.1,2,3

Added EDIT:

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life without having most of the effects of DS. But this can significantly predispose to leukemias shown here, which is an interesting area of study.  Thanks to @The Nightman.


What are these small, indoor bugs? I live in Switzerland and have noticed these small bugs appear in my bedroom, either slowly crawling on the parquet flooring, lazily buzzing around or dead on my windowsill (as pictured):

I'm not sure if these bugs are currently appearing more often – or if I just notice them more because of the fact that I'm spending a lot of time in my bedroom due to Corona lockdown.
The only hint I've got is a friend saying that they live in wooden floors. No idea if that's correct.
Thanks for any help or hints!

I doubt you'll get a positive ID from that photo. It might be some woodboring beetle, maybe genus Anobium or Hedobia. FTR, if they are chewing on your wooden floors, you might be able to hear them if you listen carefully.
I suggest you collect some, maybe even living, in a small tube and ask a specialist. My first idea would be someone at a nearby university or natural history museum working in entomology, and specifically on Coleoptera if possible.


What's a good and reliable database on the pharmacodynamic and pharmacokinetic data of drugs both approved and unapproved? What's a good and reliable database for the pharmacodynamic and pharmacokinetic data of drugs both approved (in the US and elsewhere) and unapproved?

For approved drugs, the Drugs @FDA database at CDER (Center for Drug Evaluation and Research) aggregates labeling information (which includes at least a cursory PD explanation and a listing of or reference to common PK data for the substance) for most modern drugs.

Unapproved drugs may be a bit trickier to find out about, but the FDA maintains a list of contract research organizations (CROs) who are running trials here, and the actual trials can be found on http://www.clinicaltrials.gov/, which will have citations for the papers that have been published.

Drugs in their earliest stages of development, i.e., internal to a pharma company, are likely to be kept pretty tightly under wraps.

I don't know enough about the governing bodies in other countries to know where any international data would be, but I assume you can find published papers for substances in those countries as well.


What are the long term consequences of settling an isolated territory with an extremely limited gene pool? I remember reading about a discredited theory - I'm afraid that, despite some frantic Googling, I've been unable to track down a link - which stated that Australia was first settled by a woman, pregnant with a son, who washed up on a beach. It struck me as surprising that such a theory was ever proposed; I know very little about genetics, but it seemed implausible that all Aboriginal Australians, who seem about as physically healthy as any other race, are descended from just a mother and her son. But could just one woman be the progenitor of a healthy nation? And, if not, what is the minimum number of distantly-related individuals required?
As was stated in the answers to a related question: the more immediate consequences of inbreeding are a dramatic rise in inherited diseases, as well as, perhaps, some mild intellectual disabilities. But what are the consequences over several generations? The Pitcairn Islands and Easter Island/Rapa Nui spring to mind when thinking of historical examples of isolated territories with limited gene pools: both seem to have been settled by around two dozen individuals. Did either community experience specific problems over the centuries due to a small gene pool?

The above, obviously, is concerned with our own species, but I'd be very interested to hear about this topic with respect to other species too. I seem to remember, in one of his "Dark Horse" podcasts, Bret Weinstein talked about how a particular species of Hawaiian bat colonised those islands by way of a single pregnant female being blown off course and/or washing up on a beach. Again, is such a thing plausible, and, if so, what would be the long term consquences for the colonisers?

Minimum number of individuals needed to start a population

But could just one woman be the progenitor of a healthy nation? And,
if not, what is the minimum number of distantly-related individuals
required?

Healthy is a pretty subjective term, and it's perhaps easier to think of things in terms of a minimum viable population, which is more about straight survival than population health. However, Marin & Beluffi (2018) performed some simulations of humans in a multi-generational space exploration scenario, using 'healthy population' as a desired outcome and found:

A initial amount of 25 breeding pairs of settlers drives the mission
towards extinction in 50 +/- 15% of cases if we completely forbid
inbreeding. Under the set of parameters described in this publication,
we find that a minimum crew of 98 people is necessary ensure a 100%
success rate for a 6300-year space travel towards the closest telluric
exoplanet known so far.

So according to this simulation, it seems quite unlikely that a single woman could be the progenitor for some kind of colony. However, as I discuss a bit further down, some human populations went through bottlenecks of ~20 individuals and remained viable. They may have incurred some health costs, but they would be able to propagate the population.
Long term consequences of founder effects
There are several different case studies of modern human populations relating to the founder effect.
Achromatopsia Pingelap
The atoll of Pingelap in the Pacific Ocean is extremely remote, and up until the late 18th century had around 500 inhabitants. Around then, it was hit by a devastating typhoon which reduced the population size to around 20 individuals. In following generations, it was estimated by that 10% of the estimated 3,000 Pinglapese had Achromatopsia (Carr et al 1971), an autosomal recessive form of colour blindness that otherwise has an extremely low frequency of about 0.003% in other populations (Thiadens 2011).
Subsequent studies used homozygosity mapping in order to determine the genetic basis of the high levels of Achromatopsia. Sundin et al (2000) demonstrated that Pingelapese achromats are homozygous for a missense mutation (serine to phenylalanine) in a highly conserved membrane-spanning domain. This is quite solid evidence for the deleterious consequences of the founder effect in modern human populations.
Jewish populations
There is also reasonable evidence of a severe bottleneck in the ancestors of the global Ashkenazi Jew population. Carmi et al (2014) estimated that the total population fell as low as 350 individuals:

The AJ population is much larger and/or experienced a more severe
bottleneck than other founder populations, such as Amish, Hutterites
or Icelanders.

Other studies have suggested that the high incidence of particular diseases found in Ashkenazi Jew populations was the result of genetic drift following the bottleneck, rather than subsequent co-sanguinity (Bray et al 2010):

We identified genomic regions under selection that account for lactose
and alcohol tolerance, and although we found evidence for positive
selection at some AJ-prevalent disease loci, the higher incidence of
the majority of these diseases is likely the result of genetic drift
following a bottleneck

Rapa Nui
Since you asked about Rapa Nui. Gonzalez-Martin et al (2006) have this to say:

The population of Easter Island is one of the most interesting extant
human communities due to its unique demographic history, its geographic
isolation, and the development of an incomparable culture
charac-terized by the towering ‘‘Moais’’ and its enigmatic writing.
Following the colonization of its population by Polynesians from the
Mangarevan Islands in the 5th century AD, the island remained isolated
up until the middle ofthe 20th century. Under these conditions, with
endogamy levels ﬂuctuating between 61.04–96.54% and given such a small
population, a high rate of inbreeding, and consequently, an elevated
level of genetic relationships would be expected. Using data from
church and civil records, we calculated the consanguinity of the
population of Rapa Nui. The results of this analysis do not support
the hypothesis of a high level of consanguinity.

That said, I have heard some unverified rumours that there was a high incidence of having 6 toes on Rapa Nui, but I can't find anything solid to back it up with.
Norfolk Island
One last example. I've taken this text from a nice paper by Macgregor et al (2009):

The population of Norfolk Island, located off the eastern coast of
Australia, possesses an unusual and fascinating history. Most
present-day islanders are related to a small number of the ‘Bounty’
mutineer founders. These founders consisted of Caucasian males and
Polynesian females and led to an admixed present-day population. By
examining a single large pedigree of 5742 individuals, spanning >200
years, we analyzed the influence of admixture and founder effect on
various cardiovascular disease (CVD)-related traits.

Further...

Marker-derived homozygosity was computed and agreed with measures of
inbreeding derived from pedigree information. Founder effect
(inbreeding and marker-derived homozygosity) significantly influenced
height

Non-human species
I think the last part of your answer is referring to the Hoary Bat, which colonised Hawaii from mainland USA. It was originally hypothesised that the population was the result of a single founding event, but this has been disputed by mtDNA markers (Russell et al, 2015):

Our results point to the colonization of Hawai'i by hoary bats on two
occasions by lineages that experienced distinct evolutionary
trajectories

There is some evidence of single-individual founder events occurring, however (Clegg et al 2002);

Here we undertake a genetic analysis of a series of historically
documented, natural colonization events by the silvereye
species-complex (Zosterops lateralis), a group used to illustrate the
process of island colonization in the original founder effect model.
Our results indicate that single founder events do not affect levels
of heterozygosity or allelic diversity, nor do they result in
immediate genetic differentiation between populations

Further..

A Bayesian analysis based on computer simulation allows inferences to
be made on the number of effective founders and indicates that founder
effects are weak because island populations are established from
relatively large flocks.

There is a lot of literature on this in wild populations which might be of interest, e.g. https://link.springer.com/content/pdf/10.1007/s10592-010-0049-0.pdf
References
Thiadens, Alberta. "Genetic etiology and clinical consequences of cone disorders." (2011). APA
Carr, Ronald E., Newton E. Morton, and Irwin M. Siegel. "Achromatopsia in Pingelap islanders: study of a genetic isolate." American journal of ophthalmology 72.4 (1971): 746-756.
Sundin, O.H. et al. Genetic basis of total colourblindness among the Pingelapese Islanders. Nature Genet. 25, 289– 293 (2000).
Carmi, Shai, et al. "Sequencing an Ashkenazi reference panel supports population-targeted personal genomics and illuminates Jewish and European origins." Nature communications 5.1 (2014): 1-9.
Bray, Steven M., et al. "Signatures of founder effects, admixture, and selection in the Ashkenazi Jewish population." Proceedings of the National Academy of Sciences 107.37 (2010): 16222-16227.
APA
Marin, Frédéric, and Camille Beluffi. "Computing the minimal crew for a multi-generational space travel towards Proxima Centauri b." arXiv preprint arXiv:1806.03856 (2018).
Russell, Amy L., et al. "Two tickets to paradise: multiple dispersal events in the founding of hoary bat populations in Hawai'i." PLoS One 10.6 (2015): e0127912.
Clegg, Sonya M., et al. "Genetic consequences of sequential founder events by an island-colonizing bird." Proceedings of the National Academy of Sciences 99.12 (2002): 8127-8132.
Macgregor, Stuart, et al. "Legacy of mutiny on the Bounty: founder effect and admixture on Norfolk Island." European Journal of Human Genetics 18.1 (2010): 67-72.