How precisely can we sense temperature differences? We have thermoreceptors, thus we can sense temperature (both warm and cold).  I'm interested in the sensitivity of our thermoreceptors - What is the smallest temperature difference that we can sense? I assume that different parts / organs may have different sensitivity (eg. lips vs fingers), thus I'd like to narrow my focus on the palms / fingers. But if someone has comparative data, that is welcomed too.

Short answer
Temperature differences of 0.02 degrees Celcius can be distinguished, dependent on various factors including experimental conditions and bodily location.
Background
The ability to discriminate temperature differences depends on whether it is a cooling or heating pulse, the skin temperature, the duration of the temperature stimulus, age, bodily location among other factors. Unfortunately I cannot access the primary literature other than a few isolated smaller studies. However, Scholarpedia has a very nice entry and associated references, and I quote:

The thermal sensory system is extremely sensitive to very small changes in temperature and on the hairless skin at the base of the thumb, people can perceive a difference of 0.02-0.07 °C in the amplitudes of two cooling pulses or 0.03-0.09 °C of two warming pulses delivered to the hand. The threshold for detecting a change in skin temperature is larger than the threshold for discriminating between two cooling or warming pulses delivered to the skin. When the skin at the base of the thumb is at 33 °C, the threshold for detecting an increase in temperature is 0.20 °C and is 0.11 °C for detecting a decrease in temperature.
The rate that skin temperature changes influences how readily people can detect the change in temperature. If the temperature changes very slowly, for example at a rate of less than 0.5 °C per minute, then a person can be unaware of a 4-5 °C change in temperature, provided that the temperature of the skin remains within the neutral thermal region of 30-36 °C. If the temperature changes more rapidly, such as at 0.1 °C/s, then small decreases and increases in skin temperature are detected. [...]

You also were interested in the palmar skin: here average difference limens are 0.02 - 0.06 °C, dependent on the temperature step used. These values were obtained using cooling pulses. In other words, differences in two cooling pulses of 0.02 - 0.06 °C were discernible, with higher limens needed for higher pulses. Baseline temperatures (29 - 39 °C) had little effect (Darian-Smith et al., 1977).
Reference
Darian-Smith et al., J Invest Dermat 1977;69:146-53
Note
The Stevens, J. C., & Choo, K. K. (1998). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28 article as commented on by Corvus is indeed a must-read, but my uni library does not have access to it unfortunately.


Do we posses technology to rebuild sequenced DNA? Is there existing technology that would allow to rebuild DNA molecule from a digital file storing sequenced DNA?

If not, does there at least exist theory explaining how such device could be built?

Yes, in fact synthesizing short stretches of DNA and RNA is available through several commercial services. However this limited to tiny DNA fragments (say 120 base pairs or so). Longer sequences require custom laboratory work.


VPg priming of the replication of RNA viruses I'm doing a presentation on the replication of SARS-CoV-2 for my chemistry class, and I found that to replicate its RNA, the virus uses RNA-dependent RNA polymerase, which is primed by a VPg primer. Since the presentation is for a chemistry class, not a molecular biology class, I would like to know the chemistry behind the way that primers work.

I've tried searching the information on the internet, but could not locate the information I need.

Nucleic acid synthesys can occur two ways, with a template or without. In most biological systems the template synthesis is the one that occurs since it is the only way to replicate genomic information. For template based nucleic acid synthesis in biological systems (being of DNA or RNA) the enzymes performing the reactions can use single stranded material (in the case of virus ssDNA or ssRNA virus) however they still need a small region of double stranded nucleic acid to bind and start polymerizing, otherwise synthesis could start anywhere in the template strand which wouldn't be particulartly useful, hence the primers, the polymerases bind to the double stranded region and start polymerizing always adding new nucleotides to the 3' end of the primer strand that are complementary to the nucleotide in the template strand. Usually in living cells the synthesis of new RNA molecules won't occur with an RNA template (there is usually no RNA dependent RNA polymerase, there are exceptions but they are usually result of previous viral infections), but only with a DNA template to procuce messenger/transfer/ribossomal RNAs. In the case of COVID and othe + strand RNA virus, the virus has to encode the RNA polymerase and also produce a primer that will create a double stranded region that will allow RNA synthesis to occur.


Why is one testicle larger than the other? Why is one testicle generally larger in humans? Just due to asymmetric development, or is there a hypothesis as to some utility it serves? I read that the different heights may be attributed to attempting to keep them from hitting against one another. Is there a similar guess to the purpose for the difference in sizes?

I would strongly question whether the underlying claim that testicular asymmetry is generally true. While there is no known clinical significance of testicular asymmetry, most men probably have no noticable difference in testicular size. There have been a number of studies over several decades, and findings have been inconsistent.

Braus (1956) stated that the left testis was heavier and lower; Chang et al. (1960) determined on study of cadavers that the right testis was generally larger than the left.

A 2008 study in 0 to 6-year-old boys found no difference in testicular volume measured ultrasonographically.

Age or level of sexual activity may also play a role; it is known that testes get larger during sexual activity.

The reason for testicular asymmetry is unknown. It has been reported in many different species (see Yu, 1998). The most common explanation provided in humans is that the right testis is more commonly larger than the left due to a difference in vascular anatomy: the left testicular vein empties into the renal vein while the right testicular vein empties into the inferior vena cava. However, anatomy alone would not explain testicular asymmetry in other species as well, so there is no doubt more to this than presently understood.


Finding targets of transcription factors I'm trying to find an easy way to get a list of putative targets of a particular transcription factor (for example, STAT1). I'm interested in targets determined using both experimental and computational evidence. I thought it should be easy to obtain such a list, but I'm having a hard time. Could anyone help me with this, preferably with specific, step-by-step instructions. As a bonus, I'm also interested in the reverse problem, which is, for a given gene, obtain a list of all transcription factors for which there is evidence that it regulates that gene.

Thanks,

Jennifer

If you were interested in human targets, one easy way is GeneCards, which aggregates other resources, and combines computational and (some) experimental data:

In this case the inverse problem is particularly well accessible: e.g.: scroll down to section of Genomics (e.g.: for the gene called NOTCH http://www.genecards.org/cgi-bin/carddisp.pl?gene=NOTCH1&keywords=notch1 ).

If you you were interested in obtaining all genes of a given transcription factor, you could buy a license, costing around 150 USD per year, for the GeneALaCart service of the company that runs the free genecards ( https://genealacart.genecards.org ), upload a list of all human genes (which you could for instance obtain from ncbi's ftp server), and get a spreadsheet linking transcription factors to genes.


Why is Homologous Recombination (HR) more frequent at long sequence repeats? I'm studying plasmids in bacteria (E. coli), and trying to understand the well-cited phenomenon that recombination frequency increases with longer repetitive sequences. I think this also applies to eukaryotes.

In my (potentially misguided) current view, HR can occur between two DNA duplexes either during or after replication (?). As I imagine it, the new DNA duplex will have near identical homology to the template duplex (from which it has just been replicated), meaning that sequence homology is widespread across the entire molecule. This would mean that sufficient homology between sister chromatids can be achieved anywhere (?), negating the trend for 'long sequence repeats'.

So, why is there a focus on long repeats promoting higher recombination frequencies? Is my view on when HR happens misguided?

HR rarely occurs at all in normal somatic cells, because multiple different mechanisms try to prevent this from happening between sister chromosomes during mitosis; the implications of this recombination can be detrimental to the organism. Instead, in eukaryotes, HR normally occurs during Meiosis, in the formation of Gametes, which will recombine anyway. This actually has a beneficial effect because it increases genetic diversity of offspring, thereby promoting evolution.

As for how homologous repeats enhance HR, it is a rather simple mechanism. Basically, you have the two homologous strands side by side, and you have this extensive repeat section in the middle. The thing is, because the repeat section is so long, and because of the fact that it repeats, really any repeated sequence anywhere along that section can cross over with any repeated sequence on the other strand. This increases the availability of HR sites, as well as increases the number of possible outcomes, therefore increasing the probability that HR will occur. Plus, as the number of repeats increases, the number of possible recombinations increases exponentially, making HR on long repeats much more likely than other cases of HR

I hope that satisfactorily answers your question.


Rank-specific rules for taxonomic classification There appears to be a very specific (although not universally agreed) list of characteristics that describe what a "species" is--and the list applies to ALL species.  Are there similar generic rules or characteristics for the other taxonomic ranks that do not resort to characteristics of existing members of the rank? For example, I've seen "number of lobes on leaves" used to place a particular flower in a particular Family or Order.  Is there anything that applies across ALL Families, or across ALL Orders, etc., of the tree of life?

In short, no. Species are unique, in that they are thought to be biologically real categories that would exist whether there were humans trying to classify them or not. There are a variety of definitions for species, involving fixed characters that imply a lack of gene-flow. However, all higher categories, from genera on up are designed by humans to be able to talk about these groups. Each category is defined by phylogenetic relationships, but taxonomists have wide leeway to decide how broadly or narrowly to subdivide groups. (Lumpers vs. Splitters). For example, all ants are in the same family. Yet all it would take to change this would be for some ant taxonomist to submit a paper that divided ants into however many families s/he wanted to. The peer reviewers would then decide if such a division was reasonable, and once published, it would be the new taxonomy. There are no broad rules, other than peer review. Not age: one family could be 1 million years old, and another, 100 million. Not the magnitude of phenotypic or genotypic variation: some groups are radically different from one-another, and still in the same category, while other groups are heavily subdivided and barely distinguishable.


Do you know which is this small flower in Asturias? Was located in the Turón valley on Mieres, Asturias, Spain (https://goo.gl/maps/BMwyfWtiSdw). Found it at 900 meters of altitude. The plant is just about 8 cm high maybe. All the ones I've found were alone. Just one flower from a couple of leaves.

Kind of reminds me of a Cyclamen?

It is an Erythronium lily commonly called a "dog's-tooth-violet" or "trout lily". I see that one of the species Erythronium dens-canis is found in Spain, being native to Europe. Most of the Erythronium species are native to North America. The foliage is very attractive and they are commonly grown as ornimentals. The flower in your photo is just opening. I have included a few links that better describe these lilies.

https://en.wikipedia.org/wiki/Erythronium

https://en.wikipedia.org/wiki/Erythronium_dens-canis

http://www.srgc.org.uk/bulblog/log2008/160108/log.html


What are the biological mechanisms behind the increase in cancer risk and alcohol consumption? Alcohol consumption is known to be a risk factor for developing cancer. Compared to obvious causes like tobacco where one is exposed to known carcinogens, I don't see an obvious mechanism by which alcohol consumption would increase the risk of cancer.

Is there anything known about the mechanisms by which alchohol consumption affects cancer risk?

There aren't many studies which associate between alcohol consumption and cancer to my knowledge. The association is more with metabolic diseases because the liver is affected.

Alcohol is oxidised to acetaldehyde by alcohol dehydrogenase. Acetaldehyde may also, in turn affect the cells by DNA damage if it is not metabolized quickly to acetyl-CoA (perhaps in a manner similar to formaldehyde or by formation of Schiff's base with nucleotides). The other way by which alcohol is metabolised is through cytochrome-p450 (CYP2E1) which produces ROS (Hydrogen Peroxide), that may lead to carcinogenesis.

You might want to check this review.


Genotype -/- vs delta/delta In https://doi.org/10.1016/j.neuron.2018.07.033, Pan et al. use the designation TMC1^delta/delta to describe a mouse strain lacking a functional TMC1 gene.  What if any is the different between the delta/delta superscript and a -/- superscript in this context?

The delta refers to a mutant allele, in this case a cysteine point mutant. The -/- refers to a homozygous null allele, in this case a knockout.


In the transition to multicellularity what function becomes specialized first? It's my understanding that in the transition from single celled to multi-celled organism a lineage will transition between stages where existing in a colony of cells is optional to one where it is obligate. Integral to this process is the parts of the colony taking on specialized roles in the colony's survival. First is tissues, and eventually full blown organs.

With that as background (please correct any misconceptions), which job tends to be taken over by specialized cells first in the transition? The three main ones in every multicellular organism I can think of are: digestion, structure (including skin and any rigidity), and reproduction (please suggest roles if I missed any, or over-included). Is there a single answer to this, or does it vary between lineages?

Lyons & Kolter (2015) On the evolution of bacterial multicellularity. Curr Opin Microbiol 24: 21-28; emphasis mine:

  Multicellularity is one of the most prevalent evolutionary innovations
  and nowhere is this more apparent than in the bacterial world, which
  contains many examples of multicellular organisms in a surprising
  array of forms.

  cell-cell adhesion to form a new evolutionary unit, and intercellular
  communication leading to coordinated activity (...) are the minimal
  requirements to redefine a group of cells rather than any single cell
  as an "individual."

  [M]ulticellular magnetotactic prokaryotes (MMPs) [are the only known bacteria] without a unicellular phase in their lifecycle.

  [The key features of multicellularity are: cell differentiation,
  intercellular signaling, extracellular matrix, tight cell-cell
  junctions, coordinated movement, division of entire structure (Table
  1).]


Can axons act as receptors? In all histology books, it is stated that all sensory nerve endings (receptors) consist of dendrites that translate physical stimuli from the environment into neural signals. However, several sensory neurons seem to include axons, such as the merkel and olfactory cells shown below. They act as receptors, but feature axons as well. So is it the pictures, or the texts that are incorrect?

Short answer
The textbooks are right; the receptor part of sensory neurons is always considered to be the dendrite. Axons are nonetheless an integral part of some receptor types to send the signal to the brain. Other, more specialized sensory cells do not have an axon and therefore rely on secondary neurons to send the signal to the brain.

Background
There are three types of sensory cells, namely those with free nerve endings, those with specialized dendritic structures, and specialized receptor cells that synapse directly onto a secondary neuron (Fig. 1).

Fig. 1. Types of sensory neurons. Source: Premed HQ.

Sensory neurons with free nerve endings have an exposed dendrite that functions as receptor. Examples are nociceptors (pain receptors) and hair follicle receptors.
Other sensory neurons are complex cells that feature a dendritic region specialized for a particular receptor function. Examples are the Pacinian corpuscle and olfactory neurons.
The most common receptor type are specialized receptor neurons that have no axon and need a secondary sensory neuron to send the signal to the brain. Examples are the photoreceptor cells in the retina, the hair cells in the cochlea and Merkel cells.


Why genes are assumed to follow multivariate normal? I wonder why gene expression data are very frequently modeled by multivariate normal distributions. What is the reason for those strong assumptions that the genes follow multivariate gaussian? Are there any reasons specific for genetics other than the reasons for general gaussian assumptions (the ease of calculation, etc.)?

Usually if something is not expected to behave according to some scheme then the measured values for such a parameter are assumed to be normal. It is not just with gene expression but with all types of measurements like dimensions of an object, luminosity of an electric bulb, range of a bullet etc.
In any measurement, the random error is modeled using normal distribution. I don't have a very intuitive explanation for why random errors follow normal distribution but mathematically it comes from the central limit theorem.

Now each gene is a variable and measurement of each gene suffers some random error; so a multivariate normal distribution is used.

When we dismiss a null hypothesis in a t-test or z-test what we are actually doing is dismissing our parsimonious notion that a sample is drawn from a given normal distribution. This means two things:

The sample belongs to some other normal distribution (different $\mu$ and $\sigma$)
The sample follows some other distribution

But a t-test will never be able to point out the exact reason. All it tells you is that the sample is not from some given normal distribution.


What percent of e coli genes are necessary for survival? I would like to know, in a typical e coli genome what percent of genes the organism could not survive without. That is, if all the other genes evolved except that one, the organism would not be viable.

About 10% in rich media.

There are lots of papers that try to answer this question. The basic way you do it is you knock out one gene at a time, either in parallel experiments or (more common nowadays) in a pooled experiment, and figure out which knockouts survive and which don't.

The most recent study counts 358 essential genes (out of about 4000 genes in E. coli). http://mbio.asm.org/content/9/1/e02096-17.full . Figure 2 compares a few other papers.

The exact answer will depend on the exact conditions you grow the cells in (if you have fewer nutrients or other stressful conditions, more genes will be essential).


Any difference between inverted microscope objective vs normal microscope objective? I'm planning to build an inverted microscope and I am not sure if I can use a plane achromatic objective of a normal microscope for the inverted microscope as well. Are there any specific needs for the objective of an inverted microscope?

Apart from the way it works and certain structural differences (reference), the decision of which kind of lens you need to use is left to your own personal choice based on your needs. You can find a list of the different lenses being offered by Olympus in this link.


What is the average speed of human sneeze? I sneeze a lot, at various times and various "volumes", and often wonder about the speed of the sneeze itself, i.e. the speed of the air coming out of the nose while sneezing.

What is the average speed of that, in humans? Are there any records for such a thing?

Mainstream understanding is that a sneeze is 100 mph, or ~45 m/s. However, this isn't even close to being true..

A study in 2013 (see link below) was conducted where they investigated the airflow dynamics of sneezing and breathing, and discovered that the highest velocities of a sneeze are around 10 mph, or 4.5 m/s.

  ...the maximum sneeze velocity derived from these measured distances was 4.5 m/s.

So, about 1/10th the value of what most people believe.. just like the 10% use of our brain misconception, but reversed! (we use 100% of our brain.. not necessarily all at the same time, but we do utilize all parts of our brain)

Airflow Dynamics of Human Jets: Sneezing and Breathing - Potential Sources of Infectious Aerosols


How does decreasing surface tension of lipids help to emulsify them? According to my chemistry book, water has higher surface tension than lipids. But in my biology book it is written that "the gall forms an emulsion of water and lipids by lowering the lipid's surface tension". This will increase the difference between the two substances even more. How can this be beneficial?

There appears to be either a typo or transcription error in your textbook.

According to this Nuffield Foundation and Royal Society of Chemistry article

  Molecules of most detergents and soaps are long chain hydrocarbon
  molecules with an ionic group at one end, usually carrying a negative
  charge, thus making it an anion. This charge is balanced by the
  opposite charge of a soluble cation, for example Na+. The long
  hydrocarbon chains do not interact well with water molecules, and many
  of them are effectively ‘squeezed out’ to the interfaces between the
  water and the air or the glass sides of the beaker. The effect of
  these molecules on the water surface is to considerably weaken the
  forces between water molecules there, thus lowering the surface
  tension.

Soaps, detergents, and bile (all examples of amphiphilic compounds) act to reduce the surface tension of water, not the lipids.


Is DNA a single molecule or 46 separate pieces (out of 23 chromosome pairs)? It seems that biology books refer to DNA as 'a' molecule (implying that it is a single continuous uninterrupted double strand) ... but in those same books chromosomes are depicted as 23 separate objects (chromosome pairs) containing DNA. Are these illustrations misleading ? Are chromosomes somehow connected end-to-end or are they disjoint ? Is it a single noodle or is it 46 pieces ?

Unbroken strands of DNA are single molecules. So Yes, DNA is a molecule. However, the sequence of nucleotides allow for a near infinite variety. So unlike other molecules, like collagen, or water, they cannot be characterized with a unique descriptive name, other than by their sequence. I think this is the cause for confusion, because in this sense, DNA is a class of molecules, and we don't generally give them names. Each chromosome has two unique DNA molecules in diploid organisms (except in rare cases of highly inbred individuals where the two molecules might be identical). So if you have 23 chromosomes, you have 46 DNA molecules in each cell nucleus.


Is it possible for parsimony to estimate more state changes than stochastic character mapping I'm mapping states (geographic regions) onto a phylogeny to estimate the number of transmissions between countries.

I'm using two methods, stochastic character mapping implemented in Phytools and parsimony implemented in Mesquite.

I was expecting parsimony to give lower results than stochastic character mapping, as it doesn't attempt any simulation along branches. This is generally true, and the number of transitions between states is generally lower estimated by parsimony. However, in a couple of cases, the number of transitions estimated by parsimony is higher than by stochastic character mapping.

I'm still developing an intuition in this type of analysis, so could someone tell me if this is feasible, or should I be looking for a technical problem somewhere?

If the number of taxa is large enough, an exhaustive search is not possible, and parsimony methods use heuristics to explore the tree space. It is therefore not guaranteed that the most parsimonious tree will be encountered.

This might explain your observation if your tree has a high number of taxa (> 20).

According to wikipedia:

  However, although it is easy to score a phylogenetic tree (by counting the number of character-state changes), there is no algorithm to quickly generate the most-parsimonious tree. Instead, the most-parsimonious tree must be found in "tree space" (i.e., amongst all possible trees). For a small number of taxa (i.e., fewer than nine) it is possible to do an exhaustive search, in which every possible tree is scored, and the best one is selected. For nine to twenty taxa, it will generally be preferable to use branch-and-bound, which is also guaranteed to return the best tree. For greater numbers of taxa, a heuristic search must be performed.

How many taxa do you have?


Examples of points in evolution where two species stopped being interfertile? Apologies in advance for not using the right terminology here; I'm not a biologist. This isn't for homework or anything; just curiosity.

I'm wondering: at what point do two divergent species stop being able to breed with one another, and what factors typically come into play to cause that change toward reproductive incompatibility?

I think the question above is maybe too broad, so instead I figured I'd ask for some examples of specific places in the evolutionary tree of life where this divergence occurred. I'm hoping this will give me some direction about where to start researching to find our how this typically happens in nature.

So:

Could you guys give me some examples of specific points in evolutionary history where a species was born which was suddenly unable to interbreed with its cousin species/grandparent species/etc?

Bonus points for answers with the following characteristics:

The incompatible species are very near one another in the evolutionary tree.
The species and its near-relative exist in common knowledge.
The reproductive differences between this species and its relative are significant and easy to understand.

Two obvious answers are genome doubling in plants, and Wolbachia-mediated infertility in insects. Both can cause one-generation speciation as measured by lack of interfertility.

  Polyploidy, which arises through complex genetic and ecological processes, is an important mode of plant speciation. This review provides an overview of recent advances in understanding why plant polyploid species are so ubiquitous and diverse. We consider how the modern framework for understanding genetic mechanisms of speciation could be used to study allopolyploid speciation that occurs through hybrid genome doubling, that is, whole genome doubling of interspecific F1 hybrids by the union of male and female unreduced gametes.

--Genetic Mechanisms of Allopolyploid Speciation Through Hybrid Genome Doubling: Novel Insights from Wheat (Triticum and Aegilops) Studies

  Bacteria of the genus Wolbachia are reproductive parasites of arthropods. They are cytoplasmically inherited (i.e. from mothers to daughters, like mitochondria) and their phenotypic effects on their hosts range from induction of parthenogenesis in certain hymenopteran groups, to feminization of genetic males in isopod crustaceans and to induction of cytoplasmic incompatibility in many insects  ... Three ways have been suggested4. The first suggestion is induction of parthenogenesis (assuming that the infection becomes fixed in the species). This process appears to occur in the hymenopteran Encarsia formosa7; males in this species can be obtained when mothers are treated with antibiotics, however, they are incapable of mating. The second way is offered by bidirectional incompatibility (Box 1). If a population is infected with two different strains of Wolbachia that are incompatible with each other, then bidirectional incompatibility will act as a post-zygotic reproductive barrier. A promising candidate is the species complex of the wasp genus Nasonia2, 3. The third way is offered by unidirectional incompatibility (Box 1). In this case, Wolbachia is acting as just one of the reproductive barriers enhancing speciation between two taxa.

--Wolbachia as a speciation agent

In general, though, the question seems to reflect a misunderstanding. Evolutionary theory doesn't suggest, let alone require, a sudden loss of interfertility during speciation. In many cases the lack of interfertility is incidental, and isn't selected; even in cases where it is selected, you expect to see the common gradual changes rather than abrupt transitions.


Can a carnivorous animal consume plants with no adverse effects? While I know that in nature, carnivorous animals are poorly suited to eat plants (largely due to having sharp teeth, not grinding teeth, as far as I know), I was wondering if, in an emergency situation such as imminent starvation, could a carnivorous animal such as a wolf survive solely on plant life, maybe requiring it to be ground up before hand? Could an herbivore survive on meat, if the meat was prepared in a manner that would allow the herbivore to eat it? Would a wild animal voluntarily consume food that it is not suited for if it would stave off certain death, or would it require force feeding or training?

Also, I am interested in the other side of this question: if an animal cannot safely consume food outside of its normal diet (carnivore eating plants, herbivores consuming meat), what negative effects would this action have on the animal?

Just a note, this is purely a hypothetical question, and I am only asking out of curiosity. I am in no way planning on doing this, nor do I advise anyone else doing this if there is a high chance of it harming the animal.

This is kind of a weird/trick question.  How long do you want the animal to live?  If the lifespan is shortened or compromised does that fit....   Obligate carnivores (cats, dogs) do eat plant material.  In the wild cats mainly eat grass to get rid of hairballs.  Cats are more impacted by phytotoxins than dogs.  However, both, are extremely vulnerable to compounds that don't bother humans (xanthines like theobromine, caffine, compounds in garlic, onions, broccoli, mushrooms).  Cats can't convert plant fats into what they need (we can) as a result they can go blind if they don't get the animal fats they need.  Likewise, herbivores will suffer increased cancer, heart disease, renal failure from diets with animal fats / protein.  Your mention of "wolf" is interesting because there is a South American wolf that supplements its diet with a tomato relative (called something like "fruit for wolves" in Spanish).  This is probably only "good" for it in that it keeps the wolf from otherwise starving.  I don't know that it has a strong deleterious effect (probably not, but it could be more sensitive to trace alkaloids in the fruit) but it could hurt it in a minor way.


Do all cells produce the same proteins? If DNA is more or less the same in all cells, and DNA is used to produce proteins from aminoacids, then do all cells produce the same proteins or are they specialised/controlled by something?

Each cell will indeed have the same DNA sequences and ability to produce any given protein. However, there are certain factors (transcription factors) and cellular conditions within a cell that dictate which proteins are produced. If the conditions are right then only certain proteins will be produced depending on what type of cell it is. This process by which a cell continues to express selected proteins and becomes specialized for a specific function, is called differentiation. Expression of proteins that are not required can be prevented by transcriptional repressors (or by epigenetic mechanisms such as methylation of DNA sequences). So to answer your question, while cells contain the instructions (DNA sequences) to produce potentially any protein, not every type of protein will always be produced.

Keep in mind that my answer is very basic; the answer isn't as simplistic as I'm making it out to be.


Why do living organisms replicate itself or procreate Why do living organisms spontaneously replicate itself or "procreate" (my understanding is that it does).

From a uni-cellular and micro-organism point of view. Is there some sort of stimulant in the environment? A chemical reaction that causes it? Is is there a physical or emotional motivation? Is it by choice?

Note: I may have some terms used wrongly as I am not a biologist. In this question, I am interested at living organism nearer the forms of single smallest unit of life form.

This is a very interesting question but the answer (or as much of the answer as is known) can fill a few books. There are many many signals that control cell division.

As a horrible simplification, the cell can be compared to a car parked on a slope with a driver's foot on the brake. If she lifts her foot, the car will roll downhill. In the cell, there are various proteins (P53 is the most famous) that have their metaphorical foot on the brake. Various external and internal stimuli can cause these proteins to stop suppressing replication and the cell will then continue its cycle and replicate.

So, a cell's "natural state" is to replicate, there is a complex network of interacting factors (primarily proteins) that actively block replication in resting cells. When the conditions are "right" (what that means depends on the cell in question) the block is removed and the cell replicates.


DNA sequencing problem First off, let me start by outlining the problem:

Your laboratory has established a technique for examining DNA replication in a cellular extract. To the cellular protein extract, you add nucleotides, a small amount of radiolabeled 32P-dGTP to aid visualization of the synthesized DNA, and a 4000-base-pair linear double-stranded DNA molecule that contains an origin of replication in the middle. After allowing the reaction to proceed for 30 minutes at 30°C, you boil the mixture to denature the proteins and the DNA strands, separate the components on an acrylamide gel, and detect the radiolabeled DNA products. This complete reaction is shown in lane 2 on the gel in the Figure below.

Problem A:

You perform the assay by yourself for the first time with no one else is in lab. The tube labeled “nucleotide mixture” has only enough for a single reaction, but you find a tube with a label that reads “dATP, dTTP, dGTP, dCTP” and you use this in a second reaction. You find the first reaction looks like lane 2 and the second reaction looks like lane 3. Why was no DNA synthesized in the second reaction?

My answer:

Because deoxyribose triphosphates do not have a –OH group to attach. You essentially can’t build with them.

Problem B:

Your lab partner has recently isolated a mutant strain that can replicate its DNA normally at 30°C but exhibit no DNA replication at 40°C. He calls the mutant tsr1, for Temperature Sensitive Replication. The wild-type strain replicates efficiently at both temperatures. You believe that you can use the biochemical assay of cell extracts to identify which genes are defective in the mutant. You grow wild-type cells and tsr1 cells at 40°C, make the extracts, incubate the DNA replication reaction at 40°C, and detect the products on a gel. You observe the pattern shown in lanes 4 and 5. You are so excited by the results that you run to your lab partner and tell him that you know what enzyme is defective. He is delighted by your results but says that there are three different enzymes that can account for your results. What are they?

I am 100% lost on this one.

I understand from the figure that the wild-type at 40 degrees has 4000 nucleotides so it's not being cut off. The mutant, trs1 is being cut off one into two slices of 2000 and one of these slices has been cut off into slices of 500? Am I understanding this correctly?
I also don't understand why the 500 line is so thick compared to the others?

Anyhow I feel really confused on this. I've been learning about Sanger sequencing and it makes 100% sense with ddXTP added into the mix to view the length of each sequence and therefore be able to read the sequence, but I'm not even sure if that's what's happening here.

Even though you - or the problem did not clarify, I assume in my answer that you work with eukaryote system, even though the principle of the replication is the same.

dNTPs do have an OH group on their 3rd carbon atom (for eg. check this wiki-page for dCTP) so I don't think that's the issue here. My guess is that the first tube contains the radio labeled GTP and the second does not, so even the DNA is there, you cannot see it - even though the question specifically asked why DNA was not synthesized, my opinion is that it's a tricky question to confuse you.

For the second problem we need to dig into the replication process a little bit:

In the replication fork the two strands are synthesized differently. The so called leading strand is made continuously, without interruptions, however the other strand - the so called lagging strand is synthesized by ligating small fragments - aka Okazaki fragments. These small fragments require their own RNA primers that need to be removed after synthesis is done.
Now since the origin of replication is in the middle and replication can proceed both ways, on a linear fragment such as yours you can get two 2000bp fragment from the two leading strands. Would it be a circular DNA, then you could still get 4kbp fragments since the replication could go around the DNA circle.
The smaller 500bp fragments that are quite abundant in the tsr1 lane, are the fragments that cannot be ligated. That being said I must admit that 500bp Okazaki-fragments would by atypical for eukaryotes (usual is around 100-200bp). So the enzymes responsible for this could be:

DNA Ligase - the one responsible for ligating (joining ) the lagging strand's fragments.
Polymerase delta (Pol δ): That is responsible for lagging strand synthesis and primer removal - in this case the primer removal function might be defective, this causes that the primers stay on the DNA and complete synthesis and ligation cannot occur.
The last protein although it is not quite an enzyme is the DNA clamp complex (PCNA). This complex stabilizes the polymerase to DNA, but when reaching a previous fragment the polymerase should dissociate. But if the clamp is dysfunctional than the polymerase gets stuck on the end of the fragment thus no primer removal and ligation can occur.

If need more info read this wiki-page.


What are some examples of coupled reactions in the cell? Except DNA Synthesis that requires ATP hydrolysis, which other reactions require activated carriers?

All the anabolic reaction inside our body require energy. The majority of those reactions use the hydrolysis of ATP as source of energy.

To cite a few reaction that require ATP:

Gluconeogenesis where 4 ATP, 2 GTP and 2 NADH2 are consume to produce glucose from pyruvate.
Formation of peptide bond between two amino acids.  Here the amino acid have to be first activate by binding to the tRNAc consuming ATP, as explain here (from wikipedia)

  Polymerization of amino acids is what creates proteins. This condensation reaction yields the newly formed peptide bond and a molecule of water. In cells, this reaction does not occur directly; instead, the amino acid is first activated by attachment to a transfer RNA molecule through an ester bond. This aminoacyl-tRNA is produced in an ATP-dependent reaction carried out by an aminoacyl tRNA synthetase

Ubiquitin ligase, that require ATP to activate ubiquitin for conjugaison and it transfer to an E2 enzyme. This pathway is mediate by the E1 enzyme, as suggested here

  There is one major E1 enzyme, shared by all ubiquitin ligases, that uses ATP to activate ubiquitin for conjugation and transfers it to an E2 enzyme. The E2 enzyme interacts with a specific E3 partner and transfers the ubiquitin to the target protein.

Hope that it helps.


Why do we go blind for a few seconds after switching off the light? At night, when I switch off the lights, I always seem to go blind for a while. The room becomes pitch black and I am unable to see anything. After a while, however, my vision slowly recovers and I start to see things around me again. I always have to wait a while before my vision returns to that functional state.

I am interested in knowing the mechanism behind this phenomenon. What do we call it?

Short answer
The eyes need to adapt to the low lighting condition after you switch off the lights, a process called dark adaptation.

Background
The process behind the reduced visual function when going from bright ambient light to low-lighting conditions is caused by a process called dark adaptation. The visual system works on a huge intensity scale. The only way to do that is by adapting to ambient lighting intensity.

The sensitivity of our eye can be measured by determining the absolute intensity threshold, i.e., the minimum luminance of a stimulus to produce a visual sensation. This can be measured by placing a subject in a dark room, and increasing the luminance of the test spot until the subject reports its presence.

Dark adaptation refers to how the eye recovers its sensitivity in the dark following exposure to bright light. The sensitivity of the visual system increases approximately 35 times after dark adaptation.

Dark adaptation forms the basis of the Duplicity Theory which states that above a certain luminance level (about 0.03 cd/m2), the cone mechanism is involved in mediating vision, called photopic vision. Below this level, the rod mechanism comes into play providing scotopic (night) vision. The range where two mechanisms are working together is called the mesopic range, as there is not an abrupt transition between the two mechanism.

The dark adaptation curve shown below (Fig. 1) depicts this duplex nature of our visual system. The sensitivity of the rod pathway improves considerably after 5-10 minutes in the dark. Because after you switch off the light the rod system is still inactive, you are unable to perceive much. The reason why rods are inactive is because they are said to be photo bleached. Photo bleaching refers to the visual pigments in the rods and cones to become used up because of the high light intensities when the light was still on. The pigment needs to be regenerated and that takes time.

Fig. 1. Dark adaptation curves of rods and cones. Source: Webvision

Reference
- Kolb et al (eds). Webvision. The organization of the retina and the visual system (2012)


What does 'pedigree information' mean? This paper uses Pied Flycatcher as a study species. For the population of Pied Flycatchers they studied, 'pedigree information' was available. What exactly does this 'pedigree information' mean?

It means that they recorded family information for the traits that they were investigating in the paper, i.e., they had plumage characteristics for siblings or parent-offspring pairs. Look for this phrase in the paper: "phenotypic data usually available for one or two generations, mostly from parent-offspring pairs or siblings."


Are CoA and CoAS the same thing in a compound? Is CoA-S-R the same as CoA-R, and is CH3C(=O)CoA the same as CH3C(=O)SCoA? Eg. Above is the compound on the right just coenzyme A or is it actually another compound and not just notation?

To understand the nomenclature here it is very helpful to think about how Coenzyme A works. It has a thiol group (-SH) which can form a thioester bond to an acyl group.

So the sulphur in "CoA-S-R" is part of the CoA, and in "CoA-R" the sulfur is just not explicitly named. Those two mean exactly the same thing: Coenzyme A linked to R via a thioester on the thiol group.

One specific variant that is very important in biology is acetyl CoA. The chemical formula you mentioned (CH3C(=O)CoA) is acetyl CoA, and here the same as above applies and the sulphur is explicitly mentioned in the second one and implied in the first one.


Can life subsist on anything else but water? Inspired by an answer to a previous question.

It's hypothesized that extraterrestrial life could be based on silicon rather than carbon as its main structural element.

Are there similar theories about an alternative "life solvent" rather than water?

This may not completely answer your question, but provide some information.

Looking at this Wikipedia outline Non water solvents, other possible candidates are ammonia, hydrocarbons even hydrogen fluoride.

Digging a little deeper, this abstract of the article: "Many chemistries could be used to build living systems." (Abstract only) describes the possibilities of ammonia and liquid nitrogen as being potential suitable solvents.  Page 678 onwards of the article: "Is there a common chemical model for life in the universe?" also describes other solvents such as ammonia (I should say that there quite a lot of Star Trek references in that paper).

I hope this goes part of the way to help.


How to pipette accurate volumes from BSA solution without air bubbles? I'm new to immunohistochemistry and there's one step I'm having problems with. Generally I can pipet volumes pretty accurately and avoid air bubbles, but:

1) The BSA solution that I made (with PBS and BSA crystals - then vortexing) had a lot of air bubbles that wouldn't settle over time

2) I couldn't avoid air bubbles in my pipet even though I placed the tip under the layer of bubbles

How should I improve my technique? (Also, will having slightly different concentrations of the blocking and primary antibody serums greatly affect the result?)

Thanks,
L

Never vortex the BSA solution. The best way to prepare a BSA solution is to put the BSA powder on the buffer solution (or water) instead of the other way round. Tap or rock the tube to dissolve the BSA. If there are some tiny clumps then pipette very gently (use 1ml tips; cut the tips if needed) but tapping/rocking should usually do the job.

From CSHL protocols:

  For a 10% (100 mg/mL) stock solution of BSA, dissolve 1 g powdered
  Fraction V or molecular biology grade BSA in 10 mL of distilled H2O;
  to avoid clumping, dissolve by layering the powder on the surface of
  the liquid. Gently rock the capped tube until the BSA has dissolved
  completely. Do not stir. Store in aliquots at −20°C.


How is olfactory acuity rated/measured? Acuity of one's sight is rated on the 20/20 scale. An online search appeared to indicate there is no comparable 'standard' to rate olfactory acuity.

How is acuity of the olfactory system rated?

One olfactory acuity rating method that has found acceptance in some studies (despite the commercial-sounding name) is based on "Sniffin' Sticks,"

"a test of nasal chemosensory performance that is based on penlike odor-dispensing devices. It is comprised of three tests of olfactory function: tests for odor threshold, discrimination and identification. Previous work has already established its test-retest reliability and validity in comparison to established measures of olfactory sensitivity. The results of this test are presented as a composite TDI score--i.e., the sum of results obtained for threshold, discrimination and identification measures."

In the paper from which this abstract portion was taken$^1$, subjects were assigned a score based on their thresholds, ability to discriminate, etc., and the findings were said to be internally replicable (consistent from one test to the next).

This is probably not the only rating available but it has been used on other studies and seems to be taken seriously by M.D.s and others who measure such things.

There is no absolute measure of olfactory acuity. People are classed as 'anosmic' if they do poorly enough on the test but that doesn't mean they have no sense of smell (although that might be the case). Likewise people who get a high TDI score are--by definition--people who got the "Sniffin Sticks" right. They might be poor at discriminating a good coffee from a bad one based on smell.

The test seems to do what it was intended to do: quantify relative olfactory acuity in a replicable way.

An earlier study is somewhat reserved. From an abstract: "It is concluded that ‘Sniffin’ Sticks’ may be suited for the routine clinical assessment of olfactory performance."

$^1$ Eur. Arch. Otorhinolaryngol. (2000) 257(4):205-11. Multicenter investigation of 1,036 subjects using a standardized method for the assessment of olfactory function combining tests of odor identification, odor discrimination, and olfactory thresholds. Kobal et al.


Is there a formal definition of `nature` in Biology? I've been discussing with a friend about Earth Day and at a certain point came out the question

  What do you call "nature"?

He said that he considers "nature" basically all matter, including plastics and all kind of man-made materials.

I said that as far as I understand, "nature" is the ensemble of all Earth's ecosystems, thus if something is not part of an ecosystem, it is not "nature".

Is there an official definition of what is considered to be "nature"?
If yes, what is it? If no, is there a reason?

Is there a definition of "nature"?

I don't think there is any commonly accepted definition of "nature" in biology. To my experience, the term "nature" is actually relatively rarely used in conferences or peer-reviewed papers.

Why is there no formal definition of nature?

The concept of "nature" has been developed outside the field of science or philosophy. As often concepts in the popular culture are used without a proper, complete definition. Even if there is an vague intuition that correspond to a concept, it does not mean that there is any way to make an objective definition of this concept. I think the absence of formal definition of nature mainly come from the fact that nature as used in the population culture does not mean much.

Is the term "nature" used in Biology and with which definition?

I just did a quick review of the use of the term "nature" in peer-reviewed articles. It seems that the term "nature" is rarely used or only in the abstract r in the first two paragraphs of the introduction to convey very general (and somewhat inaccurate) ideas.

Often, the term "nature" holds for "essence", "origin" or "intrinsic characteristic" rather than referring to "outside the lab", "landscape" or "ecosystems". Here are some examples of where I found the term nature

"Nature" as "Essence"

From the abstract of Gibson and Dworkin 2004

  [..] we highlight recent progress in determining the nature and identity of genes that underlie cryptic genetic effects [..]

From the first paragraph of Woolhouse et al. 2002

  Failure to recognize the dynamic nature of the interaction could result in misinterpretation [..]

"Nature" as "outside the lab"

First sentence of the second paragraph of Elena and Lenski 2003

  Since Darwin’s day, many examples of evolution in action have been studied in nature [..]

Note btw that there is no good (objective) definition of life either. One might want to have a look at Why isn't a virus alive? for a discussion on the definition of life.


Tight Junctions in Cell Types I took a quiz today on cell structure basics, which included cell junction types. I disagree with the "correct answer" according to the teacher.

Here is the question:

Which cell type would have the most tight junctions?

a) Pancrease cells
b) Ovarian cells
c) Epithelial cells (in the intestine)
d) Muscle cells (skeletal)

According to my teacher, muscle cells is the correct answer.

I argued that the answer should be epithelial cells, as muscles cells (according to the text) primarily use desmosomes for cell-to-cell adhesion, while epithelial cells rely on tight junctions primarily.

I searched it up quickly on Google, and from what I have found, epithelial cells is the correct answer.

Is my teacher incorrect?

Tight junctions are very specifically a structure found in epithelial cells, so your teacher is incorrect. Tight junctions are what allow epithelial cells to form a selective barrier between compartments. Fibroblasts can be induced to form tight junctions under certain experimental conditions, but I'm not aware of any case where a skeletal muscle cell expresses a tight junction. Regardless, it would not be normal physiology.

You can read more about tight junctions here, in the online Albert's Molecular Biology of the Cell. This figure from that Chapter illustrates the barrier function.

If you want to get into more of the details re: what we know about the various proteins involved in creating and regulating tight junctions, this is a good review.

One small correction to your reasoning, though, I wouldn't say the primary purpose of tight junctions is cell-to-cell adhesion, per se, it's selective permeability. These junctions may help the cells to hold together, but the tissues can resist shear stress in knock-out models. A knockout model without a necessary tight junction protein, however, will not maintain selective permeability.


What do the intervals between groups of arrays in microarray gene expression data images mean? This can be a dummy question, but I am not familiar with microarray experiments at all. In this image, what does each of 16 big squares mean, and what are the black intervals between them are? I know each small square corresponds to a gene expression value, but I don't know what each separated group of expression values means. Oftentimes I see those separated expression values in microarray dataset images. I would be happy if someone can explain. Thanks!

The borders provide visual cues for the image analysis software to know which spot is which. The spots are also not printed all at once, but by a series of print heads, and the spaces allow for a small amount of error in the alignment of the print heads. It also allows for humans to more easily eyeball the results - the chip map can be printed in groups, and if you're looking to see what gene X did in your experiment, and know it's in the 2nd row, in the 2nd block, row 8, column 4, you can find it more easily than just knowing it's in row 73, column 27.


Genetics and blue eyes Blue eyes are a recessive trait in humans. I read an article recently which stated:

  People with blue eyes have a single, common ancestor, according to new research.

  A team of scientists has tracked down a genetic mutation that leads to blue eyes. The mutation occurred between 6,000 and 10,000 years ago. Before then, there were no blue eyes.

  "Originally, we all had brown eyes," said Hans Eiberg from the Department of Cellular and Molecular Medicine at the University of Copenhagen.

Which appears to be a mainstream hypothesis today. My question is, if there is a genetic mutation that occurred in one individual which made their eyes blue, and the rest of the population is brown eyed, how does this make so many individuals blue eyed? If the blue eyes are recessive, the individual's children would mix with the other brown-eyed individuals and their offspring will be brown-eyed. How does anyone treat this theory seriously?

@another 'Homo sapien' is basically correct, and what they were getting at, is that in just the F1 generation, you're right, any recessive traits are masked. However, if you continue this onward, in subsequent breeding, recessive traits are unmasked. (This is basically why inbreeding is a bad thing).

If we use the traditional Punnet square method for determining genotype:

if A is a Brown-eye dominant allele, but a is a blue-eye recessive allele:

F1:

You can see that a single recessive allele is now present in 50% of the offspring of a given pair of parents.

Now, if in F2, we assume that 2 of those recessive offspring were to mate, the recessive gene would be unmasked in 1 quarter of the offspring (statistically speaking), and 50% would be carriers.

F2:

Now it gets a little more complicated. Our double recessive F2 member has blue eyes phenotypically, they aren't just a recessive allele carrier.

F3:

So, if in F3, our aa mates with another aa, (ignoring spontaneous mutation for simplicity) it should be obvious that all of their offspring in F3 would have blue eyes (and I can't quickly find a Punnett square in Google showing this).

However, if our aa now mates with an AA (homozygous dominant brown), we will get 100% offspring with a heterozygous Aa genotype - in other words, all blue eye carriers, but with brown eyes phenotypically.

If aa mates with a heterozygous individual though (Aa), we have the following:

And thus, 50% blue eye individuals, with 50% brown heterozygous dominant. And so on and so forth, ad infinitum.

Hopefully that explains how a recessive allele can go to fixation despite only occurring once.


How to Diagnose this hepatitis A, B and C case? Male patient who is working in the hospital and may be infected with contaminated blood had hepatitis
with genome IA 5 years ago. His hepatitis A at that time was confirmed with the rise of anti.HAV IgM and
later with anti-HAV IgG type antibodies. His wife is known to have antibodies against C hepatitits. The
patient had icteric illness in about three weeks ago. Which are the best indicators in
diagnosing his hepatitis?

Right answer is: Detection of HBsAg and anti-HCV antibodies.

I think this is because

to check if he has hepatitis B by HBsAg
to check if he has HepC by the antibody

Serum antigen of HB tells us about the levels of IgM and IgG.
If vaccinated, then IgG should be positive, I think?
What does HBsAg tell you?

Why do we need to detect anti-HCV?
If they are found, what does it mean?
I think that then it means if found that he does not have hepatitis C then.

The last sentence of the question doesn't make it clear what's being asked. But it seems to be asking: What version of Hepatitis did he get from the contaminated blood?

To that end...

  Serum antigen of HB tells us about the levels of IgM and IgG. If vaccinated, then IgG should be positive, I think? What does HBsAg tell you?

HBsAg gives you the knowledge of whether or not there's an acute infection of Hep-B. Hep-B IgM antibodies indicate an acute infection, whilst IgG antibodies would show up due to his previous exposure/immunization. If the patient has Hep-B IgM, the icteric illness was probably a re-infection of Hep-B.

  Why do we need to detect anti-HCV? If they are found, what does it mean? I think that then it means if found that he does not have hepatitis C then.

That would my assumption as well.

You run the HBsAg and can get two outcomes: IgM(+)/IgG(+) or IgM(-)/IgG(+). The former indicates the icteric illness was probably a reinfection of Hep-B.

You run the anti-HCV and get two outcomes: (+) or (-). The former indicates a present infection, the latter indicates no Hep-C.

What might throw you off is the wife's anti-HepC antibodies. If she was formerly infected and infected the patient (or vice versa) then you'd expect to find a (+) anti-HCV result.

I might come back to this after thinking on it a bit more, but that's the best I have for now.


Dendrodendritic synapse through axodendritic synapse at same dendrite? Reading Wikipedia's article of dendrodendritic synapse, I find that:

  Dendrodendritic synapses are activated in a similar fashion to axodendritic synapses in respects to using a chemical synapse. These chemical synapses receive a depolarizing signal from an incoming action potential which results in an influx of calcium ions that permit release of Neurotransmitters to propagate the signal the post synaptic cell. There is also evidence of bi-directionality in signaling at dendrodendritic synapses. Ordinarily, one of the dendrites will display inhibitory effects while the other will display excitatory effects.

Now I was wondering, does dendrodendritic synapse occur only when the neuron reaches the threshold action potential and "fires" or is it possible that dendrodendritic synapse occurs as a result of, for example, an axodendritic synapse at the same dendrite? (even though the neuron doesn't fire)

Edit

Clearly, we can see that the dendrite has multiple 'endings'. I was under the impression that a synapse can happen at any such 'ending'. Assuming that a synapse happens at one ending of the dendrite, is it viable that anything happens to a neighbouring neuron that is connected with a dendrodendritic synaptic connection to the other ending of the dendrite?

I'm not sure if you are asking if an axon that sends a signal to a dendrite would then be released from that dendrite to another dendrite?

I don't see how this is possible seeing as the dendrite is already paired with the axon and downstream of said dendrite there would be a neuron.

A dendrodenritic synapse is two dendrites of two different neurons in contact with each other. For there to be a signal an action potential must have been reached.

Synapse is a junction between two neurons where chemical signaling occurs, but it is not the definition of a signal occurring. If that makes sense.

It seems like you are confused on the location and anatomy of a synapse.

There wouldn't be an axodendritic synapse followed by a dendrodendritic synapse then the neuron. It would either be axodendritic or dendrodendritic. Now there can be multitudes of connections between neurons but I don't think that is what you were asking.

Edit: Seeing your edit makes your question much clearer.

If the signal from the axodendritic synapse excites the neuron enough to reach action potential then that signal would be sent out through its synapses, including the dendrodendritic ones. So I guess in this way it was a "consequence" of the axodendritic synapse.

Though I would rather you think about it in that the action potential of one neuron sent a signal through it's connections to the neighborhing neuron, thus causing that neuron to reach action potential and further send out the signal. It's not really a "consequence" of the synapse, the synapse is more a pathway for the signal to travel.

The stimulus for the action potential is what causes a signal to fire and travel through a synapse.

Hopefully that answers your question.


What does the end of DNA look like? EcoR I ........ 5'-GAATCC-3'
  BamH I ....... 5'-GGATCC-3'
  Hind III........ 5'-AAGCTT-3'

  The enzyme BamHI recognizes a palindromic sequence and leaves one strand longer than the other. A piece of DNA is cleaved by BahM I. What does the end of the DNA look like?

  A. ...GATCC-3'
       ...C-5'

  B. ...C-3'
       ...GATCC-5'

  C. ...G-3'
  ...C-5'

  D. ...G-3'
  ...CCTAG-5'

  E. ...CTAGG-3'
  ...GATCC-5'"

I understood that one strand should be longer than the other, that's why I eliminated the "C" and "E" answer choices.

Then, I thought the answer choice is the "A" one. The first strand is similar to that in the data in the task, while the second is palindromic to it.

But this answer choice is incorrect. Then, I chose the "B" one. I thought: if we are given the sequence 5'-GGATCC-3', then the sequence 3'-GGATCC-5' is palindromic to it. (In this case, we have different letters near each number. That probably means they are vise versa versions of one another.)

It turned out the correct answer choice is the "D" one. I found such an explanation:

  The end of the DNA cleaved by BamH I is complementary to the
  recognition site sequence shown in the table. One strand must also be
  longer than the other. The sequence CCTAG-5' is complementary to
  GATCC-3'.

But I can't understand this explanation... Please tell me what I do wrong..

Here is a quick drawing of how BamHI cuts the DNA:

As you can see, after cutting, the two ends are actually the same (always read sequences from 5' to 3').


Isn't sexy son hypothesis circular? Sexy son hypothesis.

It states that females are attracted to certain traits in males, because these traits will be attractive in her sons either. But isn't this circular?

Like "I'm attracted to that male because he is the son of an [formerly] attractive male". And you can repeat the process infinitely, going through granddad, great-granddad and so on. Doesn't this hypothesis presuppose some sexy traits that are sexy with no cause?

The process is self-reinforcing but the argument is not circular (no tautology implied).

As soon as some male traits are considered more sexy than others, then there is selection for females to like those traits even more, which causes those traits to raise in frequency, which increases the selection for liking these traits. In other words, in this model, the state where there are no sexy traits in males is an unstable equilibrium.


Why when measuring turbidity do we use the minimum wavelength? As a preface, I read a few other related posts and was able to gather some knowledge, though without any background in physics I am having some trouble here piecing together a coherent view. I looked up videos of Beer-Lambert law on Khan academy and it gave a relationship between transmittance and absorbance as
$$Transmittance (T)=\frac{I_1}{I_0}$$ $$Absorbance(A)=-log_{10}(T)$$
Further, this post points out that turbidity is absorbance, and describes to be in relation to diffuse-reflected and scattered light?
Taking a step back, we see okay, turbidity is really just a measure of 'murkiness' and the amount of light that is scattered as a consequence. What about this diffuse-reflected light? And then this post says scattering is really just the sum of refraction and reflection. I don't think that is correct though, as this video shows refraction and reflection and scattering are different concepts, in so much as refraction is the bending of light as it passes through one medium to another, reflection occurs when light hits a smooth or shiny surface and bounces off, and scattering happens when the surface is rough sending the light in different directions. Then this post here. appears to detail out what would be a satisfying explanation but I haven't taken physics. Are there any good videos that might help better explain these topics?
Then, thinking about absorption my chemistry textbook talks about radiation and I had this concept in my head about light being absorbed then admitted at different wavelengths and I feel like that is true and perhaps that is where we are getting the relationship between transmittance and absorbance?
Bringing it back to the question that brought all this up, through other questions we were able to determine the answers to be To measure levels of pigment production it would be best to use the light of 450 nm, and to measure it turbidity would be best to use the light of 560 nm. In other words, for pigment production, we use the maximum value of absorbance and for turbidity the minimum value. The question we have is why this is the case? The most we were able to come up with is that the color of the Chlorella bacteria is green and that things are green because that wavelength of light is reflected, and that the wavelength of green light is 560 nm. I guess we can't use green light to measure the amount of green pigment because the light that would be returned would be a combination of reflected light (how much green pigment) + scattered light(not green pigment but returns green light) + (some combination of absorbed and reradiated light??). So we wouldn't be isolating the information we are after? If we want to know how much "green" is present this would be best measured by measuring the wavelength of light that is the least reflected, or the most absorbed, so the green pigment absorbs most of this light and the light that is not absorbed will tell of how much green stuff was there to absorb it. When it comes to the why for turbidity I am a tad stuck and I think it is because we appear to have a mixture of definitions above. Perhaps some more concise definitions will shed light. It appears the answer to "why can't we use green light" may help to give a possible answer, as the scattered light is the measure of turbidity and that would be with some margin of error, what we have isolated?

Usually when measuring materials in a spectrophotometer we want to use the absorption maxima to minimize the signal-to-noise ratio, that's why for pigment measurement you'll use the maximum point. But when you measure two materials you want to take two measurements with as little correlation as possible, that is to avoid one material influencing  your measurements of the other.
Imagine you are trying to breed C. marina for more pigment. Obviously more algae = more pigment so you want to measure how much algae you have and normalize by it. If you'd measure alga density in a wavelength correlated with chlorophyll content you'll get inaccurate results.
I think the question is ill-worded. You should measure at the pigment's absorption minima and not at the alga absorption minima. As the alga can have other peaks unrelated to chlorophyll. When doing this you should remember that chlorophyll and many other pigments are insoluble in water but your measurements of live cells are, usually, in water media.
The best in my opinion and that is the method I'm currently using is to build your own curve by counting cells in some manner (like hemacytometer) and measuring the full spectrum (Your graph stops at 750nm, I got up to 1000nm).


Oregon - Tree Identification Western cascade forest, definitely was planted. In a clearing in the forest along with some western red cedars. I couldn't find anything that would match it when looking for native Oregon trees.

I'm thinking this is a Taxus brevifolia, otherwise known as a "Western Yew". They're most commonly found in the northwest region of the United States; so, even if the tree was planted, it's quite probable that it was still acquired (somewhat) locally.

I had a difficult time finding an image that so directly matches the bark image you provide, just from where that tree is so young, but I was able to find a matured version of the tree, which still has a similiar color and bark pattern. I believe that when the tree matures, the vien-like bark sheds, which results in the "scarring" that can be seen in the following image.

And then here's a few images that show the foliage. Notice the similarities in how the pines flare out, and the coloration of the branches. Once your tree matures, it'll get darker in color and develop small red berries, as can be seen in the following images.

The mature tree is on the left, and the right is still developing (which is most accurate to your images).

There is a small chance that the species provided by this answer is inaccurate, but I'm sure it's at least within the Taxaceae family.


books for beginners in research in mathematical biology I am a M.SC(mathematics) student. I have no subject like mathematically modelling.But  i'm interesting in research in mathematical biology.Initially which book i should study.
Please guide me.THANKS...

Probably the best contemporary book taking a broad view of mathematical biology modeling is Otto and Day's 2007 book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution published by Princeton University Press.

There are also a number of books that focus on more specific areas e.g. mathematical population genetics, ecological modeling, infectious disease epidemiology, etc. But without knowing which areas of modeling interest you it is difficult to recommend at this level.


Do humans emit more carbon through respiration or defecation? Where does most of the carbon we ingest go? I understand that a large amount is exhaled as carbon dioxide, but what percent is defecated (and theoretically deposited in the ground)?

The short answer
In a comparison between exhaled and faecal carbon, exhaled carbon wins.

The long answer
Warning: Assumptions, approximations and averages ahead.
Calculating faecal carbon excretion
The average human being produces about $29 \text{ g}$ faeces (dry weight) per day, the major component of which is bacteria [1]. For now, neglect variations with fibre and other dietary components. Also, assume that all of it is bacteria.
Now, carbon makes up about $50 \%$ of bacterial dry weight [2]. Thus daily carbon excretion in faeces is about $15 \text{ g}$.
Calculating carbon exhalation
An adult human being breathes about $20$ times a minute [3]. Each breath has a volume of about $500 \text{ mL}$ [4]. Thus the exhaled volume per day is $20 \times 60 \times 24 \times 500 \text{ mL} = 1.44 \times 10^7 \text{ mL}$.
Exhaled air is about $4 \%$ carbon dioxide [5]. The density of carbon dioxide at $37 \  ^{\circ} \text{C}$ and $1  \text{ bar}$ is $1.713 \text{ kg m}^{-3} = 1.713 \times 10 ^{-3} \text { g mL}^{-1}$ [6].
Hence, the mass of carbon dioxide exhaled per day is $0.04 \times \left(1.44 \times 10^7 \right) \times \left(1.713 \times 10^{-3} \right) \text{ g} \approx 987 \text{ g}$.
And since $\text{CO}_2$ is $\frac{12}{44}$ carbon, the mass of carbon exhaled per day comes out to be $\frac{12}{44} \times 987 \text{ g} = 269 \text{ g}$, which is at least an order of magnitude greater than the figure we got for faecal carbon.
References

Rose C, Parker A, Jefferson B, Cartmell E. The characterization of feces and urine: a review of the literature to inform advanced treatment technology. Crit Rev Environ Sci Technol. 2015 Sep 2;45(17):1827-1879. https://doi.org/10.1080/10643389.2014.1000761.

Lawford H, Rousseau J. Studies on nutrient requirements and cost-effective supplements for ethanol production by recombinant E. coli. Appl. Biochem. Biotechnol. 1996 Mar 1;57-58(1):307-326. https://doi.org/10.1007/BF02941710.

Hooker EA, O'Brien DJ, Danzl DF, Barefoot JA, Brown JE. Respiratory rates in emergency department patients. J Emerg Med. 1989;7(2):129‐132. https://doi.org/10.1016/0736-4679(89)90257-6.

https://en.m.wikipedia.org/wiki/Tidal_volume

https://www.bbc.co.uk/bitesize/guides/z9hycdm/revision/3

https://www.engineeringtoolbox.com/carbon-dioxide-density-specific-weight-temperature-pressure-d_2018.html


Why can ATP not be stored in excess? I just learned that ATP can not be stored in excess and is only made by the body when it is needed. What makes ATP, like glucose and fat is what is stored under the skin or wherever. Now why cant the body just produce ATP and store it for heavy, heavy exercise when it would advantageous for it to be ready rather than it going through the production phase and then used. When I say ATP storage I mean in large amounts.

Let's compare ATP, glucose and fatty acids in terms of energy storage.

ATP has a molecular weight of 507 Da
Glucose has a molecular weight of 180 Da, and contains the same amount of energy as 31 ATP molecules
Fatty acids vary in size, but a gram of fat contains about twice as much energy as a gram of glucose (or glycogen)

The difference in energy density is huge, you would need enormous amounts of ATP to replace glucose/glycogen as energy storage mechanism, not to speak of fat. You can't put an arbitrary amount of ATP molecules into a cell, you 'll get into problems due to the osmotic pressure lots of molecules inside the cell would cause. Glucose is stored as glycogen in cells due to this effect, which makes one large glycogen molecule out of lots of glucose molecules.

The energy density difference is even larger if you take into account that ATP and glucose bind water, while fat is stored without surrounding water. The actual difference in energy density of glycogen and fat is around 6 times.

ATP is also not as stable as fat, it can get hydrolized in water. This would be a problem for long-term storage of energy.

You'll find some more details in Albert's "Molecular Biology of the Cell"


What exactly is this small puffer fish doing and how did it manage to accomplish such a feat? I recently saw a video on youtube  where it shows a puffer fish making intricate designs in the sand:

OZZY MAN VIDEO

The puffer fish made this design on the sand:

What exactly is the puffer fish doing and how is it capable of accomplishing such a feat?  Is this behavior learnt, or innate?

A tiny Japanese puffer fish creates a grand sand sculpture on the featureless seabed by using his fins to dig furrows. He uses this to attract the attention of passing females.

  Why do puffer fish build sandcastles? (BBC)

  Further observation revealed that this “mysterious circle” was not just there to make the ocean floor look pretty. Attracted by the grooves and ridges, female puffer fish would find their way along the dark seabed to the male puffer fish where they would mate and lay eggs in the center of the circle. In fact, the scientists observed that the more ridges the circle contained, the more likely it was that the female would mate with the male. The little sea shells weren’t just in vain either. The observers believe that they serve as vital nutrients to the eggs as they hatch, and to the newborns.

  http://www.spoon-tamago.com/2012/09/18/deep-sea-mystery-circle-love-story/

Here is the source of the video:

Puffer Fish Constructs A Masterpiece of Love - BBC Earth (YouTube)

The following papers analyse said structures and the ethology in more depth:

  We report that male pufferfishes (Torquigener sp., Tetraodontidae) constructed large geometric circular structures on the seabed that played an important role in female mate choice. Males dug valleys at various angles in a radial direction, constructing nests surrounded by radially aligned peaks and valleys. Furthermore, they created irregular patterns in the nest comprising fine sand particles. The circular structure not only influences female mate choice but also functions to gather fine sand particles in nests, which are important in female mate choice. Strangely enough, the males never reuse the nest, always constructing a new circular structure at the huge cost of construction. This is because the valleys may not contain sufficient fine sand particles for multiple reproductive cycles.

  Role of Huge Geometric Circular Structures in the Reproduction of a Marine Pufferfish (2013)

  Here, we examined the process of the outer ring construction, and extracted the ‘rules’ followed by the pufferfish. During construction, the pufferfish repeatedly excavates ditches from the outside in. Generally, excavation starts at lower positions, and occurs in straight lines... A simulation program based on these data successfully reproduced the circle pattern, suggesting that the complex circle structure can be created by the repetition of simple actions by the pufferfish.

  Simple rules for construction of a geometric nest structure by pufferfish (2018)


What is a "homologous pair" of chromosomes in cross joining or cross over? I never understand if the chromatids attached at the centromere is a homologous pair, or the male and female chromosomes?

The term sister chromatids refers to the pair of chromosomes which have been produced from a single parent chromatid by DNA replication, while a homologous pair refers to chromosomes which are more distantly related (e.g. those inherited from one's mother and father, which I guess is what you mean by 'male and female chromosome').

So the two options you give are identical, and neither are joined together by a centromere. The sister chromatids are joined by the centromere, while the homologous chromosomes exchange material during recombination (cross over).


The arrangement of retinal cells? The section of retina shows a layered arrangement of the various retinal cells. Starting from the inside (where the light strikes first) is the nerve fibre layer, ganglionic layer, amacrine cell layer, bipolar cell layer, horizontal cell layer and finally rods and cones (and that too in inverted position, i.e. the actual receptor portions are farther inwards).

  Why is this stratification inverted? If the receptors would have been the innermost cells, they could have received the maximum
  quantity of unaltered light. Does this "inverted" arrangement, i.e.
  arrangement with the receptor cell behind a screen of several other
  layers not hinder the process of photoreception by blocking a lot of
  incident light and hence the formed image? What is, if any,
  advantage of this reverse arrangement?

I don't have an other explanation than pointing to evolution. It was obviously not a problem to evolve the way it did. One article I found (see "The Inverted Retina: Maladaptation or Pre-adaptation?") called it a sign of pre-adaptation, where forms exist before they get their final function.
Another pretty comprehensive review can be found here: "Evolution of Phototransduction, Vertebrate Photoreceptors and Retina."


What kind of spider is this from Nova Scotia, Canada? What kind of spider is this? It was found in Nova Scotia, Canada and is about the size of a quarter.

That is an Araneus diadematus, a kind of garden orb-web spider.

Orb-weaving spiders are quite common, and can be found nearly anywhere in the world, excluding Greenland. The following is a distribution map for the species A. diadematus, of which, as you can see, is mostly contained to North America & Canada.

Dark gray: present; Light gray: no record. (source)


What happens to the red blood cell in CaCl₂ solution? Here's the problem:

One red blood cell is placed in a hypertonic solution of NaCl, another is
placed in a solution of CaCl2 equimolar with the NaCl solution. What
would you expect to happen and why?

My reasoning is that the red blood cell will shrink due to water loss by osmosis when placed in hypertonic NaCl. It will shrink even further due to the larger osmosis gradient due to there being such low concentration of Ca2+ normally in the cell. However, I'm not sure if this is right so could someone please explain the correct answer?

The reason why the cell would shrink more in CaCl2 solution is because it has a higher van't Hoff factor i.e. total number of dissociated ionic species per solute molecule (it is 2 for NaCl whereas it is 3 for CaCl2).

(Nonionic solutes do not dissociate and will therefore have a van't Hoff factor of 1)

Osmotic pressure (and other colligative properties) are proportional to van't Hoff factor. Therefore osmotic pressure in CaCl2 solution will be 3/2 times of that in an equimolar NaCl solution.

Note that the ionic chemical potential is not what drives osmosis; it is the differential concentration of water (or any other solvent) that drives it.


Implications of what the discovery of Naia means Recently a discovery was made of a ~12,000 year old girl in Hoyo Negro in Mexico.

This has been covered by many different news agencies.

I'm confused however by many of the reports.  Does it strengthen the hypothesis that the ancestors to the Native Americans came over the Bering Strait?  Or is there still some doubt on the matter?

Additionally, what are the arguments against the Bering Strait migration?

The discovery strengthens the bering strait land bridge hypothesis because if I remember right they did genetic analysis and her ancestors were almost certainly east asian. As for opposing migration models, they involve boats. Some evidence exists for polynesians reaching the west coast of south america, but probably in small numbers and not before humans walked in from the north. There is more information here: https://en.wikipedia.org/wiki/Models_of_migration_to_the_New_World


How to validate the regulatory interactions inferred from gene expression data? My algorithm learns regulatory interaction between genes using Bayesian Network approach from gene expression data. After the algorithm has converged to a network of interacting genes, how to validate that the interactions are correct? I have used Lung Cancer dataset from NCBI GEO with ID: GDS2771. Also, how to get the set of genes responsible for a disease (in this case lung cancer) , and how to quantify their expression levels as over or under expressed?

You can validate the interactions by knockding down (KD) or overexpressing (OE) a gene and checking the change in expression levels of the downstream nodes. You can do this in a high throughput fashion using microarray or RNAseq. For protein you can do an LC-MS. However this method cannot help you in:

Differentiating direct vs indirect interactions
Finding regulation in case of loops and other non-linear interactions in the network

Loops are tricky but sampling at multiple time intervals can let you know if oscillations exist or not. For most usual cases this approach works out.

Usually this is followed by another round of validation using a relatively low throughput but sensitive technique such as

Real-time PCR (KD vs OE)
Western blots (KD vs OE)
Reporter assays (KD vs OE) would detect direct interactions. For e.g. possible promoter for a (Transcription Factor) TF (upstream of gene-Y) is used to express GFP to see if GFP responds to the TF; thereby validating the effect of TF on Gene-Y via the promoter.

In some cases you may have to do ChIP-seq to find out if a gene has binding sites for a TF in its promoter/enhancer. You may also use predictions for TF binding sites. For finding regulation by miRNAs you can see this post.

For finding complex dynamics such as pulses and oscillations you have to collect time-course data.

  how to quantify their expression levels as over or under expressed?

For that you first need to define your control (up/down regulated wrt what?). Having done that you can compare the expression and use right statistical tests to check differential regulation. If you have just one sample then most tests won't work. For RNAseq,  EM algorithms are used which use a bayesian model to obtain likelihoods and p-value (I have used cufflinks and eXpress). Then a FDR correction can be performed when comparing the test vs control. I am not very sure about algorithms used for comparing LC-MS data for proteins.


Is lysergic acid diethylamide (LSD) metabolized in the body? Is LSD broken down into other compounds by enzymes or hormones? If so, at what point and where in the body does this happen? I researched several papers appearing in a google search, but unfortunately I did not understand most of it.

Short answer
LSD appears to be enzymatically broken down in the liver.

Background
First off, hormones do not break down anything; enzymes are the work horses that mediate metabolism.

According to a review paper (Passie et al., 2008), humans metabolize LSD into structurally similar metabolites (Fig. 1) by NADH-dependent microsomal liver enzymes to the inactive 2-oxy-LSD and 2-oxo-3-hydroxy LSD. LAE is formed through enzymatic N-dealkylation of the diethylamide
radical at side chain position 8. Di-hydroxy-LSD and nor-LSD are also metabolites, as well as 2-oxo-LSD, 13- and 14-hydroxy-LSD as glucoronides, lysergic acid ethyl-2-hydroxyethylamide (LEO), and trioxylated LSD.

Note that the monoamine oxidase (MAO) system is unlikely to break down LSD. MAO are enzymes that catalyze the oxidation of monoamines. Monoamine neurotransmitters contain one amino group that is connected to an aromatic ring by a two-carbon chain (such as -CH2-CH2-). This structure is not present in LSD (fig. 1). A cursory Google Scholar search did not yield any relevant hits ('LSD' + 'monoamine oxidase'), loosely indicating that MAO is unlikely to be involved in LSD metabolism. However, as I suspect some self-help here - I am unsure about MAOI and LSD interactions, and I highly discourage any toying around with MAO inhibitors and any drug in general. For example, 5-HT is a typical example of an MAO substrate and LSD impinges on 5-HT2A receptors. Hence, interactions in pharmacodynamics with combined LSD and MAOI intake are likely to occur.

Fig. 1. LSD metabolites. source: Passie et al. (2008)

Reference
- Passie et al., CNS Neuroscience & Therapeutics (2008); 14: 295–314


What portions of the brain have drastic changes in activation when we "sense" someone is there? I was watching an old Arnold Schwarzenegger movie ("Commando") where he plays an elite soldier (surprise).  An enemy tries to sneak up on him, and Arnold says that he smelled the other guy approaching.  While this is possible, I find it to be more hyperbole than truth, but what modalities and areas of the brain would he would harness for this detection task?

All of us not being super soldiers, we do occasionally get a feeling when someone has entered a room silently behind us.  Is it audible clues that fall below a certain threshold, is it the sensation of air moving in a the room, some sort of vibrational or proprioceptive sensation, or a combination of all three of these?

First of all one should tell that one can attribute the activation of certain brain zones with some indepent events only when the activation takes place along the signal input (receptors, sensory pathways towards the cortex and the sensory areas in cortex) or motor action (=output) (along the motox cortex => motor neuron => target organ). Those zones in brain are also termed as primary ones, for there is a clear mapping between the event/action and the activity here.

In case of your "sneak feeling" as you describe in your post, there seems to be more not the sensory input from some unknown type of receptor, but rather a subconscious processing of the complete sensory input that reveals some potential danger and is percepted as a kind of "smell of danger". Since this processing happens in secondary zones and can be well distributed throughout the whole brain, there is no possibility to find a single focus with high activity change here (in my opinion, of course) -- those changes in activity are beyond the measuring/imaging capabilities of modern examination methods.

Possible sensory inputs here might include (but not limited to):

Optical (some shades, moving asyncronously etc).
Acustic (some sneaking sounds, normally disguised by the background sound).
Air move, air stream blocking sense etc (tactile feeling).

So, everything you suggest might apply here.


Are there any theories why such an imbalance in chirality of molluscs? Most gastropods exhibit sinistral  (right hand) winding of their shells. But very few species are anti sinistral. Have there been any theories as to why such a great difference?

Why so many molluscs exhibit sinistral winding?

The estimates of the number of molluscs vary quite greatly between 50,000 and 200,000 species. Of those molluscs species, about 70'000 are Gasteropoda. Gasteropa is most diverse Mollusca phylum.

The winding you describe is present in all Gasteropoda and is often called the torsion. So the answer to why there are so many molluscs that make a torsion is simply, because of phylogenetic independence. The torsion evolved only once in the gastropods. The answer to the more specific question, why is the torsion right handed rather than left handed in all gastropods is 1) phylogenetic independence again. The torsion evolved only once and was therefore either sinistral or anti-sinistral. There is no need for an explanation of why they are all sinistral because the observations are not independent.

Why has the torsion evolved at first place?

One may ask but why did the torsion evolved at first place?. I think the reasons are still to be discovered. The following is a summary of what I read on wikipedia (torsion#evolution)

"Why torsion is bad"

As a result of this torsion, the anus is found next to the mouth which is an obvious hygiene issue and therefore seems rather deleterious. Moreover, there are a whole bunch of issues about organs spinning around and entwining. Also, ventilation seems to be reduced by the torsion which is pretty deleterious.

"Why torsion is good"

However, because there's no "hole" left in the posterior position, the torsion may help preventing sediments. Some have suggested that the torsion may allow to move sensory organs closer to the head. The most likely explanation is that the torsion might have evolved as a defense mechanisms against predation as torsion allow an organism to hide its head behind its shell. Finally, citing from wikipedia:

  The evolution of an asymmetrical conispiral shell allowed gastropods to grow larger but resulted in an unbalanced shell. Torsion allows repositioning of the shell, bringing the centre of gravity back to the middle of the gastropod’s body, and thus helps prevent the animal or the shell from falling over.

Note also that

  Whatever original advantage resulted in the initial evolutionary success of torsion, subsequent adaptations linked to torsion have provided modern gastropods with further advantages.

Why sinistral rather than anti-sinistral

To repeat myself, we only have one single observation of torsion (as it evolved only once) and this observation is either sinistral or anti-sinistral. It sounds therefore quite likely that stochastic processes have driven the evolution of sinistral (rather than anti-sinistral) torsion. In other words, the first mutation allowing for some degree of torsion was probably causing a sinistral torsion and this is it.

But there might eventually be a more functional reason for why torsion evolved to be sinistral. The reasons would then be related to the already existing asymmetry of organs. For example, anti-sinistral torsion may yield to more entwining between the gut and the respiratory system, or to not squeeze too much the one lung, who'd be smaller than the other one due to the presence of circulatory organs. I don't have enough knowledge in the anatomy of the molluscs ancestors to have a good intuition of whether I'd expect sinistral or anti-sinistral torsion to be more beneficial.


The Ancient Kingdom of Monera Why exactly were bacteria and archaea kingdoms separated from the now unused kingdom of Monera? Aren't they the same? They are both prokaryotes, so what is the difference?

I'm surprised this term shows up much anymore. Though it's a part of history now, the following paper by Woese demonstrated the three domain system long ago.

This, however, is the net result of the sequenced genomes of eukaryotes, archaea and bacteria:

Source: Toward automatic reconstruction of a highly resolved tree of life.

The phylogenetic differences between these organisms shed light that bacteria and archaebacteria were not as closely related as was initially though, hence the abolishment of Monera.


Help identifying a weird creature Okay, so there is this weird creature, which has been crawling around our house.
I can hear it moving around, and it's especially active in the dark. I've however been able to take a picture of it.
If it helps, it's a carnivore (I've thrown some hot dogs and such).
This weird thing is 25-30cm long, and the picture of it was taken from a balcony on the second floor. I've only been able to photograph it once, but never came close to it otherwise. We live in central Europe, in a small town that somehow resembles a village. As for the ecosystem, I don't quite know. Fields, rivers and forests are all in proximity of our house.

Thank you for your anwsers,

The black and white colours on the front and the grey back as well as the overall shape make me think it could be a badger. Given the location, it could be the European badger (Meles meles). The size matches, and badgers are omnivorous, so they can eat meat.


What's the technical terminology for call-and-respond type behaviour? The groups of some species such as water birds display a behavior that once out of line-of-sight a member will periodically initiate an interaction by make some type of sound, which will be followed up by responses from all the other members - presumably to confirm they haven't been silently snatched by a predator. I have observed this in person at a local botanical garden where the water birds sound off like this every 10 minutes or so all day long.

What is the technical term for this behavior and some examples of species that demonstrate it?

if you are referring to call and response in rapid succession, ethologist use the terminology "turn-taking" or "antiphonal calling".
Many species do it with different degrees of precision.
A rapid research on google scholar will give you several results.
I do not know whether it would apply specifically to your case, which might be more general and it could be simply "contact calling".

Regarding the hypothesis you formulated ("(...)presumably to confirm they haven't been silently snatched by a predator"),   it would be nice to know if actually everyone respond, who is calling first (always the same individual?) and if they would behave different if someone does not reply.

Hope it helps and have fun with your observations.