What exactly are genes, DNA and chromosomes. How do they relate to each other and what is their function? So I am new to biology and I have been reading, and searching the web, but I couldn't understand the whole framework of a cell. So as I understood:

A DNA, is a double chain of Nucleotides (A,T,G,C and a sugar) and a phosphate residue. Some parts of a DNA code a gene and some do not, exons and introns accordingly. As I understand it these the sequences of exons hold genes and the whole sequence is called genome. Now I read in the book Introduction to Computational Molecular Biology by J. C. Setubal and J. Meidanis. that I cite Each cell of an organism has a few very long DNA molecules. Each such molecule is called a chromosome. So each X shaped thing called a chromosome holds one DNA molecule?

Or is each "hand" of the chromosome one complete double helix of DNA so we have 23 pairs of such chromosomes? or is it that each we 23 pairs Xs?

Shouldn't we have just one uniquely identifiable DNA sequence? I am asking this, because I have also read that each chromosome encodes a different part of one's genome. Does this mean we have several DNA sequences?

This is really bothering me, since I can't figure out the correct structure of a cell.

EDIT:
Now if each chromosome contains a pair of DNA helices. We have 46 chromosomes so overall within the cell there are 92 DNA sequences? All of which are the same? Or are they different? If they are different how do they code for different aspects of one's genome?

Your understanding of DNA is correct. DNA is a heteropolymer of monomers called nucleotides and each nucleotide is made up of a sugar (deoxyribose), phosphate and a "base" (A, T, G, C).

As you already know, DNA is organized as a double helix with the Watson-Crick pairing rules.

A chromosome contains a single DNA double helix. Many organisms have multiple chromosomes which are very different in their DNA sequence. In diploid cells (such as the somatic cells in humans), each chromosome has two copies. The two copies are almost identical and are called "homologous chromosomes". As you know each parent contributes to one of the homologous chromosomes.

During eukaryotic cell division, each chromosome is duplicated. The duplicates (or sister chromatids), are joined at a region which is called the centromere. Centromere is an attachment point for spindle fibres that pull the sister chromatids apart.

Each chromosome has multiple genes. A gene is a region of DNA that is transcribed i.e. it can give rise to an RNA (which can either be a mRNA that in turn codes for proteins or a non-coding RNA). There are other regions of DNA that are not transcribed and these are generally referred to as intergenic regions. In many eukaryotic genes some parts of the transcribed RNAs are removed as a result of splicing. The retained parts are called exons and the removed parts are called introns.

Some organelles like mitochondria and chloroplasts also have a unique genome within themselves. A genome is the entire set of chromosomes including the homologous chromosomes and the organellar chromosomes.

However, when talking about a reference genome, which is just a bioinformatic information and not an actual genome, we just have one sequence for each unique chromosome (for example, in humans, chromosomes 1-22, X-chromosome, Y-chromosome and the mitochondrial DNA). A reference genome is used as a basal set and in a population genomics study, differences from the references are highlighted instead of presenting the entire sequences.

  Picture source: https://cnx.org/contents/9TxHOD3O@4/The-Nucleus-and-DNA-Replicatio  Note that paired chromosomes (X shape) are found only during replication. Usually the chromosome is like a single thread. Chromatin is the name of the assembly (for e.g., we don't say chromatin-21).

Bottomline: We have 46 chromosomes then it means we technically have 92 DNA sequences. However you should consider the double helix as one entity (or a metamolecule) because the strands always stay together. For more details you should read a book. Genes by Benjamin Lewin and Molecular Biology of the Gene by James Watson et al. are good books on this topic.


Why was not RNA completely replaced by DNA when the RNA world evolved into a DNA and protein world? If DNA just has a slightly different chemical composition from RNA, why can't DNA act as a catalyst and why hasn't it replaced RNA? Here, I am talking in terms of evolution, shouldn't evolution just replace all the RNA with DNA?

A related question is Why do some bad traits evolve, and good ones don't? Basically a strong selection pressure is necessary to filter out a trait.

Having said that, there is no strong argument in support of transcription being disadvantageous.

RNA has unique properties that makes it suitable for certain functions. RNA can adopt different secondary/tertiary structures that an equivalent ssDNA cannot. One of the reasons is that GU wobble pairs are stable in RNAs but not in DNA thereby allowing structural flexibility to the former. See https://chemistry.stackexchange.com/a/35224/5295

RNA also has a high turnover because of different RNAses. If there was DNA instead of RNA for carrying temporary messages and there were equivalent DNAses to increase the turnover of the "mDNAs", then the genomic DNA would also become susceptible to degradation by these DNAses, which would cause genomic instability. You can argue that protein synthesis could directly begin on DNA as a template instead of mRNA. I guess that it would crowd the DNA and clash with replication. Even transcription machinery clashes with the replication machinery; this is called Transcription Replication Conflict which leads to genomic instability. A hypothetical situation in which there are multiple ribosomes on a DNA, is likely to have higher chances of the conflicts with replication than transcription-replication conflicts, thereby causing higher degree of genomic instability. I am assuming so because a large number of ribosomes need to simultaneously be progressing through the gene in order to produce sufficient amount of corresponding protein (like in case of polysomes).

Another possibility is based on the RNA world hypothesis. If it is really true that RNA preceded DNA as a functional as well as a hereditary molecule then it is difficult to get rid of all RNAs that easily. Even if most of the functions of the archaic RNAs were taken over by DNA and proteins, they are still performing some vital functions. To replace RNA from these roles, an alternative should exist which performs much better than the RNAs.

These are just guesses. An absolute reason can not easily be attributed to many biological observations. This is because we do not know the actual evolutionary trajectory of how things happened. However, what is important to keep in mind is that evolution does to proceed towards some kind of global optimum. Evolution does not "aim" for perfection.


In the context of heterotrophic theory of abiogenesis, what is an organism that eats other organisms called? In the heterotrophic theory for the origin of life, we imagine a primordial soup that is rich in organic compounds and the first organisms emerge eating those compounds. Since these organic compounds are external to this early organism, this early organism is a heterotroph. But it is not like any current heterotroph since it doesn't eat other organisms or their byproducts. Is there a special name for this 'type-0' heterotroph?

At some point, some organisms emerge that eat other organisms (i.e. eat those 'type-0' heterotrophs that are already around). These new organisms are more like the standard heterotrophs of today. Is there a special name for this 'type-1' heterotroph?

I am looking for the terminology that distinguishes the heterotroph that eats only organic compounds that are non-organisms in the primordial soup ('type-0')  versus the heterotroph that eats other organisms ('type-1').

Normally, I could call the 'type-0' a primary heterotroph and the 'type-1' a secondary heterotroph. But we usually think of primary heterotrophs as things that eat autotrophs and at the start of the heterotropic theory, there are no autotrophs to eat. The primordial soup of the environment itself is the 'producer'.

If there is no standard name, would it be strange to call the 'type-0' heterotrophs as 'nullary heterotrophs' and the organisms that eat other organisms as 'non-nullary heterotrophs'?

@Artem, it's been a while! Good to see you back on Biology.SE.

I doubt that any rigorous terminology exist to describe these "type-0 heterotrophs" living on "non-organismic" organic compounds.

You might be assuming that early organic matters can naturally be categorized as being fundamentally alive vs fundamentally non-living. It is more a question of philosophy of the definition of life than anything else but, to my experience, most authors who wrote about the definition of life tend to consider early life as a spectrum from "definitely not living" to "definitely a living thing". The existence of this spectrum questions the need for the terminology you are looking for.


Relation between carbon dioxide assimilation and the ambient and intercellular partial pressures of carbon dioxide So, water-use efficiency (and carbon assimilation rate) is correlated with ambient CO₂ concentration (Ca), and  carbon isotope discrimination Δ is correlated with Pi/Pa (partial CO₂ pressure, intercellular and atmospheric, respectively) in C3 species. If the Ca increased, would that result in decreasing Δ? In other words, would increasing ambient CO₂ levels result in less discrimination towards the ¹³C isotope, in C3 species? And if that's true, is my math sound?

After more research, I've found this to be true and the reason why. Discrimination against ¹³CO₂ isotope comes from two reasons; kinetic effects (diffusion and enzyme fractionation), and thermodynamic effects (1). ¹²CO₂ and ¹³CO₂'s diffusion rates are different, carboxylation reaction's discrimination value is 30 per million, and the diffusivity of ¹³CO₂ is 4.4 per million less than that of ¹²CO₂ (2).

When stomata are fully open

  they place no place no limitation on diffusion of CO₂, C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere. When stomata are sufficiently closed that they become the sole source of limitation, the discrimination should be 4 per million. Intermediate cases give intermediate discriminations. (2)

It's known that when CO₂ is abundant in the atmosphere, stomata start to close because their job is to balance the CO₂ uptake and water loss by transpiration. This, combined with the previously mentioned information, to my understanding, means that, when they are more closed, CO₂ in the intercellular space gets consumed more. This lessens the carboxylation reaction's effect on the ¹³CO₂ discrimination because the CO₂ in intercellular space becomes more limited compared to the free diffusion of fully open stomata. In other words, carboxylation reaction has less CO₂ molecules to choose from intercellular space because free diffusion doesn't supply a constant flow of CO₂ molecules, making it use more ¹³CO₂.

(1) Farquhar et al., 1989, Annual Rev. Plant Physiol, Carbon Isotope Discrimination and Photosynthesis

(2) Farquhar et al., 1982, Aust. J. Plant Physiol, On the Relationship between Carbon Isotope Discrimination and the Intercellular Carbon Dioxide Concentration in Leaves


Asexual Reproduction Of sponges through endogenous or exogenous budding? I was studying asexual reproduction in sponges and came across two website

Wikipedia of Gemmule and there is a line....

Only Endogenous Types of Buds develop into New Sponges.

Then as I was reading this Website Sponges there is a Section 9.1. iii) Budding, in which, there is Two Parts i.e (a) Exogenous Budding and (b) Endogenous Budding
So now, I am a bit confused..... if only Endogenous Bud can give rise to New Sponges then why there is a section of exogenous budding i.e reproducing through exogenous buds,in the reproduction section of sponges, in this website sponges ? ISN'T that Contradiction?

I would say that the quoted sentence from the Wikipedia gemmule article is wrong.  The first sentence of the containing paragraph says:

Asexual reproduction in sponges occurs via budding, either by external or internal buds.

At face value, the two sentences together imply that sponges can reproduce by external budding, but that the external budding "reproduction" does not produce "new sponges"(!). Note that the most recent edit to the article (on 10 March) was by an anonymous user who changed the sentence you quoted from "Both types" to "Only endogenous types", so this was a somewhat recent corruption.


Surrogacy Post Fertilization The wikipedia page on surrogacy highlights two main forms of surrogacy: Traditional Surrogacy and Gestational Surrogacy. Traditional surrogacy inseminates the surrogate mother with sperm, while gestational surrogacy uses in vitro fertilization to form an embryo from egg and sperm, which is then transferred into the surrogate mother.

It does not discuss whether surrogacy is possible after a natural fertilization has already taken place, such as if a woman becomes pregnant and then wishes, for whatever reason, to have a surrogate take the baby to term. Is this biologically possible? If it is possible, what is the mechanism? Also, if possible, is heightened risk a major reason it is not more common?

No, it is not possible. The problem is the fertilization which takes place near the ovary. It takes the new forming blastocyst about 4-5 days to wander through the fallopian tube to reach the uterus and 8-9 days in total to implant itself into the uterine wall. See the picture below (from the Wikipedia article on fertilization):

You would have to get the blastocyst out of the right fallopian tube, make sure it survives the procedure and then implant it into the uterus of a woman which is about in the same phase of their period (otherwise the uterus is not ready to allow implantation).
It is already hard enough to do in vitro fertilization where you can control the environment.


Survival curve in early humans The survival curve/function describes the probability of a given individual to survive to age $x$. In humans, today's survival function is very much influenced by medicine. This leads me to wonder what the survival function looked like before modern medicine. Typically I wonder what the survival function looked like during the paleolithic age.

What did the survival function looked like during the paleolithic age?

Why did the survival function looked like that? What were the major causes of mortality for males and for females?

To obtain a full survival curve (basically a full life table) you would need to make quite a number of assumptions, since the data for paleolithic societies is scattered and probably biased. This is however not a field I know well, but I can point you to one recent paper (White, 2014) that explores how the ratio of young and old individuals in a population relates to demographic rates, using agent-based models. Using such a model you can obtain smooth survival curves and also explore how different assumptions will affect the survival curves.

There are also data from recent or current hunter-gatherer societies that can be used to approximate what the survival curves looked like during the paleolithic. For instance,  Hewlett (1991) (pdf here) has compiled survival rate data for individual hunter-gatherer societies (along with other demographic rates and data from other types of pre-industrial societies). The child mortality rate (deaths before age 15) often lie in the range 40-50% in active (mobile) and sedentary hunter-gatherer societies, with an infant mortality rate usually between 10-30% (death before 12 months of age). This indicates a fairly steep survival curve, which is the reason why the average age of paleolithic people is often estimated to ~25 years. This doesn't mean that most people died around the age of 25, just that the distribution of ages was very skewed and non-normal. Many died young, but people that survived to adulthood could become much older than 25.


Laparoscopic surgery: Why did the gas cause pain in my shoulder, and how did it escape my body? I recently had Laparoscopic surgery, and the nurse told me I would experience pain in my shoulder and burping as the gas escapes my system. I looked up a bit of information on the "pain in my shoulder" claim, and its due to the CO2 gas irritating my phrenic nerve. So my first question is:

Why was the pain only in my right shoulder when there is a right and left phrenic nerve? Is it common for patients to experience pain in one or both shoulders? If CO2 causes pain/irritation, why not switch to another gas?

My second question revolves around the burping and the gas escaping my system. Basically, how? How is it that gas in my abdominal area escapes through my mouth? Is it through some absorption mechanism?

Thank you!

Does CO2 cause pain?

CO2 can cause pain by applying pressure on the diaphragm; also stretching of the diaphragm due to the body position can irritate the phrenic nerve (Indian Journal of Surgery).

ALSO:

  It was once believed the resultant shoulder pain was simply due to
  reaction of the gas combining with water; or that it was merely
  trapped CO2. The actual cause of this irritation is the result of
  cellular death caused by the combination of a temperature change from the gas at 70oF and the drying effect of the gas at
  .0002%. Much of this irritation is centered on the diaphragmatic
  region. Experiments with gases other than CO2 i.e. helium, nitrous
  oxide and argon have all produced the same or similar effect (Center
  for Endometriosis Care).

Why they use CO2?

  To begin, during Laparoscopy, CO2 (carbon dioxide) gas is injected
  through a special needle inserted just below your navel. This is done
  to create and maintain a distended abdomen; a condition called
  "pneumoperitoneum."  For safety, cost and convenience, CO2 is used
  almost exclusively for this purpose (Center for Endometriosis Care).

Why is pain in the right shoulder?

  The mechanism of laparoscopy-induced shoulder pain is mainly derived
  from carbon dioxide retention within the abdomen, subsequently
  irritating the phrenic nerve and causing referred pain in the C4
  dermatome. Moreover, carbon dioxide trapped between the liver and the
  right diaphragm, irritating the diaphragm, also causes upper abdominal pain (JAMA Surgery).

BUT

  In such hiatal surgeries including LAGB and in few gynecological
  surgeries, pain occurs preferentially on the left shoulder. This
  difference suggests that the region of surgery and position of the
  patient have an important influence on the site of pain. The cause is
  that in laparoscopic cholecystectomy the liver is separated from the
  undersurface of the diaphragm because of the reverse Trendelenburg
  with a right side up position of the patient. This leads to
  stretching of the right hemidiaphragm and the gas to be potentially trapped below the right diaphragm. Reverse is true for
  hiatal surgeries (Indian Journal of Surgery).

Where does CO2 go after surgery?

Most of the gas passively leaves the abdominal cavity through the surgical wounds immediately after the procedure. What happens with the rest:

  Carbon dioxide readily dissolves in water and forms carbonic acid.
  Carbonic acid is then absorbed into the intravascular space...(JAMA Surgery)

CO2 is not released through the mouth and is not a direct cause of burping. Burping may result from the pressure of gas applied on the stomach and intestine.


What sounds deter sharks? Have any studies been done to find sounds that alienate sharks?

Sharks hear from 10-800hz.
Sharks jump out of water for fun, which makes  huge noise pressure next to their ears. Sound weapons aren't very renowned in Darpa or defence tech. i'd say, you play any kind of patterns to a shark at any frequency, you'll have a tough time upsetting it.  you may have a very good effect at attracting them from afar and delaying predatory response as they assess/avoid the prey. LF takes huge batteries compared to HF. curiously, dolpins hear up to 100khz, whales as low as 2-3 hz for booming across the ocean. precise answer here : https://scholar.google.fr/scholar?hl=en&q=shark+sonic+deterrent&btnG=&as_sdt=1%2C5&as_sdtp=


Questions about Cohesin - what does the ATPase domain do, and any suggested PDBs to look at? I've been reading about cohesin lately, and I'm confused about the head subunit interactions.  I've read a few papers, and also found this nice figure from wiki that demonstrates the crux of my question (note: SMC here corresponds to Cohesin, or am I mistaken?  I'm pretty sure this is correct, or pretty much correct):
From reading around, I'm aware generally the head subunit is an ATPase, yet from this diagram (and from the typical putative "use" of Cohesin in TAD maintenance), I'm not sure what exactly is the ATPase motif so useful for, it seems that the ATP is sort of "glueing" the the two head domains together, but that seems opposite of what ATPase would typically do, ie catalyze ATP -> ADP.  This makes me think I'm just misunderstanding something, and wondering what is the function of the Walker A/B ATPase motif.
Also, I'm wondering if there are any nice PDB files that show a cohesin loop, or elsewise are generally the most instructive about Cohesin.  I've searched through a few, but would like more informed advice about some good structures, and maybe why they are nice.

This article :
Prakash Arumugam, Stephan Gruber, Koichi Tanaka, Christian H. Haering, Karl Mechtler, Kim Nasmyth,
"ATP Hydrolysis Is Required for Cohesin's Association with Chromosomes",
Current Biology,
Volume 13, Issue 22,
2003,
at
https://www.sciencedirect.com/science/article/pii/S0960982203008042
Their conclusion is:
"Conclusions: Cohesin complexes whose heads have been connected by Scc1 must hydrolyze ATP in order to associate stably with chromosomes. If chromosomal association is mediated by the topological entrapment of DNA inside cohesin's ring, then ATP hydrolysis may be responsible for creating a gate through which DNA can enter. We suggest that ATP hydrolysis drives the temporary disconnection of Scc1 from Smc heads that are needed for DNA entrapment and that this process is promoted by Scc2/4."


What causes instinctive behaviour? Some actions, almost behaviour, exist that are common across a species. For instance, based on personal observation, human babies try to taste anything new they encounter until they are a few score months old. Similarly most dogs will go round-and-round before they finally settle down to sleep.

We probably use the term 'instinctive' to indicate there is no conscious thought behind that action, albeit the action is not a reflex either. Anyway, what causes instinctive behaviour? Is it genetic in nature? Are there some basic rules/behaviour hard-coded into our brains sort of like BIOS in a computer?

This stuff is so interesting! The instinctive behaviour is also known as a fixed action pattern or FAP which is a collection of well-defined motor patterns that are activated in response to a stimulus, i.e. a group more eleborate reflexes [2]. FAPs allow the brain to concentrate on other things as they don't need require time or energy to be thought about. The theory is they've been selected for because they decrease choice and decision time, which can be particularly important to survival.

There are some cool examples here (http://www.cerebromente.org.br/n09/fastfacts/comportold_i.htm).

the bird is continues to perform parental instinctive behaviour in the absence of a brood of chicks because the similar stimulus of hungry open-mouthed fish is present.

Another article draws comparisons between different animals as to how much of their behaviour is fixed/pre-determined [3]. There can be a correlation between the size of the cerebral cortex, used for thinking and problem solving, and the amount of innate behaviour (i.e. the bigger your cortex the less you need to rely on pre-determined behaviours in certain situations).

These patterns seem to be for the most part genetically determined, however some studies with song-birds in the 70's demonstrated that a learning aspect can modify the innate behviour. Birds which have been reared in an environemnt where they cannot hear other birds of the same species sing still sing their typical song, but when allowed to hear others sing the song becomes more complex.

Investigating the genetic basis behind innate behaviours involve searching for Quantitative Trait Loci (QTLs) or stretches of DNA that contain genes (complex traits require the concerted actions of multiple genes) or are linked to genes that are involved in determining a specifc trait (in this case a behaviour). Classically this involves crossing two animals that differ in the trait you're interested in and looking at the segregation patterns in the offspring to try and pinpoint the specifc region of DNA/collection of genes that control the trait. I think quite a lot of this has been done in insects and mice which have high breeding rates and can be studied easily in the lab.

...at this risk of making this answer ridiculously long I've just included a snippet from another website on behavioural genetics which details the OMIM and some of the traits you can search for[4]:

  Online Mendelian Inheritance in Man (OMIM) is a large, searchable, up-to-date database of human genes, genetic traits, and disorders. Each OMIM record contains bibliographic references and a summary of the scientific literature describing what is known about a particular gene, trait, or disorder. The following behavioral traits are included in OMIM. The six-digit number MIM number is used to uniquely identify each record.

Hand skill, relative (handedness): (139900)
Hand clasping pattern: (139800)
Arm folding preference: (107850)
Ears, ability to move: (129100)
Tongue curling, folding, or rolling: (189300)
Musical perfect pitch: (159300)

[2] http://books.google.co.uk/books?id=aQvGXLPjMPAC&pg=PA44&lpg=PA44&dq=fixed+action+patterns+difference+reflex&source=bl&ots=TxaSYeIpTs&sig=RfsmHLWVlNiF8B-dH928-F0I5M8&hl=en&sa=X&ei=Bs1WUZeCFYiZtAbZ_IHYBw&ved=0CDcQ6AEwAA#v=onepage&q=fixed%20action%20patterns%20difference%20reflex&f=false

[3] http://www.grandin.com/references/genetics.html

[4] http://www.ornl.gov/sci/techresources/Human_Genome/elsi/behavior.shtml


Braquio-abduction illusion explanation and references Illusion: Lying down on a hard flat floor move arms up and down (as when doing a snow angel) while keeping them touching the floor. While repeating it a few times the floor begins to appear concave, with the deepest part where the arms as perpendicular to the rest of the body.

Questions: What is the origin of this illusion?

My guess: I think it might be related to the arms being harder to extend towards the back when they are perpendicular to the body than when they are at other angles.

Note: The name above is only the way I like to call it. I found this illusion when I was a kid, but I am sure others might have noticed it as well.

It may be because, when we move our shoulders towards our the body, also know as abduction (Fig 1.) gives the central part of the body an elevation. when we rotate our arms more upwards (Adduction), the elevation will be lost.

So in other words, when we are making snow angels,

Start Normal position (hands near thighs) = Back and shoulders on ground
Middle position      (hands in middle)   = Back elevated and shoulders on ground
Final Position        (hands upward) = Back and shoulders on ground again.

Due to this motion, it seems as if the ground become concave.

Source:

Anatomical Terms of Movement

Articulating the Importance of Joints in Anatomy


Sister chromatids during meiosis Sister chromatids

  $A)$ Cross over during prophase I of meiosis

  $B)$ separate during the first mitotic division

  $C)$ are produced during $S$ phase between cell divisions

  $D)$ cross over during prophase II of meiosis

  $E)$ are also called homologous chromosomes

My thoughts:

  $A$ is incorrect because it's nonsister chromatids that cross over
  $B$ is incorrect because they separate during the second mitotic division
  Don't know about choice $C$
  $D$ is incorrect because there is no crossing over during Meiosis II
  $E$ is incorrect because well...it's just not true

So is the answer $C$?

It is C. During S-phase the DNA of each chromosome duplicate and the two sister chromatids formed get attached by cohesin proteins. These sister chromatids separate at Anaphase-II of Meiosis.

From wikipedia:

  A sister chromatid refers to either of the two identical copies (chromatids) formed by the replication of a single chromosome, with both copies joined together by a common centromere. In other words, a sister chromatid may also be said as 'one-half' of the duplicated chromosome. A full set of sister chromatids is created during the synthesis (S) phase of interphase, when all the chromosomes in a cell are replicated.


What cells in mosses behave analogously to mammalian embryonic stem cells? The Washington Post article Ancient life awakens amid thawing ice caps and permafrost describes the work of Peter Convey, an ecologist with the British Antarctic Survey and his team, and includes a discussion of some mosses that have survived over 1000 years in permafrost, and sprung to life once "revived" in a laboratory setting.
This passage caught my eye:

It’s not easy to survive being frozen solid. Jagged ice crystals can shred cell membranes and other vital biological machinery. Many plants and animals simply succumb to the cold at winter’s onset, willing their seeds or eggs to spawn a new generation come spring.
Mosses have forged a tougher path. They desiccate when temperatures plummet, sidestepping the potential hazard of ice forming in their tissues. And if parts of the plant do sustain damage, certain cells can divide and differentiate into all the various tissue types that comprise a complete moss, similar to stem cells in human embryos.

What are these cells in moss called, and how similar are their functions to mammalian embryonic stem cells?

Convey and his team announced that they had awakened 1,500-year-old moss that had been buried more than three feet underground in the Antarctic permafrost. (P. Boelen/BAS)

The growing tips of roots and shoots contain regions of rapidly dividing cells in all plants that are called apical meristems. Apical meristems contain the plant's stem cells, which are not fundamentally different from the stem cells of animals.

You can begin learning more about this subject from this Nature scitable article.


In a fitness landscape, is fitness relative or absolute? I was asked if the fitness of a fitness landscape is absolute or relative.

Fitness landscapes are usually graphed with a fitness function that uses either phenotypes or genotypes in relation to fitness or one of its component.

More specifically, if the fitness measured is survival, and it's computed based on a quadratic model, does that means that every individual survival probability is an absolute measure of "fitness" (survival)?

Or since it's computed from a model, would it be better to find the relative contribution of a variable on the predictor in the model and say that the "fitness" is relative to a trait if it's computed with multiple traits?

How does the mean fitness of the population influence the model, which will determinate the fitness of all individuals? Is this "mean contribution of the population's fitness" a relative measure of fitness?

My specific questions are:

What type (relative vs absolute) of fitness is shown in a fitness landscape?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
When using a mark recapture model (you use the survival of each individual to find a fitness function) is the survival estimated by the model relative or absolute? Does the mathematical formulation of the model changes something?

In the image below, I've graphed all the points (black line) and I've removed the 3 lowest values of y for the 3 largest x values (red line). If I was calculating the fitness of the individuals with or without the 3 smallest points for the 3 largest x values, then the fitness of all the other individuals would be affected (except at x~38 and y~38).

x = c(1:100,101,102,103)
y =  c(x[1:100]+rnorm(100, sd = 6), 50,60,30)

x = c(1:100,101,102,103)
y =  c(x+rnorm(103, sd = 6))

summary(lm(y~x))
plot(y~x)
abline(lm(y~x),col = "red")
points(38,38,col="blue")

Another example with crossbills:

Would you say it's relative or absolute fitness. Here the fitness measure is "performance" of eating certain types of seed.

In this article they are saying (Morrissey & Sakrejda 2013):

  Regression analyses are central to characterization of the form and
  strength of natural selection in nature. Two common analyses that are
  currently used to characterize selection are (1) least squares–based
  approximation of the individual relative fitness surface for the
  purpose of obtaining quantitatively useful selection gradients, and
  (2) spline-based estimation of (absolute) fitness functions to obtain
  flexible inference of the shape of functions by which fitness and
  phenotype are related. These two sets of methodologies are often
  implemented in parallel to provide complementary inferences of the
  form of natural selection.

Are least squares-based approximation of the individual always computing relative fitness surfaces? For spline, is it always absolute values?

By experience, most of the time, authors are talking about relative fitness. To
confirm my feeling, I looked at the three randomly chosen theory papers from the first page of results that Google Scholar returned when searching for fitness landscape and they all use fitness as a relative measure. The papers are Derrida and Peliti (1991), Merz and Freisleben (2000) and Woodcock and Higgs (1995).

However, I do not think this is in the definition of a fitness landscape. One could work with absolute fitness and still call his model a fitness landscape. I think that therefore the answer is specific to every model considered. Note that even the "landscape axes" for which a fitness value is assigned can be of different nature. Typically, one can associate phenotypic or genotypic and/or even environmental axes.


Help me identify this insect from Bangladesh I have seen this insect flying literally everywhere in Dhaka city (Bangladesh) over the last two months. It's small -- around 1-1.5 inches long. It's not an agile flyer and can be easily grabbed by hand during flight.

This is actually the flying adult of a scale insect (superfamily Coccoidea). Specifically, this appears to be some species of the genus Drosicha.

Here is a picture resembling your specimen:

 Source: John Horstman

And another from Vietnam that looks very similar:

 Source: Dan Doucette

I can only find info on a closely related species, Drosicha corpulenta, and here's a tree of related species.

Scalenet provides numerous keys and references that could be useful for positively IDing this specimen.

I will keep searching for more details, but this might be the best you get without asking a scale insect expert.


T7 Tagging in Synthetic Biology What is a T7 tag and can if be used to purify synthesized proteins? Is it charge based like a His tag?

The T7 tag is the first 11 amino acids of the T7 gene 10 protein. Basically, if you engineer a protein with the T7 tag, you've engineered a small, known epitope to the protein of interest which may be detected immunologically. The small size of the epitope reduces the chance it will disrupt the protein's normal function (to which it's tagged). If we look at the affinity purification kit on the following product page we can see that specific vectors can be used to express T7-tagged proteins, and an immunoaffinity column can be used to purify the protein of interest. The T7 tag chemical structure is denoted here.


Why do Bee stings cause swelling? Why is it that when a bee stings, a little area around it gets swelled?

I think it is some sort of defense mechanism of the body.  But how does it help?

Bee, or other insect stings/bites, will cause a reaction to occur due to chemicals being released from your immune system.  This can result in anywhere from a small bump to anaphylaxis, which can be life-threatening if not treated right away.

From Southern Cross Medical Library:

  An anaphylactic reaction occurs when the body's antibodies respond to the insect venom by releasing chemicals such as histamine and serotonin that trigger the allergic reaction.

Whatever the reaction, it is correct to say that the reaction to an insect sting/bite is a defense mechanism of the body.  An interesting study done by Stanford University School of Medicine was done and discusses these immune mechanisms:

  Innate immune responses occur in subjects exposed to a foreign substance, such as a pathogen or a toxic material like venom, for the first time. [...] Immune cells called mast cells, which reside in most of the body’s tissues, are poised to unleash signals that turn on defense responses when a pathogen or toxin intrudes.  Prior immunization is not required for these types of innate immune responses, nor is the development of specific antibodies. In contrast, during an adaptive immune response, the immune system creates antibodies that can recognize the toxin or pathogen that is invading the animal’s system. Adaptive immunity is typically a faster, more specified and more effective form of defense than innate immunity, the research team explained.

More explanation of the non-specific immune response:

  If a bee stings you, the presence of the bee venom triggers a nonspecific immune response. White blood cells arrive first on the scene to rid the body of bee venom antigens. As war wages between antigens and white blood cells, battle signs may appear on the affected skin. Inflammation (redness, swelling, heat, and pain) results as the body wards off invaders.

  If the body detects an antigen that it previously met, a specific immune response occurs. In this response, the body has been trained to recognize and neutralize a familiar specific antigen; its immune system "remembers" the antigen. Such systemic (not restricted to the initial infection site) immunity enables a faster, longer lasting immune response than does a nonspecific response.

Therefore, these reactions to bee stings and other foreign toxins help us to better develop our immune system to protect against potential future encounters with these insects.


How exactly does a prion cause disease? During my study of the immune system,  I came across 2 very contrasting explanation as to how prions work.

Firstly, scientific American pointed out this:

link here:

  "A major breakthrough occurred when researchers discovered that the infectious agent consists primarily of a protein found in the membranes of normal cells, but in this case the protein has an altered shape, or conformation. Some scientists hypothesized that the distorted protein could bind to other proteins of the same type and induce them to change their conformation as well, producing a chain reaction that propagates the disease and generates new infectious material. Since then, the gene for this protein has been successfully cloned, and studies using transgenic mice have bolstered the prion hypothesis. The evidence in support of the hypothesis is now very strong, though not incontrovertible

However based on this website

  The guess was that they infected cells by causing normal prions to become misshapen, too. That theory, though, has been proven false, though it is still commonly believed. (See Sanctuary: Bad Bad Prions from Discover, dated 9 January of this year for an example of the ongoing belief.) The first serious attack on the prion-as-infectious-agent theory was reported in Medical Hypotheses in 1997. The article makes the case that prions trigger an autoimmune response.(1) As becomes clear the more one looks into the issue, this makes sense and fits the facts as known.

The problem right now is that my campbell 11th edition textbook, which is the newest edition and just recently revised also points to the same explanation as the first source.

Which source is correct in showing the method in which prions cause diseases?

I agree with commenter Martin Klvana, but there are a couple things going on here I wanted to touch on:

I think that your second quote is making an error in saying that if prions cause immune responses that means they aren't "infectious" in the sense of propagating misfolding of homologous proteins. The standard understanding is that prions work biochemically by refolding prionogenic proteins to make more infection prion particles (see e.g. wikipedia), similar to your source 1 and your textbook. It's completely possible that these newly infectious prion particles lead to immune reactions in additional to the "infecting" particle. The key here is to separate the biochemical phenomenon (propagated misfolding of proteins) from the medical phenomenon (disease, immunological response).
To more directly answer the question: as far as I can tell from scanning a couple of articles (here, here), immune responses are not a prominent part of the best-known prion diseases, but I'm not an expert and could be wrong. I was unable to easily locate the 1997 Medical Hypotheses paper referenced by your source 2.
I haven't looked deeply into this, but that website appears to be run by an advocacy group and the "read full article" link is broken. So... I would put less stock in that source. Advocacy groups are fine and all but I don't think that their blog posts are good sources of biomedical science information.

Hope that helps.


To have a drug travel to a specific place in the body can you just coat the drug in extracellular signals recognized by target cells? In a lecture of mine the professor was talking about the issue faced in regards to drug therapy when it comes to targeting lung cells in cystic fibrosis. It was said that if unless the drug gets targeted just for the lungs it could simply travel randomly throughout the body and thus not effectively treat the disease. My question is if cells internalize extracellular signals and travel/respond accordingly why can we simply not coat a drug for cystic fibrosis in extracellular signals that specifically bind to lung cell surface receptors?

Yes you can, in principle, coat the drug particle with ligands such that it will be targeted to specific cell types. This is being considered and actively worked upon for development of targeted drug delivery. However, you should also bear in mind that doing these kinds of coatings would be costly and it would greatly increase the cost of the drug.

At least, in the case of cystic fibrosis or any other disease of the lungs, an easy method of restricting the drug to lungs would be by taking the drug in the form of aerosol, using inhalers.

  Mechanism of inhalers.   Picture source: http://www.globalasthmareport.org/management/inhalers.php


Can we remove impacted teeth by key hole surgery? Can we remove impacted teeth by key hole surgery, rather than an open technique, like lithotripsy?

The impacted tooth is partially or fully enclosed in the bone. Even if accessed by a drill hole to reach the tooth. The tooth is too hard to be cut up into smaller sections with any of the conventional equipments available through an endoscope.

Tooth is a composite of three highly organized, mineralised tissues. The bulk of the tooth is formed by dentin and has around 30% organic content almost similar to that of bone. A large part of the organic content is collagen a tough fibre. Where as kidney stones etc are aggregates of minerals etc and are much more susceptible for pulverisation by shock waves from a lithotripter.

Besides an impacted tooth is either partially of fully inclosed in bone. So that too rules out the use of a lithotripter.


How to synthesize and isolate single stranded cDNA from an RNA template? I would like to have pure single stranded cDNA of my choice. I am thinking of reverse transcription from RNA (obtained by in vitro transcription), degrading RNA from RNA-DNA hybrid with RNase-H, heating to 65C to remove any oligoribonucleotides still bound to DNA and pass the solution through G50 sephadex column buffered with elution buffer. This is what I have in mind but are there any efficient ways that are tried before? Or do you have any suggestions over this protocol?

Sure that will work, or gel purify the ss cDNA, or treat the rxn with alkali to degrade RNA.  The real questions in my mind are:

What will you use as a primer for the RT?
What are you going to do with this pure ss cDNA?

If you already have the target cloned (how else would you transcribe it in vitro?), then why not just do a linear PCR where you cut the plasmid to linearize it at the site of your choosing, and then throw it in a PCR machine with just one primer?

Why bother going through the T7 RNA pol and RT steps (if you don't need to)?


Is humans' height ideal? More or less we humans are around 1.70 meters tall.

My question is, would it be possible to scale us? that is, is it in principle possible having humans 1 cm tall, or 10 meters tall or is there some reason that makes our height somehow ideal?

Humans can, to some extent, be scaled: While most humans are two meters tall; the human body essentially works throughout the entire range from around a meter to around two and a half meters, although you tend to run into problems at the extremes.

However, outside of that range you run into the tyranny of the square-cube law:

As you scale a creature (or, in fact, anything), it's mass increases proportionally to the cube of the scale, while its surface area increases proportionally to the square of the scale.

This means that as you scale humans down, their mass, and hence their ability to generate heat would drop faster than their skin area, and hence their ability to dissipate heat; meaning that if unaltered, smaller humans would rapidly run into problems of freezing to death.

(Small animals typically solve this through a number of methods: Higher metabolic rates, rounder bodies, and more fur. Small humans, i.e. babies also suffer under this, and solve it by having what is typically referred to as "baby fat", a blubber that, among other things, aids thermoregulation.)

Similarly, as the human body is scaled up, the opposite problem arises: The body becomes unable to dissipate heat quickly enough. Larger animals solve this problems with giant organs specifically suited to radiate heat, such as elephant ears; or through submersion in water, as seen is cetaceans and hippopotamuses; or simply through living in cold climates, such as the polar bear. (All of this is typically augmented by lower metabolic rates.)

Heat economy isn't the only problem with size, however:

Especially when scaling up, the strength of various structures in the body become problematic. Unusually (yet not even freakishly) tall humans generally have some manner of bone problems, and also often have problems with too small hearts, leading to low blood pressure, or too big ones, leading to heart failure.

If the change was gradual enough, with sufficient adaptation, this wouldn't necessarily be a problem. After all, giraffes and elephants get on perfectly well; but a pump-valve heart such as we have cannot be scaled up indefinitely.

With a continuous-flow heart, this limit could probably be stretched, but how that would even begin to work biologically I have no idea.

Further problems with very large humans include getting enough air flow through the lungs, the enormous chore it would be to stand up or sit down, and of course, just getting enough food to drive the enormous body.

The long and short of it is: Anything less than about half a meter would probably leave us freezing to death; and anything more than two and a half meters is quite frankly a stretch (if you'll pardon the pun).

(There are people alive now that are more than two and a half meters tall, but they are not generally speaking in good health, although some do get on.)

Of course, all of this is predicated on the specific gravitational and atmospheric conditions on Earth.

On another planet with a greater or lesser gravity, a different proportion of oxygen in the air, or just a denser atmosphere; many of these limits and limitations would be quite different indeed. (Which is why whales, living in such an alien world as the sea, can be an order of magnitude bigger than any animal that lives on land.)


What species is this rabbit-like animal? This image was included in something I was browsing through.
It reminds me of my lion head rabbit, but the head shape doesn't match.
Is this some kind of Siberian wild rabbit?

Thanks to @Satwik's tip about google image search, I was able to figure out that the animal in question is a Viscacha. Though the source answer is thanks to reddit, so take that as you will.

  Viscachas or vizcachas are rodents of two genera (Lagidium and Lagostomus) in the family Chinchillidae. They are closely related to chinchillas, and look similar to rabbits, apart from their longer tails


How does the tRNA recognise the first methionine during translation? The process of translation starts with the initiator tRNA identifying the codon coding for methionine (AUG). However my textbook also says that there are various untranslated regions present on the mRNA. It was then this question had occurred to me.How does the tRNA actually differentiate between the regions that are ought to be coded and that are not ?One may say that translation always start with the methionine; but my question is different.For example,if the code is
5'...GUAUGCAUGAUC...3'
then when the tRNA arrives it reads from which of them? Does it leave the first two nucleotides and read it as AUG CAU GAU and so on or does it leave out the first six nucleotides and read it as AUG AUC and so on?

There are different processes for recognising the initiator site in prokaryotes and eukaryotes.

In prokaryotes the process relies upon the Shine-Dalgarno sequence, this is a well conserved sequence throughout prokaryotes found upstream of the start codon. It interacts with the 16s ribosomal RNA to place the initiator codon in the A site of the ribosome.

In eukaryotes the process is somewhat more complex and relies upon a large protein complex which assembles on the 5' cap of mRNAs. This complex mediates an interaction between the mRNA and the ribosome, the ribosome then scans (using GTP for energy) 5' to 3' to detect the start codon.

One final process which is unusual but does occur is cap independent initiation mediated by internal ribosome entry sites (IRES). These are sequences which form structured loops which can mimic the interactions usually formed by the cap complex. These sequences appear in viral mRNAs allowing viruses to bipass anitviral mechanisms in cells.

You will need to do some reasonably extensive reading if you want to uderstand fully these processes and how they may be manipulated by cells to alter expression.


What is the state-of-the-art algorithm for multiple sequence alignment? Which algorithm or algorithms are considered the standard or state-of-the-art for multiple sequence alignment?

How big is the need for better algorithms? How many sequences need to be alignment in a typical test? I am trying to understand how important problem this is in bioinformatics.

My Vote goes to Mafft(insi) as it have ~86% accuracy and results in ~1.2 hour. Though fastest will be kalign takes only ~3 minutes to finish with an accuracy of 74.3%.

For testing:

  For each of the 218 reference alignments in the benchmark, we applied
  eight alignment programs, resulting in a total of 1744 automatically
  constructed MSAs. The overall quality of these automatic alignments
  was measured using the Column Score (CS) described in Methods.

FIGURE 1: Overall alignment performance for each of the MSA programs tested.

(A) Overall Accuracy

(B) Total run time for constructing all alignments (a log10 scale is used for display purposes).

doi:10.1371/journal.pone.0018093.g003

Compared Tools

http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0018093.t001&representation=PNG_L

Source and Photo Credits:

A Comprehensive Benchmark Study of Multiple Sequence Alignment Methods: Current Challenges and Future Perspectives

PS: This is from an old paper of 2011. If you want the new statistics you can always test on your own, by the process described in the source paper.


Cysticercoids of Eucestoda I have found the following pictures representing cysticercoids of Eucestoda.

If I correctly understand the right part of the picture, I would say that the development of the scolex is portrayed on the right, as the formation of what I think to be two acetabula shows. Nevertheless, with respect to the images on the left, it is totally unclear to me, since the text says nothing about it, what the structure that seems to be encapsulating the animal is.

I know that cysticercoids develops from an oncosphere, but I do not know whether that sort of capsule that seems to be enveloping the animal is a part of what was the oncosphere's tegument -the embrionophore- that it can have gone out of and is entering again...

Does anybody reading this question know more about it? I thank you very much for any answer!

I would say that the left part of the picture depicts 2 stages of the development of cysticercoid, while the right part shows the consecutive stages in the development of cysticercus. These two parts represent different species of tapeworms in the same stage of their developments.


Is PCR a DNA cloning technique? According to Genomes

PCR is

  A technique that results in exponential amplification of a selected region of a DNA molecule [in test tube].

DNA cloning is

  Insertion of a fragment of DNA into a cloning vector, and subsequent propagation of the recombinant DNA molecule in a host organism.

While, Molecular Biology of the Cell, Sixth Edition says in a summary:

  DNA cloning (through the use of either cloning vectors or the polymerase chain reaction) in which portion of a genome (often an individual gene) is purified away from the remainder of the genome by repeatedly copying to generate many billions of identical molecules.

Here DNA cloning has been used to mean DNA replication in general.

Question: Which author's view is correct, or at least provides the most accepted definitions?

Short answer
All of your sources are correct as they are not mutually exclusive. PCR is used to isolate and amplify DNA to yield small quantities of pure target product. Gene cloning can subsequently be applied to scale the production of the fragment up. PCR thus can be part of the DNA cloning process.

Background
Cloning in general simply means duplicating. Cloning in Biology refers to

  [Making] an exact copy of an animal or plant created in a laboratory from the
  animal’s or plant’s DNA

source: McMillan Dictionary

Gene cloning, as far as I understand refers specifically to the isolation of one single gene and inserting it into cells to amplify it:

  The production of a lineage of cells all of which contain one kind of DNA fragment of interest derived from a population of many kinds of DNA fragments.

source: Northwestern University

PCR is a technique to amplify a specific strand of DNA that can be used to subsequently clone DNA into host cells (source: New England Biolabs). The cloning is done to upscale the quantity of DNA. PCR uses primers and can be used to isolate and amplify the DNA up to the scale it is easily clonable.


What specific mutations can cause an apoptosis mechanism to malfunction? What specific mutations can cause the apoptosis mechanisms in a cell to malfunction? Are any such mutations 'reversible' , somehow or are they generally permanent? what kind of mutations can happen without disrupting the apoptosis mechanisms?

There are lots and lots of specific single mutations that cause problems with apoptosis.

Some of the most common are in P53, PTEN, MYC, APC, and KRAS. If you want a specific amino acid change, KRAS G12D is particularly potent. It works by disabling a regulatory domain and causing KRAS to be constitutively active.

These aren't "reversible" in a strict sense (except, I guess, for the struck-by-lightning-while-holding-a-winning-lottery-ticket level improbability of a second replication error in the same place back to the original base) but in many cases the cells will upregulate compensatory pathways or activate senescence pathways instead, rather than instantaneously becoming full-blown malignant.

As for mutations that don't cause disruptions to apoptosis,there are almost an infinite number, in that silent mutations or mutations to genes that aren't involved in apoptosis would count.

If you mean what kind of non-silent mutations can happen to genes that are important to apoptosis without causing problems, there are still a lot: swapping similar amino acids in non-active parts of proteins are unlikely to have huge effects.


Can platypuses communicate via electroreception? I know at least some electroreceptive fish are capable of basic communication with other members of their species via varying their own bioelectric signals.  However, I can't find any information as to whether platypuses (or, for that matter, any of the handful of other electroreceptive mammals) are capable of communicating in a similar manner.  Does anyone know if they're able to do this?

Electrocommunication is used by weakly electric fish only and it is limited to aquatic environments where the electrical conductivity of the medium allows to transmit electric signals. The best studied fish species that use this communication method are The African Mormyriformes (which comprise the Mormyridae or elephantfish and the Gymnarchidae with Gymnarchus niloticus as the only species) and the South American Gymnotiformes (or Neotropical knifefish).[1]

The mammals that are capable of electroreception use it for passive electrolocation which means locating the prey by detecting the weak electric fields of the prey with electroreceptors. These mammals are the three living species of monotreme; the Australian duck-billed platypus (Ornithorhynchus anatinus), the Australian short-beaked echidna (Tachyglossus aculeatus) and the Western long-beaked echidna (Zaglossus bruijnii) of New Guinea; and more recently discovered, the Guiana dolphin (Sotalia guianensis) from the cetacean order.[2][3]

Note: Electroreception was reported in star-nosed mole, Condylura cristata, based on limited behavioral data (Gould et al., 1993) but the theory remains unexplained physiologically.[4]

The electrosensory system of platypus (and probably other mammals) is evolved independently and the electroreceptors belong to the trigeminal system. The physiology of the electosensory system of mammals reveal why they can't use their electroreception for conspecific communication.

  In African mormyriform and South American gymnotiform fishes this sense has evolved to an additional active system using an electric organ as a source for a.c. impedance measurement of the environment and for communication. All electroreceptors found in fishes and amphibians that do not have electric organs are of the ampullary receptor type and probably form part of the acoustico-lateralis system. In contrast, the electroreceptors in platypus belong to the trigeminal system. Their sensitivity to d.c. as well as to high-frequency pulses [2] contrasts with the mostly d.c. or lowfrequency responsiveness of ampullary receptors, which are less well-adapted to detect rapid muscle action potentials.

  Langner, Gerald & Scheich, Henning. (2009). Electric Senses in Monotremes: Electroreception and Electrolocation in the Platypus and the Echidna. 1056-1060. 10.1007/978-3-540-29678-2_2919.
  https://www.researchgate.net/publication/299656487_Electric_Senses_in_Monotremes_Electroreception_and_Electrolocation_in_the_Platypus_and_the_Echidna

References:

1. Map of Life - "Electrolocation and electrocommunication in weakly electric fish"
http://www.mapoflife.org/topics/topic_578_electrolocation-and-electrocommunication-in-weakly-electric-fish/
January 24, 2018

2. Passive electroreception in aquatic mammals.
Czech-Damal NU, Dehnhardt G, Manger P, Hanke W.
https://www.ncbi.nlm.nih.gov/pubmed/23187861

3. Electroreception in the Guiana dolphin (Sotalia guianensis)
Nicole U. Czech-Damal, Alexander Liebschner, Lars Miersch, Gertrud Klauer, Frederike D. Hanke, Christopher Marshall, Guido Dehnhardt, and Wolf Hanke
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248726/

4. Edwin Gould, William McShea, Theodore Grand; Function of the Star in the Star-Nosed Mole, Condylura cristata, Journal of Mammalogy, Volume 74, Issue 1, 19 February 1993, Pages 108–116, https://doi.org/10.2307/1381909

Further reading:

1. Electroreception (edited by Theodore Holmes Bullock, Carl D. Hopkins, Richard R. Fay)

2. Neurobiology of Monotremes: Brain Evolution in Our Distant Mammalian Cousins
(edited by Ken Ashwell)

3. Sensory receptors in monotremes ( Proske U, Gregory JE, Iggo A.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692308/

4. Electroreception in monotremes (John D. Pettigrew)
https://jeb.biologists.org:2083/content/jexbio/202/10/1447.full.pdf

5. Perceiving in Depth, Volume 3: Other Mechanisms of Depth Perception (By Ian P. Howard)

6. Electroreception and Electrogenesis (James S. Albert and William G.R. Crampton) http://www.ucs.louisiana.edu/~jxa4003/Albert%20PDF%27s/Albert-Crampton-Electroreception-proofs.pdf


Are there specific non-protein substances that pathogens release into their host? Reading research articles, I have found out that proteins called effectors get released into the host cell when a pathogen attacks a host. My question is, whether pathogens also release non-protein substances?

Have these substances been extensively studied and classified? Is there a list of such compounds? Are these compounds unique to pathogens?

Sticking my neck out (and expecting it to be bitten by a black swan) it appears that all the examples of toxins secreted by bacterial pathogens when they infect an animal host (exotoxins) are proteins.

However fungi secrete a variety of exotic (and often very nasty) small non-protein molecules (mycotoxins). It’s not clear from the question whether you would be interested in these systems as they differ somewhat from those involving bacteria. One difference from bacterial toxins is that fungal toxins not secreted inside an infected cell, but just into their environment. Thus, cercosporin is secreted onto the surface of plants on which Cercospora reside and may be taken up through lesions in the plant. However it is not clear whether the plant is the main target of such toxins, rather than bacterial ‘foes’. So the host/pathogen concept is less clear in this context.

A similarly ambiguous host/pathogen situation would appear to exists with toxins such as saxitoxin, the paralytic shellfish toxin secreted by certain marine algae and cyanobacteria.


How to surpass cell death? Is it possible to surpass/decay cell death.  For example to disable the process muscles cells death, by tweaking the transduction pathways:

If it's not possible in our age Medicine, what it would take to do such thing in theory. The idea is to tweak the cell dying mechanisms for example to preserve neural and muscle cells for longer time. I am also curious how to disable a pathway or part of it.

Yes; It is possible to inhibit cell death.

There are several possibilities, of which many - as correctly recognized by you - involve changes in the activity of the cell death pathway (or related ones);

For a long (but still incomplete) list of commercially available drugs that inhibit cell death, please see: https://www.sigmaaldrich.com/life-science/cell-biology/cell-biology-products.html?TablePage=9559839

P.S.: Note that selectively inhibiting a pathway (note: not only cell-death) in only one cell type (or tissue - as you hinted at) usually requires a lot of tests and experimentation and isn't trivial.


Why are superantigens not "MHC-restricted", and what's the significance? MHC restriction is the requirement to recognize an antigen in association with a self-MHC molecule; CD4+ cells can only respond to an antigen if it's presented with a self-MHC II molecule, and the same goes for CD8+ cells and self-MHC I.

Various sources say that super antigens require an MHCII+ antigen presenting cell to activate a T-cell, but they're not MHC-restricted. I've found one "clarification" on what this could mean, and it's that various MHC II molecules can present a superantigen. Does this mean that MHC II from different hosts can activate a clone of T-cells if a superantigen is involved? What's the significance of that in a single host, e.g., someone infected by a microbe that produces one of these things?

Normal, "non-super" antigens activate T-cells in the following manner: they are first engulfed and processed by a professional antigen presenting cell (APC), e.g., a macrophage. The processed antigen is then presented along with an MHC class II molecule on the surface of this cell. The T-cell's T Cell Receptor (TCR) then binds this complex; it must be able to recognize both the MHC class II and the antigen, and in addition to this "main signal" other co-simulatory signals are also needed. The important thing to remember is that a T-cell will only react to a specific antigen it's specific with when it's present with an MHC class II molecule it can recognize. This is known as MHC restriction

A person has 3 genes (each having 2 alleles,for a total of 6 alleles) for MHC class I: HLA A, B and C, and 3 genes for MHC class II: HLA DR, DQ and DP. These alleles are highly polymorphic, i.e., varied, with each of these 6 genes having hundreds or thousands of different alleles, and the combination of alleles differs from individual to individual; it's very unlikely that two people who aren't identical twins would have the same combination of HLA alleles.

MHC molecules can only bind peptides, and in addition, they cant bind ALL peptides; of all the peptides that can possibly be bound by an MHC molecule, a particular MHC molecule can only bind a select number of those peptides. Different MHC molecular forms, be they class I or II, can bind, and thus present, a different set of peptides. Having different HLA alleles at your immune system's disposal means there's a larger pool of possible peptides your APCs can present with the different MHC class II isoforms they have, allowing defense against a larger pool of antigens.

A normal antigen has 2 "restrictions" on its ability to activate a T-cell clone: it must be presented by an MHC class II isoform that can bind it, and it must be recognized by a T-cell with a compatible TCR.

Superantigens activate T-cells in an unconventional manner: They have a domain that binds to the TCR, though not at the usual antigen binding site, and a domain that binds to the MHC class II molecule, but not in the usual peptide-binding site these molecules possess. Since it binds outside of these regions that are specific to particular molecules, they're not restricted by the antigen specificity of the TCR nor are they restricted by the MHC class II isoform they're utilizing. Hence why, even if they do need MHC class II-positive cells to be able to activate a T-cell clone, they're not MHC-restricted.

Readings:

Immunobiology by Charles Janeway, Sections 5-13, 5-15 and 5-16.


Are there any animals that are unable to hear the human voice? Humans and animals have different hearing ranges. The frequency range of a human, for example, is stated with 20 Hz to 20 kHz, whereas the fundamental voice frequency is stated with 125 Hz for men, 250 for women and 440 for children.

Now if I understand correctly, the hearing range of bats, for example, is commonly stated with 1 kHz to 200 kHz (depending on species). The hearing range of mice is stated with 1 kHz to 70 kHz.

Are there (apart from those with no sense of hearing at all) any animals that are unable to hear human voices at all?

(Edited in reaction to the first and the second comment below. Humans can obviously realise speech with energy at much higher frequencies. My examples are in this respect misleading.)

Are there (apart from those with no sense of hearing at all) any
  animals that are unable to hear human voices at all?

I don't know of any examples off the top of my head, but let's think about this systematically.

The voiced speech of a typical adult male will have a fundamental frequency from 85 to 180 Hz, and that of a typical adult female from 165 to 255 Hz.

These are fundamental tones, and DO NOT include overtones (harmonics) of higher frequencies, that are actually responsible for the timbre of the voice, i.e. its characteristic sound and full content sonic content.

Here is a Fourier transformation of an audio clip of a female voice (a plot of frequency vs. amplitude, whereby the original recording was broken down into its constituent sine waves).

As you can see, the vocal cords produce overtones up to - and beyond - 7.5kHz. These overtones theoretically go to infinity in frequency, but are very negligibly quiet past around 10kHz in our case. Certainly very low in terms of decibels (though do not confuse real decibels with the -70dB sensitivity on the graph; with audio processing gear, 0dB is at which the signal is maximally saturated, or 'clips'). Let's assume 10kHz is the upper limit for normal female speech.

Keep in mind this does NOT mean that one could not perhaps sing a high note, and produce overtones past 10kHz - this is in fact doable. But let's stick with regular speech in our case.

Below you'll find the hearing ranges of some animals (source).

You'll find that all animals listed (save one) can hear some significant range of a regular (female) human voice. The little brown bat would not be able to hear the upper harmonics of a typical female speaker, given that they speak in a monotone.

Lastly, please keep in mind the difference between decibels ('loudness') and frequency (ability to sense a pitch). Some of the extreme high overtones are very quiet, so even if an animal would be able to sense them, they may not have a sensitive enough ear to pick up how quiet these sounds would be.

And really lastly, remember that sound produces vibrations and resonates through objects that sound waves hit. These resonate at different frequencies, so your voice can be sensed indirectly too through these resonating frequencies.


Help in identifying an unknown arthropod I'm not even sure it's an insect:  the best I can do is identify it as an arthropod.  I captured this slow-moving organism and after a period of observation under high magnification, I concluded that it appears to construct a "shell" from miscellaneous particles or debris.  With a scalpel, I carefully cut this outer casing open to observe the organism, and the pictures show what I found.  It seems to have six legs, like an insect, but is oddly worm-like and wingless.  Total length is approximately 1 cm.  I do not believe that this is a juvenile/larval/instar form.  I've seen several of these where I live, and they always look like this (with maybe a +/- 20% size variation).

Edit:  This specimen was found in San Diego County, California, United States.

It is the larva of household casebearer moth (a Lepidoptera), named after the larval stage. It is scientifically called Phereoeca uterella.

It is found through out South and North America.

  The larva constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings.

References:

Wikipedia
bugguide

Further reading: Household Casebearer, Phereoeca uterella by
Juan A. Villanueva-Jimenez and Thomas R. Fasulo


Is my terminology for proteins correct? Statement: Protein X consists of 20 amino acids.

Question 1: Is it necessary to write "Functional" Protein X or is it already implied, that it is functional?

Question 2: Referring to question #1 - Does "Active," "Functional", "Native", "Mature," and "Stable" all serve as the same as synonym?

Question 3: How would I refer to the 16th, 17th, 18th, 19th amino acids?

Option 1: AA-16 through AA 19
Option 2: (Subscript) A16A17A18A19
Option 3: The 16th through 19th amino acids ...

1) I don't think so. I would not assume functionality.

2) People may diverge a bit on the semantics, but here's what I would say (my background is more cell bio and structural bio than biochem or genetics).

Active - Has enzymatic or signalling activity (or some other functional capability). Often proteins have multiple activities, or different active sites, so activity should be with respect to a specific function.
Functional - I interpret this to mean has all of its native activities intact. (I don't take this to mean anything structurally). One could also use this as a synonym for active, especially for a specific functionality.
Native - I take this to mean the protein has not been altered from its form found in nature. This implies it is functional.
Mature - My natural feeling for this is that it means the protein is structurally mature, i.e. it has been folded properly, transported to the correct cellular compartment, post-translational modifications completed, etc... For a non-functional mutant protein, I would hesitate to call it mature though, even if it were not semantically incorrect.
Stable - I interpret this entirely structurally. i.e whether the protein has folded to an energetic minimum or their natural structural state (incl. proteins with disordered domains). People might say, though, that stable means it has a natural lifetime, i.e. the cellular environment or the enzymes present are not destroying it at an abnormal rate.

I'm not quite sure what (3) is asking; if you edit, maybe I can comment.


Is there is difference between "homozygosity" and "homozygosis"? Are these just two terms for the same phenomenon, i.e., the state of being homozygous? Merriam-Webster says so, but I know dictionaries sometimes miss the nuance of scientific terms. If they are indeed synonyms, it seems homozygosity has won out, according to Ngrams

Homozygosis and homozygosity are NOT synonymous. The two terms refer to the same concept though.

Homozygote

An indivdidual or a cell is said to be homozygote for a particular gene (or any DNA sequence) when identical alleles of the gene are present on both homologous chromosomes. (Wikipedia > Zygosity).

Homozygosis

Homozygosis is the state of being homozygote (Wright 1933) for a particular gene (or any DNA sequence). According to freedictionary.com, homozygosis may also refer to the process of formation of a homozygote. I have never encountered this sense in the literature though. As you found out by yourself, Homozygosis is a term that is rarely used in the literature (in comparison to homozygote and homozygosity)

Expected Homozygosity

Expected Homozygosity is the probability of two randomly sampled alleles (in a population and at a given locus) to be identical by descent.

Expected homozygosity and Expected heterozygosity

As shown in Nei 1973, the mathematical expression of expected homozygosity $Ho$ is

$$Ho = \sum_{a=1}^{n} x_a^2$$

where $n$ is the number of alleles and $x_a$ is the frequency of the allele $a$.

It is more common to use the concept of expected heterozygosity $He$ (a.k.a. gene diversity) rather than the one of expected homozygosity $Ho$. By definition, $He=1-Ho$, that is

$$He =1- \sum_{a=1}^{n} x_a^2$$

In the special case of a bi-allelic locus, and replacing the two allele frequencies $x=1$ and $x=2$ by $p$ and $q=1-p$, the above formulations becomes

$$Ho = p^2 + q^2$$
$$He = 1 - (p^2 + q^2) = 2pq$$

Hardy-Weinberg equilibrium

Under the Hardy-Weinberg assumptions, the observed frequency of heterozygote (a.k.a. observed heterozygosity) is equal to the expected heterozygosity and observed frequency of homozygotes (a.k.a. observed homozygosity) is equal to the expected homozygosity.


Carrying out a BlastP on ORF and achieving hits but 2 have the exact same score, evalue and query cover? I'm working on a project in my university and we were all given different sequences to work off of. I am meant to compare my blastN to my blastP result. However, when I carried out my blasP I got many hits but the top 2 hits had 100 percent cover, 100 percent identity and 0.0 evalue. I am meant to work off of one of the species I achieved from blastp to compare to blastN. How do I know which one to compare to see what's most significant to my blastn species? I have to continue on and use clustalw and phylogeny after so I need to be sure.

If I understand it correctly, you have two subject protein sequences that are exactly the same as your query. You say they are different species, so I guess you made sure they are not the same species and different strains, or subspecies.

I would suggest to now query your nucleotide sequence using blastn against both results (since a priori it could be either species, or neither), and focus on the one that gets a higher score using blastn in your phylogenetic analysis. Due to codon degeneracy, it could be that your blastn results differ between the two.


Why do proteins targeted for chloroplasts require two signal peptides? Question #11 of the GRE Biology Practice Test says that proteins targeted for chloroplasts require two signal peptides:

Targeting of a newly synthesized protein is most likely to require two different signal peptides for which of the following destinations?

(A) Plasma membrane

(B) Lysosome

(C) Cytosol

(D) Chloroplast (Correct Answer)

(E) Endoplasmic reticulum

I can't find a reference for this.

I understand that a ribosome starts the synthesis of a protein in the cytosol and a signal peptide takes that to the endoplasmic reticulum (ER) which finishes protein synthesis in the ER lumen and then the protein is secreted in a vesicle to its destination (if it doesn't become an ER membrane protein). What's the purpose of the second signal peptide to enter a chloroplast?

Protein import to chloroplasts (and also mitochondria) can still have multiple destinations, because these structures themselves have sub-compartments:

both have an inter-membrane space as well as an 'inner space' (the stroma in chloroplasts, matrix in mitochondria).
proteins can also be targeted towards either of the two membranes
additionally chloroplasts have the Thylakoid stacks in the stroma which are separated by another membrane layer.

Due to this complex structure you need multiple signal peptides to properly target proteins to their destination.

I don't remember (or can find) all the details now but basically you (can) have:

a 'main' signal peptide that targets proteins directly towards the stroma (which will be removed there by the stromal processing peptidase (SPP)).
an additional signal peptide for import to the the thylakoid stacks (which will be 'made avaibalble' by cleavage of the first peptide)
there should be other signal peptides or at least variants that allow import to the intermembrande space and the inner membrane (via the TIC23 complex). [I couldn't find any sources for this right now]

Sources I could find:

TIC/TOC complex in wikipedia
in-depth scientific review


How exactly are genes swapped during the process of recombination? I am studying recombination in Meiosis and the idea of crossing over doesn't make sense. My understanding is that 46 chromosomes in our germ-cell (23 from mom + 23 from dad) line up next to each other and recombine (swap areas of DNA). My confusion is that, since, for example, Chromosome 1 from mom is same as Chromosome 1 from dad, how is swapping areas of DNA going to exchange any information. Brown eye gene from dad would just be swapped with brown eye gene from mom. How will have any affect on the offspring? OR is it that if mom has brown eyes, the brown eye color gene in mom has something attached to it?
OR is my understanding of genes incorrect and not every nucleus has all possible genes? (except the difference of X and Y chromosome.)?

There is quite a few misunderstanding in your question. So, I'll shortly give you some (simplified) definitions and then point you to another post.

Definitions and Basic Concepts

A locus (plur. loci) is a position along a chromosome. A some loci, there are  genes. To make things easy a gene is any sequence which is transcribed into RNA and translated into proteins.

Now at any locus, you might see different individuals having different variants. For example an individual may have the sequence ATTCT while another individual may have the sequence ATTGT. Those different variants are called alleles. It is key to understand that there is genetic variation in populations. This genetic variation is a big part of the reason why people around you look different and why you ressemble more your siblings (if you have any) than a random person in the population.

How does recombination have any impact?

To understand the effect of recombination you necessarily have to picture a several loci model. As you now understand the above definitions you will find your answer at this post: Why do we need two markers to measure a recombination rate?

Further readings

The following posts will also be of interest to you:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Chromosome and chromatid numbers during cell cycle phases


Why does the amount of adipose tissue contribute the most to the total body water amount in humans? I don't quite get this concept. An obese individual will have a greater fat content in their body, and thus will have 45% water in their bodies (for example), versus a slim person that will have 75% of body water and a much lower fat level.
Is this because fat is made up of about 10% water, so the more fat you have in your body, the more water it "takes up" from the entire body water supply of your body?

Fat mass does not take up water.  It brings with it less water percentage than lean mass and so a person with more fat mass will have relatively less % body water.  Additional mass as fat contributed relatively less water than additional mass as lean tissue.

Consider a 50 kg individual who is extremely lean.  From your numbers, if this individual is 75% water (will will assume lean tissue is 75% water) that is 50 * .75 = 37.5kg water and 12.5kg nonwater body mass.

Now this 50 kg individual puts on 50 kg of fat.  The fat is 10% water (from your numbers) so an additional 10 kg of water.  This individual its now 47.5kg water and 52.5 nonwater; since this obese person weighs 100 kg now she has 47.5% water, similar to your example.

Suppose instead your 50kg person grew up into a 100 kg performance athlete.  Still no fat.  She is still 75% water because the lean tissue has 75% water.

It has to do with the % water each type of body mass brings with it.  This is with no special knowledge; using just the numbers in your example which is what your professor wants you to use.


Why are 3 nucleotides used as codons for amino-acid mapping in DNA? DNA is made of 4 unique nucleotides. When coding for a protein, a sequence of 3 nucleotides is used to code for each amino acid. Why are codons 3 nucleotides in length?

A related question can be found here: why-are-there-exactly-four-nucleobases-in-dna

The central dogma of molecular biology: DNA makes RNA makes Protein

DNA is a reference for proteins*, which are the functional molecules in cells. These are comprised of 20 unique amino acids, and each is coded for by a stretch of DNA known as a codon. Codons are always 3 base-pairs (nucleotides) in length.

DNA is made of 4 unique nucleotides; (A)denine, (G)uanine, (C)ytosine and (T)hymine. This means that there are 64 unique codons that can be made with these 4 bases (4*4*4).

Theory One - evolvability

If codons were only 2 bases in length then the variety of codons that could be created would be less (only 16 unique sequences if there are still 4 nucleotides). More unique nucleotides would be required to get enough unique sequences to code for the 20 amino acids (as well as the STOP codons). For instance, to get 64 unique sequences using a 2-bases-per-codon system there would need to be 8 unique nucleotides.

We cannot ever 'know' what happened in evolutionary terms, but it seems likely that the 3-base (nucleotide) codon system would have arisen after a period of a 2-base system, as the biological systems became more complex. This would have allowed a lot more variation in the amino-acids used, and thus more "evolvability", which would have been very advantageous to early organisms.

However as the 4-unique-nucleotide/3-codon system is ubiquitous to all life we have discovered on earth, it seems likely that, back at the start of DNA (in fact probably RNA), this was the system that worked, or at least, this is the one that survived (although as Kevin rightly points out, we don't know whether there ever were any other systems). Variations may have arisen over the years, but it is this 1 system that has prevailed here on Earth.

See this question for some more interesting info: why-20-amino-acids-instead-of-64?

Theory Two - "redundancy" of codons conveys additional information

This theory is not mutually exclusive to the one described above. In a recent paper D'Onofrio and Abel [1] state that ribosomes pause for different lengths of time at different codons (even if the codon codes for the same amino acid), and that this pausing affects the 3-dimensional structure of the final protein.

Therefore the nucleotide sequence contains at least two "layers" of information: firstly which amino-acid should be added, and second the specific codon used for that amino acid can impact on the final structure of the protein. This could not be done with fewer nucleotides, but arguably even more control could be exerted with more nucleotides, but perhaps this comes back to my first point that this system evolved such a long time ago that more nucleotides were not necessary for life to "work" and proliferate into everything we see today.

D'Onofrio and Abel, 2014. Frontiers in Genetics. Redundancy of the genetic code enables translational pausing

*only around 1% of our genome is actually protein-coding, and many non-protein-coding RNA products have very important functions, but I won't go into this here. Suffice it to say I am referring to the protein-coding regions of the DNA.


Metrics or operations on genome sequences in human genomic research? Edit distance may be an important metric for measuring the similarity of two genome sequences.  For example, if A = GCAATT and B= CGAATA, then the edit distance of A and B is 3. Such a metric is intuitive and may be useful in comparing the similarity of two sequences.

I wonder is there any more complex or advanced metrics used in human genomic research?

The question of how similar two DNA or protein sequences are, is one of the most important problems in bioinformatics. While there is no definitive answer Bayseian statistics are often used to group sequences. There is a good explanation of the theory on this wikipedia page.

Alternatively one of the most commonly used programs to find similar sequences is BLAST. It is getting a little bit dated but you can find an overview on the statistics used by this program on this page

But there are many other methods out there.


Possible moth identification There's a flying insect being caught indoors today in Sydney Australia. Before it is being caught, it basically flies like a moth. However googling of Tinea pellionella and other cloth moths does not suggest it is a cloth moth as hair is missing from its very small sized head.

It is also known to be very common every year when spring approaches in australia

To assist identification, the bug was caught in a plastic jar to allow multiple angles of it to be photographed

Measured body length (not including long antennae): 1.1 cm
Color: Brown an golden brown with lustre
Legs: 6 (front pair very short, middle pair is forked, hind legs have some golden brown feathery structure)
Head is black, very small and have no hair

Here one can easily see the hindlegs are covered by some bristle like golden brown feathery structures, and also its shiny golden segmented abdomen

The camera is not fast enough to capture it unblur when it is flying, but the few moments when it opened its wings can be seen here extracted from a video

And these are our best shots using the iphone camera in capturing its flight with its wings fully opened.

  Is this a type of moth, is it a pest or is it neutral. What is the species?

This is a Bogong Moth,the migration point was really helpful !!
They migrate in masses around the
 1. Victorian alps
 2. southern Australia (Sydney,Canberra)
 3. New Zealand..
Agrotis infusa,
These are pests which affect many plants,they're not neutral and they
Cause some attentive damage

More on this and the site which helped me


Why do cells not spread on soft substrates? I recently read a paper discussing how cells (primary mouse embryo fibroblasts) fail to spread and proliferate properly when plated on a soft substrate (i.e. soft PDMS pillars with stiffness k = 2.3 nN$\mu$m$^{-1}$), but spreading and proliferation can be restored with cyclic stretching of cells.

http://www.nature.com/ncomms/2015/150223/ncomms7333/full/ncomms7333.html

My question is if we understand why cells need to be on a hard surface to do normal operations (proliferate and spread)? It doesn't seem to me that a soft surface would be any more difficult for a cell to attach to. I would think that a "slippery" (I'm not sure of a correct biological term for this) surface may have this effect, but I wouldn't expect this from a soft surface.

As both @MattDMo and @WYSIWYG have already so succinctly answered this question in their comments I'm just going to attempt to expand a bit on their answers.

@MattDMo and @WYSIWYG have explained that the aforementioned paper from the question has results that are "not extensible to all cell types and environments" and "Some cells need a matrix to adhere. Adherence relays proliferative signals in these cells."

I'm just going to expand a little bit on these points... I know this addressing an erroneous assumption in the question rather than the question itself but bear with me.

Ok, so as has already been mentioned, different cell types in a multicellular eukaryote (like a mouse, or a human) only grow in certain environments and this is really important . Think about it like this, a mouse's body is made up of many different cell types all working together to create functional organs and systems and to ultimately make up the mouse. The individual cells don't know they are all coming together to make an entire animal and a cell is designed to grow and proliferate in order to make more copies of itself and spread. So why don't all cells just grow all over the place, on top of each other and spread to all parts of the body.

The reason you and the mouse aren't a formless mass of undifferentiated cells - like a big soft tumour - is because different cell types develop in such a manner that they can only grow in a restricted, structured way in a certain environment in your body. There are mechanical and chemical signals along with unique sets of growth factors that are found in different environments in the body that make it possible for certain cell types to grow in one area while not in another. It's why only blood cells can survive suspended in the blood not adhered to anything and your fibroblast cells (they make up your structured connective tissue can't, they need to adhere to a surface to grow. The different cell types only get their signal to keep growing when they are in their proper environment.

This is why when scientists are growing various mammalian cell cultures they have to be aware of what environment and growth factors the specific cell type they are working with requires in order to grow. Some mammalian (e.g. mouse) cells need a structured scaffold to grow them in culture and some can grow in soft or liquid culture.

Source: Hallmarks of Cancer: The Next Generation http://www.cell.com/cell/abstract/S0092-8674(11)00127-9?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867411001279%3Fshowall%3Dtrue [This is a classic paper that explains this far better than I can hope to - look for the section 'Sustaining Proliferative Signaling'.]


To what extent is Ebola airborne? (aerosols) Recently, CIDRAP at the University of Minnesota announced that Ebola may be more transmissible through aerosols than previously thought.

I lack the familiarity with the field to critically evaluate this release. They also seem to more interested in making the point that there is a risk of aerosol transmission, not to settle whether it does transmit by air or not.

What is the simple answer? Can Ebola really be transmitted by aerosols?
If so, how come nobody realized this before? Is this a general phenomenon allowing any pathogen to become airborne? I don't see why you couldn't aerosolize a great many pathogenic objects, not just Ebola virus.
How does the number of virions necessary for successful infection compare to what you could get from aerosols?

Interesting question and hard to answer definitively. First of all: It seems still pretty clear that the major (and by far most important) infection route comes from direct contact with infected people or their body fluids and that aerosol transmission is of far less significance. Ebola is infecting cells of the immune system (mostly macrophages and dendritic cells) which are located in the skin which makes the route through the respiratory organs pretty uneffecient, but it is possible.

However, there are reports for Ebola transmissions (or at least unclear cases in which a direct contact could be excluded), which suggest that the aerosl transmission is possible. There are reports of Ebola infections which spread among experimental animals between infected and non-infected (and without direct contact) control groups. This has been observed between rhesus monkeys and pigs. It was also possible for the pigs to infect non-human primates (see references 1-4 for details).

This results should be seen with some caution: At least for pigs an Ebola infection seems to be pretty much different than one in humans. There it looks more like a respiratory disease with all what comes along with it: Extended sneezing and coughing - which makes a lot of aerosol droplets. See reference 3 for the original paper and 5 and 6 for a summary and a classification. I think it is also possible that anatomical differences to the humans make such an infection route easier or harder.

Finally there are some reports of infected people which had no direct contact to people (see reference 7). However, this is rare and mostly restricted to people which where involved in health care for infected persons. These people come in close contact to the infected people which raises their chance of getting infected by aerosols. This underlines the importance for health care workers to get the right protective equipment.

References:

Transmission of Ebola virus (Zaire strain) to uninfected control
monkeys in a biocontainment laboratory.
Replication, Pathogenicity, Shedding, and Transmission of Zaire
ebolavirus in Pigs
Transmission of Ebola virus from pigs to non-human primates
Aerosol exposure to Zaire ebolavirus in three nonhuman primate
species: differences in disease course and clinical pathology
Pig-to-monkey Ebola: is there something in the air?
New paper on Ebola–no primate-to-primate transmission seen
Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo,
1995: Risk Factors for Patients without a Reported Exposure