Can a cell start a mitosis if it lacks energy or molecules to complete it? I'm wondering whether a cell can start a mitosis if it lack molecules or energy to fully complete it. From what I'm reading on wikipedia the cell passes most of its time in the interphase in which the DNA is replicated and then there's the G2 checkpoint to make sure mitosis can start.

However I'm not sure all of this is enough to ensure that the cell has sufficient energy to fully complete the mitosis (is the cell "fueled" in energy and molecules during the mitosis or does it has everything needed before starting it?).

Edit: I'm considering this question for humans in particular, or animals in general if the answer is the same.

When I speak about "molecules" I mean any atom or molecule. In other words, whether the cell needs some material intake from the external environment during the mitosis or not. If not, I consider that it has all the necessary atoms/molecules to fully complete the mitosis without any external need.

The short answer: no. First, let's get an understanding of the cell cycle control system, as there are some important molecules involved in this system that regulate mitosis. Think of the control system as a series of stoplights: as you mention, there is one stoplight at the G2 phase. There are two additional checkpoints: one at G1 and one in the M (mitotic) phase, just before Anaphase. Why before anaphase? At this stage in mitosis, the cell checks to determine if all of the kinetochores of the duplicated sister chromatids have microtubules attached to them. This is to ensure proper distribution of chromatids in anaphase.

Ok, so back to your question: what are some of the molecules involved, or what are some molecules that the cell might need before it proceeds?

Cyclins - these are proteins that are produced in the late S-G2 phases of Interphase. They activate cyclin dependent kinases (Cdks)
Cyclin Dependent Kinases - as the name suggests, these proteins (kinases) are dependent on cyclin in order to operate. The best known Cdk is called MPF, short for maturation promoting factor.

Throughout the cell cycle, these Cdks, together with their bound cyclins, are able to phosphorylate various proteins in the cell as it undergoes mitosis. For instance, the MPF would phosphorylate lamins, which are proteins on the nuclear envelope that can initiate degradation of the laminar matrix. This is essential in Prophase, when the nucleus is disassembling. There are many other things it can phosphorylate. For a more complete list, look under "Targets of MPF" in the above link for MPF. Take a look at this diagram, taken from Campbell's Biology (9th Ed):

There is one other molecule worth mentioning:

Growth factors - these are proteins specifically released by neighboring cells (relative to the cell that is preparing to undergo mitosis). These are crucial for mitosis to even initiate. A great example of a growth factor is PDGF, which stands for "Platelet Derived Growth Factor". These PDGFs are released by platelets at sites of injury, such as a cut on your knee. The PDGFs stimulate cell division and help your skin to reheal!

There are many other essential nutrients that cells require before they can initiate mitosis; not all have been listed here. Also, I know I didn't necessarily answer the "energy" part of your question, but I hope this helps for your first part.


Do plants need sleep? Turns out that you can do indoor farming these days via hydroponics and specialised LED lights. My mother, who has a large garden, warns me from exploring this as a hobby. She mentions that 'plants need to sleep too' and that having a LED light on them 100% of the time might be bad for them.

Is there any sense in this? Is it true that plants would grow suboptimally if the sun was on them 100% of the time or would they in fact grow quicker? Is there any research on this?

The quote as phrased is a bit non-sensical really because it mostly hinges on what you define as 'sleep' or 'rest'. Plants, like most living things, including us, are far from dormant at night.

It's true that diurnal patterns govern the behaviour of most, if not all, living things that are exposed to them (1). Plants are no exception to this.

For example, photosynthesis is a 2-component process. With the so called 'dark' and 'light' reactions of photosynthesis (more correctly "light-dependent" and "light-independent"). Though both happen during the day and night, it is at it's peak during peak sunlight.

In CAM plants, to avoid dessication, there is differential carbon fixation because the stomata are kept shut during the hot daylight hours.

Respiration however, where the produced food is converted to energy, primarily happens at night.

The Khan Academy has a great 'walkthrough' of the steps of photosynthesis:
https://www.khanacademy.org/science/biology/photosynthesis-in-plants/the-light-dependent-reactions-of-photosynthesis/a/light-dependent-reactions

(1). The diurnal course of plant water potential, stomatal conductance and transpiration in a papyrus (Cyperus papyrus L.) canopy
https://link.springer.com/article/10.1007/BF00379885


Why Crocodiles don't eat Hippos? I have been following documentaries about crocodiles and amazingly, crocodiles and hippos apparently seem to live happily in the same pond together without attacking each other.

Why is it so? Like no matter how strong hippo is, its soft skin is no match to the brutal jaws of a crocodile?

Skin

First, you are being misled by your wrong assumption that hippos have soft skin. Hippos have a 5 cm thick skin! For fun, here is a picture of a hippo skin.

They are big and pretty fast

An adult hippo weighs on average 1.5 and 1.3 tons for males and females respectively (with a record at 4.5 tons) and can run up to 30 km/h on land and up to 8 km/h in water (according to wikipedia > hippopotamus).

They have an aggressive nature

Hippos are aggressive animals (esp. males). Hippos kill about 500 people a year (against 1000 for crocodiles) according to this BBC article (but estimates seem to vary quite a bit from source to source).

They have serious teeth

Hippos have a big mouth with very long teeth. Lower canines are 50cm (19.7 inches) long (see wikipedia citing Estes 1991)!

Hippos live in herd

As suggested by @ChinmayKanchi in the comments, because hippos live in a herd, a crocodile that attacks a hippopotamus might have to deal with more than one enemy.

Videos

You can find here a video fight between a crocodile and a hippopotamus (thanks to @TahlaIrfan) and here is a video of a lion waking up a hippo. You will easily find other videos on YouTube.


What is this flying animal that hovers like a hummingbird? What is this animal?

Characteristics:

Has a long curved bill.
Has green upper body and a dark black lower body.
Likes petunias.
Hovers like a hummingbird but is a bit smaller.
Has small rear feather-like tufts and is very odd shaped.
Moved quickly from flower to flower.

That's a lepidopteran insect called hummingbird moth.

There are several species of hummingbird moths. Their more distinctive feature, as the name implies, is that they hover just like a hummingbird.

Your photo is not the best one for identification, but it seems to be a hummingbird hawk-moth, from the Genus Macroglossum, specially because the rear feather like tufts (which are just elongated setae).

Here is a better photo, for comparison:

Macroglossum stellatarum

However, according to the colors you described, your species is probably different from that in the photo above.

Here is one flying (from a different species):


What type of bird is this? Can someone identify this white colour bird?

Location: unknown (image taken from someone's profile pic).

From the picture, it looks like Cacatua sulphurea

[Source: Wikipedia]

  The yellow-crested cockatoo (Cacatua sulphurea) also known as the lesser sulphur-crested cockatoo, is a medium-sized (approximately 34 cm long) cockatoo with white plumage, bluish-white bare orbital skin, grey feet, a black bill, and a retractile yellow or orange crest. The sexes are similar.[Source]

Habitat and ecology:

It mostly inhabits evergreen, deciduous, monsoon and semi-evergreen forests.
It nests in tree cavities or a pre-existing hole made by any another species.(Nandika et al.)
Observations made on Masakabing Island suggests that it's favourite diet include male fruits of Artocarpus communis, flowers and fruits of Cocos nucifera, Young leaves and flowers of Ceiba petandra, mangroves and male fruits of Brassus sudaica.(Metz et al.)
It mostly nests on C. nucifera, A. communis, C. petandra, Tamarindus indica and Avicennia sp. (Nandika et al.)
[Source]

Why it is not Cacatua galerita?

The plumage is different and the skin around the eyes are more white. [Source: In description part]
In the picture of the OP there is a blue ring over the eyes and it is also known as blue-eyed cockatoo. [Source: In the description part]


Species that have evolved to be near identical? Are there any species that are near identical in outward appearance but are separate species?
When I say species I mean can’t interbreed.

Simple answer: yes, an uncounted number of them.  You need to read up on two topics: convergent evolution and mimicry.
Convergent evolution is when environmental factors cause different creatures to evolve similar appearance and lifestyle.  Perhaps the classic example of this are the dolphins and ichthyosaurs.  Despite being of different groups - mammals vs reptiles - they both evolved from land-dwelling creatures that adopted a marine lifestyle, and as a consequence a similiar appearance.
Mimicry is when one creature evolves to appear similar to another because that gives them some advantage.  Here the classic example is the viceroy butterfly, which supposedly evolved a similar appearance to the monarch because the latter tastes bad, so that birds avoid eating it.


Plating 96-well bacterial transformations I need to clone 96 different inserts into the same backbone in arrayed format. I am planning to perform Gibson assembly reactions in a 96 well plate, and then do chemical transformations in a 96 well format.
However, I am not sure how to plate 96 well transformations in the most efficient way. I could just plate them one by one onto petri dishes, dividing each petri dish into 4 sectors. However, I suppose there could be a better way of doing it. Any suggestions?

I think your approach very much depends on how essential it is that you get discrete single colonies, and if this is a one off or a regular process. To preface, similar to what Maximilian Press said, using a single welled plate like a nunc omnitray would be your best bet.
The main consideration you need to take into account for high-throughput transformations is the transformation efficiency (TrE). Naturally in a big petri dish, 100 µL of a single 1:10 or 1:100 dilution of your recovery culture can bring out nice discrete colonies. When you start reducing surface area and volumes, the chance of discrete colonies obviously diminish.
The best way I've found is to do a test transformation using the backbone of your choice and gauge the average TrE over a few runs to hone in on a 'one size fits all' dilution/volume, then apply that to your full high-throughput run. Assuming your inserts are of similar size, you should see a relatively similar TrE between them (bar edge cases). Another option would be set up three 96-well plates and do three separate dilutions, 1:10, 1:100 and 1:200 at 100 µL a pop so you at least get some fudge factor.
In terms of the chemical transformation itself, doing them in a 96 well plate format will guarantee lower TrE simply due to the characteristics of the plate itself. Thicker plastic and sub-optimal heating (if you aren't using a thermocycler and PCR plate) requires a slightly longer heat shock, and recovery in media requires much more vigorous shaking due to the mixing characteristics within the wells.
If you don't care about plating out in 96 well plates, like Maximillian Press said, use a single welled plate and format it in a 96/48 well fashion. Will save a massive headache when pouring. Just make sure you leave it to dry to prevent any running culture.
In terms of actually growing the colonies in a 96 well plate, if you're making the agar yourself I'd recommend adding an extra 0.5% agarose to thicken it up (I doubt you'll be using one, but make sure your plate is non-tissue culture treated). Wait for it to cool just above its solidifying temperature (around 45 °C in my experience) and then transfer out using a pipette or low volume serological pipette to reduce the meniscus formation. If the agar forms a high angled meniscus, your colonies may form smears and will not be discrete. Leave the plate out to dry as well, colonies may also smear from the agar being moist.


R/Bioconductor query for a gene? I'm fairly new to bioinformatics, so please be gentle ;0

Is there a way to query a particular gene using a script in R/Bioconductor? I'm particularly interested in Gene Ontology terms. There are many websites that, given the gene name, will return relevant GO terms. My question is, can it be automated?

Take a look at the biomaRt package. This package allows you to access some databases in R directly. Quote from the user's guide:

  The package enables retrieval of large amounts of data
  in a uniform way without the need to know the underlying database schemas
  or write complex SQL queries. Examples of BioMart databases are Ensembl,
  Uniprot  and  HapMap.   These  major  databases  give  biomaRt  users  direct
  access to a diverse set of data and enable a wide range of powerful online
  queries from R.

In the user's guide you will find anything you need, i.e. description and example tasks, for doing queries on HGNC symbols, GO terms, and more.


Current scientific theories for evolution of Cucurbita I'm attempting to find research on scientific theories surrounding the evolution of certain plants, and am unable to find any footing with respect to a certain genus.

In this case, I am researching Cucurbita (ie: squash, pumpkins, etc), and can't find any basis for how it survives inherently without outside manual intervention. Unlike hot peppers (eg: Capsicum annuum), it is not easily ingested by birds, who do not suffer from the painful effects of capsaicin, and effectively transport the seeds, undigested, to new areas to spread the plant.

Also, unlike fruit growing on a tree, such as apples, it doesn't (seem) to provide a means to transport seeds any meaningful distance.

Finally, it seems most animals; ruminants, scavengers, and insects alike, would consume and digest the seeds.

Are there any generally-accepted (or at this point, plausible) theories with research to back it with respect to how such plants could survive long term without being manually grown and harvested by a species which eats them? While I understand (and acknowledge) the scientific theory of evolution, I'm not sure how the survival of such plants seems to be a special case.

Thanks!

You're right that modern species would have a hard time spreading group seeds, though you're not quite right about the reasons.  Cucurbita rinds are extremely bitter, so that modern mammals are reluctant to (or unable to) process the rinds to access the seeds.

According to a recent article (Gourds and squashes (Cucurbita spp.) adapted to megafaunal extinction and ecological anachronism through domestication), the explanation is that wild Cucurbita first co-evolved with North American megafauna, like mammoths and mastodons, who could tolerate the toxic/bitter rind. (The authors also suggest that megafauna also produced suitable habitats for their growth.)

Following the extinction of these megafauna, humans picked up the slack, with most wild Cucurbita going extinct and only domesticated versions remaining.

  Collectively, these results point to wild-type declines coinciding with widespread domestication. ...megafauna consumed Cucurbita fruits and dispersed their seeds; wild Cucurbita were likely left without mutualistic dispersal partners in the Holocene because they are unpalatable to smaller surviving mammals with more bitter taste receptor genes. ... Thus, anthropogenic landscapes provided favorable growth habitats and willing dispersal partners in the wake of ecological upheaval.


Is the chitin in an insect's exoskeleton cross-linked? This answer to the question How to clean and preserve a cicada's molted exoskeleton (exuvia)? states:

  The exuvia is made of cross-liked chitin, and will not decay. You don't need any special preservatives as all. If you need to get the mud off, just rinse it as you said, in soapy water, let it dry, and you are done. Simple.

Wikipedia's Chitin says only:

  Chitin is a modified polysaccharide that contains nitrogen; it is synthesized from units of N-acetyl-D-glucosamine (to be precise, 2-(acetylamino)-2-deoxy-D-glucose). These units form covalent β-(1→4)-linkages (like the linkages between glucose units forming cellulose). Therefore, chitin may be described as cellulose with one hydroxyl group on each monomer replaced with an acetyl amine group. This allows for increased hydrogen bonding between adjacent polymers, giving the chitin-polymer matrix increased strength.

I'm not a chemist, but "increased hydrogen bonding between adjacent polymers" doesn't sound the same as cross-linked polymers. So I would like to ask for an answer based on sources other than Wikipedia:

Question: Is the chitin in an insect's exoskeleton cross-linked? If it depends on the type of insect, then the focus should be on "a cicada's molted exoskeleton (exuvia)" as discussed in the linked answer.

much like cellulose, chitin strands are bonded to other strands by hydrogen bonds. here is a slide share with a breakdown of the structure.

It is crosslinked in the sense strands are linked to other strands in such a way that most enzymes cannot access it to break it down. this is the same thing that makes wood last untreated. In a strictly chemistry sense it is not a crosslinked polymer (which requires covalent or ionic bonding) but it still has crosslinking. Your hitting a difficulty in jargon.

source.


Is ability to easily pollinate desirable? In Mendel's crosses was it desirable for the plants to be able to cross-pollinate and self pollinate easily ?

Yes, the fact that pea plants were easy to pollinate was desirable and helpful in understanding the effects of Mendelian factors (genes) but for the proper study of the factors expressed CROSS POLLINATION of homozygous plants having different phenotype and genotype ( e.g. cross between RR and rr) was preffered rather than self pollination.


What kind of hot pink eggs are these? I saw a dozen or more clusters of what I think are insect eggs attached to a few vertical sticks protruding from a small pond, and a few more to stalks of grass nearby. Location is in Hsinchu County, Taiwan, end of March, fairly good weather these days in the neighborhood of 15-22 C.

Each cluster consist of a group of roughly 150 spherical hot pink colored eggs stuck to a surface, each about 2.5 to 3 mm in diameter. One group was deposited almost completely around a stalk of grass on land next to the pond, and several others were deposited on the side of a stick from a fallen branch sticking out of the water.

Questions:

Is it possible to identify what kind of insect produces such clusters of eggs?
Is there any explanation possible for the "hot pink" color? I suppose it could be a general "don't eat me" signal like these big juicy red bugs but it's such an artificial looking color, I've never seen it anywhere in nature, at least that I can remember.

click images below for full size:

update: This answer suggests that snails are the likely culprits, and so I returned to the scene of the crime today and caught them red-handed, or in this case "pink-footed".

Click for full size; the larger snail is about 5 centimeters in diameter.

 caught red-handed, or in this case "pink-footed"

Those appear to be the eggs of a species of apple snail in the genus Pomacea, probably the introduced invasive golden apple snail (Pomacea canaliculata), but there are at least two other candidates1,2.
You can learn more about this species and the problems it causes from this Columbia University webpage.
For comparison — Figure 3 from "The identity, distribution, and impacts of non-native apple snails in the continental United States"3.

Egg masses of introduced and native Pomacea in the continental U.S. a. P. haustrum, b. P. diffusa, c. P. canaliculata, d. P. paludosa, e. P. insularum. Scale Bar:5 cm.
References:
1: Yang, Q. Q., Liu, S. W., He, C., & Yu, X. P. (2018). Distribution and the origin of invasive apple snails, Pomacea canaliculata and P. maculata (Gastropoda: Ampullariidae) in China. Scientific reports, 8(1), 1-8.
2: Yang, Q. Q., & Yu, X. P. (2019). A New Species of Apple Snail in the Genus Pomacea (Gastropoda: Caenogastropoda: Ampullariidae). Zoological Studies, 58(13).
3: Rawlings, T. A., Hayes, K. A., Cowie, R. H., & Collins, T. M. (2007). The identity, distribution, and impacts of non-native apple snails in the continental United States. BMC Evolutionary Biology, 7(1), 97.


Do genes play a role in the athleticism and shape of a person? I am an Indian with a small thin stature with some deposition of fat around my belly.I was wondering if genes play a role in fat deposition in the body for Indian, Chinese, European or African people. Fat deposition may differ among all these people around the belly, thighs etc.
These people also differ in their stamina and speed naturally.

  For example here in India in the game of cricket there has been no
  fast bowler out of 1.2 billion people who can do fast bowling
  because it requires a lot of strength and stamina.Also on field
  athleticism is also very bad compared to Australian or South African
  players.I assume that may be its because of some cultural or genetic
  problem.

All these characteristics you observe (speed, ability to play cricket, belly size, height, etc…) are what what we call in biology a list of phenotypic traits. Basically, the phenotype is a characteristic of an organism that we can eventually measure or describe (physiological, behavioural, morphological, and life history are four common classes).

In a given population the phenotypic variance (the variance in height for example) can be expressed as the sum of the genetic variance (=the genetic variance underlying the phenotypic trait of interest), the environmental variance (=the environmental variance underlying the phenotypic trait of interest) and the variance due to the interactions between genes and environment (the variance due to the interaction that is underlying the phenotypic trait of interest).

Mathematically expressed it gives:

$$V_{phenotype} = V_{genetic}+V_{environment} + V_{gen X env}$$

Therefore, for each trait there is a given part of the variance that is explained by the environment and a given part that is explained by the genes. We might go a bit further and defined the concept of heritability (in the narrow sense, see wikipedia article for more info). The heritability (in the narrow sense) is the ratio of the phenotypic variance to the additive genetic variance. Mathematically expressed it gives:

$$h^2 = \frac{V_{additive}}{V_{phenotype}}$$

Each trait has it's given heritability. The heritability can be defined only for a trait in a population (which defines $V_{genetic}$) and its environment (which defines $V_{environment}$).

For example, the heritability of height in human is around 0.8 (non-peer reviewed source). Which means that 80% of the variance in height in the world-wide population is explained by the genetic variance. See this post for more info about the concept of heritability

In your question, you also used (before your question was re-edited!) the word fitness (also it is not really present in your question). The fitness is a very important concept in biology, it is the ability of an individual to survive and sire offsprings. Our phenotypic traits influence our ability to sire offsprings and therefore our genes influence our fitness. If the whole phenotypic variance is explained by the environmental variance only, then, even the the trait is under selection, there will be no change in allele frequency due to selection. Note: an allele is a gene variant. If eye color is a gene, brown eyes and blue eyes are alleles (to make it easy). This change in allele frequency is called a response $R$ to selection $S$. This link between selection, the response and the narrow sense heritability $h^2$ is given by:

$$R=S\cdot h^2 $$

So to answer your question. Yes, part of the variance in height, belly size, cricket playing ability, etc… is genetically coded. As the fitness depends on phenotypic traits, Yes, the fitness is genetically coded (otherwise there would have no response to selection). Therefore we're not all equal to playing crickets!


Why is a lack of oxygen fatal to cells? In animals temporary anaerobic respiration leads to the breakdown of the pyruvate formed by glycolysis into lactate.  The buildup of lactate in the bloodstream is accompanied by a large number of protons causing lactic acidosis, which is detrimental to the health of the organism.  This is one of the main suggestions I have come across for why a lack of oxygen is fatal to cells, however the LD50 for lactic acid as referenced by the COSHH MSDS seem awfully high (even if the route is by ingestion rather than directly into the bloodstream) for this to be a cause of cell death:

  Toxicological Data on Ingredients:
  ORAL (LD50): Acute:

  3543 mg/kg [Rat (Lactic Acid (CAS no. 50-21-5))].

  4875 mg/kg [Mouse (Lactic Acid (CAS no. 50-21-5))].

I also wonder if this is a larger problem for an organism as a whole rather than on a cellular level.

The alternative, I suppose, is that glycolysis alone does not provide sufficient ATP for vital cellular processes to occur.  If this is the case, which ATP requiring processes are most vital for the short term survival for a cell?

Here's an illustrated example in neurons:

ATP, of course, is generated by aerobic respiration. The critical biochemical reaction in the brain that is halted due to lack of ATP (and therefore O2) is the glutmaine synthetase reaction, which is very important for the metabolism and excretion of nitrogenous wastes:

The body uses this reaction to dump excess ammonia (which is a metabolic waste product) on glutamate to make glutamine. The glutamine is then transported via the circulatory system to the kidney, where the terminal amino group is hydrolyzed by glutaminase, and the free ammonium ion is excreted in the urine.

Therefore, as you'd expect, under hypoxic conditions in the brain, excess ammonia builds up which is very toxic to the cells. Neurons are also highly metabolically active, which means they generate more waste products. A buildup of nitrogenous waste products in the cell (and bloodstream) can be potentially fatal due to it's effects on pH (screws up enzymes and a whole slew of biochemical reactions).

In addition, the buildup of ammonia will cause glutamate dehydrogenase to convert ammonia + aKG to glutamate, which depletes the brain of alpha-ketoglutarate (key intermediate in TCA cycle). This basically creates a logjam in the central metabolic cycle which further depletes the cell of energy.

This is just one example of many. Of course, there are many, many other critical metabolic processes that require ATP (i.e. the Na+/K+ ATPase pump that regulates neuronal firing and osmotic pressure), but nitrogen metabolism was the first that came to mind :)


What is the correct classification of population groups of homo sapiens? The classification system of the United States census into various races of humans is a bad way to classify population groups of humans, because both East Asians and South Asians are classified the same, yet they look different and are genetically distinct. So, has anyone proposed a more scientifically accurate classification of population groups of homo sapiens?

Basically all the genetic variation of humans is inside the native african populations.  A norwegian and a australian native are more closely related  to each other than two random native Africans are. So the only accurate way to do it would not only group those two asians together but also group them with europeans and native americans. If you split people up enough to get two groups of "asians" then you end up with more than a hundred races the vast majority of whom would be split among the native african populations.

Humans have very low genetic diversity in the first place, and most of our diversity is within our populations not between them, so splitting us up does not make a lot of sense. We end up doing it mostly on superficial variations.
Source


Spread of malaria from an infected person If a person is infected with malaria, how can that person be a part of spreading malaria? As in, if a female anopheles mosquito sucks blood out of that infected individual, how is it possible that malarial schizonts will be only sucked by the mosquito and not pure blood? The point is, out of such a huge volume of blood, how can only malarial parasites enter the suckling mosquito?

With humans infected with malaria, the parasite load in the blood can be quite high. It ranges from 10 to 108 Plasmodium falciparum parasites per ml .

When a female Anopheles mosquito bites an infected human, they take in infected blood, not just the parasite. They take in a few micro liters of blood, which in usually enough to get themselves infected, and the next time they bite a human (about one week later), the infection is spread.

You can learn more at the CDC malaria FAQ and their overview of the malaria transmission cycle.


Population genetics and the fitness probability distribution. Why is the arithmetic mean all we need? When recording change in allele frequency in diploid, bi-allelic, infinite and panmixic population we usually use this kind of equation:

$\delta_p = \frac{p * q *( p (w11 - w12) + q * (w12 - w22))}{\bar{w}}$

$\bar{w} = p^2 * w11 + 2*p*q*w12+q^2*w22$

$\delta_p$ = change of $p$ (frequency of one of the allele) from one time step to another

$w11$ is the mean fitness of individuals of genotype 11. $p$ and $q$ are the allele frequencies.

The only indicators for the fitness distribution is the arithmetic mean. Why don't we include other indicator of the probability distribution of fitness? The skew, the sd, the median for examples. Could you argue why we don't need to care about the probability distribution of fitness of individuals with genotypes 11 (for example)? In other words, why is the mean fitness (=w11) a sufficient statistics?

I wouldn't be able to answer if one asks me:

Why don't you take the median instead of the arithmetic mean?"
Why don't you care about the variance, the skew (or any other moment) of your distribution?
What if the traits were not countinuous but discrete (sex is a discrete trait for example)?

It's simplest to think about a haploid population with size $N$. Say there are two alleles, $A$ and $a$, with $A$ having frequency $p$ in this generation. Each $A$ individual will have some realized fitness (i.e., number of offspring) in this generation; let's call this number $w_A^{(i)}$ for the $i^\text{th}$ individual. The total number of $A$ individuals in the next generation is then $\sum_{i=1}^{Np}w_A^{(i)}=Npw_A$, where $w_A$ is the arithmetic mean of the fitness distribution, $w_A\equiv\sum_{i=1}^{Np}w_A^{(i)}/(Np)$. So regardless of how weird the distribution of the $w_A^{(i)}$ was, all that matters (in the large-$N$ limit) is the arithmetic mean.


Our muscles give us the ability to move our arms but....? I have a strange question, but let me tell you something first.

If you think of this carefully, then you realize something, please try this right now:

Contract your muscles only so that your arms move without you doing it. You can't.
The way it happens is that you move your arm (or you do something or whatever you call it), then your muscles contract.
If our muscles weren't there, then we wouldn't be able to move our arms.

We don't contract our muscles, we move our arms, then our muscles contract automatically. So the muscles contract themselves, but what gives us the ability to make our arms move after deciding when we want to move our arm?

We can't contract our muscles so that our arm moves, we make that movement, then our muscles contract, but you can't even feel it because it's so light.
This is hard to explain.

So what gives us the ability to make our arms move, but not the muscles? I'm telling you, some people won't even understand, but this is real.

Thank you.

I am a bit confused as to what you are asking. You don't move your arm, like your suggesting, ever. No one does, and no one can. You contract your muscles which happen to move your arm. The movement of the arm is the result of your muscles contracting, not the cause.

How it happens is that your brain sends a signal to your muscles (which you cant feel). The muscles get excited and they contract. The instant your muscle contracts your hand begins to move. In the end your bones are like sticks, and your muscles are the ones that pull the stick in different directions, in order to achieve flexion and extension.

Might i suggest you read up on the musculoskeletal system (http://kidshealth.org/teen/your_body/body_basics/bones_muscles_joints.html) ?


Is funnel web spider venom poisonous? Does the venom of the Sydney funnel web spider have to be injected into the bloodstream to have an effect? If the venom was swallowed (e.g. if a spider was eaten), would it still have an effect? Or wouldn't it be able to pass through the gut lining, or be broken down in the gut?

I understand that the funnel web's venom is different to most spiders', but would this answer apply to spider venom in general?

The Sydney Funnel Web Spider's venom is called δ-atracotoxin and it is especially toxic to primates. It is a peptide toxin, which means that it has the potential to be digested in the stomach before having any physiological affect. However, many peptide toxins are not inactivated by swallowing--you don't want to be eating any Botulinum toxin.
Characterization of insecticidal peptides from venom Australian funnel-Web spiders (Vonorax et al. 2006) harvested venom from Hadronyche infensa, the Darling Downs funnel-web spider. This spider is closely related to the Sydney Funnel Web spider and also produces δ-atracotoxin.

An oral ingestion activity test was undertaken using crude H. infensa venom.

The ingestion test was performed with insect larvae, which are susceptible to the venom when injected. (Aside: there's a lot of interesting research on the toxin's effect in insects). They didn't find much:

Oral ingestion activity test of crude H. infensa venom
No effect was observed in this test, even though approximately 4 times the dose required for lethality by injection was orally consumed by the larvae.

I don't think anyone has performed a study of toxin ingestion in primates (if they have, I couldn't find it). The researchers don't speculate as to why the toxin has no effect when ingested. As expected, the toxin had no effect on (non-primate) mice:

Effect of atracotoxin-Hv1 on newborn mice
All mice in both test and control groups survived without apparent toxic effect beyond 24h post injection.

Whether this is applicable to other spider venom depends on the nature of the venom. A non-peptide, low molecular weight venom able to be absorbed by the lining of the esophagus could be very toxic by ingestion.

Further reading:
Scanning Mutagenesis of ω-Atracotoxin-Hv1a Reveals a Spatially Restricted Epitope That Confers Selective Activity against Insect Calcium Channels (Tedford et al. 2004)
Isolation and pharmacological characterisation of δ-atracotoxin-Hv1b, a vertebrate-selective sodium channel toxin (Szeto et al. 2000)
(for more info on peptide toxins): Cyanobacterial Peptide Toxins


Meaning of arrows in 3D representation of proteins Below is a three-dimensional representation of the protein, CD4. I would like to know what the arrows and the thin wires between them mean.

The flat arrows are a cartoon representation of β-strands (one type of regular hydrogen-bonded secondary structure). The direction of the arrow is the direction of the amino acid sequence (arrow head pointing towards the C-terminus).

The thin wires are regions with no regular structure.

There are also two small green spiral ribbons in the foreground left and right, which represent α-helices (the other main regular secondary structure).


What is a triglyceride? I'm confused on what a triglyceride is, from what my text book it says its a type of gylercide, then from a website it said

  Glycerides can be subdivided into two categories. The first group, the neutral glycerides are nonionic and nonpolar. The second group, the phosphoglycerides contain a polar region, the phosphoryl group.

Which makes triglyceride not a directly under a glyceride but under one of these groups. Then it says

  Esterification may occur at one, two or all three positions producing monoglycerides (monoacylglycerols), diglycerides (diacylglycerols), or triglycerides (triacylglycerols). The most prevalent and most important are the triglycerides.

So does that mean that triglyceride can be produced by either of the two groups phosphoglycerides and neutral glycerides. And if that's correct then how are monoglycerides and diglycerides produced.

Source

The following answer was giving by Michael D. Dryden from https://chemistry.stackexchange.com/questions/24797/what-is-a-triglyceride/24799#24799

There is some minor argument as far as nomenclature goes for these lipids. Most sources I can find, including IUPAC have glycerides as only including esters of glycerol with fatty acids. Monoglycerides have a single fatty acid ester with two free OH groups, diglycerides have two fatty acid esters, and triglycerides have three. Phosphoglycerides are defined separately as esterified derivatives of phosphatidic acids, so you can think of them like glycerides where for one of the substituents, instead of a fatty acid, some derivative of phosphoric acid is present. However, the way the two terms are defined, they don't encompass any common molecules, i.e. there are no molecules that are both glycerides and phosphoglicerides and neither group is a subset of the other.

So: mono-, di-, and triglycerides are subsets of glycerides while phosphoglycerides are a different group altogether, though structurally similar.


What's the aim of genetically modifying of foods/organisms? On news, articles etc. experts talking about Genetically Modified Foods and Organisms often mentions about their disadvantages like,

their potential to harm human health
allergies may become more intense, new allergy types may develop
possible damages to the environment

So I wonder, what's the aim of genetically modifying of foods/organisms? In other words, what are advantages of that?

GMO foods have a huge potential to make food cheaper to produce and more nutritious.

The most common GMO foods have at least one gene added to them - an enzyme that makes the plant resistant to RoundUp - an herbicide made by the same company (Monsanto).  this makes the farmers able to grow their crops with much less intensive labor to keep the plants healthy. It does cost some money and people wonder whether using so much roundUp is good.  I won't come down on the benefits of this, but you can see how it might be more economical way to grow crops.  roundUp is biodegradable and does break down in about 3 weeks, just FYI.

Other GMO foods can make the crops more resistant to drought, disease or insects. This might enable crops to be grown in areas and or with longer growing seasons - a big advantage for thirsy crops like tomatos or rice. Other GMO project may allow us to make the crops more nutritious.  A famous example of this is golden rice, which has been enhanced to produce pro-vitaminA, which will help malnutrition in millions of children who can die annually because of a lack of vitamins in their diet.

There is also an effort in nutriceuticals, where vaccines and common drugs maybe produced by edible plants for easily processing or even direct distribution of pharmaceuticals.

For people who can afford organic food and free range beef, I think its great that its available, but at for a hungry world, GMO foods can help solve some vital problems.


Does eating beans of a mother cause flatulence on babies? Is it true that if you eat beans it could cause flatulence on babies (when breastfeeding them)?

I can't find any research or scientific facts about that topic.
I thought the body of the mother would filter "bad" ingedients.

When the mother eat beans, the fiber (oligosaccharides) from them is not digested in the small intestine, so it travels to the large intestine, where normal intestinal bacteria break it down to some absorbable nutrients (like short-chain fatty acids) and gas that is largerly expelled (fao.org). Some gas can be absorbed into the blood and then removed by the lungs (PubMed).

This means that neither the fiber nor the resulting gas ends up in the mothers breast milk, so it cannot give gas to the baby.

Breast milk contains human milk oligosaccharides (HMO). HMO is undigestible, but bacteria in the infant's intestine can break it down and produce gas. However, the amount of HMO in the breast milk is not likely related to the amount of beans or other high-fiber foods the mother consumes, but is genetically determined (PubMed).


Evolution of the energy generating system in mitochondria Both yeast and humans have mitochondria. Given that yeast have a much shorter time between generation I would expect evolution to have had more time to optimize mitochondria of yeast.

The main function of mitochondria in yeast is essentially similar to that in human cells.

Is their efficiency roughly the same or did the stronger evolutionary pressure allow yeast to evolve much better mitochondria? Is there empirical research about mitochondria that studies the difference between the mitochondria of different species that includes metrics of their efficiency?

ANSWER SUMMARY

The criterion of efficiency of mitochondria is taken as the yield of ATP per carbohydrate molecule oxidized using the electron transport chain and oxidative phosphorylation. Experimental values for this are similar for yeast and humans, whereas theoretical values derived from differences in the structures of the ATP synthases actually imply a higher yield for mammalian mitochondria.

It is argued that it is not surprising that the difference in generation times did not produce the result expected by the poster. First, the period after the separation of eukaryotes from prokaryotes is no longer than the period between the origin of eukaryotes and that of the aerobic bacteria from which their mitochondria arose. Second, the stage would have been reached when there were mechanistic limitations on further increases in efficiency of this complex system. If the differences between mammalian and yeast bacterial ATP synthases is real (and an even ‘worse’ yield for bacteria, that have an even shorter generation time), this suggests that the main evolutionary pressure on this system varies between organisms, rather than being simply to maximize the yield of ATP.

ANSWER ELABORATION

Criterion of efficiency

The main function of mitochondria is to use molecular oxygen to oxidize NADH and FADH2 via the electron transport chain and oxidative phosphorylation to produce ATP. A suitable and generally accepted measure of efficiency — reminiscent of that applied to man-made mechanical devices — would be the percentage of the energy of this oxidation that is converted to ATP (rather than being released as heat). Any reader not familiar with the biochemistry of this system is advised to read the footnote* before proceeding further.

Is there any difference?

The traditional way in which the yield of ATP in oxidative phosphorylation has been measured is by the P/O ratio (the ratio of ATP produced to oxygen consumed). Results obtained over the years have varied becauase of technical problems — see review by Hinkle (2005). As summarized more recently (2010) by SJ Ferguson,  the historical controversy was not about differences between species — they were no indications of differences even between bacteria (the precursors of mitochondria, performing oxidative phosphorylation in their intermembrane space) — but merely about the true value of the P/O ratio.

As Ferguson goes on to say, the gradual elucidation of the structure of the ATP synthase and the elucidation of its mechanism led to a believe that deductions from this were a more reliable indication of the stoichiometry than the experimental measurements. Specifically, a 360˚ rotation of the F0 component of the ATP synthase could be seen to result in the synthesis of one molecule of ATP, and that this required on hydrogen ion bound to each of its c subunits (see diagram from Wikipedia article, below).

He describes the results with yeast as follows:

  X-ray crystallography of yeast ATP synthase revealed a ring of c subunits attached to F1 even in the absence of other subunits of the F0 sector (9). This work not only suggested that a and b were not interdigitated with c but also revealed the surprising stoichiometry of c10. The C-terminal helix of the hairpin c subunit is at the outside of the ring and contains an essential aspartate or glutamate residue. This residue is believed to pick up an H+ and rotate away from an interaction with the α subunit. Thus, 10 protons should drive a 360° rotation of the c ring, which is structurally connected to γ, giving synthesis of 3 ATPs as γ rotates through 360° within F1; the H+/ATP ratio would be 10/3 = 3.3. The P/O ratio for NADH would be 10/(3.3 + 1) = 10/4.3 ≈ 2.3, thus moving below the range of values directly determined.

It was assumed that ATP synthases other than yeast would also have 10 c subunits, but, surprisingly, although bacterial ATP synthases also have 10 subunits, the bovine (and other vertebrate) one has only 8, suggesting a higher P/O ratio than yeast — greater, not poorer, efficiency.

Mitochondrial evolution in context

Whatever the actual P/O ratios in different aerobes, the more rapidly-dividing species do not show a clear increase in efficiency in this respect. I suggest that in this respect the evolutionary timescale shown below (adapted from The Cell: A Molecular Approach) should be considered.

What is clear is that the time for an improvement in efficiency of energy production to occur between the divergence of yeast and animals (A) is much less than that between the time at which mitochondria were acquired from bacteria by the first aerobic eukaryote (B–A). Note also the long period the system had to evolve in the aerobic bacterium that gave rise to mitochondria (C–B). My argument is that by the time of appearance of mitochondria, the system had time to evolve to the optimum that mechanistic considerations would allow. Otherwise one would have expected those bacteria to further evolve a system much superior to yeast or mammals in the C–B timescale.

Other aspects of the evolution of the mitochondrial energy generating system

It should be noted that there have been changes in the mitochondrial energy generating system over evolutionary time. For example, in the cytochrome oxidase system the same set of core subunits are found in prokaryotes and eukaryotes. However additional subunits have been acquired in primates. Rather than being concerned with the catalytic efficiency of the system, these additional subunits are thought to be concerned with regulation.

Better systems to study the effect of division time on evolution of eukaryotic ‘efficiency’?

Because mitochondria had probably reached optimal mechanistic efficiency in energy generation when they were acquired, they do not appear to be a good choice for studies of the type the poster envisages. Perhaps he might do better with something related to nuclei, which are not present in bacteria. However there are problems of interpretation. For example, if it were found  that some aspect of the DNA replication machinery in yeast allowed this process to proceed faster than that in mammals, could one conclude that this was due to the shorter generation time of yeast? No! One could equally argue (and it would seem to me more likely) that the lower generation time resulted from an evolutionary pressure for faster DNA replication, a pressure that does not exist in the more slowly dividing mammals.

FOOTNOTE *

ATP in mitochondria (and the inner membrane of aerobic bacteria) is synthesized from ADP using the free energy released by the oxidation of the reduced cofactors, NADH and FADH2 (produced from the oxidation of particular carbohydrates), by molecular oxygen. The mechanism of this, rather than involving simple coupled chemical reactions, involves the movement of hydrogen ions across a membrane in which there is a concentration gradient (strictly through a proton motive force, to which membrane charge also contributes) using an ATP synthase, a molecular machine, the structure of which clearly indicates the stoichiometry of input hydrogen ions to ATP synthesized. The hydrogen ion gradient results from three stages in the electron transport chain (complexes I, III and IV) where a hydrogen ion is translocated into the inner mitochondrial intermembrane space. This is described in standard text books of biochemistry such as Berg et al..


Alternative dyes for Gram staining In the Gram stain, is there any replacement for primary stain, secondary stain, decolourizer and mordant? What results will the replacements produce?
I found that crystal violet can be replaced with methylene blue but in that case, what will the secondary stain, mordant etc. be? Please also explain what result we might get.

As you may have realized, crystal violet can be replaced by a lot of dyes since the ethanol will wash out the dye from the gram negative cells. Methylene blue is a nice choice - malachite green may also work.
A weak concentration of hydrochloric acid (3%) is also a possible replacement for the ethanol. A 3% HCl solution is used in the acid-fast stain but it may be too strong for non-acid fast cells. It would be worth testing it out and trying it to see if it could replace the ethanol step.


Why doesn't copper affect human skin? It's been known for a long time that copper has antimicrobial properties, but if it is so potent, why does it seem to have no effect on human skin or really any large animal?

The outermost layer of your skin consists mostly of dead cells, the Stratum corneum. Copper can't kill what's already dead.


What is known about major events of pre-LUCA evolution? All organisms share many common biochemical features (including 20 amino acid genetic code) and are believed to have a common ancestor (so-called LUCA). According to wikipedia article, this common ancestor was quite complex organism with advanced biochemistry. Are there an knowledge about evolutionary events occurred during pre-LUCA era? Namely, which of biochemical pathways already present in LUCA were evolved earlier than anothers?

There is an awful lot of literature and debate about what happened before LUCA consequently here are some key words to read more about, first on Wikipedia, then on review papers and then on the many papers...

According to the Oparin-Haldane hypothesis life formed from an abiotic primoridal soup.
These abiotic building blocks were formed by lightning, meteorites, UV or other processes (see Miller–Urey experiment and the Murchison meteorite)
Not all metabolites we know today existed and many that do not have a use today existed (non-proteogenic amino acids on Wikipedia is an article/list on the topic).
The genetic code is a frozen accident (Crick), but many believe it went in waves and was rather promiscuous (e.g. 3rd position pairs came later) and may have included ornithine and norleucine, which were "usurped".
Ignoring the temperature/location aspect, from a chemical point of view, life arises from a hypercycle process and requires gradients.
DNA did not form as is. The ribose may have been glycol and the nucleobase glycine: many metabolites in nucleotide metabolism are able to base pair.
The RNA world came first, then DNA with chromosomes came later. This has an odd effect in that early enzymes had to be highly multifunctional.
To have evolution, you need compartmentalisation.
Tar is gloop that forms easily abiotically. Tarrification is a threat to early life, but could have helped with compartmentalisation.
Montmorillonite clay can act as a scaffold for DNA polymerisation.
Ribozymes are RNA enzymes. The most core cellular processes is still RNA operated: the ribosome and tRNAs.
Many cofactors are primordial and are attached to riboses, e.g. NADH, FADH and arguably cobalamins.
Proteins came later, but still today the catalytic power of protein comes from their cofactors or from a single amino acid (e.g. cysteine as a nucleophile).
Once you have potentially RNA-encoded proto-enzymes you can start building more of the useful compounds that were available in the primordial soup but were depleted. Most pathways will therefore form by retrograde pathway evolution.
Enzyme activities can only be evolved if there is a pre-existing activity to select. Luckily accidental activities happen, called promiscuous activities (this term a century ago had no sexual meaning and used mean "being muddled").
Modern enzyme are highly specific and evolved to work at a high turnover (fast) and work at physiological substrate concentrations. But still have promiscuous activities because the substrate chemistry is similar. If the enzyme has never see a given compound the enzyme will not be evolved to not act on it and maybe the activity has no detrimental effect (neutral). When an enzyme evolves into a new activity an intermediate form is seem with higher promiscuity. These are often argued to be primordial-like.
Many pathways have a common origin, for example the Krebs cycle and the branched chain amino acid pathways and actually experiments in E. coli have found that the enzymes can rescue "deficiency" (auxotrophies) in the other pathway albeit slowly. Therefore, as enzymes could act on different similar substrates a set of overlapping pathways arose (patchwork hypothesis).
LUCA is the last common ancestor. It was likely thermophilic and lived in thermal vents as seen in every documentary. If life started there is debated.
Early enzyme were like very unstable, very very slow and may have often broken good metabolites in a futile manner. Given the problem of segregating with a chromosome and the need for high promiscuity, they had to be multifunctional. Not to mention that similar-ish amino acids were used interchangeably —isoleucine and valine say are hard to tell apart to modern tRNA synthases, go figure for the early ones.
Enzymes generally fall under a few families, which share a common ancestor. Rossmann fold enzymes for example bind NADH. TIM barrels are a ubiquitous fold.

So to answer your question, between the RNA world and LUCA, enzymes were slow and were selected upon to remake the more complex metabolites in the soup and then the simpler ones and thanks to their poor selectivity a patchwork of pathways arose. Once simple core pathways started and all metabolites could be made, more complex compounds that cannot arise abiotically such as the amino acids tryptophan and arginine were made. The enzymes became more selective and stuff like straight chain hydrophobic amino acids were selected against and the genetic code was fixed. Then you can make stuff like chromosomes and everything happens fast and efficiently.

Caveat. Early life was messy, really not efficient (it had no competition) and happened a long time ago. As time machines are physically impossible, all this is conjecture (sensu Popper), but the words theory and hypothesis are used happily in the field of origin of life.


Regarding cancer cells and telomeres If cancer cells have telomeres are they different than the telomeres in non-cancerous cells? Would cancer cell telomeres be somehow 'set-up' to function almost indefinitely; in other words are 'they' very 'robust' or 'durable'? If these cancer cell telomeres are 'durable could their functioning cause any apoptosis mechanisms to 'shut down'?

In a normal cell, during each replication the telomere is shortened slightly due to the end replication problem, as you probably know. As mutations occur and a normal cell begins to exhibit cancerous characteristics, it needs a way to stop the self-destruction which happens when the telomeres become too short. In fact it is the cancer cells themselves which 'short-circuit' the shortening process and cause the telomeres to stay long enough.

90% of tumors do this by activating telomerase, an enzyme complex which elongates telomeres and keeps them from getting too short, so that the cell is effectively immortal from this sort of destruction. Usually telomerase is not active in most cells, except for stem, germ, and hair follicle cells, but cancer cells use this to their advantage and activate it to stay immortal. The other 10% or so employ a method called ALT, or Alternative Telomere Lengthening, a not yet thoroughly understood process which involves the recombination of tandem repeats between sister chromatids.

This page explains how cancer cells bypass the telomere shortening process well, and also provides a series of further reading on telomeres and telomere shortening.


Macromolecule levels in daughter cells after fission When a prokaryote undergoes binary fission, how are the non-DNA macromolecules distributed between the two daughter cells? This is motivated by comments on a previous question and a G+ discussion. I am primarily interested in explicit mathematical models.

Naive model
For DNA, each copy is attached to a different part of the cell membrane, to ensure each of the daughters receives a copy. As far as I understand, there isn't such specific mechanism in place for other macromolecules. If we are allowed to assume that non-DNA macromolecules are distributed uniformly through the parent cell than this would mean the two daughter cells would receive half the proteins within statistical fluctuation. This has a specific meaning: if there are $N$ molecules of type A in the parent, then the difference in number of type A molecules in the two daughters after fission will be on the order of $\sqrt{N}$.
However, this model might be wrong. For instance, as the new cell-wall is being formed it could have in it specific pumps that either balance the protein levels below chance (producing an average difference lower than $\sqrt{N}$) or to create asymmetries higher than chance. Altenrnatively, the initial distribution of macromolecules in the parent could be far from symmetric for some other reasons. Which is the case?
If the naive model is correct, is there experimental evidence explicitly showing this?

Many years ago I worked in the field of bacterial chemotaxis, and your question brought this paper to mind:

  JL Spudich & DE Koshland Jr. (1976) Non-genetic individuality: chance in the single cell. Nature 262:467-471.

The authors report an analysis of the chemotactic behaviour of individual bacterial cells from a single homogeneous culture. They find marked differences between individuals, and their favoured model is what they refer to as a Poissonian variation in the inheritance of key proteins that are present in small numbers.

According to ISI Web of Science this paper has been cited 241 times - presumably at least some of those papers might be about other more recent examples of this type of phenomenon.


Inheritance of Huntington's disease People with Huntington's disease have HTT genes with more than 37 copies of CAG repeat. The risk of extra copies being generated is higher during sperm formation than during ovum formation. Why is it so?

Interesting fact: People with HD allele inherited from father develop symptoms earlier than if that allele is inherited from mother.

Excellent question. The answer is that, in general, there is a higher rate of mutation in spermatogenesis compared to oogenesis. This is because there are more cell divisions during spermatogenesis, which allows for opportunities for mutation.

In addition, repeat diseases like Huntington’s sometimes have a phenomenon known as anticipation. This is when the disease gets phenotypically (and genetically) more severe with each successive generation. The exact molecular basis of this is not completely understood, but it is just well known that DNA polymerase tends to make more mistakes in large repeat regions, causing an expansion of the repeat. Anticipation is not linked to gender, I just wanted to point out that these repeats are prone to mutations that will expand the repeat and cause disease

You can see anticipation in this graph. This example is for Fragile X. The higher the repeat number in the parent, the greater the chance the child develops the disease. The parent doesnt have the disease, but what happens is the repeat mutates and gets expanded to the point where the disease will develop.

So, put these two facts together and you have your answer. A male's sperm tends to have a higher overall mutation rate, and the region responsible for Huntingtons is already prone to disease causing mutations as it is. The result ends up being the disease gets ‘inherited’ more often from the father

Picture from here


What are the internal surfaces of body cavities actually made of? In Ross's book of histology it says that the mesothelium that includes all body cavities is made of simple squamous epithelium but in other places it says that in the gastrointestinal tract it is made of simple columnar epithelium. Is it that the trachea and the the gastrointestinal tract are not classed as cavities?

The peritoneum, the pleura, the pericardium, the tunica vaginalis testis and the tunica serosa uteri are made of mesothelium (simple squamous epithelium) [1].

The GI tube is made of a specialized tissue composed from four layers: mucosa, submucosa, muscularis externa and adventitia. The innermost layer (mucosa) has an epithelium that is stratified, squamous and non-keratinising, for protective purposes. The internal organs in the peritoneal cavity are covered with the visceral sheet of peritoneum which is the adventita layer [2].

Trachea is made of respiratory epithelium, which serves to moisten and protect the airways. It is lined with pseudostratified columnar epithelium with goblet cells that produce mucus [3].

Trachea, stomach and intestines are considered cavitary organs as opposed to parenchymatous organs (lung, kidney, liver).

References:

Wikipedia contributors, "Mesothelium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mesothelium&oldid=598055771 (accessed June 26, 2014).
Wikipedia contributors, "Gastrointestinal wall," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Gastrointestinal_wall&oldid=598338180 (accessed June 26, 2014).
Wikipedia contributors, "Trachea," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Trachea&oldid=613017631 (accessed June 26, 2014).


Does pepsin enzyme digest other enzymes like other pepsin molecules Pepsin digests proteins, as we know, but can it digest other enzymes that are actually made up of proteins, like digesting other pepsin molecules?

Pepsin does cleave itself (Ingram, 1951) - this is termed autolysis. Pepsin (and other proteases) act on proteins with the right amino acid sequences. Pepsin prefers to cleave at phenylalanine, tryptophan or tyrosine residues (Lehninger, A. Principles of Biochemistry).

* Pepsin can also cleave inactive 'zymogen' enzymes to activate them. One of these zymogens is pepsinogen (an inactive form of pepsin itself). So you could argue that pepsin is cleaving itself here but I personally wouldn't, since pepsinogen isn't really pepsin.


Why Egg shell is not called a cell wall? Egg is a single cell and has a outer hard covering outside inside which there is a cell membrane. Then why isn't the egg shell a cell wall?
Is it because no exchange of materials take place through it?

Egg shells are actually porous so that the organism inside can aquire oxygen and get rid of carbon dioxide as it develops (http://www.scientificamerican.com/article/bring-science-home-chick-breathe-inside-shell/).

Although gametes (eggs and sperm) are single cells, an egg shell (or "wall" if you like) is created by the mother (therefore external to the egg cell) and contains many compartments separated by protein membranes:

https://www.exploratorium.edu/cooking/eggs/eggcomposition.html

The initial egg cell is a tiny fraction of a size of the egg visualised here, so it would therefore be incorrect to call the egg shell a "cell wall" as it is a structure independent of the egg cell itself.


What do "reduced antipredator defense" and "reduced antipredator vigilance" mean? The book BIOMAT 2010 (International Symposium on Mathematical and Computational Biology, edited by Rubem P. Mondaini) mentions the terms reduced antipredator defense and reduced antipredator vigilance.
Can you help me to make sense of them?

When groups of prey use certain mechanisms to defend against predators, those mechanisms are known as antipredator defenses. For example, groups of tuna and starlings flock together to confuse predators. A reduction in this defense would be 'reduced antipredator defense'.

Groups of prey also exhibit shared antipredator vigilance, as in certain members of a group will look out for predators to protect the group. This is seen most predominantly in meerkats. A reduction is said vigilance would be a 'reduced antipredator vigilance'.

With reference to the Allee effect, which is what you appear to be reading about, this reduced antipredator defense and vigilance can significantly effect the population and the population growth.

Some related links:

On the ecological mechanism of the Allee effect.
Vigilance, predation risk, and the Allee effect in desert Bighorn sheep, a recent research paper.


Protein structure prediction using PSSM? Or not? I have been studying protein structure prediction algorithms. A lot of recent work uses something called the PSSM, the position-specific scoring matrix.

I think that what a PSSM does is to build a 2-D matrix of all possible residue pairs in a protein, then scores how likely it is that the two residues mutate in tandem. Co-evolution of two positions which are far from each other in the primary sequence are an indication that they are in contact. When one residue in a contact pair changes, that generally destabilizes the protein, and the other residue in the pair is under selective pressure to compensate. Knowing this gives you a good start on building the protein contact map.

Do I have that right?

If that is correct, then this technique of protein structure prediction depends on having many examples of proteins in a homologous family. You need nature to do a lot of sampling for you. And you need to dredge up massive numbers of homologs from genomics projects. I've read that creating the multiple sequence alignments for PSSM work is computationally intensive. If I understand the process correctly, I can see why.

My main question is: what can protein structure prediction models built using PSSM do, when there isn't a PSSM?

For example, the Top7 protein is a fully-novel protein fold that does not have any homologs in nature. It was created in 2003 using RosettaDesign software. Rosetta's protein structure prediction algorithms predate PSSM as far as I know. Sixteen years later, there are exactly six variants of Top7, all of which have been made in the laboratory. That hardly sounds like enough data for a statistically-valid PSSM, and in any case, the variants were not naturally selected.

If you don't have a PSSM, is it even possible to enter your sequence into a model that expects one?

Thanks for your input.

I think you are making PSSMs out to be much more sophisticated than they really are.

A PSSM is merely a scoring matrix — it gives position specific scores for each residue at a given location.

There is no explicit pairing of interacting residues though that does sound like an interesting approach ...

You can learn more about PSSMs from many sources on bioinformatics including NCBI.


Why is glycerol the backbone of fat? Fats are fatty acids joined onto the backbone of a glyercol (propane-1,2,3-triol).

Why was glycerol seemingly chosen by nature to be the backbone of fats? Why can't it have been a butane -1,2,3,4- tetraol or pentane with 5 alcohol groups or almost any other molecule?

So my question boils down to, is it just pure chance that glycerol is the backbone of fats or is there a deeper underlying reason?

Chance should always be high on our list of explanations of why the history of life turned out in some specific way. As James A. Coffman has described, there are a couple of different notions of chance. Evolutionary biochemistry is quite difficult because today's diversity of biochemical genotypes and phenotypes are a biased representation of the ancient past.

However, I think a case can be made that it was not 'pure' chance.

As your question itself suggests, the chemistry requires alcohols for the esterification with fatty acids to form acyl glycerols. I think that is 'sufficient' to say it is not 'pure' chance that among molecules that it was glycerol, but since you're also questioning "why glycerol?" over other alcohols, let's look at what glycerol has going for it compared to other alcohols.

Glycerol is relatively small. All else being equal, fulfilling a biological function with a smaller molecule requires less energy than larger ones. Compared to polyphenols, for example, this is a no-brainer because (1) building polyphenol would be expensive energetically, and (2) would be difficult to transport.
Glycerol is flexible. The two outer alcohols have the ability to move with respect to the central carbon so that as we go from glycerol to mono-acylglycerol, di-acylglycerol, and finally triacylglycerol, the outer groups' motion can reduce steric hinderance.
Glycerol can be converted into a lot of other things that form a part of metabolism. While it is conceivable that an extremely different metabolism without glycerol could have come to be, the fact that glycerol is directly and indirectly convertable into a large number of molecules with structural and energetic functions does give it better candidacy than molecules that are relatively unreactive or require large numbers of reactions to build anything useful biologically.
While glycerol doesn't have the greatest number of alcohol groups for its size (size in terms of carbon backbone, not necessarily molecular weight), it doesn't have the least number either. Steric hinderance or difficulty to synthesize of alcohols with the same size would make glycerol a better choice.

Hopefully that convinces you that glycerol was not completely random with respect to all other molecules or even all other alcohols. That is, not all the possibilities in those sets are equally good for the biochemical role that we now see glycerol fulfilling, and glycerol is defintely not the worst. However, there may have been other subsets of alcohols/molecules in existence at that time for which we don't have specific reasons for glycerol being better.

In conclusion, no, not 'purely' random.

UPDATE

Reading my answer above, I can see why someone reading my list of glycerol traits may think I am making a just so story on why it is specifically glycerol that we have today fulfilling a biochemical role of joining together fatty acids via acylation. To be clear, I am not addressing 'why' glycerol is the molecule fulfilling this role but rather whether it is purely random that glycerol is the molecule fulfilling this role. In my vernacular, 'purely random' implies a uniform probability distribution, which is to say that in this context each molecule was as likely as any other to fulfill the role that we see glycerol fulfilling in biochemical systems today. By citing reasons why some molecules are better suited in their properties, we show that the distribution cannot be uniform. We don't need to even place where glycerol sits on this distribution to determine that it is not purely random. We only need non-uniformity. The fact that glycerol has traits that make it more likely than others is an additional suggestion that among the molecules under consideration, glycerol was not the least likely.


Do ants feel acceleration? The organ we have to provide us with current acceleration information is quite complicated. Because an ant queen didn't seem to notice when I picked up the bottle she was in, I have a suspicion that ants don't really care about acceleration and therefore can't tell where it's up and where it's down.

Am I right? If not, how do they sense acceleration?

According to Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Vicente Honrubia, page 8, the vestibular system (animals' "accelerometer") is as old as 600 million years and is present in invertebrates.

I assume (without a precise source) that this is especially important for flying insects (after all, accelerometers were engineered for flying machines in the first place!) and that the ant didn't respond because the acceleration to which you submitted it was not deemed harmful.


How does the body survive Ebola? Because Ebola takes over the immune system and uses it to replicate more and more of the virus, how does the body survive?

Is it a case of the virus being self-limiting and eventually just getting 'too big for its britches' so to speak? Or does the body somehow eventually start producing antibodies to fight it off?

While the ebola virus infects a lot of human cells, immune system cells it infects are mainly monocytes and macrophages. The cells in our body mainly responsible for adaptive immunity, T cells, are at least not completely infected:

  Our data indicate that 20–30% of CD4 and CD8 T cells died during the course of infection1

That's a lot, but the ones that survive get activated and it's apparantly enough that between 80 and 10% of the infected (depending on the strain) can survive the infection. Little is known about the details of the immune reaction to ebola, but the immune system does get activated. The immune system even remains on "high alert" for quite some time after infection and recovery.

And the antibodies do stick around, at least for 10 years. Whether they confer immunity against all strains of ebola, we don't seem to know - ebola isn't very well-researched yet.


Modern alternatives of DNA footprinting Since DNA footprinting is an old method I thought there may be some more recent and effective methods to identify a DNA sequence, do you know any of them?

DNAse-seq is the most obvious choice. It uses the same idea as DNAse footprinting but measures output using high-throughput sequencing, so it can be done on a whole genome in one shot.


Weighing 2 vertical halves of the human body I had this thought while bathing:

Assume a perfectly developed physical human body and anatomy in terms of size, dimensions and proportions. In theory, if I cut the body vertically into two exact halves from the center of the head downwards, would the two halves weigh the same?

I tend to think that the 2 halves would weigh differently, and if so, I find this quite interesting because it is strange to me that our body would - perhaps unecessarily - evolve in such a manner that requires it to balance itself on a symmetrical skeleton.

Are there any topics that touches on this... phenomenon?

The two halves likely do weigh approximately the same. Since the density of most tissues that are not filled with air is basically equal, it doesn't matter that, e.g., heart, spleen, and stomach are on the left and liver is (mostly) on the right. In the left/right axis, it evens out.

As for the location of the center of mass of a human: it's located about 10 cm below the navel, at the level of the S2 vertebra approximately midway between dorsal and ventral surfaces of the body (assuming that the person in question is neither pregnant nor obese).


Explanation of "differential transcript usage" (DTU) This paper describes differential transcript usage as

Differential transcript usage (DTU) is a special case of alternative splicing in which a gene’s relative transcript abundance (RTA) profile, the proportion of total gene-level expression that arises from each of the gene’s transcript isoforms, differs between conditions (Soneson et al., 2016). [...] An example of DTU may be illustrated by the scenario where the total gene expression is the same between conditions A and B, but transcript isoform 1 is the predominantly expressed transcript in condition A while transcript isoform 2 is the predominantly expressed transcript in condition B.

My question is: is differential transcript usage essentially the same as the usage levels of particular codons? If not, what is the difference? I am unsure of what "transcript isoforms" are, so I'm not sure whether it's talking about codons here or something entirely different.

No, it is a completely different thing, which has to do with splicing and alternative splicing.
I refer you to some genetics text for details on splicing and alternative splicing, but I will give here a very brief and incomplete explanation fo what they are and how they fint into DTU.
Genes are composed of introns and exons. Exons are the only parts of genes that are usually composing the mature transcript (intron retention is possible, but we are not interested in that).
Splicing is the mechanism by which in a eukaryotic gene, introns are removed, and the mature transcript is assembled only using exons.
During splicing, not all exons are necessarily retained. Imagine a gene with exons 1, 2 and 3. It is possible that the main form (called isoform) is the one consisting of exons 1, 2 and 3. Let's call that Isoform 1. However, due to a phenomenon called alternative splicing, other isoforms, can be generated, for example one isoform composed by exons 1 and 3. Let's call that Isoform 2.
On average, we may imagin that the abundance of Isoform 1 compared to Isoform 2 is rather constant. However, some treatments or some changes in environmental stimuli, can give rise to a Differential Transcript Usage by which the relative abundance of the two isoforms changes.


Why does the open tree of life have 2600 species of rose? The open tree of life has 2754 species and subspecies with the prefix Rosa.

Wiki says:

  There is significant disagreement over the number of true rose
  species. Some species are so similar that they could easily be
  considered variations of a single species. Lists of rose species
  usually show between 100 and 150.

The thing is that a subspecies in the open tree taxonomy (OTT) should be written with a different latin name, and I can find at least 400 OTT rosa that are listed as individual species and not subspecies.

Is the OTT not very coherent in terms of accepted species?

There are at least three possible explanations (and quite likely more):

1) You may be correct in suggesting that the OTT isn't "very coherent."* In other words, they may have a little work to do. I don't know enough about the site to offer a solid opinion.

2) The OTT may be unintentionally repeating someone else's error(s).

3) The OTT has to work with the information that's available, and, in the realm of taxonomy, that information can be very confusing. Different authorities recognized different classification schemes. Scientific names also change over time; for example, the polar bear (Ursus maritimus) used to be Thalarctos maritimus.

I don't know enough about OTT to really understand exactly how it works. However, I typed in Ursus (a subspecies in the bear family), and it listed 22 "Descendant tips." Curiously, it didn't display a list of species and subspecies, however. When I type in Panthera (the "big cats"), it does display a list of species and subspecies. I don't know if that reflects a problem with OTT or not.

You're focusing on the genus Rosa, which, as you say, is complex. In fact, I just thought of a fourth possibility...

4) Domestication - Many species in the genus Rosa have been domesticated and/or hybridized. It's possible that OTT is including the names of cultivated species. (It shouldn't be too hard to determine if this is the case if you're familiar with the Latin names of some cultivated species.)

Ultimately, the people best qualified to answer your question are probably the people behind OTT. I'm very interested in finding a definitive answer myself, because taxonomy is a major personal interest. I also find it endlessly confusing. ;)

P.S. I once wrote an article about a particular phylum of marine invertebrates. I stated that there were X number of species in the phylum, using a similar website as a reference. However, a specialist later told me I was way off base. I can't remember the details, but I believe there was either an error with the "master database" or there were conflicts between two or more databases. Like I said, taxonomy is confusing.

*Regarding coherence, we might also consider the target audience. This definitely is not what I would call a user-friendly site. I'm a lifelong naturalist with a degree in ecology/biology, and I find it very confusing. But rather than call it "incoherent," we might just say it isn't user-friendly.


Was there a time in Earth's history when some animal life existed on land but humans could not have breathed? I understand that higher oxygen content allowed insects and arachnids to grow much larger than today and I wonder if this additional oxygen would have been toxic or unhealthy for modern humans?

There isn't evidence that the worldwide air has ever been toxic compared to today since animals came to land 530+ million years ago.

At some times in history, there has been lots of mercury vapor and perhaps other poisons in the atmosphere, for example recent research indicates that the late dinosaurs had at least 10 times as much environmental mercury from the Deccan traps eruptions which give most of southern india it's current geology. That said, the air would have been breathable, but some apex predators would have had mercury poisoning from their diets. Imprecise studies have found mercury levels in sediment go up to 1000 ppb for hundreds of years, compared to perhaps 100 ppb as they are today... other studies may find that there were higher mercury spikes, up to 30 times those of today perhaps. https://www.researchgate.net/figure/Temporal-correlation-of-mercury-records-with-other-indicators-of-Large-Igneous-Province_fig15_328051765

For oxygen, ever since the first insects emerged on land 530 million years ago, the oxygen levels have been safe for humans. https://en.wikipedia.org/wiki/Timeline_of_the_evolutionary_history_of_life


Understanding ancestry testing mathematically Forgive me if this question has been asked here before, because it is something which should be very easy to find, but I can't seem to find an answer no matter where I search.

The question is simply where to learn the mathematics that goes into things like popular ancestry tests, and also more academic things like determining ancestry components of historical groups (e.g. usage of the terms Ancient North Eurasian, Eastern European Hunter-Gatherers and all that).

It is clear that if someone gets an ancestry test saying say 32% Scandinavian, then of course that doesn't mean 32% of their base pairs have a convenient "Scandinavian" label attached to them, rather there is some statistical inference going on behind these percentages, and I would like to understand that.

Suppose I have the raw data of my own fully sequenced genome, and also a database of the genomes of many individuals from various populations (of course grouping them into populations is already something that involves some assumptions that I would like to learn more about). Where would I learn how to analyze that myself to produce something like the results of an ancestry test? Is there a textbook someone could recommend that gets into the actual algorithms used?

I'll give here a simple, non-technical answer because I'm assuming you don't need to actually perform an analysis of ancestry.

So, detecting ancestry is a non-trivial task. Given your genome sequence, you would need to compare some "informative" regions of the genome with the homologous sequences of some population (say, of a database with other genomes). These informative regions are usually some parts of the genome that vary across individuals (variation is used because differences are informative: some populations vary on particular sites, distinct from other populations). At the core, this is a question on how to compare "character strings" (DNA is composed of 4 characters, namely, A, T, C, and G). But these strings exist in a complicated structure: a human genome is partitioned in 23 pairs of chromosomes, within each individual. However, the question of ancestry is not about individual sequences really, but about population-level changes in DNA composition. So, in fact, you need to consider population-level factors: size of the populations to consider, the rates of recombination (DNA exchange across chromosomic pairs), mutation rates, and even population structure (people move geographically!).

Given these (and, many other) factors, people build models of "coalescence": given a sequence of interest, how likely is that it shares some ancestor with another query sequence? So, the models try to relate these two sequences (say, the one you are interested), with a query (say, a "consensus" Scandinavian sequence), and then make a model of a 3rd sequence (the ancestor!). This process is repeated to test many hypothesis, so you end up with many probabilities. On top of this, you can estimate the ancestry for any given part of your genome, and this is what most companies do (say, 23 and me).

In summary, you are correct that a "% Scandinavian" does not mean sequence similarity per se. It implies an estimation of common ancestry. This estimation comes from models of shared ancestry. If you're unsatisfied with this simple answer, and want a more technical answer, I recommend reading this paper. An intermediate-level explanation is found here.


Michaelis-Menten Kinetics: Does measuring apparent Km and Vmax take into account competing reactions? I am learning about why it is important to measure Km and Vmax for each experimental setup because measuring the "apparent" Km and Vmax includes enzyme inhibitions of which one might not be aware.

However, what if there are entire reactions going on that are consuming the product or substrate that are not known? Are these accurately aggregated into the Km and Vmax measurements?

Here are some of the links that I read through:
http://www.bio.upenn.edu/media/pdf/courses/F02/BIOL202/Handouts/BIOL202.ApparentKmandVmax.pdf

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

Have you heard of something known as "Occam's Razor" ?

It says when you have multiple possible explanations/hypotheses then select the one which is simplest (i.e least number of assumptions)

Same with mathematical models. Chemical kinetics models usually assume first order unless there is some evidence against it. Similarly, for enzyme kinetics, as long as you don't think there is something anomalous going on, use Michaelis-Menten model.

  What if there are entire reactions going on that are consuming the
  product or substrate that are not known

Many physiological enzyme catalysed reaction are not Michaelis-Menten. If you happen to have an insight about it or if the simulations dont match the experimental data, you can revise the model.

However, Michaelis-Menten model for for competitive inhibition exists, as you yourself indicate in the link.


Can your immune system's cells destroy you? (Critical thinking and Fictional sense) In an imaginary sense, If you alone were replicated into 2 so that there should now be 2 of "you" (meaning you both have the same DNA). Then let's say one of you shrunk to the size of a bacteria, and was placed inside the other you (normal human size. Let's call this the actual you).

The question is how would your immune system affect the bacterial sized you in your own body?

Would white blood/T cells try to get rid of the smaller you?
If so, how? And could the smaller you die from this?

This is a very interesting question. As others have alluded to, the body generally recognises self and non-self. However, as with any biology it's not that simple. Even leaving aside autoimmune disorders, the body doesn't always attack non-self and doesn't always leave self alone. Think of a pregnancy - the foetus is non-self, and yet the body doesn't reject it. The same can be said for a whole host of molecules that enter the body, such as food or things breathed in (e.g. pollen).  For this reason, Charles Janeway put forward the infectious non-self theory. This postulated that the body had a degree of leniency towards non-self, and would only attack if the macrophages became activated. This is done through recognition of Pathogen Associated Molecular Patterns, or PAMPs, binding to Pattern Recognition Receptors, PRRs. These PRRs are receptors present on immune cell surfaces, though most relevantly on macrophage surfaces, and when they bind to PAMPs it sends a message to the cell that it's likely in contact with a pathogen (or at least there is likely a pathogen in the area somewhere). This causes activation, and starts an immune response.

However, it's also too simplistic to suggest that the immune system always leaves self alone, and in fact one of the key jobs of macrophages is to clean up self cells that are damaged, and undergoing apoptosis - programmed cell death. (You can read more on macrophages here and more on apoptosis/other methods of cell death here). Therefore Polly Matzinger put forward what is known as the "Danger Model". This basically speculates that in order for an immune response to occur, the body has to recognise certian molecules that are evolutionarily associated with danger. PAMPs would indeed count, but there could also be endogenous molecules such as HSPs - proteins produced when a cell is under duress through heat, pH, cold, irradiation, viral infection etc. This tells the immune cell that detects it that the body is in danger, and allows activation and mobilisation of an immune response.

So the question here is, would the body respond to a miniature version of yourself? That would depend on a number of factors:

Where in the body would you go? If you were to stay in the digestive tract, so get swallowed and 'passed through' the body, I would say it's very unlikely you would be attacked. The body has a high tolerance for places such as the gut, because it's constantly exposed to external and non-self molecules. If it were in the blood stream, it's more likely because you're more likely to come across immune cells.
How is this 'shrinkage' achieved? Growth comes in two ways, through increase in cell size and increase in cell number. Which of these are you reducing? Are the cells the same size, but there are many fewer of them (unlikely, especially given that the opening question specifies to bacterium size, which are many times smaller than human cells already) or do you have the same number of cells but each cell is shrunk to a much smaller size (given that the entire body is the size of a bacterium, each cell would have to be many times smaller than a bacterium). If the cells were the same size, or even a bacterium-sized each, then an immune response is much more likely. If the whole organism is the size of a bacterium, the cells are going to be far too small to elicit an immune response.
Are you causing danger signals? As mentioned above, if no danger signals are present then it's unlikely an immune response will be launched regardless of anything else. Provided you're not killing or injuring cells, the body will pretty much ignore you.

I would say you wouldn't be attacked if you shrunk down as far as you've suggested. Everything would be too small for the body to recognise. However, if you didn't shrink down nearly as far, so your cells remained a size the body could recognise, and then started blundering about causing all manner of danger signals around you, the body may pick up some of your antigen and launch a response against you. On the other hand, the body is likely to have become tolerant to your antigens so even if this was the case, a full immune response is unlikely.


Are bacteria necessary for an individual's life, or, how long could a person live without bacteria? Bacteria are essential to life in that they are responsible for breakdown of organic substances, etc. but are bacteria necessary for an individual's life?

In other words, how long would a human survive if they took a super-antibiotic which killed all the bacteria in their body, with the current state of medical technology? If they died what would be the most likely cause of death?

Assume bacteria don't recolonize your body.

Background: I call bacteria the "Lords of the Earth" both to remind myself to be humble and (rather more) as a conversation-starter. I'd like to be able to underline their importance in the ensuing discussions.

You might need to demote your single-celled 'lords' to 'squires'. They're not essential to an individual's life. You wouldn't die (dispensing with the "how" right off the bat.) You'd be just fine if no bacteria reentered your body. Your fecal output would be greater; you would derive somewhat less nutrition from your food, you would need to take vitamin K, and there would be an adjustment period, but theoretically, you'd be just fine. You might even be healthier.

Your hypothetical is impossible, of course, because experimentation on humans is unethical. However, it might surprise you to learn that there are colonies of germ-free animals (also called gnotobiotic) used to study the effect of certain bacteria on animals.

The derivation of such subjects was initially fairly gruesome.

  The process of engineering biology and machine began by removing intact uteruses from near- to full-term pregnant animals within a purpose-built germ-free "surgical isolator." The uterus was subsequently passed through various disinfection procedures, involving total immersion in germicide-filled "dunk tanks," before the progeny were surgically released and hand reared within a second microbially sterile isolator.

These animals are costly to keep, as you can imagine. The originals must be delivered by Cesarean section, and housed and raised in sterile conditions. But once you can do that, they can multiply.

  To start a germ-free colony, one must remove a young animal from its mother’s womb through a careful surgical procedure to avoid exposing it to the microorganisms in the mother’s vagina and skin. Then, the animal is raised in a sterile cage and only exposed to food, water, and other equipment that has also been sterilized. On a weekly basis—or more often—a technician swabs cages and animal feces to ensure that no bacteria have contaminated the sterile housing. Once the colony has been created, it becomes easier to rear new germ-free animals; a germ-free mother can give birth naturally without exposing her newborns to any bacteria.

By the 1950s, researchers were rearing germ-free mice, rats, guinea pigs, and chicks inside sterile stainless steel (and later, plastic) housings. Germ-free animals are especially useful in researching, among other things, diabetes, auto-immune diseases, obesity, genetic engineering, cancer, immunology, nutrition, and the effects of normal intestinal flora on health.

Vitamin K must be added to their diets, and it is important to sterilize their food without destroying nutrients, but otherwise they do well in their environments. Their feces, of course, are sterile. Everything is microbe-free. They also have no "normal" antibodies.

Since generations of germ-free animals can exist and multiply, it is not only possible but quite likely that germ-free humans can exist as well.

Which is not to say that gut (and skin, etc.) microbiomes are unimportant. If you release a germ-free animal into a normal environment, it can die if it picks up pathogenic bacteria before more normal gut flora. To do this safely, a germ-free animal is first given a cocktail of bacteria to colonize the gut. After a while, they can be in a normal environment without problems. But your hypothetical human wouldn't even have this problem.

Germ-Free Mice
Gnotobiotics
Technology Highlights：ESTABLISHMENT OF THE FIRST GERMFREE MOUSE AND RAT COLONIES IN TAIWAN
"Life in a Germ-Free World":
Isolating Life from the Laboratory Animal to the Bubble Boy


What are the purposes of granulocytes in acute inflammation? I heard the phrase

  Neutrophilic leucocytes are kings in the acute inflammation.

Neutrophils are granulocytes, while leucocytes are not granulocytes.
I think this statement refers to the fact that leucocytes have neutrophilic properties, instead of being neutrophils itself.

Acute inflammation players are, I think

Granulocytes, monocytes and leucocytes

while in chronic inflammation similar player but the main factor is macrophages so the phrase which I heard

  Macrophages are the kings of chronic inflammation.

I think granulocytes are related to the Healing and Proliferation.
Eosinophils for instance in the allergic responses of acute inflammation.
I think granulocytes are phagocytosed by the macrophages and this way spread their functions through macrophages around.
Probably, neutrophiles are attached to the leucocytes such that they spread their function through leucocytes (so called neutrophilic leucocytes).

Let's cover first this, since we can after understanding it go to the chronic one.
What is the purposes of granulocytes in acute inflammation?

MattDMo's answer

  Essentially, [neutrophilic granulocytes] are the first infiltrating
  cells to arrive at the site of injury at the beginning of acute
  inflammation (bacterial infection, environmental exposure, etc.).

which I agree with.