How is the urea cycle regulated with respect to protein deficit? Proteins cannot be stored in the body. Excess proteins from the diet are deaminated in the urea cycle that takes place in the liver. The liver is the first contact since these amino acids are delivered through the portal circulation.

What I do not understand is what controls the extent of amino acid breakdown in the liver. For example, suppose there is a man who hasn't had protein in a month, and has a net protein deficit, what determines that there shouldn’t be much deamination in the liver?

For carbohydrates and sugars, insulin and glucagon balance regulate the main enzymes controlling the steps in glucose phosphorylation hence maintaining homeostasis. Since this is at an organismal level and not the cellular level, like glucose, I would expect the control of urea cycle also to be hormonal. Since there is no hormone that reflects protein status (at least to my knowledge), what determines the activity of the urea cycle?

Preamble

This question is extremely broad because, rather than there being a ‘one-click’ answer, whole areas of amino acid metabolism need to be considered. This is both inappropriate and impossible to do here — even if I understood everthing about it (which I certainly don’t). However I shall provide a specific biochemical answer (or partial answer, as all is not understood) regarding the regulation of the urea cycle, after commenting on some of the assumptions implicit in the question.

Comments on the assumptions of the question

I am not sure that ‘protein deficit’ is a useful metabolic construct. From the point of view of a clinician, yes, one can say that someone is suffering from protein deficiency or malnutrition, but in metabolic terms protein is a not the highest priority and will be broken down to provide glucose for the brain during long-term starvation. And it is well established that protein synthesis is under the control of hormones and growth factors (reviewed here), and this will affect the fate of dietary amino acids or those produced by protein turnover. In addition, the emphasis on hormones in the question seems to ignore the role of the concentration of amino acids and other intermediates in regulating metabolic pathways. Finally, there is control of the expression of the genes encoding enzymes of the urea cycle, which operates over a longer time period.

The Medical Biochemistry site provides a wider perspective on amino acid metabolism and nitrogen metabolism and the urea cycle.

Regulation of the Urea Cycle

The first point that should be emphasized is that the urea cycle does not exist in isolation from other metabolic pathways, but is intimately connected to them. This is shown in the diagram below:

It should be remembered that ammonia for the urea cycle only comes from the deamination of glutamate by glutamate dehydrogenase, and the transamination of other amino acids to produce this depends on a pool of α-ketoglutarate (2-oxo glutarate). A requirement for α-ketoglutarate also exists in relation to the regeneration of aspartate for the cycle itself.

The entry point of ammonia into the urea cycle is the reaction catalysed by carbamoyl phosphate synthetase:

It turns out that this reaction requires N-acetyl glutamate (NAG) for activity, and it is thought that this plays a regulatory role in the urea cycle, as increased intake of protein has been found to increase the hepatic content of NAG. Although aspects of this remain to be clarified or resolved, it is thought that the regulation occurs at the point at which NAG is synthesized from glutamate in a reaction catalysed by the enzyme N-acetyl glutamate synthase:

This enzyme is activated by arginine, giving rise to a model for regulation described more fully in a review by Caldovic and Tuchman, from which I quote the following:

  “… the hypothesis that NAG is a regulator of ureagenesis… If this hypothesis is correct, mitochondrial concentrations of glutamate and/or arginine may reflect the need for nitrogen disposal through their effect on the production of NAG by NAG synthase, glutamate as a substrate and arginine as an effector.”


Does chromosomal crossover result in a mutation? Is chromosomal crossover considered a mutation? Would this be a large-scale mutation?

There are many different ways a DNA sequence can change. Labeling a change as a mutation implies that there was a biological process in which DNA was damaged then not properly repaired.

Crossing over during the formation of gametes does not result in a mutation.
Crossing over during repair of a double stranded DNA break does result in a mutation.


Why did whales end up larger than most sauropods and what is a whale's limits? I understand that due to the square-cube law (when something grows 2 times but its volume grows 4 times and it goes on) sauropods were massive but not enough when compared to whales because whales got around the square-cube law by using the buoyant force to balance their bodies in the water. In addition, being mammals allowed them to breathe, oxygen-rich air while fish were limited to oxygen-poor water, this thenceforth allowed whales to grow many times more than the largest fish. So my question is what is the limit to whale size and if there is one what is their true potential?
A question presented by the scientific community and given to the public.

As best we can tell food availability is the relevant limits in whales.  its true that the bigger an animal gets the more energy efficient it is, it needs less food proportionally but still needs more total amounts of food. There is a limit to how much food you can find and eat, especially in the lean parts of the year. This is actually why we see dwarfism on islands lower food availability favors smaller size (less overall food needs). Finding food and even feeding itself takes energy and it reaches a point where the energy you expend is equal to or less than the energy you can extract from your food.
There are other limits like blood pressure, internal surface area, digestion time, heat buildup, but whales have not reached any of these.
https://science.sciencemag.org/content/366/6471/1367


How do you calculate or predict the charge of a protein at pH 7? How do you calculate or predict the charge of a protein at pH 7 given a fasta sequence?

Any papers or online servers to do this is well appreciated.

ExPASy to the rescue! Although I didn't comb through all the tools, this nifty website provides quite the myriad of bioinformatics resources which most certainly contains the tool to calculate what you want.

Bear in mind though, most tools will tell you the isoelectric point of your protein. However, bearing in mind the relationship between pI and pH (i.e. if pI < pH, then protein is - charged, and vice versa), you can easily figure out the charge of a protein at pH 7.

http://expasy.org/tools/

*Update

Here's the exact tool to calculate isoelectric points: http://web.expasy.org/compute_pi/


How does the original ionic distribution restore after synaptic transmission During synaptic transmission the calcium ions around the presynaptic membrane diffuse in due to the influx of Na+ ions and the resulting depolarization. This happens because the calcium channels are voltage regulated ones. At the same time on the other side of the membrane there is efflux of K+ ions in order to repolarize the membrane. My question is how does the original ionic distribution restore which is more K+ on the inside and more Ca2+ on the outside? What kind of pump does this job and what is the exact mechanism? As contrast to the nerve membrane where the Na+/K+ pump does this. I don't find a pump like K+/Ca2+ pump to do this.

Most of the depolarization in the presynaptic terminal is still sodium-based, it's just that there are also calcium channels there. Very little calcium actually moves, as these channels are closely coupled to the synaptic release machinery (see for example Stanley 1993 Single calcium channels and acetylcholine release at a presynaptic nerve terminal).
The calcium concentration gradient has to be established everywhere in cells that have this gradient (all animal cells, as far as I know), not just at a synapse, since calcium is typically a powerful "second-messenger" signal.
The two common mechanisms for transport are by using the gradient of sodium via calcium antiporters (this mechanism: using sodium or proton gradients to move other ions/molecules, is quite ubiquitous in biology), and via a calcium ATPase. Calcium transport involves both the external space and intracellular calcium stores such as within the endoplasmic/sarcoplasmic reticulum.
In the short term, calcium concentrations are also dealt with via chelation by calcium-binding proteins.


From a purely biological perspective, how does an optimal human diet look? There is hardly any subject as contested in the media as what humans should eat. Usually, such discussions are devoid of actual scientific reasoning, though they all claim to be backed by scientific studies (typically without naming those studies). The colorful spectrum of suggestions ranges from eating only bananas, to avoiding "refined" sugars and red meats, to avoiding meat altogether, to eating as much meat as possible etc. Clearly, many of them are completely contradictory.

From a purely biological, evidence-based perspective, how does an optimal human diet look? In particular, I'm interested in the following questions:

Is there a single diet that can be recommended to all humans, regardless of lifestyle, which only needs to be scaled in quantity (i.e. more physically active people should eat more of it) but not content?
Excluding diseases, does the optimal diet for an individual depend not only on their lifestyle but also on their genetic makeup?
Knowing nothing about their genetic makeup and living an average industrialized-society lifestyle, what is the best guess for what a human should eat?

Answers should be backed by solid reasoning and (ideally) references to verified (meta-)studies published in actual scientific journals supporting the claim. It seems strange to have to ask such a question, as one might expect it to have been answered thousands of times already, and of course it has, but the answers vary so wildly that I suspect I'm being fed hogwash mostly.

No, there isn't a single diet that can be recommended from a biological perspective.

The most popular diet from a pseudo-scientific perspective is the Paleo diet, saying we should eat what our ancestors in the Paleolithic were eating, but it makes a mistake of forgetting that our metabolism has evolved since then. There are also numerous other flaws in the Paleo diet but I won't go through them all.

The most notable example to use here would be dairy products, as we're among the few species that can drink milk at adult age. Drinking milk as an adult isn't normal, and yet we evolved the ability to do so. Some individuals can't drink milk, same goes for consuming gluten, nuts, and several other things, but the species as a whole can consume all of the above. Some people must avoid certain foods because of their individual genetic makeup though. Most evolved to process gluten and this ability is greatly responsible for the fact that there are 7 billion of us now. If you read an article "gluten is bad", remember that gluten grew the human race and without it at least a third of the world's population would die through starvation. If you read an article about the Paleo diet, remember we wouldn't be here if the agricultural revolution didn't happen.

The correct answer would be - humans can consume everything that isn't toxic and provides them with energy. We're very capable omnivores, which is probably one of the reasons why we've done so well as a species. In other words, you won't die from eating processed sugar. There are healthier and less healthy foods, but none will kill you.

You are correct, there are numerous answers (or attempts to answer) to this question, and the way the research is concluded definitely doesn't help. Research is mostly conducted through polls designed to prove the scientist's original unverified claim, and virtually no research is conducted on the biological level, e.g. what happens to the body when you consume a certain carbohydrate. The whole field became pseudoscientific. The "food pyramid" is...pretty much wrong.

Body needs proteins, body needs carbohydrates, body needs fat. You could come up with a vague answer if you eliminate the foods that body doesn't need, such as processed sugars, but it's still energy and you won't die from consuming it.

There is no scientific research that consumation of any food, or elimination of any food, affects life span. Meaning, there's no differential survival rate depending on what you eat.

To put things in perspective, imagine a lion preoccupied with attempting to answer whether it would be better for his body to eat an antilope or a gazelle. 10.000 calories is 10.000 calories and if he eats either he'll live another day.


Is this question about limiting factors answerable? This is from a Singapore-Cambridge GCE O-level Biology exam (a national exam for 16-year-olds). The exam board maintains that the question is "correct and accurate"—but isn't there a typo in option C?

Here's my argument:

Merely increasing the light intensity at either Points 1 or 2 speeds up photosynthesis, but varying the light intensity at Points 3 and 4 doesn't.
Therefore, light intensity is limiting photosynthesis at only Points 1 & 2.

At Point 3, merely doubling the $\ce{CO2}$ concentration speeds up photosynthesis; on the other hand, the graph shows no evidence that varying the $\ce{CO2}$ concentrations at Points 1, 2 or 4 speeds up photosynthesis.
Therefore, $\ce{CO2}$ concentration is limiting photosynthesis conclusively at only Point 3.

As this is a data-inference question, all the four answer choices are invalid deductions.
(Asserting that $\ce{CO2}$ concentration is a limiting factor at Point 4 requires assuming that raising $\ce{CO2}$ concentration beyond 0.08% continues speeding up photosynthesis.)
Excluding Point 4 from Option C will render this question finally answerable.

I think your thinking is fine, but you're being a bit pedantic about it. I don't think there is any typo.
The purpose of the question is for you to understand that there are two limiting factors here: light and CO2.
You can identify points in the graph where light is limiting because there is a slope with increasing light, and you can identify points in the graph where CO2 is limiting because light no longer increases the rate, and that the plateau level changes with different CO2 levels.
Yes, you are right, there could be other yet-unrevealed-to-you limiting factors here, but there is nothing in the graph to show this. You would need to see another set of lines where increasing CO2 further does not change the plateau level, and/or where the shape changes.
Chalk it up to Occam's razor. Without further information besides what is on this graph, if I asked you to draw your prediction about what the line would look like at 0.12% CO2, you should draw another line that follows the other and then plateaus at a third, higher level.


What happens to H+ when Glycerate 3-Phosphate is converted to Triose Phosphate? The conversion from Glycerate 3-Phosphate to Triose Phosphate requires:

$ATP \rightarrow ADP + P_i$

$NADPH \rightarrow NADP + H^+$

So what happens to the $H^+$?

Is it in-effect "recycled" back to the Light Dependent reaction.

First off, I believe you have the production/consumption of the proton off, at least for the reaction with NADPH. Most reactions with NAD(P)H go like NADPH + H+ + (oxidized compound) --> NAD(P)+ + (reduced compound). In fact, in most reaction mechanisms the hydrogen that's actually on the NADPH is ends up covalently bonded to the reduced compound.

That said, acid-base reactions are some of the fastest reactions that can occur in the cell. The cellular environment is pH buffered, so any excess H+ ions would be rapidly taken up by the excess of buffering agents which are floating around in the cell. Likewise, when a hydrogen ion is needed in a reaction, it's pulled from the general pool of free hydrogen ions, and it is rapidly replaced from that same pool of buffering agents. As a consequence of this, it normally doesn't make much sense to talk about where hydrogen ions flow in the cell - there's just a general hydrogen ion pool which supplies and takes up any hydrogen ions that are needed/produced by the reactions in the cell.

The big exception to this is where hydrogen ion movement is restricted by things like membranes. The TCA cycle and the light-dependent reactions of photosynthesis being major examples of this. In those situations hydrogen ions are pumped across the membrane during the reaction, and there is a distinction between hydrogen ions "inside" and "outside" the membrane. But there isn't any distinction between any of the hydrogens on one particular side of the membrane.

The light independent reactions of the Calvin cycle, though, happen within the chloroplast stroma and don't pump hydrogen ions across the membrane. So the hydrogen ions generated/consumed by these reactions go into/come from the general stromal pool of hydrogen ions. Here they can be used by any reaction that requires/generates hydrogen ions - a major one of these would be the light-dependent reactions, which take hydrogen ions from the stroma and pump them to the lumen (and then release them back to capture the energy for phosphorylation). But the hydrogen atoms from the Calvin cycle enzymes aren't in any way "earmarked" for the light dependent reactions.


Is addiction adaptive? Addiction and addictive traits seem common amongst animals.  A pubmed query shows it's been studied in everything from humans to worms.

My personal favorite of these is: "Individual Consistency of Feather Pecking Behavior in Laying Hens: Once a Feather Pecker Always a Feather Pecker?"

Is there/was there something adaptive about addictive behaviour?
Alternatively, how it is that addictive behaviour survived/persists if it is not adaptive?

Albeit used in the keywords of the paper, feather pecking is not an addiction, but normal behavior turned pathological in artificial (overcrowded) environments.

Addiction typically arises through overstimulation of reward centers in the brain, most notably the dopaminergic pathways involving the nucleus accumbens. Massive dopamine release, e.g. through cocaïne or meth intake, results in euphoria (Wise & Bozarth, 1985). When the drug's effects wear off it is followed by the 'crash', characterized by dysphoria and a longing for more drugs (CSAT, 1999). Gambling addiction works much in the same way.

Addiction develops because of an interplay of dependence and tolerance. Dependence is caused by downregulation of dopaminergic responses in the reward centers. Notably, dopamine receptors are downregulated when dopamine agonists like stimulant drugs of abuse are chronically administered. Downregulation of dopaminergic responses causes the physiology of the reward pathway to adapt to the presence of dopamine agonists. While the drug is in the system, everything is OK. However, once the levels of the dopamine agonist wears off, the body enters a state of lack of dopaminergic responses, causing dysphoria and depression. Tolerance develops as the liver and other tissues start breaking down the drug more efficiently due to upregulation of the necessary catabolic enzymes. Hence, more of the drug is needed, and the user becomes more and more tolerant. The interplay of dependence and tolerance form the dreaded vicious, downward spiral of addiction.

The reward centers have been crucial in evolution, as they provide motivation to vital acts of life, including eating and sex (University of Colorado, Boulder). Without a proper reward system, why eat or reproduce? However, drugs and other addictive acts such as gambling also activate the reward system.

Highly purified drugs such as crystal meth and cocaïne result in massive dopamine release that is unparalleled by normal physiologic processes such as eating. Before the occurrence of stimulants and things like gambling, the reward system was nothing but essential to life and evolution. Now, things are different and man needs to adapt to these novel, artificial pleasures in life.

References
- Treatment Improvement Protocol (TIP) Series, No. 33. Center for Substance Abuse Treatment. Rockville (MD); 1999
- Wise & Bozarth, Psychiatr Med (1985); 3(4): 445-60


Are there any online resources for finding the signaling pathways that two proteins both belong to? I am studying the proteins GSK3 and AMPK and I am trying to identify the signaling pathways that both of these proteins belong to. From reading journal papers I have found out that both of these proteins belong to the mTOR signaling pathway. I know on KEGG if you type the name of a gene involved in a signaling pathway (e.g. GSK3B) in the search bar on the page showing a signaling pathway (e.g. the mTOR pathway), you can find more information about that gene. However, I was wondering if there are any resources online where you can type the names of multiple genes and you can find out the signaling pathways that all of the genes are in?
Any insights are appreciated.

I would try "gsk3" AND "AMPK" at WikiPathways .
Here are some pathways where both GSK3 and AMPK are participants, such as:

And


What prevents a pregnant woman's immune system from recognizing her fetus as nonself (and attacking)? I'm familiar with the scenario of Rh- mother with Rh+ fetus having complications (more so after her first child), but that's not what I'm curious about. I want to know mechanistically why a pregnant woman's body does not display a reaction similar to what we see with rejection from a mismatched organ transplant. On the most basic level, I feel as though the fetus should be recognized as "nonself" due to paternal genetic contribution.

I feel as though if this mechanism could be understood, it could be harnessed for other situations (e.g., organ transplants).

Just so that someone answers this question so that the moderators have less work to do:

The fundamental reason why embryos don't get massacred by the maternal immune system is because of the placenta and several of its functions. Three mechanisms are:

1) Secretion of neurokinin B, which is also secreted by parasites to avoid detection of the host.
2) The placenta has developed immunoevasive actions from a virus. It creates a syncytium to limit transaction of mobile immune cells.
3)It only allows specific antibodies,(IgG) to enter and bind infection. (IgG being the only isotype here).

Yay  for biology


Oxygen uptake with gills from water vs lungs from atmosphere The concentration of oxygen in water tends to be around 6.5-8 mg/L. In the atmosphere, it is 21%, one liter of air weighs roughly 1.25 gram, so, oxygen concentration is 0.25 g/L or 250 mg/L. So, lungs can access 50x higher concentration of oxygen than gills can. This suggests, sort of, that maximum oxygen uptake possible should have a significant increase when lungs evolved. Is that trend observed and a topic that is often talked about?

The assumption in the question was corroborated by this article here, and is correct. The downvote is unnecessary, it is a valid question, and was easily answered with strong scientific consensus.

  As a precondition for the coevolution of eurythermy and life with high energy turnover, oxygen availability had to be maximized and the
  capacity of oxygen supply mechanisms selected high (Fig. 2). Such
  preconditions were met with atmospheric oxygen levels always above a
  minimum of 13%–15% during animal evolution (Fig. 4). Moreover, such
  preconditions were most ideally met in terrestrial environments since
  breathing air rather than water implies a reduction by one order of
  magnitude in the energy cost of ventilation at 30–35 times higher
  levels of ambient oxygen and about 103 times lower viscosity of the
  respiratory medium. However, new and largely different ventilatory
  systems had to be developed in air (lungs instead of gills in
  vertebrates) in most cases (except for terrestrial crabs) to exploit
  the excess amount of oxygen. At the same time, thermal conductivity in
  air is more than 20 times less and specific heat about four times less
  than in water, reflecting that thermal buffering is much less in the
  968 H. O. Po¨rtner terrestrial than in the aquatic environment. As a
  consequence, temperature changes occur on shorter timescales and at
  larger amplitudes in terrestrial than in aquatic environments.
  Therefore, terrestrial organisms at the same latitude are likely to
  experience much larger temperature fluctuations than aquatic
  organisms. Opposite to the marine realm, where temperature
  oscillations are less in polar and tropical than in temperate areas,
  those in air increase at high, especially Northern, latitudes, as
  estimated for mainland locations in the Americas (Gaston and Chown
  1999). According to these considerations, extreme stenotherms
  comparable to Antarctic marine species are highly unlikely to exist in
  (cold) terrestrial environments. Eurytherms will predominate instead.

Pörtner, H. O. (2004). Climate Variability and the Energetic Pathways of Evolution: The Origin of Endothermy in Mammals and Birds. Physiological and Biochemical Zoology, 77(6), 959–981. https://doi.org/10.1086/423742


Why does a fetus drink and urinate into the amniotic fluid? I was reading this website saying that fetuses urinate into the amniotic fluid. It also mentioned that, because we drink the amniotic fluid, we’ve been drinking our urine for months.

However, why do we produce urine as fetuses? I always believed the placenta was our source of waste removal; then why have fetuses the need for filtering their blood through their own kidneys?

In addition, why would fetuses drink the amniotic fluid? Is there a benefit for doing that?

In utero, the growing little human is getting ready to be an independently functioning individual. While it is everything but that, it must be able to obtain fluids and nutrients through its mother's milk, and that from pretty much the first hour of its life.

To develop proper kidney function, the growing fetus needs to ingest fluids just as it will do post partum. Because a mini bar isn't available, it has to drink whatever is available, i.e., amniotic fluid and indeed, its own urine. Shortly after the kidneys start to produce urine, the fetal swallowing commences.

Amniotic fluid is 98% water and 2% salts and cells from the baby. Until the fetal kidneys start working during month four, amniotic fluid is made by the mother’s body. But after month 4, the fetus starts to make his contribution to the amniotic fluid by urinating into it (Penn Medicine). Production of amniotic fluid is then predominately accomplished by excretion of fetal urine (300 ml/kg fetal weight/day or 600 to 1200 ml/day near term) and the secretion of oral, nasal, tracheal, and pulmonary fluids (60 to 100 ml/kg fetal weight/day). Fetal breathing movements also contribute by efflux of lung fluid into the amniotic fluid. Removal of AF is predominately accomplished by fetal swallowing (200 to 250 ml/kg fetal weight/day) (Underwood et al., 2005).

The water in amniotic fluid originally comes from maternal plasma and passes through the fetal membranes. As the placenta develops, water and solutes from maternal plasma pass across the placenta to the fetus and then to the amniotic fluid (Underwood et al., 2005), see Fig. 1.

Swallowing its own urine is not only not dangerous, it is essential to proper development. A decrease in fetal urine production or excretion can result in a reduced amount of amniotic fluid (oligohydramnios). Oligohydramnios can result in fetal lung deformations (pulmonary hypoplasia) and increased risk of infection.  Fetal mortality rates as high as 80-90% have been reported with oligohydramnios diagnosed in the second trimester (Source: Patient Info).

If the fetus would have to prevent the production of urine in utero, the kidneys would have to remain nonfunctional during development, which would be disastrous once it is born. Renal failure is in fact pretty common in newborns, but can be fatal without proper treatment (Andreoli, 2004).

Fig. 1. After month 4, amniotic fluid is derived from maternal plasma that passes via the placenta, to the fetus and then to the amnionic fluid. Source: Underwood et al., (2005).

References
- Andreoli, Semin Perinatol (2004); 28(2): 112-23)
- Underwood et al., J Perinatol (2005); 25: 341–48


How does eutrophication yield lower levels of dissolved oxygen? Where do the oxygen go? Is it consumed by a particular species? Is just not enough being made? Please explain.

From Wikipedia:

  Eutrophication arises from the oversupply of nutrients, which leads to over growth of plants and algae. After such organisms die, the bacterial degradation of their biomass consumes the oxygen in the water, thereby creating the state of hypoxia.


Why does bed bugs not carry disease? Whenever I look up this topic, all I get is articles that say "Bed bugs don't carry disease...", but they never explain why?  Is it something in their saliva that kills microbes?  Something in their gut maybe?  When they are crawling over the floor wouldn't it be logical that they would carry microbes, I mean cockroaches do?

It's not entirely true.
For example, a 2014 study demonstrates bed bugs can transmit Chagas disease. From Penn Medicine News:

  The bed bug may be just as dangerous as its sinister cousin, the triatomine, or “kissing” bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

(I'll update with more details when I get off the road)


Spider identification Delaware It looks like a wolf spider, but I've not seen these exact markings.

That's a nice female Dolomedes tenebrosus - the upland Fishing Spider that lives in similar habitat to Wolf Spiders, and eats the same sort of foods.
The way it holds its long, stripey legs together (the front pair, anyway) is pretty standard for the Pisauridae, and the pattern on the body (while a bit variable in this species) is pretty distinctive.

https://bugguide.net/node/view/2011


How many human proteins have a solved 3D structure? I was wondering how many human proteins have a solved 3D structure. Is there a database with only human proteins? I looked at pdb but couldn't find a filter.

6405 proteins mapping to 5220 genes, according to Ensembl.

In Ensembl's BioMart, you can select the PDB ID as external reference. Export the results and count the unique proteins/genes that have a PDB ID.


Statistically, why is the number of mutated genes in eggs treated with chemical mutagenesis one? Excerpted from the Guide to Research Techniques in Neuroscience [1]:

  In chemical mutagenesis, a scientist applies a mutagenizing chemical, such as ethyl methane sulfonate (EMS) or N-ethyl-N-nitrosourea (ENU), to thousands of eggs/larvae, which statistically creates lines of ani- mals with mutations in a single gene in the genome.

My hypothesis is that the discrete probability distribution of the number of mutated genes can be approximated by a normal distribution with mean=1, thus it is said statistically the number of mutated genes is one. But how can the scientists know which organism or cells contains only one mutated gene, or for that matter one mutated gene that is caused only by chemical mutagenesis?

[1] Carter, Matt, and Jennifer C. Shieh. Guide to Research Techniques in Neuroscience. Academic Press, 2015. ISBN: 978-0-12-374849-2

The expected number of mutation would not follow normal distribution (ND) as you speculated because a ND would have negative values too as it ranges from $(-\infty,\infty)$, as Remi has also pointed out. In many cases a ND can be approximated because the variance would be so less that you can practically find no negative values. However, it is a wrong assumption to consider all biological statistics as ND by default. Please see this post. Basically, ND approximations can be made on multiple measurements that follow the central limit theorem. Now, in your case of a ND centered at 1, I'll tell you how that is impossible. You can have 2 and more than 2 mutations but you cannot have less than 0 mutations. The distribution is not symmetric and is skewed towards right. You also cannot have fractional mutations and therefore the distribution has to be discrete and not continuous.

Mutagenesis itself can be modelled as a Poisson process. For more information on this please see this post. So the probability of $k$ mutations in a time window, $t$, can be represented by the following equation:

$$P(n=k)=\frac{(\lambda t)^ke^{-\lambda t}}{k!}$$

Where $\lambda$ is the rate of mutagenesis.

The mean number of mutations (and also the variance for a Poisson distribution) would be $\lambda t$.

Now, the rate of mutagenesis would be proportional to the concentration of the mutagen. I speculate that the relationship between them would follow a saturation kinetics (like Michaelis-Menten) but at lower concentrations it would be essentially linear.

Moreover, the rate of mutagenesis would also depend on the cell type.

Therefore, standardization is required and labs working in this area for a long time develop standardized protocols (with specific mutagen concentrations and treatment times) which would let them avoid multiple mutations. Even then, they have to screen a lot of individuals to filter out the non-mutants.

Basically, there is no magic number.


How copy number variation thresholds are defined in GISTIC I am having trouble trying to understand how GISTIC discretize copy number variation to values -2, -1, 0, 1, 2. I am using TCGA copy number variation for ColoRectal Adenocarcinoma.
In cBioPortal FAQ it is written that:

For TCGA studies, the table in all_thresholded.by_genes.txt (which is the part of the GISTIC output that is used to determine the copy-number status of each gene in each sample in cBioPortal) is obtained by applying both low- and high-level thresholds to to the gene copy levels of all the samples. The entries with value +/- 2 exceed the high-level thresholds for amps/dels, and those with +/- 1 exceed the low-level thresholds but not the high-level thresholds. The low-level thresholds are just the 'amp_thresh' and 'del_thresh' noise threshold input values to GISTIC (typically 0.1 or 0.3) and are the same for every thresholds.
By contrast, the high-level thresholds are calculated on a sample-by-sample basis and are based on the maximum (or minimum) median arm-level amplification (or deletion) copy number found in the sample. The idea, for deletions anyway, is that this level is a good approximation for hemizygous given the purity and ploidy of the sample.

The low-level thresholds are quite clear, while the high-level threshold not (the ones used to label +/-2 values).
I tried to reverse engineer the discretization function (the cutoffs are not available on firebrowse). The best solution I found is, for each sample, to:

split the copy number values in two groups (amplified - positive values, deleted - negative values)

for each group (amplified - deleted)

compute the median copy number value inside each chromosome arm
take the maximum (minimum for deleted group) median value across arms and use it as higher (lower) threshold

I tested it using the files:

all_data_by_genes.txt
all_thresholded.by_genes.txt

trying to get the correct discretized value (-2, -1, 0, 1, 2) of the second file from the first. However, a small part of the values are not correctly mapped. Am I missing something?

The best solution is to use only the broad alterations, using the file broad_values_by_arm.txt.

In particular, for each sample, the highest threshold is computed as the sum of the noise (low-level) threshold (e.g. 0.1) plus the maximum value of copy number variation for the sample over all the arms. Similarly, the lowest threshold is the minimum value for the sample over all the arms plus the negative noise (low-level) threshold (e.g. -0.1).


How does the brain cool itself? Thoughout life everyone tells you that brain is essentially a computer but just like computers your brain would create immense amounts of heat by being in use, so if that's the case how does it cool down.

Is like liquid cooling where the blood transfers the heat away? and if so what is the critical temperature when your blood can no longer cool your brain? Also at what temperature are you at risk of brain damage?

Computers rely on cooling mechanisms like heat sinks( an aluminum alloy mounted over the micro integrated chip) and fan. So far none of these mechanisms are utilized by nature, but analogies like cooling mechanisms in elephants which are in turn considered to be a model quite like the fan.
As the largest land animal, elephant's ears have crucial role in regulating homeostasis. When we see an elephant, it always wave its ears in order to reduce the brain temperature. On the other hand humming birds which are very smaller in size reduces its temperature by flowing blood to its wings. Humming birds wings flutter 90 times a second and it allows them to exchange much of its heat to the environment and the cooled blood is driven back to the brain.
The  carotid rete or rete mirabile in birds have been developed for heat exchange. In mammals, a pool of the cool venous
blood  returns from the nose or
head skin, exchanges the heat with
warm arterial blood of the carotid artery.
These arteries are sub divided into hundreds of
small arteries forming a net like structure which significantly improve the
heat transfer in brain.

Vascular retia mirabilia are also found in the limbs of a range of
mammals. These reduce the temperature in the extremities. Some of
these probably function to prevent heat loss in cold conditions by
reducing the temperature gradient between the limb and the
environment. Others reduce the temperature of the testes increasing
their productivity. In the neck of the dog, a rete mirabile protects
the brain when the body overheats during hunting; the venous blood is
cooled down by panting before entering the net.Reference

In Humans,

The net effect of heat production in the brain and brain cooling
keeps the brain cooler than the rest of the body and is achieved by
surrounding and bathing the brain with venous blood that has been
cooled outside the cranial vault, by bone and fat acting as
insulation, by the veins of the face and scalp through conduction,
convection, sweat and evaporation and by cooled venous blood flowing
through the cavernous and suboccipital cavernous sinuses cooling
incoming blood in the internal carotid and vertebral arteries before
it enters the brain. The combined effect of the brain cooling system
keeps the temperature inside the vault and brain about two to three
degrees cooler than the rest of the body. The effect is important
enough that some physical anthropologists attribute the extra-large
size of the human brain more to its exceptional cooling capacity than
to the increase in arterial blood flow that comes with upright
posture. Anthropologists refer to human encephalization due to
enhanced brain cooling capacity as the "radiator theory".
Reference

Also yawning and panting are considered to be mechanisms to reduce brain temperature.


What is this 2-3cm insect found in Slovakia? Noted in the West Slovakia at the garden

You have with you a Carpenter bee, which are species of the genus Xylocopa  of the subfamily Xylocopinae

Xylocopa violacea, the violet carpenter bee, is the common European species of carpenter bee, and one of the largest bees in Europe. It is also native to Asia.

Here is a link to a youtube video documentary about the bees.


How does temperature influence the rate of protein degradation? For computer modeling purposes, I am looking for some referenced quantitative measurements of the effect(s) of temperature on biochemical reactions.

Question

In particular, my question is:

How does temperature influence the rate of protein degradation?

Reducing the scope of my question

My question might be too broad in the sense that there might have too much variance in how different proteins respond to temperature in order to draw in general tendency. If this is so, someone willing to answer may reduce the question to transcription factor, to General Transcription Factor (GTF) or even to TFIIA.

I am NOT looking for..

I am not looking for a theoretical explanation of how temperature influences this process (I have basic understanding of the importance of the activation energy as displayed on a Maxwell-Boltzman distribution and of the Michaelis-Menten equation).

I am looking for..

I am looking for a function that I can plug in my algorithms to incorporate the influence of various temperatures on the process I want to simulate. I want to simulate the average gene network from an average standard eukaryote. For other purpose, I chose parameter values coming from the yeast. A index such as the Q10 would be very useful as well.

Similar already-answered question

Similar questions have been asked and answered here and here

This is a general answer for all three of your related questions:

This one
How does Temperature influences the rate of protein turnover?
How is the rate of transcription influenced by temperature?

Since you said:

  I want to simulate the evolution of genetic architecture when after a
  sudden change in temperature or in an environment that is temporally
  heterogeneous in terms of the temperature

You should see this paper. They have studied the dependence of growth rate on temperature. This was measured for different organisms (all poikilotherms).

See this figure:

Figure S1 from Dell et. al 2011. PNAS

  The unimodal thermal response of radial growth rate of sac fungi (m/(colony*s)). Green and brown curves are OLS regressions to the Boltzmann-Arrhenius model (Eq. 1) for the subset of data that are the rise and fall components, respectively. These components were extracted by the algorithm described in the Materials and Methods. For
  this particular response, the rise was obtained by the algorithm
  through removal of the measurements at the 4 highest temperatures and
  the fall through removal of measurements at the 5 lowest temperatures.
  The blue curve is the best fit to the Johnson & Lewin model (SI
  Methods) (1). Values shown are estimated activation energies with 95%
  confidence intervals for the respective response components. Dotted
  vertical arrows are estimated temperatures for Topt –the temperature
  at which the trait value is optimal–calculated from the direct method
  (red) and Johnson & Lewin model (blue). See SI for more details. Data
  are from Fargues et al. (9)

As you can see, the curve is skewed. The left side of the curve from Topt follows the activation energy model (Arrhenius/Boltzmann). The right side, though they say in the figure legend also fits the model, it seems to me that the phenomenon is somewhat different. The steepness of the curve is perhaps because of denaturation of enzyme active site and therefore a loss of activity. For different enzymes the denaturation kinetics would vary.

I happened to stumble into the author of this paper and that is how I got to know of this work. He seemed to agree that the right half steepness might be because of enzyme denaturation.

Also have a look at this article which is about the temperature dependence of the activity of the proteasome of a thermophile (same principles apply for mesophiles).

Figure 2 of the article:

  Normalized Cbz-Ala-Ala-Leu-pNA hydrolysis activity of (filled squares)
  purified native and (filled circles) 70°C heat-purified recombinant (α
  + β) Mj proteasome. To normalize recombinant activity to native activity a multiplier of 1.92 was used. Error bars for the native
  sample represent one standard deviation for triplicate assays.
  Measured temperature errors were ±2°C.

Bottomline (From my comments)

You can assume that the enzymes are at their optimum. You can model the loss of activity due to increased temperature (protein denaturation) as gamma/chi square or exponential function (or the fitted function on the denaturation kinetics) and the effect of low temperature using the chemical thermodynamic equations. But the point is that we don't know if they are at their optimum or not or how each of they may perform at different temperatures.


What are the criteria for determining the origin and end of muscle anatomically? For example the pectoralis muscle starts from sternum region and ends on the acromion or coracoid process. Why you can't say that it starts acromion process and ends on the sternum?

This is more of a convention.

The start point or origin is considered to be:

bone which is proximal
bone with higher mass
bone with higher stability during muscle contraction

The end point or insertion is:

the structure that tends to be moved by contraction
tendon
distal end of a bone

Reference: Wikipedia - Anatomical terms of muscle


Question about microaerophilic parasite tolerance for oxygen Does anyone know what is the maximal concentration of oxygen that can be tolerated by the parasite Giardia intestinalis?

Short answer: 50-60 µM O2 is ok; 80 µM is toxic.

Giardia lamblia (aka intestinalis) is a microaerophilic intestinal parasite.

According to:

  Lloyd et al. (2000) The microaerophilic flagellate Giardia intestinalis: oxygen and its reaction products collapse membrane potential and cause cytotoxicity. Microbiology 146: 3109 - 3118

Giardia colonises the upper intestine, and the oxygen concentration there has been measured at 60 µM. At oxygen concentrations up to 50 µM the organism can scavenge oxygen; above 80 µM oxygen inhibits the oxygen-scavenging process. In this paper the authors used 10% air (equivalent to 25 µM oxygen) to characterise  oxygen toxicity.

The source of oxygen sensitivity was investigated by:

  Li and Wang (2006) A likely molecular basis of the susceptibility of Giardia lamblia towards oxygen Molecular Microbiology 59: 202 - 211

These authors propose that the enzyme DT-diaphorase, previously suggested as a component of the oxygen detoxification system promotes the formation of reactive oxygen species which lead to death. Thus they found that overproduction increased sensitivity to oxygen, whereas a knock-down decreased sensitivity. This work does not, however, use controlled microaerophilic conditions.


Is numbness the absence of one or all touch sensations? I am studying the effects of tetrodotoxin and its symptoms when consumed. Numbness is one of the first sensations reported.

But I googled numbness and I couldn't find information about whether this means all touch sensations (e.g. thermal, mechano, etc) have to be absent for numbness or just one specific kind.

My Question:

Can someone

Define numbness
Explain whether numbness is the absence of one or more than one or all touch sensations.

The definition of numbness has been answered by yourself, and I will focus on the second part of the question.

In terms of the underlying physiological mechanism behind numbness I think it's good to narrow the question down and focus on local anesthetics, which numb a local area of the body for minor surgical procedures. Cocaine and related compounds have been shown to block not only pain, but also warmth, cold and touch perception, as well as blocking motor function. Cocain and related compounds are basically voltage-gated Na+ channel blockers, but also block K+ channels to some extent. Their affinity to various different channels differs, explaining the differential effects. E.g., pain is blocked more effectively than motor functions (Scholz, 2002).

We all know the feeling of numbness when our limbs are asleep due to restriction of blood flow. Likely all neural activity is blocked here too, as the cutting off of oxygen affects all neurons.

Given the broad range of effects of local anesthetics and restriction of blood flow, I would tentatively conclude that numbness can be interpreted as a reduction of sensitivity of all the senses.

Reference
- Scholz, Br J Anaesth (2002); 89; 52-61


Does Spinning dancer has anything to do with your eyesight I came across the spinning dancer as part of the brain test to determine left brain vs right brain dominance.

I saw the dancer is turning clockwise. The other people around me saw it turning clockwise for the first time, but soon they got confused and said they saw it turning it in both direction.

I know the tips of how to see it anti clockwise, but no matter what I do I always see it clockwise. I have shown it to a number of people and all of them could see it spinning in both direction after looking at it for longer time.

I am the only person who has never see the dancer turning in both direction.

My question is does this has anything to do with my eyesight? I have very limited(almost blind) eyesight in my left eyes. This is from birth.

Does my visual impairment has anything to do with this or does this mean anything else?

For a bit of background, this test was devised by Nobuyuki Kayahara and it was originally thought that it shows the dominance of one part of the brain to the other. This was later on discarded as a misconception (reference). It is now widely believed that the clockwise - counter-clockwise rotation is a phenomenon called Bistable perception (Reference 1 and reference 2).

  Multistable perceptual phenomena are a form of perceptual phenomena in
  which there are unpredictable sequences of spontaneous subjective
  changes. While usually associated with visual perception, such
  phenomena can be found for auditory and olfactory percepts. Famous
  examples include the Necker cube, structure from motion, monocular
  rivalry and binocular rivalry, but many more visually ambiguous
  patterns are known. Since most of these images lead to an alternation
  between two mutually exclusive perceptual states, they are sometimes
  also referred to as bistable perception(reference 1 and
  reference 2).

No, the fact that you can only see her turn clockwise has not got anything to with your vision (for the record, I have never been able to see the girl go counter- clockwise myself).

  Sometimes, a person will stare at an image and it will never reverse.
  Dr. Toppino advises staring at one part of the image, such as the
  foot, and most of the time it will eventually flip. In people who
  can’t see the reversal, it may be that one underlying neural structure
  is more dominant, but once someone finally manages to see the flip, it
  will start to happen more often (reference).

This image would help you watch her rotate counter-clockwise.

Here she is spinning clockwise.


Meaning of PAM matrix values If PAM-1 matrix refers to time or evolutionary event for 1% change in amino acid sequence of a protein then how come there is PAM250? shouldn't PAM 100 be the highest where the two concerned sequences are 100% different

You misunderstood slightly what PAM1 means; it's actually (from Wikipedia) "1 [PAM] mutation to occur per 100 amino acids". So PAMn makes sense for any n, as in the 100 amino acids may mutate more than once each, on average.

Or if you put it in terms of PAM distance...

  Is possible for two sequences to be more than 100 PAM
  apart?
  Yes: One position can mutate multiple times.

An attempted analogy: what does 600% casualty rate (for soldiers) mean? Well it means not only the original guy died, but his 5 replacements got (successively) killed as well.


How did the Chromosome #2 Fusion propagate? There is strong evidence that chromosome 2 in humans is a fusion of two chromosomes of a common ancestor of chimps and humans as explained at wikipedia here

Was it necessary for the common ancestor with fused chromosome 2 to mate with another creature whose 2 chromosomes fused in a similar manner?

If yes, what would their offspring look like? would they also need to mate within themselves or could they mate with the chimp population?

if possible, also, how in the world could a genetic disadvantage take over the population? doesn't this contradict natural selection?

Was it necessary for the common ancestor with fused chromosome 2 to
  mate with another creature whose 2 chromosomes fused in a similar
  manner?

Of course not.  People with balanced translocations have kids with people with the wild-type chromosome arrangement all the time.  Such people have some fertility problems, due to problematic meiosis leading to more inviable gametes, but they can still reproduce.

Someone already mentioned Robertsonian translocations to you in your previous question.  Didn't you look it up?

  would they also need to mate within themselves or could they mate with
  the chimp population?

What chimp population?  There were no modern chimps when the fusion happened.

Look, you could ask a million questions here, and still learn nothing.  This board is helpful for people who have a good, accurate framework of the facts of biology, but who want specific holes in their knowledge base filled.  I don't think that's you.  I think you think you know the right answers to your questions, based not on science, but on other things, have imbibed or made up a whole slew of very wrong stuff about biology, and are asking questions here expecting people to confirm your wrong beliefs, trying to trick people in to confessing that mainstream biology is wrong, and you are right.

Picking at one bit or another of evolutionary biology is not going to help you.  You need to start by assuming that a lot of what you think you know about the scientific facts is wrong, and learn the real stuff.  It is not at all easy to get wrong information out of our brains, but until you do, this exercise isn't going to educate you much at all.


How does the bladder transition from releasing urine at night to being able to hold urine at night? I wonder about this.  What's the biology of the transition from wetting the bed at night to holding urine at night?  Is there a chemical change with how the bladder muscles contract?

The bladder is controlled by both the autonomic and somatic nervous systems. This means that part of the bladder activity is voluntary and another part is involuntary - more precisely, the detrusor (which is the smooth muscle in the bladder wall) is controlled involuntarily, while the external sphincter (the muscle around the bladder neck) is controlled voluntarily (see picture, this is the female bladder).

I found all kinds of references that describe the maturation process of the bladder during infancy. This paper, from Pheonix Children's Hospital, is about voiding disorders in children. It notes in the first paragraph three conditions that make up the bladder's maturation process (the rest of the paper discusses voiding disorders):

The bladder capacity must increase.
The child must develop voluntary control over the sphincter muscle in order to start and stop voiding.
the child must develop voluntary control
over the infantile voiding reflex which allows the child to stop involuntary bladder contractions.

This article discusses the topic of bladder maturation in greater detail (see the first section titled: MATURATION OF BLADDER CONTINENCE). From the article: "As bladder urine increases, a critical volume is reached (functional bladder capacity), which initiates a spontaneous reflex contraction that is mediated by the sacrospinal ganglia. As the bladder contraction ensues, the increased bladder pressure overcomes the detrusor muscles at the bladder neck and spontaneous emptying occurs. As the infant grows and matures, control centres in the pons and medulla initiate inhibitory signals that slowly dampen this reflex over a period of years ... Nighttime continence is achieved in association with the abolition of spontaneous bladder contractions, mediated by the pons and medulla; a nocturnal bladder volume less than the nocturnal functional bladder capacity (NFBC), which is ADH-dependent; and the achievement of prolonged rapid eye movement (REM) sleep and attainment of sleep arousal."


Why does this plum/apricot hybrid look like brains? Why does this plum/apricot hybrid look like brains?

Notes:

Here's a photo of what a normal fruit on the tree looks like.
Location is Zone 5, east of Toronto.
There are about 20 other fruits on the tree. This the only fruit on the tree that has this problem.
The date is June 26, 2019 (although plants have been delayed by about 3 weeks this year due to unusually cool and rainy weather).
I have had lots of disease problems on my prunus this year due to the wet weather.

It is difficult to say, but it is likely due to disease. Many plant diseases have the effect of convincing plant tissues that they are some other organ than what they actually are, which leads to deformations.

I was not able to find anything that looked as dramatic as the image that you show, but there are similar diseases in stone fruits that deform fruit:

Plum pox potyvirus: http://download.ceris.purdue.edu/file/1424
Plum pocket fungus/"Bent banana disease": https://pnwhandbooks.org/plantdisease/host-disease/prune-plum-prunus-spp-plum-pockets, http://shropshireprunedamson.com/a-bad-case-of-bent-banana-disease/

I hope that this is helpful.


Epilepsy explained by computational neuroscience A few years ago, on my maths masters, I did a module in theoretical neuroscience. I was shown that the mathematical framework the course developed for neurons, with a small adjustment in the parameters, would produce spike trains similar to those observed during epileptic kindling. These parametric tweaks could be attributed to mutations in ion channel/receptor structures. This was one of the highlights of the course, and when I came to apply for a math/bio interdisciplinary doctoral program, I cited it as such in my personal statement.

Now the interview is fast approaching, and I'm pretty sure it's going to come up, but for the life of me I can't track down a reference. After four years out of the game, my memory is hazy at best.

As I recall, this had something to do with short term plasticity. Normal neurons' response to unrelentingly high frequency spike trains decayes over time, while pathological neurons' does not. This may however be entirely wrong.

What is a reference for the model I describe above? An introductory/educational treatement is prefered, but the original paper is fine.

Unfortunately, epileptic spiking can occur very easily in many neural modeling studies, and therefore one should be very careful in asserting the possibility of certain aspects of model as a cause for epileptic activity. One possibility, as you mentioned, is the lack of short-term depression which prevents long sustained firing. But again, a simple increase in the global excitatory coupling can also exhibit similar dynamics.

Good luck on your interview.


Are there birds with knees instead of elbows? Are there any birds whose legs fold the same way human legs do, in a knee, instead of an elbow which is what all the birds I know have?

The joint you are thinking of is not a knee, nor is it an elbow, instead it is an ankle which is bending the same way as us humans. You can see from the below diagram that the knee - the joint between the femur and tibia - is just further up the leg normally hidden by feathers.

Birds have a comparatively elongated metatarsus which gives the impression that the knee bends backwards more like an elbow, but it's just the ankle. (Image from here)

I also liked this diagram from a blogpost on a similar theme...

To follow up there appears to be no animals whose ankles bend the "wrong" way.

http://www.answers.com/Q/Which_animal_has_backward_knees

http://qi.com/infocloud/knees

http://www.ehow.com/info_12317202_birds-knees-backwards.html#page=1

Though these are far from conclusive resources. I'd guess the way knee is defined (it means something to humans but not to nature (a bit like the species being a concept which has weak biological bounds)) has something to do with that


Rabies transmission via barking According to CDC, non-bite exposure includes scratches, abrasion, and contamination of the mucous membrane from a rabid animal's saliva.

So, is it possible to catch rabies if a rapid animal barks near you? I mean, it can have some tiny droplets of saliva on it, right? Or the contamination of the mucous membrane should come from licks as stated by WHO?

Between 1956 and 1977, 4 human cases of rabies virus infection were
  attributed to aerosolized rabies virus;

Possible but very rare.

https://academic.oup.com/jid/article/195/8/1144/816583


Why is there an extended delay before G.M. liver cells are attacked by the immune system? In this BBC article a trial is described where patients with B-Haemophillia are infected with modified Adeno-associated Virus 8 which contained the genes for Factor IX clotting protein.  Trials seemed to be successful, however the article later mentions

  There was an immune response against the infected liver cells around seven to nine weeks after the virus was injected.

I am interested to know why there was a delay period of such length?  Would this be true of all cells and is it due to a long duration of clonal selection in the humoral immune response or is something else at play?  Also, I'm presuming that the Adeno Virus would be attacked long before the cells it has infected?

The delay in immune attack is common for many viral infectious deceases where auto-immune response plays substantial to significant role in pathogenesis of the decease. The classical example here are the viral hepatitis B, C and D where it is auto-immune attack that causes the massive death of liver cells (hepatocytes).

The delay in immune attack is explained by the following mechanisms:

The immune attack is developed against the surface antigen, in case of hepatitis it is the HbS Antigen. "Surface" means that this antigen has to appear on the cell surface in order to elicit immune response: the virus itself as well as the parts of destroyed cells are not immunogenic enough for this.

The second point explaining why the attack takes so long to develop is that it is primarily cell-mediated attack, the humoral factors play the secondary role here.

So, the usual "workflow" in this case is the following:

Contamination with hepatitis virus.
Virus propagation to hepatic cells and their infection.
Processing of the viral DNA (either as DNA or first reversed-transcripted from RNA) so that it is integrated into cell normal processing pathways.
Expression of viral proteins (=antigenes) and their anchoring in the cell membrane.
Surface antigenes are detected by macrophagues, processed and expressed on their membrane for T-helpers
... (continuation of the usual cell-mediated immune response via T4 and T8 lymphocytes).

Every stage takes some time, the total duration can sum up to 4 to 12 weeks depending upon the viral activity and the immune system status.


Can Bioluminescence drive photosynthesis? I'm trying to construct an anaerobic kitchen-waste digester at home.

The major output from the digester is methane - with a significant component of carbon dioxide. To scrub/reduce the CO2 I was thinking of passing the methane through a freshwater container charged with algae ... then it occurred to me to also think of introducing some bioluminescent algae to drive the photosynthesis & absorb some of the oxygen released by the other algae. Understandably this would be an unbalanced system.

But ... can bioluminescence drive photosynthesis?

Yes and no. Yes as in the energetics do work out and you will be going down a small but non-trivial driving force as long as you continue to provide the luciferin to the algae.

However, the wavelengths of light by which photosynthesis absorbs its energy are well defined and narrow. As a result, light sources for photosynthetic organisms have to be fairly strong and bright to cover the whole spectrum to provide the necessary light. As a result, your bioluminescent algae will also have to emit light at the desired wavelength to achieve a high photochemical efficiency and provide light to both Photosystem II and Photosystem I which have different wavelength requirements.

(source: gsu.edu)


How to compute CNV from TCGA data TCGA provide CNV data for each cases like this.

I want to know, how can I calculate CNVs from this data? What are standard  algorithms and methods used?

Copy number variation (CNV) has traditionally been detected in the wet lab via FISH, fluorescent in-situ hybridization. By combining targeted DNA oligos to fluorescent reporter proteins, a region with high CNV will "glow more brightly" than a region that doesn't have as many repeats.

More recently, with next-generation sequencing, a common approach is to align sequencing reads to the reference genome. If a particular region in the sequenced sample has a large CNV, then there should be disproportionately many reads (2x, 3x, etc) reads mapping to the CNV locus in the reference genome compared to the rest of the genome.

For example, if our sequenced sample has a 3-CNV for region B:

$$A-B-B-B-C$$

then aligning our sequenced reads to the reference genome, which is:

$$A-B-C$$

will yield 1x coverage at region A, 3x coverage at region B, and 1x coverage at region C.

There are, of course, more sophisticated approaches. For a good review, refer to
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059128


Can two denatured DNA strands reassociate? What matter if I increase the temperature to 95°C. So double-strand DNA denatured into two ssDNA, and then I decrease the temperature to room temperature. Are they able to reassociate after denaturation?

Yes, heating the DNA above 94°C for some length of time will melt, or denature, dsDNA into two ssDNA strands. Upon cooling, the complementary strands will come back to anneal. The degree and completeness of annealing, or association, is dependent on a number of factors including the rate of cooling and structural properties of the DNA itself (%GC content, secondary structure). I would not expect that the majority of ssDNA strands will completely anneal to a single, complementary dsDNA strand. What is more likely is that the DNA mix will look more like spaghetti with one strand partly annealed to two other strands. When performing PCR, the primers are designed to be specific, and added in excess, so that you bias the odds of annealing to favour a primer:ssDNA association. If this weren't the case, we could not possibly have efficient PCR amplification.


Determination of animal and vegetal pole How do we determine which is an animal pole and which is a vegetal pole in a zygote?

My professor said that the zygote can be divided into two hemispheres, vegetal and animal poles. The hemisphere with yolk is the vegetal pole and the one without is the animal pole.

But I couldn't find an authentic book that I have access to saying anything about the polarity of the zygote. However I stumbled upon this paragraph from Objective Zoology and I'm not sure if it's right.

  Zygote or egg of frog is spherical and measures about 1.6mm in diameter. The upper half of the zygote is black (pigmented) and contains nucleus and cytoplasm. The lower part of the zygote is white or light yellow in colour and contains the reserve food in the form of yolk. The upper pigmented part is called the animal pole and the lower part vegetal pole.

Do you have any reason to doubt this statement? The wikipedia article says pretty much the same thing. When reading the folllowing, don't forget that one can talk about such poles at different stages of development.

  The animal pole consists of small cells that divide rapidly, in contrast with the vegetal pole below it. In some cases, the animal pole is thought to differentiate into the later embryo itself, forming the three primary germ layers and participating in gastrulation. [..] The vegetal pole contains large yolky cells that divide very slowly, in contrast with the animal pole above it. [..] The animal hemisphere is dark brown, and the vegetal hemisphere is only weakly pigmented.

and it comes with the following picture


Can 12 mitotic divisions produce 6000 nuclei? The following quote is from "Principles of Development" by Tickle & Wolpert:

  "After fertilization and fusion of the sperm and egg nuclei, the zygote nucleus undergoes a series of rapid mitotic divisions [...] The result after 12 nuclear divisions is a syncytium in which around 6000 nuclei are present in a common cytoplasm"

12 divisions (starting from 1 zygote nucleus) should produce no more than 212=4096 nuclei, not 6000. Is this just a simple error in the textbook? Alternatively, is there a biological explanation that makes the 212 estimation invalid?

There are indeed some mistakes in that excerpt from Wolpert & Tickle. First of all, the blastoderm is not a syncytium, it is a cenocyte instead (have a look at my answer here). By the way, that's a wrong nomenclature used by all books on developmental biology I'm aware of... therefore, being so well established, that wrong nomenclature probably won't change anytime soon. We have to get used to it.

Back to the numbers:

The second mistake in that excerpt (also reproduced by most books on developmental biology) is the number of divisions: it's not 12, but 13. And that would give us 213, or 8192 nuclei. As you can see, that's more than the ubiquitous "6000" we see everywhere in the literature.

Now the question becomes inverted: what's the reason for the blastoderm having a smaller amount of nuclei compared to the expected number?

According to Miles et al. (2010), the number of nuclei depends on the size of the egg:

  The number of nuclei at the cellular blastoderm stage also changed in response to selection, with large-egg selected lines having more than 1000 additional nuclei relative to small-egg lines. This increase in nuclear number in larger eggs does not scale with egg size, however, as nuclear density is inversely correlated with egg length. (emphasis mine)

And the most important part of that paper, which addresses your (now inverted) question:

  After 13 mitotic divisions the maximum possible number of nuclei at the blastoderm stage is 213 or 8192 nuclei, considerably more than the classic value of ~6000 given in the literature (Zalokar and Erk 1976; Turner and Mahowald 1983). We found that cell number is not anywhere near constant at 6000 nuclei in the cycle 14 embryo, but rather is positively correlated with egg size. On average, our large-egg selected treatment had more than 1000 additional nuclei than the small-egg selected treatment, a difference that arose as a correlated response to selection for egg size. Yet, in comparing cell numbers in other (nonselected) lines and species, we conclude that cell number must not be entirely a consequence of egg size, but rather must itself be a genetically variable trait. For example, D. sechellia (mean cell number = 7448.7, some embryos approaching the 213 limit) and the Ind strain of D. melanogaster (mean cell number = 6569.1) have nearly non-overlapping distributions of cell number despite having almost identical egg length. (emphases mine)

Conclusion

213 (or 8192) is the upper limit when considering 13 divisions. The real number of nuclei is less than that and varies from blastoderm to blastoderm. The mechanical explanation for that smaller number is, probably, that some nuclei fail to divide.

Also, it's worth mentioning that, from the 14th cycle on, the divisions become asynchronous, that is, the nuclei do not divide at the same time: some of them divide faster and some of them divide slower, and the exponential 2n (where n is the number of divisions) for the total number of nuclei doesn't apply anymore (because, at a given moment, you have several different values for n).

Source:

Miles, C., Lott, S., Luengo Hendriks, C., Ludwig, M., Manu, Williams, C. and Kreitman, M. (2010). ARTIFICIAL SELECTION ON EGG SIZE PERTURBS EARLY PATTERN FORMATION IN DROSOPHILA MELANOGASTER. Evolution, 65(1), pp.33-42.


How do viruses provide selective advantage I've heard in many talks as a passing, well-known fact that viruses(e.g. pathogenic HPV strains) offer selective advantage for the infected cell to multiply. But I'm not able to quite wrap my head around this.
I assume this has something do with episomal qualities of viruses, but how exactly does that does translate to selective advantage.
My intuition says that if there is an uneven segregation of the viral genomes to the daughter cells, than that heterogeneity can cause give selective advantage. But given no preface of the heterogeneity of a virus during cell division, how is one able to claim that viruses offer selective advantage?
Background: I am not a biology person, but rather computational scientist who works with biologists.
one example source

See the instances of "selective advantage / pressure" from the source provided by Jonathan, emphasis mine:

Persistent infection with HPV leads to an environment of genomic instability and local immune suppression, which can lead to both the accumulation of genomic alterations in the host cell, as well as to the integration of the viral genome into the host genome. When these additional alterations provide a selective growth advantage to the cell, carcinogenesis may ensue.

Furthermore, the integrated viral transcripts confer stronger transforming capacity than those derived from episomes, due to longer half-life of transcripts (32). This promotes immortalization and transformation of these cells and provides a selective growth advantage (3, 8, 30, 33). Integration may, however, confer a selective growth advantage to the host cells not only through its effects on the viral genome (i.e., enhanced/deregulated expression of viral oncoproteins), but also through its effects on the host genome (i.e., by affecting key cellular genes).

Several mechanisms by which HPV integration may confer a selective advantage have been described (Fig. 3).

This environment is also amenable to accumulation of genetic alterations and viral integration, and subsequent tumor formation. Integration affects both the viral genome and the host genome, likely conferring additional neoplastic selective pressure, by one or more of the following mechanisms: (i) enhanced expression of viral oncoproteins, (ii) alteration of critical cellular genes (leading to increased expression of oncogenic proteins, decreased expression of tumor suppressor proteins, altered DNA repair mechanisms, or modulation of the immune system), and (iii) changes in global promoter methylation and transcription.

In biology, "selection" often refers to natural selection -- in short, genetic diversity in a population manifests as different traits in individuals, which result in differences in relative fitness in a given environment that, through time, result in evolution.  The quoted excerpts refer not to the environment acting on different traits but rather to the (potential) enhanced growth characteristics of HPV-infected cells, relative to non-infected cells.  So, the use of "selective" here is misleading.  Yes, viral integration may lead to enhanced growth of a cell population by disruption of certain cell cycle checkpoint genes, but the organism on the whole will certainly be less fit when that unrestricted growth leads to cancer.
In my opinion, the text could read "growth advantage" or "enhanced growth" in all instances and do away with "selective" entirely.


Can controlled dose of Codeine improve brain's functionality? What I know so far about drugs (codeine, heroin, etc) is, the first time you take them you will feel better, think sharper, and act better, just like a supercharged engine. But as this goes on a regular basis, it will stop being efficient and causes addiction.

So what I can understand of this, is that our brain can function better but for some unknown reason (to me) it doesn't. However its functionality increases for a period of time after you take a dose of these drugs.

Now I have a few questions about this:

If our brain can function faster than normal, then why it demands additional drugs to do so?
Can we inject a controlled dose to brain (not by needle to the brain obviously, I mean pills, tablets, etc) of these drugs to keep the brains functionality at a higher rate?
When a drug actually charges our brain, is it taking any damage? The same way you overclock a CPU and it might cause damage to it over the time.

PS: I'm asking this on Biology instead of Health since I'm talking about brain's behavior about addiction, not just to confirm whether or not i can use drugs on a regular basis.

the first time you take them you will feel better, think sharper, and
  act better

You are probably thinking of amphetamines, not opiates. Militaries have used amphetamines for just that purpose for decades, particularly for situations where long periods of attention are necessary. The problems are addiction, adaptation (lessening effects over time), withdrawal, side effects, etc.

Caffeine has very different cellular effects, but is also a stimulant, albeit a much weaker one. People around the globe use caffeine to achieve much of what you are suggesting on a daily basis. I actually think caffeine is a great example of what you are proposing, because (at least for people who tolerate it well and don't have any other conditions) it is safe, effective, and has less serious withdrawal symptoms and is somewhat less addictive than many other drugs. That said, among people who use caffeine regularly, some of the benefits begin to wane, and people start needing caffeine to maintain their normal level of alertness.

People with ADHD (and some others without, particularly students) also take amphetamines to help with attention (Adderall is an amphetamine; Ritalin/methylphenidate is closely related). There is a bit of controversy over whether that's a good idea or not. All of these things have side effects, including potential for changes in personality, anxiety, and various peripheral side effects, as well as the risks of dependency and symptoms of withdrawal.

Codeine and other opiates, on the other hand, are primarily useful for blocking pain. They are often associated with euphoria, but their other psychological effects are mostly depressant: drowsiness, respiratory depression, suppression of gut motility leading to constipation, etc. I'm not aware of any cognitive enhancement from codeine, unless the cognitive task you are trying to perform is sleep.


What is the advantage of the way eukaryotes initiate translation? The eukaryote and prokaryote mechanism for translation is slightly different. Is there any advantage of the eukaryote translation mechanism ?

Edit : I specifically want to know why eukaryotic ribosome first attaches to tRNA and then to mRNA but prokaryotic ribosome can do this in either order. Is there any advantage of the former ?

As far as I understand it (and I'll preface this by saying that initiation is not my strongest point), but prokaryotes utilize the beautiful AGGAGG Shine-Dalgarno sequence.  Usually around 8bp upstream of the start codon, it is this sequence that the prokaryotic ribosome seeks out to initiate translation.  It does this through a complementary region in the 3' sequence of the ribosomal RNA.  Upon complementary binding, the ribosome and mRNA are correctly bound.  Convenient!

In eukaryotes, however, there is no consensus SD sequence, so a different mechanism must be used; the complex of 40S and Methionine tRNA serves this purpose.  The two together scan the mRNA, looking for an AUG start codon which the tRNA is complementary to.  This eventually brings the full ribosome (40S + 60S) together to start translation.


Text Book Recommendation: Cell & Molecular Biology + Organic Chemistry I am studying undergraduate biology course and I have cell biology and molecular biology in my next semester. Our college recommends three books : Cooper, Lodish & Bruce Alberts. It would be really helpful if you give me your opinion on which of these (or your own recommended book) would be the best to learn these subjects properly. The only thing I need is the book to be easy to understand because it will most probably be totally self taught because our instructors are not always helpful in explaining stuff properly.
We also have an organic chemistry class and the recommended books are Solomon's&Fryhle & LG Wade. It would be helpful if you help me choose between these as well, my requirement stays the same. Book should be easy for self learning.
If you know about online video lectures about organic chemistry and molecular biology do let me know. MIT OCW doesnt really have good bio videos. I cant seem to find video lectures anywhere for gre preparation. Thank you

Given your requirements I would go for the Alberts for molecular cell biology.

For organic chemistry, in my opinion, there is no better book then the Clayden. It is targeted at OC students but I - as a biologist - learned a lot from it and still sometimes love to browse through it even though my work is far away from organic chemistry.

In general, I would advise you to go to your local library and take a look at the different choices before getting one. Take your time to get a feel for the writing and teaching styles and pick the one you find most access to (and maybe give feedback as a comment/an own answer to your post which book you took and why, for future reference).


How does the body "know" how to metabolize foreign substances As a freshman biochemistry major, I find myself befuddled by our body's ability to perform complex chemical reactions to break down foreign substances. I can see how we would evolve explicit pathways to deal with substances we would find often in our environment of evolutionary adaptedness, but we also process things we would never have encountered before. How does the human (or any organism's) body do that without explicit programming?

One strategy for xenobiotic metabolism seems to be making a lot of similar enzymes with different substrate specifities. Lets take the cytochrome p450s as an example. These are a class of enzymes with 57 genes identified for humans, and I don't know how many alternative splicing products are made from those genes. As a class, they are responsible for about 75% of drug metabolism and are predominantly found in the liver. They work by using a heme group with a carbon monoxide to add oxygens to xenobiotics. Here is a diagram of the mechanism:

It's been too long since my drug metabolism class to go into more detail on these enzymes, but there are other classes of enzyme that fit this multiple enzyme strategy such as the 2 monoamine oxidases, 5 flavin containing mono-oxygenases, and 4 epoxide hydrolases. So the body doesn't really know how to break down xenobiotics, but has a wide array of enzymes with broad and overlapping substrate specificities that work on whatever they happen to bind to, whether it's an endogenous hormone or pharmaceutical compound or toxin.


Are there eukaryotes with fully working mitochondria but without mitochondrial genes? Are there eukaryotic organisms with fully working mitochondria that do not have genes in the mitochondria?  By fully working, I mean ones which can carry out oxidative phosphorylation, unlike reduced mitochondria like organelles such as mitosomes in Giardia lamblia.

Is it possible to transfer all mitochondrial genes to the nuclear DNA and still have fully-functioning mitochondria?

No there aren't any organisms with fully functional mitochondria which (the latter) do not retain the minigenome.

On whether it is theoretically possible to transfer all the mitochondrial genes to the nucleus:

Perhaps it is possible and mitochondria may work just like lysosomes and ER, but I think that the responses will be greatly delayed. At present there are no mathematical models that can provide a better understanding of that possibility. Nonetheless, some studies have shown that chloroplasts and mitochondria also have redox dependent gene regulation by which the expression of some components of the ETC is regulated by the redox state of the quinone. This helps in optimization of the ETC; if all genes were in the nucleus then this would not be possible. This pheonomenon is, however, better studied in chloroplasts. See this review.


What is the darkest color human bowel movement can become? I assume a healthy human, with usual nutrition, without using any drugs or supplements.

The darkest stool in a healthy human is black. It can result from eating black licorice, blueberries, blood sausages, Oreo cookies or grape juice.

Other foods that may cause almost black stools: dark chocolate, beets, cranberries, prunes, dark green leafy vegetables, such as spinach or kale.

They are not nutrients, but natural or artificial dyes in the food, that can turn stool black.

Black, tarry and smelly stool is suspicious for bleeding from the upper gastrointestinal stomach (from mouth to stomach), since the acid in the stomach turns blood black.

Sources: (Medline Plus, OU Medicine, 25Doctors.com)


How do parasites "reprogram" brains? Dicrocoelium dendriticum is a parasite that uses ants as a second intermediate host (which means that ants aren't its primary host/target, but are rather a temporary host to help reach their main/definitive host: sheep).

When ants are infected, this parasite causes them to climb onto the top of grass blades, which increases the chance that sheep will devour the ant along with the grass, helping the parasite reach the sheep.

My question is: how do parasites such as (but not limited to) that described above "reprogram" the minds of the hosts? I know that brains are incredibly complex, so I'm fascinated and curious about how a parasite can change the behavior of its hosts - which I'm assuming is only possible by modifying its brain? If so, how do they do this?

Not much is known about the mechanisms involved, but they do appear to differ significantly from parasite to parasite. I'll discuss a few different examples here, and try to provide as much information as is currently known about how the parasites are doing it.

There are likely to be many more different examples and mechanisms than these, and researchers may well revise the below hypotheses over time. For this reason, I'm thinking about either splitting this answer into multiple separate answers or changing it into a community wiki.

Example 1 - Toxoplasma gondii and rats as an intermediate host

The Toxoplasma gondii parasite infects multiple hosts during its lifecycle. At one stage, it is hosted by a rodent, which must be eaten by a cat if the parasite is to use the feline's gut in the next stage of its life cycle. Somehow, the parasite causes the rodent (I know that rats are affected, but I don't know if mice or other rodent species are) to behave in a less risk-averse way around cats, making it more likely to be eaten by them.

Exactly how Toxoplasma influences its rodent hosts is unclear. An article in Nature ("Parasite makes mice lose fear of cats permanently") mentions that the parasite creates cysts within the rodent's brain cells, increasing their production of dopamine, which may be one of the causes for the change in behaviour. However, the researchers quoted in the article found that the risk-taking behaviour persisted even without the cysts and dopamine.

Link to that research paper: "Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance".

One theory is that the parasite simultaneously infects the ovaries/testes of the rodent, causing increased testosterone levels in the male and thereby causing it to engage in more risk-taking behaviour. A lot of the literature relevant to this theory is behind paywalls, but as far as I can tell studies have shown that:

Male rats with their testes removed are not affected by the behavioural changes, although I do not know if the orchiectomies were performed before or after infection.
Male rats in general are affected.
Female rats are affected by the behavioural changes, whether or not their ovaries have been removed.

This suggests that the parasite has more than one means of inducing the behavioural changes in the rodent, and that the behavioural changes in female rats have a different cause to the same behavioural changes in males. In the case of the male, it is believed that epigenetics play a part. The increased testosterone levels lead to reduced methylation in genes in a certain area of the brain, and this in turn leads to increased production of the chemical "arginine vasopressin" (AVP). I know nothing about AVP, but the increased levels of it are supposed to cause the behavioural changes, according to this theory.

As I mentioned, the presence of paywalls is giving me some difficulty in studying the relevant research for this particular theory, but a link to one paper is provided in the "Sources" list below.

Another theory is that the parasite infects the white blood cells and causes them to produce excess quantities of a chemical that acts as a neurotransmitter, affecting the brain through the increased levels of said chemical. The research paper is "GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii".

There's also a New Scientist article: "Parasite makes mice fearless by hijacking immune cells")

Example 2 - Ophiocordyceps unilateralis (fungus) and carpenter ants

A recent article in Ars Technica ("Zombifying fungus bypasses the brain to make ants its puppets, study finds") described research into another example, the Ophiocordyceps unilateralis fungus that parasitizes carpenter ants. The researchers had found that the fungal cells in the ant's body effectively disconnected its brain and linked up to act as a replacement brain to move the host's limbs.

Link to the research paper: "Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants"

(If I understand correctly, the brain's disconnection might be due to damage caused to it by chemicals emitted by the fungus. It may be the case that the original brain and fungal network are both able to move the ant's limbs during the early stages of infection, I'm not sure.)

Even then, one piece at least of the host's altered behaviour wasn't in fact due to this, but due to the fungus destroying a protective membrane on the ants' jaw muscles - leading to the famously strong "death grip" as the infected ant bites a high leaf, dies, and is held in place by the grip of its jaws.

The O. unilateralis fungus extending soma stalks and fruting heads from the bodies of dead ants. Image taken from https://en.wikipedia.org/wiki/File:Ophiocordyceps_unilateralis.png. The image was posted under a Creative Commons Attribution 2.5 Generic license and is credited to David P. Hughes and Maj-Britt Pontoppidan.

The research paper for the jaw membrane is, unfortunately, behind a paywall. If you have access: "Zombie ant death grip due to hypercontracted mandibular muscles"

The "cut off and replace the brain" part of this was also covered by a 2017 article in The Atlantic ("How the Zombie Fungus Takes Over Ants’ Bodies to Control Their Minds").

Example 3 - Dicrocoelium dendriticum and ants

For the actual host/parasite pairing that OP was asking about, not as much is known. One fascinating aspect of this infection is that the ant's behaviour is only changed during the evening/nighttime hours. As day approaches, if the ant has not already been eaten, and if the temperature exceeds a certain threshold, the ant climbs back down to ground level. It rejoins the colony (which does not reject it) and continues to function normally until night falls again, whereupon it climbs back up to the top of the blade of grass.

(In some situations, it may climb up a flower stem and attach itself to a petal.)

A team of researchers used micro-CT scanning to examine the brains of infected ants, publishing their results in a 2018 Nature article ("3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host")

Most of the parasites are situated in a region of the ant's abdomen known as the "gaster". At this stage in their lifecycle, they are known as "metacercariae". At least one of the parasites, however, will enter a region of the ant's nervous system known as the "suboesophageal ganglion" (SOG). In the brains examined by the researchers, one (and only one) of the parasites in that area would attach its "oral sucker" to the brain tissue of the host ant. This would occur in "the ventral-anteriormost region of the SOG".

The parasites in the gaster are contained within cysts. Some or all of the ones in the brain may not be. The parasite that has attached its oral sucker is not. This one is informally nicknamed "the brain worm".

What is so significant about the SOG region? For one thing:

  dendrites of the 10–12 motor neurons that stimulate the fast muscle fibres of the mandibular closure muscles in ants share the same neuropil in the ventral-anteriormost region of the SOG24 – the precise location where non-encysted D. dendriticum metacercariae are located. Thus, by targeting this region of the SOG, D. dendriticum has the potential to directly interfere with ... the action of the mandibles.

Thus we see another mechanism used by a parasite to force its ant host to grip something tightly with its mandibles.

The SOG also has some connection to locomotive activity - presumably getting the ant to climb the blade of grass and/or stopping it from climbing down too soon:

  Site-selection and development of non-encysted metacercariae within the SOG can provide a direct pathway for the manipulation of locomotory activity.

And even more...

  The SOG is a major part of the nervous system-wide network for neuromodulation in insects, evidenced by the many different neuromodulators expressed in neurons that reside in this region of the brain [25,26,27]. The effects of these neuromodulators ... are diverse and far reaching, from flight modulation, visual dishabituation and olfactory learning to mediation of the fight-or-flight response and the control of aggression ... FMRFamide-like peptide is implicated both as a neurotransmitter and a neuromodulator and affects the nervous system as well as skeletal muscle [25]. Thus, any influence exerted by metacercariae on the activity of neuromodulatory neurons in the SOG could have far reaching consequences for the behaviour of infected ants.

The researchers noted that they did not know if the "brain worm" was in contact with the SOG all the time, or just when the temperature was low enough to induce the changed behaviour. Further research was needed.

Sources:

Ingram WM, Goodrich LM, Robey EA, Eisen MB (2013). Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance. PLoS ONE 8(9): e75246. https://doi.org/10.1371/journal.pone.0075246
Abdulai-Saiku, S., Vyas, A. Loss of predator aversion in female rats after Toxoplasma gondii infection is not dependent on
ovarian steroids. Brain Behav. Immun. (2017), http://dx.doi.org/10.1016/j.bbi.2017.04.005
Fuks JM, Arrighi RBG, Weidner JM, Kumar Mendu S, Jin Z, Wallin RPA, et al. (2012). GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii. PLoS Pathog 8(12): e1003051. https://doi.org/10.1371/journal.ppat.1003051
Fredericksen MA, Zhang Y, Hazen ML, Loreto RG, Mangold CA, Chen DZ and Hughes DP. (2017). Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants. Proceedings of the National Academy of Sciences Nov 2017, 114 (47) 12590-12595; DOI: 10.1073/pnas.1711673114
Mangold CA, Ishler MJ, Loreto RG, Hazen ML and Hughes DP. (2019). Zombie ant death grip due to hypercontracted mandibular muscles. Journal of Experimental Biology 2019 222: jeb200683 doi: 10.1242/jeb.200683
Martín-Vega D, Garbout A, Ahmed F. et al. 3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host. Sci Rep 8, 8587 (2018) doi:10.1038/s41598-018-26977-2


Chemoautotrophic eukaryotic cells? There are heterotrophic prokaryotes, and there are autotrophic prokaryotes. In the autotrophic prokaryotes category, there are photoautotrophic prokaryotes and chemotrophic prokaryotes.

Are there chemotrophic eukaryotes?

There are two ways of classification of Prokaryotes(on the basis of mode of nutrition) that you will generally come across:
Way 1

Way 2

The First classification is very much based on a complete segregation between respiration and photosynthesis. In the first classification, anything that needs another animal to get food is a 'Heterotroph'. (Here, chemotroph and chemoautotroph are the same things)

But Generally the 2nd Classification is preferred, because prokaryotes have some very unique nutritional habits that cannot be explained on the basis of 'Eating/Not Eating'

In a way synthesis is the creation of a carbon compound by use of some energy.
So we need to classify based on energy and carbon source. Here organic carbon source means it is a 'hetero'troph and inorganic means it is an 'auto'troph. Similarly if Light energy is the direct energy required, it is a 'Photo'troph and if a chemical compound is required it is a 'Chemo'troph

By the First Classification, there are no 'Chemotrophic/Chemoautotrophic eukaryotes' meaning no eukaryote can produce food from inorganic material using chemical energy.

But by the 2nd Classification, essentially all eukaryotes that do not photosynthesize, instead use organic compounds as a food source, all animals, fungi etc. are 'Chemoheterotrophs'*However no Eukaryote is a 'Chemoautotroph'