Do acetic acid bacteria use the electron transport chain when converting ethanol to acetic acid? Do acetic bacteria use the electron transport chain when converting ethanol to acetic acid?

And is wikipedia inconsistent here in its definition of fermentation. It says fermentation

  Fermentation takes place when the electron transport chain is unusable

(and this is consistent with (academic) microbiology books searchable on google books).
Wikipedia defines acetic acid bacteria as

  produce acetic acid during fermentation.

also

  Some genera, such as Acetobacter, can oxidize ethanol to carbon dioxide and water using Krebs cycle enzymes. Other genera, such as Gluconobacter, do not oxidize ethanol, as they do not have a full set of Krebs cycle enzymes.

I read in microbiology books on google books, that acetic acid bacteria use oxygen as the terminal electron acceptor, and have a respiratory mechanism.

Brewing Microbiology edited by Fergus Priest p165

  Acetobactor spp. possess a respiratory mechanism...Acetobactor spp. are obligately aerobic with a respiratory metabolism (O2 as the terminal electron acceptor)

So is wikipedia wrong to describe acetic acid bacteria as using fermentation?

I see mention of krebs cycle though, which I understand to be associated with respiration rather than fermentation. Also in this reaction/process :

$C_2H_6O\hspace{1mm}(ethanol) + O_2 \rightarrow C_2H_4O_2\hspace{1mm}(acetic\hspace{1mm}acid) + H_2O$

I see water mentioned but not carbon dioxide(if it had both I'd say that really looks like respiration, though it's being called oxidative fermentation).  So I still can't really see whether it's respiration or fermentation, though it's being called fermentation (oxidative fermentation), yet there is the mention of krebs cycle enzymes (krebs cycle being associated with respiration), so it makes me unsure whether the electron transport chain is used or not.

Yes

I find it somewhat ironic that in a response a recent post from the poster concerning itself with the precise definition of ‘fermentation’ I argued that this was a semantic question because of the use of the term in the English language before any biochemistry was known. I now discover that the term is used in an even looser sense than I was aware of — in an aerobic context. The conversion of ethanol to acetic acid by acetic acid bacteria is apparently referred to as oxidative fermentation as explained in this extract from a paper in The Journal of Bacteriology:

  Acetic acid bacteria are obligate aerobes that belong to the α-Proteobacteria and have a strong ability to oxidize ethanol, sugar alcohols, and sugars into their corresponding organic acids. Such oxidation reactions are traditionally called oxidative fermentation, since they involve incomplete oxidation of these compounds. These bacteria accumulate the corresponding incomplete oxidation products in large quantities in their surrounding environment.

The biochemistry is summarized by Gómez-Manzo et al.:

  Ethanol fermentation by acetic acid bacteria is carried out by two sequential reactions catalyzed by pyrroloquinolinequinone (PQQ)-dependent alcohol dehydrogenase enzymes (ADH) and aldehyde dehydrogenase (ALDH), which are located in the cytoplasmic membrane [6] and transfer electrons to ubiquinone Q10 [7]. PQQ-ADH is a periplasmic quinohemoprotein-cytochrome c complex and catalyzes the first step of ethanol oxidation by transferring electrons to Q10 and producing acetaldehyde which usually is the substrate for another enzyme (ALDH), and converted to acetic acid during the second step of ethanol fermentation.

The fact that the reduced pyrroloquinolinequinone is re-oxidised by ubiquinone, indicates that the conversion of ethanol to acetic acid requires the electron transport chain in the bacterial membrane to continue, and that the ultimate electron acceptor is oxygen.


Do changes in an organism's cell modify the genetic information it uses for reproduction? What I'm actually interested about is whether a modification in one cell during the life of an asexually reproducing organism affects its genetic information? Which cell's genetic information is used during reproduction like budding, for example in the case of Hydra.

Or does the incidental advantage it could have given rise to disappear with the death of the organism?

In multicellular organisms there are specialised cells called gametes that are responsible for sexual reproduction (sperm/ egg cells). Mutations occurring in these cells can be passed on to offspring (germ line mutations). Mutations occurring in others cells affect only the given individual (somatic mutations).

Edit:
For unicellular organisms it is pretty straight forward, the daughter cells formed through fission are identical. As for multicellular organisms here are many forms of asexual reproduction, and even these may involve the formation of specialized cells (eg. spores). So my answer is: it depends on the type of asexual reproduction and the actual cell(s) that accumulate mutation(s). For example in parthenogenesis - where the unfertilized egg cell develops into a new individual - , a mutation can be inherited if it occurs in the germ line cells generating the egg cell, but any somatic mutation would stay in the parent. You can find detailed info on asexual reproduction with details on each form on this wiki page


Different Effects of Detection Probability Between Presence and Count Data at the Same Location I'm modeling habitat suitability for a large, mobile animal using occurrence data (presence only - I have no true absence data in this case) collected from camera traps (stations with automatic motion/heat sensing cameras). At each camera trap location I have 0 to several occurrences recorded.

Typically, when such data is modeled, they are modeled as count data, and detection probability is included in order to mitigate for covariates that affect detection, which otherwise may be identified as covariates that affect suitability. For example, an area where detection is less likely due to, say, dense vegetation, may be mistaken as less suitable due to that vegetation structure when in fact that may not be the case (or even the opposite may be true).

My question is, if the count variable were to instead be used as a detection/no-detection variable (so, a binary) would the probability of detection have less of an effect on the model (*when modeling relative suitability, not probability of occurrence)? i.e. if you didn't account detection probability, would using a binary response variable give you a less biased estimate of habitat suitability than if you were to use count data? And if so, why? It doesn't seem like probability of detection would change, or would be more homogeneous across the study area with this change, but it seems like the effects would be smaller in magnitude by not reinforcing differences in detection probability with multiple occurrences.

Also, I understand that it's not desirable to toss out all the other occurrences assuming you can calculate detection probability. I'm asking this in an attempt to better understand the possible differences in outcome between these two modeling approaches when using such data, as I've seen both methods in the literature, but have not seen this question specifically addressed. If you could reference any publications that may shed light on this, I'd be very appreciative.

Disclaimed: Not really an answer, but too long for a comment

If I understand you correctly, this must depend entirely on the accumulated probablity of detection over the entire detection period (the time the cameras were out). If the accumulated probability of detection across all habitat types is high (approaching 1, given that the animal is present), then the detection probability shouldn't be a problem for the binary occurrence variable. An indication of this would be if you have sites (cameras) with either zero or a very high number of occurrences, which should indicate that the binary occurrence is rather robust. On the other hand, if sites have 0-4 occurrences in total it will be extremely difficult to separate non-occurrence from random factors or detectability. I assume that the detection probability across habitats is unknown though (as well as the accumulated probability of detection), but you might be able to make an educated guess. Also, by using a binary response, you will completely exclude the possibility to estimate e.g. an effect of habitat quality (for instance a difference in abundance between habitats), since counts of 1 or 13 will both be represented by 1 in the binary detection variable. In the Q, you talk about "modeling relative suitability" which indicates that you are indeed interested in something similar to this (relative habitat quality). In that case, I think that a binary response will be too coarse to provide useful information.

One possible toy scenario could be that you have two habitat types A and B (10 camera locations/sites of each) with a binary detection variable as:

A: 1 1 1 0 1 0 1 1 0 1  (species found in 7 sites)
B: 0 1 0 0 1 0 1 1 0 0  (species found in 4 sites)

In that case, the species can obviously exist in both habitat types (as you have categorized them), so the higher amount if zeros in B can represent (among other things) 1) lower occupancy of this habitat (in a metapop perspective), 2) that the quality of B is heterogeneous which is not captured by your habitat categorization (so parts of B is just as suitable as A), 3) lower population abundance in B compared to A (but the same detectability), or 4) lower detectability in B compared to A (but the same abundance). I don't really see how you can separate between these cases with only the binary variable, and I don't believe that using a binary detection variable will solve any specific problems compared to using the count data.

This is all very hand-wavy, but can hopefully give you some useful ideas/perspectives.


How is eye color in humans inherited? In high school we studied the inheritance of eye color, as it was explained to us in the most simple way: blue eye color is a recessive, monogenic, autosomal trait. Now I know that it is a bit more complicated than that; there are several genes which determine the inheritance of eye color. That's as far as I my knowledge goes.

Which are these genes and what do they encode for? How is the eye color trait inherited? Provided that a man with blue eyes and a woman with brown eyes have a child, can the probability of their child to have blue eyes be calculated?

It is mainly determined by the OCA2 gene, but it also likely involves several other genes, including TYR, TYRP1, HERC2, and several others. To complicate things further, it is not a "mutant/wild type" trait, but multiple normal alleles can be found in the population, and it is believed that the sum of these single nucleotide polymorphisms (SNPs) determine the final phenotype.

I took the info from a 2004 review by Sturm and Frudakis and a more recent paper from Liu et al, 2009


What promoter is required for expression of a human protein Y in bacteria? This is the actual question. It's from an entrance test for a research institute:

A scientist wants to express human protein Y in bacteria. For effective expression of this protein he should use
(A) promoter of human gene Y. (I think this is the correct one)
(B) promoter of bacterial gene.
(C) operator of any human gene.
(D) operator of any bacterial gene.

I think my answer is right although I am not sure if my thinking is entirely correct.

Canadianer has very deftly enabled me to arrive at the answer with knowledge I already had. I attempt to explain the same here.

We know that eukaryotes and prokaryotes have different RNA polymerase (enzyme responsible for transcription) enzymes. Eukaryotes have three different RNA polymerase, each responsible for synthesis of the three different types of RNAs. RNA Polymerase II is responsible for mRNA synthesis in eukaryotes. It recognises the eukaryotic (or say, human) promoter present in an eukaryotic cell. On the other hand, in prokaryotes, there's only one RNA polymerase responsible for synthesis of all the types of RNA.

Coming to the question, using a human promoter is probably logical since it would be ideal for initiation of transcription of the said human gene Y. But this is not true because a promoter is only responsible for recognition by RNA polymerase and allowing it to move further and transcribe the DNA sequence i.e. it doesn't matter what comes after a promoter. Also, prokaryotic RNA polymerase is unlikely to recognise the sequence of a human promoter. It is much more likely to recognise a bacterial promoter. Since a promoter's function is limited to allow recognition, it doesn't matter that it's a bacterial promoter as long as it can be recognised.

The two options about operators weren't a confusion for me since I already know that they don't have much to do with expression of gene as much as regulating it. Besides, any operator used would also require a promoter in any case, since that is how transcription is initiated.

Thus, the scientist should use a bacterial promoter.


Is a large tumor is more likely to develop hypoxic regions? It is known that cancerous tumors in humans can develop hypoxic regions where no blood nor oxygen arrive to some volume of its cells, creating a dead lump inside or around the tumor.
See Wikipedia - Tumor hypoxia.

  Are hypoxic regions and regions without blood supply are more common in large tumors than in small tumors?
  What is the likelyhood or frequency of hypoxic regions in small (< 2 cm) and large (> 4 cm) tumors?
  What is the typical size of an hypoxic region within a tumor?

The article in Wikipedia is too techincal and very hard to be read and understood, and doesn't have an explicit answer to my question.

The prescence of hypoxia is independent of size, grade, or histology. It occurs due to a cut off in blood supply to the tumour. Or insufficient vasculature systems, meaning the oxygen cannot diffuse all the way into the tumour. Aberrant growth of tumours can increase the likelyhood of tumours developing hypoxic regions.


What mechanisms exist for the excision of specific sequences from DNA? I already know about recombinases (specifically excisionases), but was wondering if there were other mechanisms present.

Genome editing techniques like CRISPR-Cas and TALEN use non-specific recombinases coupled to a DNA-recognizing part that can be designed to be specific for any stretch of sequence, as it is constructed out of single zinc-finger 'modules' that each specifically bind a couple of nucleotides (one nucleotide each in the case of TALEN).


Genetic networks vs genetic architectures? What is the difference between the terms genetic network and genetic architecture? I've heard both in a variety of contexts used by different people, so I am interested in what people think they mean, other than what is described in Wikipedia:

Genetic architecture refers to the underlying genetic basis of a phenotypic trait

Genetic regulatory network (GRN) is a collection of DNA segments in a cell which interact with each other indirectly and with other substances in the cell, thereby governing the rates at which genes in the network are transcribed into mRNA.

EDIT: so what I take from the answers so far is that a genetic network is the molecular wiring of all the interacting loci, whereas genetic architecture describes the phenotypic consequence(s) one would be able to see from that network. Then, trying to bring the two definitions together, if we would assume we knew all the molecular details of a genetic network, we would only need to add the other factors in the model, such as environmental perturbations, to end up with the description of the genetic architecture, right?

You can think of a genetic network as a network of interacting genes, turning each other on and off based on complex relationships and external stimuli. A genetic network is typically characterized in terms of graph theory--connectivity, density, etc.

The term genetic architecture, on the other hand, typically refers to a trait or phenotype and the characteristics of the gene(s) that contribute to that phenotype (this is what the Wikipedia article means by genotype-phenotype mapping). Characterization of a phenotype's genetic architecture involves describing how the phenotype(s) is/are related to the genotype(s). For example, for a particular trait or set of traits, is there a one-to-one relationship between gene and trait? Or do multiple genes contribute to a single trait? Or are multiple traits affected by changes in a single gene? The relevant terminology is discussed briefly in the Wikipedia article: polygeny, pleiotropy, etc.


Can a fungus become resistant to a chemical such as Potassium Permanganate? A friend used potassium permanganate solution to treat tinea on the hands/feet but after some initial success, the tinea seems to be making a comeback. Could the fungus develop resistance to potassium permanganate?

I don't think a fungus would develop resistance to something so quickly.
As Chris suggested in the comments, it could be because "The disinfective effect is based on the production of reactive oxygen species. The problem is that the solutions used for this purposes are not very stable." So, if fresh solution haven't been used, it may be ineffective.
As commented by @inf3rno, fungal infections could be much deeper and hence, "treating" them superficially may not help much.


Are there mechanisms that limit the amounts of time conjugation and F-plasmid transfer can happen? If yes, what are they? Not all bacteria have acquired F-plasmids through conjugation. Some of the mechanisms for this are unsuccesful conjugation events (mechanical disruption), no transfer due to integration in bacterial chromosome, etc (See previous question and answer).

Now I am wondering if there are also mechanisms that self-limit the conjugation and transfer of F-plasmids. For instance that a bacterium can only transfer its F-plasmid once during its lifetime.

Yes there are many such mechanisms.

One of the simplest, but perhaps most easily overlooked, is metabolism.  Conjugation requires ATP.  In environments with low levels of nutrients, heterotrophs might not have enough "extra" ATP to fuel the conjugation process.  Note that both donor and recipient need to expend ATP in conjugation.  The donor needs to make the nicking enzyme, the pilus, and extrude the DNA into the recipient, and the recipient needs to synthesize DNA from the single-strand DNA that it has received.


Is there any problem with using a single stop codon with a single CDS in prokaryotes? All protein coding sequences in the iGEM Registry are supposed to end with a double stop codon. Presumably, this is to decrease the potential for read-through, which could be problematic if one is putting together a polycistronic design.
If the design is intended to have only one CDS, however, and is targeted at a prokaryote (which have "backup" ribosome release mechanisms), then is there any problem with using only a single stop codon?

If there is only one CDS, presumably there will be a transcriptional termination directly after the CDS (after the stop codon actually), which makes any read-through coming from using a single stop codon almost negligible.


What brazilian snake is this? (1) Is it possible to identify the snake in the picture below?

If (1) cannot be answered:

(2) In view of the pattern of colors, is it possible the snake in the picture below be non-venomous? If so, what kind of non-venomous snake?

Additional informations:

Size: 62cm.
Region: South of Brazil, noutrh of Paraná.
I do not have a picture of the head.

Pictures:

The triangular pattern and the lightly colored underside resemble typical patterns of Bothrops (lancehead viper). Without the head it is quite difficult to tell which species this is. Given the location, the most common lancehead viper would be Bothrops jajaraca, simply called Jararaca by the locals.

Images can be found here


exercise of gene linkage in genetics Could you help me solve this problem:
AAbbCC is crossed with aaBBcc and the offspring re-crossed with aabbcc. Considering that A and B are linked and their distance is 12 mapping units, while the gene C is not linked to them, find the percentage of the offspring that will have phenotype aabbcc.
I used this method to solve it (I know it's not correct but I don't know where I am mistaken):
P: AAbbCC x aaBBcc
F1: AaBbCc
AbBbCc x aabbcc
Since the distance between A and B is 12, their recombinant frequency is 12%
88% then is the recombinant frequency of the parental
Dividing by 2, 44% is the RF of parental AB/ab and 44% of parental aa/bb
In conclusion, since gene C is not linked, I calculated the probability to obtain cc from CC x cc, and that's 1/2
So my final result is: 0,44 x 0,5 = 0,22 = 22%

You did right for most of the exercise, but you got confused on one of the (apparently) easiest things.
Try to reason in terms of chromosomes, and not merely of genotypes:
F1 inherit their chromosomes from two homozygous parents, so you know that they are AbC and aBc.
You can visualize the cross with the recessive homozygote as follows:
Ab C     ab c

-- -  X  -- -

aB c     ab c

The second parent will always pass abc, so in order to have an offspring with genotype aabbcc you only need that parent 1 passes abc.
Given that the parentals are Ab and aB and that RF is 12% (0.12), regarding the first two loci, the frequencies of the gametes are
Ab = 0.44
aB = 0.44
AB = 0.06
ab = 0.06

Including locus C, the frequency of the gamete abc is then simply 0.06 * 0.5 (because c is unlinked), and that corresponds to 3%.


Ways to fight black mold Is it possible to introduce a microorganism to a colony of black mold that will kill off the black mold entirely and permanently? Is there a common microorganism that likes to eat them and is harmless to us?

In other words, I ask if there's a way to get rid of the mold biologically, maybe a different mold that at least won't stink?

Alternatively, will getting a UV lamp to shine in the opening once in a while be an optimal solution?

I also read that copper sulfate is a popular fungicide with plantations, will it kill and prevent the mold from coming back? Could this ruin the AC with corrosion or be harmful to people if it will be airborne?

I ask this because I have black mold in my AC and I can't take it apart and disinfect it.

PS: it's probably Aspergillus, they're black and make these white structures like in this picture:

I write this as an answer instead of a comment because I don't have the reputation to do otherwise (frustrating!) even to edit my answer-which-is-now-a-comment

A weak vinegar solution (maybe 1:1 ratio water and vinegar) will solve your problem and will not stink up your home. Vinegar smell evaporates very quickly and are great for areas you can't reach easily to clean by hand. I promise your AC won't smell like egg salad.

Here's the first mold-cleaning with vinegar article I could find, there are plenty more where that came from


Chromatids in metaphase? Please see the following picture:

In my book, the author claims that these chromosomes are in metaphase (a metaphase stopped by cholchicin).
I don't understand why they don't have two chromatids...A chromosome looks, by everything I've learned, like TWO chromatids (http://i60.photobucket.com/albums/h1/GameMaster57/Chromosomestructure.jpg) and should be together in metaphase. These chromosomes only look like chromatids to me (1 of 2 pairs).

Have they been separated?

I am also asked to specify which chromosomes are from the father and which are from the mother. How would I go by doing that?

Thank you.

The chromosomes in your picture do have sister chromatids, they are just very close together. A chromosome needs to pass through replication before it can compact into the typical metaphase chromosome shape depicted above. When I prepare metaphase chromosomes, I usually see a mixture of chromosome sets where the chromatids are close together (like above) and clearly separated. I think this is related to the time each metaphase has spent in the colcemid block-the longer the cell has been blocked at metaphase for, the longer the enzymes that work to separate the two chromatids have acted on it. Also chromosomes keep getting more and more compacted during the colcemid block-if you leave them for too long, they become a lot smaller.  This paper has very cool pictures showing the links between the sister chromatids:
http://www.ncbi.nlm.nih.gov/pubmed/18461479


Why are there no tree-like plants that grow in lakes? Looking at aerial photos of boreal forests, with dense woods clear-cut by quiet lakes, I wondered why exactly are the woods so clear-cut at the edge of water? Why won't trees develop adaptations that will let them grow from a shallow lake bottom, with the lower part of the trunk in the water and the crown above the water?

It seems to me that this would give them some significant advantages. Lake bottoms are rich in organic nutrition, and insolation will also be plentiful above water, at least at first when there's little competition. So why are lakes' surfaces so clear and open, instead of overgrown? Of course there are aquatic and semi-aquatic plants like water lilies, Scirpus or Typha, but they are a far cry from the nearby terrestrial forests, in terms of biomass. Why don't they develop into large amphibian trees, or why don't terrestrial trees try to re-colonize lakes?

Trees need:

Deep roots to get more water and anchor their growth.
Strong trunks to support themselves against gravity.
A vascular system to move water and nutrients throughout the tree.
Small leaves that can be supported high by the trunk to compete for sunlight.

Water plants need:

Just enough root to anchor its location.
No vascular system. Water is everywhere.
Leaves that are more substantial than the stems to gather as much sunlight as possible through the cover of water.

So the kind of body that has to develop under water to thrive is in many ways the opposite of the kind of body needed to thrive on land.

Water plants would have to waste energy on

Vast roots.
A strong trunk.
A vascular system.

...Things it wouldn't need till later while receiving little sunlight on small leaves. It would have to shed its thirsty skin like a snake on the above water parts. Too complex and little or no demand for it.

If water plants had evolved a way to turn oxygen into helium and keep much of it trapped within its leaves, then we'd have tall ocean forests. The plants could grow just like they do now  but with slightly fluffy leaves. As soon as it broke water surface, the abundance of oxygen would ramp up helium production and really fluff them leaves. The slight stems would have to be scrappy instead of massive.

There would be Greek mythology that Gaia was married to Helios but left him for Poseidon the Gaia-Shaker. Poseidon and Gaia were cursed with children (the vast ocean forests) who rebel against them and adopt a lifestyle where they are always reaching out to Helios and later in life shedd their bodies to be closer to him in spirit. Some early humans tried to rob the Helium spirits of the ocean forests by inhailing them out of their plant bodies. They were cursed and turned into chipmunks with only their hands to remind them of their past humanity.

Edit to add reference: A piece by Mickey Walburg on eHow.com

Though I would call mangroves amphibian trees, I wouldn't call them large and I was trying to ascertain the spirit of what @kai teorn was asking rather than let the question sit unanswered when I believe I can answer it.
You learn something new often if you're looking and today @MattDMo introduced mangroves into my awareness. If he thought it was the answer to the spirit of the question post, he might have elaborated on it as an answer instead of a comment. I could be wrong about that.

Mangroves are mostly coastal. They are usually at the edges of the water. The ones that are a few meters in the water are usually more like shrubs than majestic boreal forest trees. They end up shooting roots everywhere and kinda lounge around compared to the typical tree standing straight reaching for the sun. Also the incidences of Mangroves in the ocean away from the shoreline are of maybe a handful bunched up, hardly a species wide return to the the oceans. Seen from aerial photos, Mangrove concentrations look like boreal forests surrounding lakes, not swamp lands.

  Why are there no tree-like plants that grow in lakes?

  Looking at aerial photos of boreal forests, with dense woods clear-cut
  by quiet lakes, I wondered why exactly are the woods so clear-cut at
  the edge of water?

I think the spirit of the next question is about trees in general in lakes. Not the few instances peppered around the world. Also some lakes grow and shrink throughout time, sometimes long enough for trees to gain a little ground and survive lake growth. But I don't think those trees as a species have developed adaptations to grow from shallow lake bottoms.

  Why won't trees develop adaptations that will let them grow from a
  shallow lake bottom, with the lower part of the trunk in the water and
  the crown above the water?

... and from the end of the post ...

  Of course there are aquatic and semi-aquatic plants like water lilies,
  Scirpus or Typha, but they are a far cry from the nearby terrestrial
  forests, in terms of biomass. Why don't they develop into large
  amphibian trees, or why don't terrestrial trees try to re-colonize
  lakes?

... I eliminated mangroves from qualification. Interesting but I still don't think it's what @kai teorn had in mind. I think @MattDMo introduced mangroves as a comment to enhance our knowledge.


Distance matrix with different length sequences In a project we're doing (in python), we want to create a distance matrix for a phylogenetic tree with multiple, different length sequences. However, what we've seen so far (AlignIO in biopython, etc.) requires the sequences' length to be equal. Is there any pythonic way to get the matrix with sequences of different length? Or any other indirect way that would get us to the same result?

There are two possibilities:

Do not use the sequences per se but a scalar metric of sequence similarity for distance values
Introduce gaps in the alignment. You can also do an end to end gapped alignment such as the Needleman-Wunsch and use the alignment scores for the distance matrix.


What causes a polypeptide to fold into an Alpha helix over a Beta pleated sheet I know how they fold, but what causes some polypeptide chains to preferably fold into Alpha-helix rather than Beta-sheets (or vice-versa). What force makes it fold into one conformation over the other?

All the residues in a polypeptide chain tends to configure into their lowest potential energy state. except the peptide bond all the other bonds are free to rotate, alpha helix makes optimal use of internal H bonds. The overall structure is stabilized by H bond between the hydrogen atom attached to the electronegative nitrogen atom of peptide linkage and the electronegative carbonyl oxygen atom. The arrangement of amino acids in the peptide plays a very important role in forming alpha helix. Different combination of amino acids results in different combination of dihedral angels, hence it determines alpha helix conformation.


Primer design for HLA locus i have designed primers for HLA locus DPA1(exon 2 region) based on Real-Time PCR (qPCR) Primer Design guidelines. primer will start from intron regions to cover full exonic region.

F-CAGCAACAGAGAATGTCAGC

R-CCCTGAAGCAGCAATTGATG

to check for amplification of only a single region  i have used in silico PCR UCSC but it shows multiple region from chr6.

pls kindly help me with solving this.

thanks

When designing rtPCR primers always check the extensive and well validated  taqman library for the ABI system, the primers for the region you want are already well characterized:

http://www.lifetechnologies.com/order/genome-database/details/gene-expression/Hs01072897_m1#more-information-section


Can anyone ID this ant queen species? It was found in Hong Kong! Below are a few basic information:

Place: Hong Kong

Habitat: Forest. I live very close to a mountain with lots of forestation.

Where Collected: Found it in my window slit of my apartment.

Coloration: Major body parts are black, but legs are light brown.

Distinguishing characteristics: Appears to have one spine in the mid-body (not sure); Huge mandibles

Length: 14mm to 15mm

Width: 3mm

Anything else distinctive: It could move incredibly fast (like a cockroach). Also, it appears to be quite aggressive. When I put in an ant (male ant with wings) of a different species to its tube, it attacked the introduced ant with its mandibles immediately. During its attack, it shook its abdomen periodically.

The species in the photo is a carpenter ant (Camponotus irritans), possibly C. i. hongkongensis. More info, photos, and video here.


Which viruses still present today caused a deadly pandemic/epidemic in the past? The current Covid-19 pandemic and its virus Sars-Cov-2 can be dangerous, especially for vulnerable groups like the elders. But however, I have seen studies that this virus become less dangerous in the future, when human population has built some immunity against it.
There are many other viruses still present and most of them produce only harmless diseases like the cold. But were some of such viruses really dangerous in the past and cause only mild symptoms on infected persons in present day (due to immunity)? Perhaps thousands of years they caused a bad epidemic?

There are a few viruses which are around for a long time and have caused recurring episodes of disease. Most of these where not pandemic, which is probably more of a problem for modern times due to fast travel/exchange of people and are also a problem of "modern" cities where many people come together in a limited space.
Among theses viruses are:

Measles: This virus is around since at least 400 BC, profiting from the first big cities. (see reference 1 and 2 for more details)

Polio: This virus has been described already in ancient Egypt, although major outbreaks didn't happen before the early 20th century. There is a nice article in Wikipedia about it, see reference 3.

Smallpox: These are only not threat anymore because mankind successfully eradicated them. They have been described first around 1500BC in India, later also in China and Egypt. See reference 4 and 5.

Not viruses but also pathogens which caused historic epidemics: Typhoid fever, Cholera and the Yersinia Pestis (also known as The Plague or the Black Death).
References:

The history of measles: from a 1912 genome to an antique origin
Measles may have emerged when large cities rose, 1500 years earlier
than thought
History of Polio
Emergence and reemergence of smallpox: the need for development of a
new generation smallpox vaccine
History of Smallpox


Spectrophotometric Values of Individual Nucleotides All around the net you will find this list giving 260/280 ratios of individual nucleotides:

Guanine: 1.15
Adenine: 4.50
Cytosine: 1.51
Uracil: 4.00
Thymine: 1.47

Yet I cannot find a reliable source for these values. One source cites a 70s version of Leninger's Biochemistry but even though I got hold of a more recent edition, I cannot find that information in there.

Does anyone happen to know a quotable source for this?

If it's so important to you that you need a quotable source for this, I'd measure it myself with the equipment I use for the real experiment.

Otherwise I'd suggest you look at a chemical database such as NIST:
http://webbook.nist.gov/cgi/cbook.cgi?ID=C58617&Mask=400 and use the spectra that can be found there.


Mechanism of DNA gyrase inhibitor Why DNA gyrase inhibitor, such as Nalidixic acid and Norfloxacin, do not stop gyrase from cutting DNA helix but only prevent them from decatenation replicating DNA?

This might be a good article to read: http://www.ncbi.nlm.nih.gov/pubmed/24497635

Robert Kerns's lab has been doing a lot of work on fluoroquinolines, so look into his other work as an entry to the literature. And apparently X-ray crystals have been done for at least parts of this complex. There is some evidence for fluoroquinolines binding to DNA, then moving into the protein as it moves along the DNA.


Comparing Shine Dalgarno scores, creating a distribution I am in the process of creating a poster for the phage that I recently annotated. The phage is an A4 and the portion of the poster I am working on is analyzing the data that we have collected. I have an excel sheet that has all the Shine Dalgarno scores for each gene that we annotated and decided was the best. Using mathematica I tallied all the data into a table and this is what I got (The x value of the list shows the score, the y value shows the amount of genes that had this score):

How can I create a distribution from this data? Would I need to use a Histogram, a plot, or some other graphic to represent the data?

Biologically speaking, can we make any observations about the genome from these scores?

I would expect to see if every gene has a strong SDS, and that every strong SDS is in a gene (and if not, an explanation of why).

Mathematically, that can be calculated using Fisher's Exact Test (since I don't see any p-values for your scores).

You should also provide a diagram of the genome showing coding sequences or genes, and mark each SDS on it.


How does a cell know what function it has within an organism? Given that all cells in a multicellular organism contain the same DNA (ignoring random mutations during mitosis), how does any given cell know what purpose it is supposed to have within an organism.

For example, how does a cell know to become a muscle cell, a neuron or a liver cell?

The answer to this question can be split into two parts: cell differentiation from stem cells and simple mitosis. Also, the answer I am providing mainly only applies to species that sexually reproduce.

During the primary stages of growth, immediately following the fertilisation of the female gamete, the zygote begins to divide. Most of these initial cells will not be specialised, they will be stem cells and these have the potential to asymmeterically divide. When they do this, each of the daughter cells will have a specific specialisation path to follow. Which path they will follow, muscular, neural etc. is determined by transcription proteins.

Once the stem cells have produced the correct daughter cells, the general structure of the organism will begin to take form. Once this happens and the cells have followed their development paths until they hit their final specialisation, mitosis takes over. This means that a muscle cell will divide, causing the organism to grow. A muscle cell, will only ever divide into a muscle cell, the same goes for all specialised cells. This is how an organism grows and maintains itself.

However, some stem cells do remain after the organism has matured. For instance, a mature neuron is unable to undergo mitosis, so stem cells are needed to allow for the production of new neurons to replace those that die, to take one example.

You can find out more here.


Where do I purchase a fly with the collagen tagged? Where can I purchase a fly with tagged collagen?  My senior undergraduate research paper is observing the collagen in larvae with normal diet compared to larvae with an experimental diet.  I need flies that have the protein tagged so I can observe the collagen under a fluorescent microscope.  Instead of using an expensive antibody (my budget is $300) to tag the protein, my advisor suggested purchasing stock flies that already have the tagged protein.

There are some more places other than what Bez has already mentioned.

See here.

However, tagging collagen may be a problem. Collagen undergoes a lot of post-translational modifications including hydroxylation and end clipping. It forms a unique structure (triplex) and adding tags may compromise its structural integrity. You can try Masson's trichome stain instead, which is used to stain collagen — a very cheap alternative.


What insect is this on the photos? What insect is this on these photos?
Found in Russia in the living room.

I think I found it. It can be Lacewings:

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


Does adding milk to cereal make it harder for our body to absorb the vitamins and minerals from the cereal? I add about 3/4 cups of Blue Diamond almond milk (unsweetened) every morning to a single serving of Cheerios. The milk contains filtered water, and I read that drinking water with food at the same time makes it harder for the small intestine to absorb the nutrients from the food. Has this been verified?

Overall, no it doesn't. Cereal is made in a way that it's expected consumers will consume it with milk. Here's a list of some important fortifications added to cereal and milk effects on absorption.

Riboflavin: No. Affected most strongly by light.

Iron: Yes. Calcium can affect absorption. Milk causing a deficiency is rare unless it is being used as a breast milk substitute in babies.

Thiamin: No. Unless you are drinking alcohol with your cereal.

Folic acid: Milk is a source of this!


Term for a leaf in a family tree Imagine a family pedigree.

Mathematically it is a graph, which consists of nodes and edges.
Nodes being family members, and edges - their relationships.

In a clinical setting, what is the proper term for the nodes? Would they be called 'leafs'?

So in a pedigree, Standardized Human Pedigree Nomenclature: Update and Assessment of the Recommendations of the National Society of Genetic Counselors notes that these "nodes" in the pedigree are the "individual symbol" denoting individuals. Although, when you read it, you'd read "Male," "Female," "Gender Unspecified," etc. instead of individual symbol.


how is the plasma membrane repaired after endocytosis? When the vesicle is swallowed of course the lipid layer internalizes. My question is how will the top segment of membrane will bind back together when that vesicle took the membrane with it inside cytoplasm. Will the plasma of the cell decrease or they will repair back and how does the membrane know that a certain substance is outside and i have to internalize myself in order to swallow. The same thing with exocytosis: How does the membrane open itself and repair back and what will happen to the membrane of the vesicle which went out?

You have one misconception about the endocytosis: In the process no hole in the membrane is generated. It works in principle like in the figure below (it is of course more complicated, but this should explain it):

The membrane forms a vesicle around the particle which shall be integrated until it is completely surrounded by a membrane. At this point the vesicle is detached from the cell membrane and inside the cell. To accomplish internalization, the particle binds to certain receptors which regulate this process. See the Wikipedia for more details.

Exocytosis works in principle the other way round. Here are the visicles detached from the Golgi apparatus (mostly at least) and are directed to the cell membrane. Here the fuse with the membrane and form a pit which has its opening to the outside, releasing what was in the vesicle. It works like this (image from here):

In this process you have to differentiate between permanent unregulated exocytosis and regulated endocytosis (for example for the release of hormones) which are regulated by signal transduction pathways.


How can I text-mine full-text articles from PubMed? I want to do a text mining study using full-text versions of articles I find on PubMed. My intended search protocol will be roughly as follows:

Search PubMed using a gene name (and any alternate names) as the query, all matching papers are subjected to Step 2; my understanding is that this will return articles that mention the gene in their abstract
Search full-text for any and all matches from a list of keywords; assign each paper a score based on the number of matching keywords; any papers that match have to be read by a human but the most relevant papers will have a higher score and get read first

The two-step search needs to be repeated many times with different genes in Step1 so an automated approach is probably worth the time it will take to develop.
I know enough about programming that I could write a script to do Step2 if I had the paper as a plain-text document (I program in Perl but I also know a little Python) but I have no idea how I could automate the process of searching for papers, downloading them, converting them to plain-text documents that my program could work on.

I considered posting this in StackOverflow but have opted for this site because I have not ruled out the possibility that this can be done without doing my programming.

UPDATE: I have found one tool that might be very useful for exactly this problem. Unfortunately, I am not in a position to ask for a free trial so I cannot evaluate it. Even if it is an appropriate tool, I will most likely not be able to use it for my study.

Below is a Python script that might help you to get started  (apologies if it fails the Pythonic test - it works!). It uses the Entrez part of the Biopython library. The script sets up a query, in this case yeast AND Saccharomyces against the pmc database. Also note that this script uses the 2 step process that NCBI likes you to use - the first part of the fetchByQuery function gets a set of results then the second part uses those results to actually obtain the data.

The output is an xml file which you get to parse with your favourite tools. In your case you will need to get out the text sections and do your token analysis. If you use Python for that I recommend the Natural Language Toolkit (NLTK).

In your case you could just set up search terms as a Python list and loop through writing each dataset to a file named from the search term.

from Bio import Entrez

import urllib
import urllib2
import sys

def fetchByQuery(query,days):
    Entrez.email = "xxx" # you must give NCBI an email address
    searchHandle=Entrez.esearch(db="pmc", reldate=days, term=query, usehistory="y")
    searchResults=Entrez.read(searchHandle)
    searchHandle.close()
    webEnv=searchResults["WebEnv"]
    queryKey=searchResults["QueryKey"]
    batchSize=10
    try:
        fetchHandle = Entrez.efetch(db="pmc", retmax=100, retmode="xml", webenv=webEnv, query_key=queryKey)
        data=fetchHandle.read()
        fetchHandle.close()
        return data
    except:
        return None

days=100 #looking for papers in the last 100 days
termList=["yeast","Saccharomyces"]

query=" AND ".join(termList)
xml_data=fetchByQuery(query,days)
if xml_data==None:
    print 80*"*"+"\n"
    print "This search returned no hits"

else:
    f=open("pmcXml.txt" ,"w")
    f.write(xml_data)
    f.close()


Do pulled hair from the root grow back? There is not much to explain, I'm wondering if pulled hair, for example of the head, normally does grow back again or not. In reddit, It says this may depend on the follicle integrity, if the follicle is  not hurt then it will grow back and viceversa. It is the case?

There's no harm in plucing a hair, but it won't do you much good

Plucking the hair will indeed get rid of the hair - but only temporarily

  "The follicle (the little tube beneath the skin that produces the
  hair) is still alive and will produce another hair to replace the one
  that was pulled out

So actually if you DON'T damage the follicle (which is really rare, this could be the case if you remove skin) the hair will definitly grow back.
To get into more depth here is a figure that shows the root and the follicle so it's clear what the difference is:

I don't know in how much depth you want this question to be answered but if you are interested in the growth stages (which can influence the hair regrowth) you should take a look at this answer, I won't copy someone else effort here..
source: Randy Schueller (link)


What is this species of angiosperm from Morocco? The flowers are about 1 cm long. The plant is about 1 metre high. Photographed in spring. The plant was found in a ruderal environment.

Look into the Symphytum genus, or related genera within Boraginaceae (the forget-me-not family). It is loosely similar to Symphytum officinale, but clearly not that species. The overall layout, size, leaves and hairyness of the stalks is similar to species in Symphytum.

Here is Symphytum officinale, as an example of the overall appearance:

Also similar from the Anchusa genus in the same family (Anchusa azurea):


What is the beneficial function of IgE antibody? Dont tell me the "function" of IgE is to cause allergy !

In whatever texts I have seen it is  written that IgE is important to cause allergies but what is the beneficial function of IgE ? Why was it ever created ? Did it have an advantage in the pre historic ages but now causes allergies ?

No, they are of course not there to cause allergies.
It is thought (although not directly proven in human) that IgE is important to fight parasites and worms. They bind to antigens from the parasites, which leads to the secretion of histamines. This causes a local immune reaction (which also is a problem in allergies) which is helpful to fight the parasites.

See these papers for example:

IgE, allergies and helminth parasites: a new perspective on an old
conundrum.
IgE Enhances Parasite Clearance and Regulates Mast Cell Responses in
Mice Infected with Trichinella spiralis
Immunology of Parasitic Helminth Infections

There is also some evidence, that IgE is involved in the immunological response to cancers:

Activity of human monocytes in IgE antibody-dependent surveillance
and killing of ovarian tumor cells.
Animal models for IgE-meditated cancer immunotherapy


Meaning of "optical" in "Optical cap, 8X Strip" (used in qPCR) I'm translating an English document that lists equipment used in a qPCR procedure:

Reagents/Materials

Optical cap, 8X Strip

I googled and found that the meaning of this line is "a strip of 8 caps for PCR tubes". What is the meaning of optical though? I'm not sure how to translate it into Russian.
Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?
Screenshot:

I'm googling but I can't seem to find any definition of "optical cap". It is used in a lot of books and documents as if the term is self-evident, while it's not.

Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?

Yes and yes. As an example of the different kinds of PCR tube caps, refer to the cap options available from Thomas Scientific:

Available with a domed, flat frosted, or flat clear caps for qPCR. [emphasis mine]

For most lab plastics, "optical" refers to the surface between the camera/detector and the sample.  Another example: for plate-based fluorescence assays where the plate reader takes measurements from below  the plate, one might use a Nunc MicroWell 96-Well Optical-Bottom Plate from ThermoFisher. Usually, such plates also have opaque walls to prevent signal bleed from adjacent wells.


Is PrEP used for anything other than HIV? In the field of HIV prevention, PrEP is an abbreviation of pre-exposure prophylaxis. This is a very generic term. Are any diseases other than HIV prevented using a similar approach? Do they use the same name?

Prophylaxis is typically prior to exposure. Condoms, for example, were historically referred to as prophylactics, in that they prevent pregnancy and many STIs. The reason the pre-exposure bit is given special attention in this context is that it refers to use of drugs with substantial risk of harm. Because of their associated risk, these drugs were previously only used for post exposure prophylaxis. Similar to rabies vaccination after an animal bite, this strategy involves preventative treatment given after exposure but before a critical point in the progress of an infection.

To more directly answer your questions

  Are any diseases other than HIV prevented using pre-exposure prophylaxis?

Many, many, many diseases. Vaccines are a good example of prophylactic treatment, typically given prior to exposure. Malaria prophylaxis is another example, where a medication (with non insignificant risk of harm) is given to healthy people traveling to an endemic area.

  Do they use a different term?

In most cases, as you can see by searching for the words used in the linked references, the term is simply prophylaxis, rather than pre-exposure prophylaxis.


General time reversible model of evolution and Felsenstein model I would like to get suggestions for the books related to General time reversible model of evolution and Felsenstein model etc. Specifically the mathematical treatment of these topics and concepts related to general balance and detailed balance etc. Can someone point out any books, links etc related to these.

The classic answer would be Joe Felsenstein's Inferring Phylogenies. It has substantial technical discussion of GTR and Felsenstein models, among others.
However, it does not have any index entries for "general balance" or "detailed balance". I was not familiar with these terms, so I googled them and they do not appear to be common terms in the phylogenetics field.
These terms do pop up in the MCMC literature a bit regarding transition probabilities, so it seems likely that it is somewhat related in terms of underlying math. However, I think that you are more likely to find phylogeneticists talking about "stationary" or "equilibrium" models rather than in terms of "balance". Possibly a difference in terminology between fields.
It might be helpful to know more about what you mean by these terms and why you are interested in them, in the form of links or otherwise.


What are the universal laws of Nature concerning animals' behaviour? I'm looking for very old (centuries) treaty or recent (20 & 21th century) research that state what some of the laws of Nature are, particularly concerning wild animals' behaviour. Such as; every animal does this, no animal does that, etc.

Laws that could be then used to simulate or reproduce natural behaviours or check against unnatural ones.

Added: I'm looking for more simple laws, such as "no (wild) animal eats cooked food". Assuming it's true then humans broke that law of Nature. It's the relation to Nature that interests me. I used the word behaviour in the large sense, as in, what are the laws that animals seem to follow (dos  and don'ts) in the world. I suppose that by looking at what the human is the only one to do we can find lots of those laws.

This seems to be rather impossible to answer! Very fundamental laws of nature are rather found in physics, mathematics or philosophy than in biology.

The theory of evolution is generally considered as a field that brings light to the whole science of biology. T. Dobzhanski famously said: "Nothing in Biology Makes Sense Except in the Light of Evolution" So I guess you might be interested to "laws" coming from that field.

I'm afraid you will some more knowledge in animal behavior than what you can acquire from this simple question before starting simulating. You can easily spend 5 years studying animal behavior and still having much things to learn from that field.

I would guess you might be interested in the concept of selfishness and altruism. I don't know your level of knowledge in biology. The following might seem a bit complicated (although it is a very brief and inaccurate summary of the real science that study these fields), if so, I would invite you learn about basic stuff in biology and evolutionary biology.

Selfishness and altruism

In order to have natural selection, you need:

variation
heritability (of the trait that present some variation)
different reproductive success (or success of copying itself) according to the trait which is heritable.

Following, this idea, an allele that behave altruistically (providing benefit (in terms of ability to copy itself) to someone else to its cost (always in the same terms)) will disappear  to the benefit of the selfish allele and therefore altruistic behavior should never be found in nature.

However, we find altruistic behavior (and that was one of the greatest flaw Darwin could think about his theory):

Because of relatedness (Hamilton's law)

An animal would always behave in order to increase its inclusive fitness (=direct fitness + indirect fitness)

Because of genetically correlated behavior
Because of upper level selection
Because behaving in a way will directly or indirectly influence the way others will behave with you

Now, that's a very big field. I can't develop everything in this answer! If you liked the discussion of selfishness and altruism, you might be interested to read the selfish gene or the extended phenotype.

If you want to go a bit deeper into mathematical formulation you might be interested in evolutionary game theory and hamilton's rule.

Here is a quick formulation of Hamilton's rule on this website

UPDATE (in reaction to your comment)

So, you're not looking for a scientific law/theory/evidence/etc... you're looking for a simple observation in the nature that fit all animals. Here are some examples:

There is no wheeled animals (see this).
There is no animal that migrate every year from Earth to Mars
All animals need a source of organic carbon
All animals possess some flagellates cells (I think)
All animals reproduce (not necessarily sexually)

If you want to talk only about behavior, then you might have some trouble to generalize things to all animals because, there are many non-motile animals, many animals that have no brain, many animals that does not even have organs, … As a side note: It is possible that if you accept that a sponge (which is at the base of the Animalia kingdom see this website if you want to learn about what is classified to be an animal) produce some kind of behavior, you will have to accept that an oak tree also have behavior

UPDATE.
Ah you meant animal in opposition to human?! Humans are included in my above list. If you look for differences then between human and all other animals, than you won't many other things than the brain and the behavior indeed. I hope nobody lost a whole life of work listing what human can do and what animals can't!

Human have a complete and articulate language (I don't fully remember what adjective we use to differentiate human to animal language)
Human are conscious that the are conscious that they are! It is quite hard to show that animals are not!
Humans are the only animals that drive a car!
etc…

You're using the word law in a weird way. You might to have a look to
http://en.wikipedia.org/wiki/Scientific_law and http://en.wikipedia.org/wiki/Scientific_law


DNA shared by octopuses and modern humans What percentage of DNA do we share with octopuses? I tried looking it up but couldn't find the answer on the internet. Could someone enlighten me on the same? To make the question more specific, I am more interested in knowing how many genes humans share with octopuses, but answers regarding how different our shared genes are or even a metric of the entire genome alignment would be helpful.

Octopuses have more chromosomes and genes

Octopuses have 28 chromosomes, and 33,638 protein-coding genes (Albertin et al 2015).
Humans have 23 chromosomes, and 20,365 protein-coding genes (Uniprot).

Octopuses had an expansion of genes in only a few protein families

There is a large number of C2H2 zinc-finger proteins (C2H2 ZNFs) (~1800), interleukin-17-like genes (IL17-like), G-protein-coupled receptors (GPCRs), chitinases and sialins paralogues in the octopus genome.

However, there does not exist a comprehensive analysis of orthologous proteins in the octopus that I can find.
This means that although we can say that there are thousands of genes we only observe in octopuses, there is currently no study comparing orthologues that exist in both humans and octopuses.


Mechanisms of extracellular stimulation of neurons When stimulating a group of neurons with an electrode, let's say we put it in a region that contains axons, what is the mechanism by which the axons are stimulated?

I've been told electrodes (usually silver or gold) must be coated with ions, usually chloride, to allow the passing of the stimulus. So I'm not sure if the stimulus is based on changing the extracellular concentration of ions by injecting chloride, therefore changing the membrane potential with a depolarization (elevating the potential, possibly generating an action potential). Let's call this idea A.

The other idea, B, that seems possible would be having the ions in the extracellular fluid conduct the current to the nearby axons, thus changing the potential but not the intra or extracellular concentration of ions.

Good question. Just to set some stuff straight: In contrast to a comment placed earlier, there is definitely a current flow between electrodes in neural tissue, as long as the impedance is not too high. The potential difference between the electrodes and impedance determines how much current flows, basically following Ohm's law: I = U/R.

As to your hypothesis (A) - I confirm  WYSIWYG's answer - electrodes indeed do not have to be coated, as long as they are conductive. For instance, Ag/AgCl coatings are used to electrically stabilize the electrode, mainly for sensitive reference electrodes used for recording purposes (see a commercial link here). For stimulation purposes chloride salts are a big no no, as AgCl or comparable chloride salts will be converted into metal (e.g. silver) + Cl2, obviously a toxic gas.

As to your hypothesis (B) - It is the electrical field that activates neurons (Basser & Roth 2000) by means of inducing current flow. For example, imagine a cathode (negative electrode) placed close to a neuron. Normally in rest, a neuron's membrane is hyperpolarized (more negative ions inside the cell, the extracellular fluid can be considered to be neutral). The negative electrode will now cause the extracellular fluid to be negatively charged. Subsequently, positive current will flow out from the cell close to the electrode and into the electrode. According to Ohm's law, the membrane voltage is thus positive (note Ohm's law: U = IxR, with I being positive and R being always positive, means U is positive). Hence, the membrane is depolarized, as the resting state is a negatively charged state (hyperpolarized). With an anodic electrode neurons can also be depolarized but due to a slightly different mechanism. Basically, the flanking regions of the now negative current flow to the positive electrode become subject to positive current, as it counterbalances the negative flow to the electrode.  The chapter of two veterans in electrical stimulation, Abbas and Miller, in (Cochlear implants) is particularly helpful, as is (Basser & Roth 2000). I can't link a pdf to Abbas and Miller, excuse me for that. I bet your university library will have access to it. Hope this helps.


Which of the cell types commonly found in mammals has the greatest number of mitochondria? This is basically a fun question, inspired by this answer on scifi.se. So, which cell type will have the greatest number of mitochondria? Obviously, I am talking about wild type, healthy individuals and am looking for a rule of thumb. I realize that the number can change under different conditions/ between different individuals.

Off the top of my head, I would say that it's sperm cells given the strenuous exercise they need to perform and their MT-packed axonemes but perhaps there are better contenders?

I am primarily interested in human cell types but answers dealing with other mammals are welcome.

It's commonly believed that it's muscle cells that have the largest amount of mitochondria, and for good reason.  Muscle cells are continually used to move the body, so they have the most mitochondria because of the large energy requirement.  If you want to be more specific, the muscle cells of a marathon runner have even more since the muscle cells involved in running need to be able to do a lot of aerobic respiration.  Another example is the cells in the heart; the amount of mitochondria makes up 40% of the cell.

The truth is, retinal cells with photoreceptors most likely have the most (80% of the cell volume) since they need to reset the potassium/sodium pump to keep the action potential in the nerves the same.

If you're curious, the cells with the least amount of mitochondria are skin cells and erythrocytes (red blood cells) since skin is just a protective barrier and red blood cells don't need to exert any effort or energy to move.

Sources:

http://hyperphysics.phy-astr.gsu.edu/hbase/biology/mitochondria.html
http://www.ncbi.nlm.nih.gov/pubmed/12511073


Are there any bacteria that can receive ultrasound signals? I'm looking for an example of bacteria that could receive ultrasound (at any ultrasound frequency) signal and possibly perform some (re)action afterwards.

I'm going to post a quick answer here, really a thought piece.

Usually to detect a sound wave you need a sounding board about the wavelength of the sound.

Bacteria are on the order of a few microns in length.

Ultrasound frequencies range from 2 to 200 MHz (and up I assume).

To have a wavelength on the order of 3 microns, a 100 MHz wave would be needed.

So only on the very high end of the range.  If bacteria make sound though, they probably are on this frequency range.

I wonder if this has been looked at?  Not sure it has.  While in biology you never say never - if a bacterium really needs to pick up a wave it might have a clever adaptation to do so, but in the 100MHz + frequency range seems more likely.


Can tubular secretion regarded as local hormone? Tubular secretion is : The process in which ions and other waste products are transported into the distal tubules of the nephron.

can it be regarded as local hormone??

First of all, I can't understand how can you regard an electrochemical process (tubular secretion) as chemical substance (hormone).

Tubular secretion is the transfer of materials from peritubular capillaries to renal tubular lumen. Tubular secretion is caused mainly by active transport.
Usually only a few substances are secreted. These substances are present in great excess, or are natural poisons. Many drugs are eliminated by tubular secretion [1].

The substances that are secreted into the tubular fluid (for removal from the body) include [2]:

Potassium ions (K+),
Hydrogen ions (H+),
Ammonium ions (NH4+),
creatinine,
urea,
some hormones, and
some drugs (e.g. penicillin).

Tubular secretion occurs from the epithelial cells that line the renal tubules and collecting ducts [2].

Uptake transporters in the basolateral membrane and export transporters in the luminal membrane of renal tubule cells are involved in tubular secretion of their substrates (organic anion transporters and organic cation transporters - these are transmembrane proteins) [3].

Despite considerable advances in the understanding of basic transport pathways and mechanisms involved in the tubular secretion of organic compounds, there is still relatively little information on the regulation of this transport [4].

References:

Wikipedia contributors, "Renal physiology," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Renal_physiology&oldid=608689347 (accessed June 26, 2014).
http://www.ivy-rose.co.uk/HumanBody/Urinary/Urinary_System_Kidneys_Actions_3.php
Müller F, Fromm MF. Transporter-mediated drug-drug interactions. Pharmacogenomics. 2011 Jul;12(7):1017-37. doi: 10.2217/pgs.11.44. PubMed PMID: 21787191.
Berkhin EB, Humphreys MH. Regulation of renal tubular secretion of organic compounds. Kidney Int. 2001 Jan;59(1):17-30. doi: 10.1046/j.1523-1755.2001.00461.x. PubMed PMID: 11135053.


Is better healthcare a bane to the long-term survival of the human race? The theory of natural selection has it that individuals with better genes tend to survive and reproduce, passing their genes to their offspring. This gradual process results in a population more adapted at survival. However, due to the advancement in medical science, humans with poorer genes tend to survive and reproduce just as well.

For example, in the past, many people, excluding those with natural immunity due to some genetic mutations, would have succumbed to illnesses such as malaria and typhoid. But with better hygiene and medical treatment, these patients tend to survive.

Now, imagine a future where all illnesses including cancer can be treated. How would it impact the survival of the human race? Would we become more and more vulnerable such that our survival hinges heavily on medical technology, analogous to how an astronaut's survival is dependent on his spacesuit?

Gene frequencies (frequencies of each allele at a given loci) in populations are affected by many things divided in to systematic and dispersive processes. Systematic process (migration, mutation, selection) affect gene frequencies in an often quite predictable manner and strength. Dispersive process (Random drift, differentiation between sub-populations, uniformity within sub-populations, increased homozygosity) are random in their direction and only predictable in their amount. Your question focusses on the systematic process called selection.

In a large population (if we ignore dispersive processes for the time being) the gene frequencies will reach an equilibrium called Hardy-Weinberg equilibrium. This means, with constant rates of the systematic processes, each locus will reach a point of stable equilibrium. Mutation and migration bringing more variation, and selection reduces it (over simplified - sometimes selection maintains variation, see my answer about why variation exists here). The frequency of each allele at equilibrium will be where these effects balance out. If selection becomes weaker against one allele it will become more frequent in the population.

By using medicine etc. to cure diseases we reduce the selection acting on a deleterious mutation thereby putting the gene frequencies in to a state of flux during which they move to new equilibrium points. So in short the answer is yes, modern medicine is decreasing our genetic fitness by allowing deleterious mutations to become more common.

I raise the question, will we ever be able to cure all genetically caused disease? In my reckoning, no, at least certainly not in our lifetimes.

It only represents a real risk if we suddenly are unable to cure diseases. This would increase selection against that allele and the gene frequencies would move back towards the equilibrium point which existed before the selection was reduced. What this means for the population is the loss (death) of those with the low fitness genotype.

The best reading you can do on this is the opening chapters of Falconer and Mackay's Introduction to Quantitative Genetics. Also read about Hardy-Weinberg equations.

HTH


Does yeast grow on LB agar plates? I would like to grow E coli cells on cellophane on top of LB plate, and then grow yeast cells on the same LB plate. Does (or how well) yeast grow on LB plates? Is there a composition media that can be good for both E. coli and yeast? Has anyone done this experiment?

Not well, they need  dextrose. Use YBT:

20 g Casein Peptone Tpe-M
10 g Yeast Extract
20 g Dextrose
17 g Agar

q.s. to 975 mls in di-water.

pH to 6.2 w 5M NaOH

q.s. to 1L with di-water.

Autoclave for 45 min at 121C

Aseptically dispense in Petri dishes.

Store at 4C for up to 12 weeks.

If you want to grow Co-culture do so in LB supplemented with 20g/L Dex.


Simple Mendelian sex-linked chromosome fruit fly question From my molecular biology textbook:

  When red-eyed flies (dominant) were mated with white-eyed flies (recessive), most, but not all, of the F1 progeny were red eyed. Furthermore, when the red-eyed males of the F1 generation were mated with their red-eyed sisters, they produced about one-quarter white-eyed males, but no white-eyed females. In other words, the eye color phenotype was sex-linked.

First, wouldn't recombination scramble the eye color alleles among the sex chromosomes?

Secondly, even without recombination, the F1 generation will be heterozygous and all F1 flies will have white and red alleles. Some F1 males will have a white X and some F1 females will have a white X, in which case it should be possibly to have an F2 white fly.

Can someone explain this?

I think the text is slightly misleading. But before going into the detail genetics of eye color let's answer your first question.

First, wouldn't recombination scramble the eye color alleles among the sex chromosomes?

Two X chromosomes do recombine but one X and one Y chromosome do not recombine (to the exception of the so-called pseudo'autosomal region).

I am not sure why recombination would change anything here. I think the eye color of flies in determined by a single locus.

How is this possible?

Let's go through the text slowly because I think the text is a little misleading. I am suggesting the only scenario I could think of that would explain the observed pattern. Note that this scenario also depends on the interpretation of the text and I would need more info on the experience to make sure my interpretation is right.

  When he mated red-eyed flies (dominant) with white-eyed flies (recessive), most, but not all, of the F1 progeny were red eyed.

Actually, only males are sometimes white eyed here. And to be more accurate, if sex was uncorrelated form eye color in the parental lines, then half of the males should have white-eyed.

What was happening here is that red is dominant, white is recessive and the locus for eye color exists only on the X chromosome. As a consequence, all F1 females are now heterozygous (and display the dominant red-eyed phenotype) and all males are hemizygous, half of them having the red-eyed phenotype while the other half have the white-eyed phenotype.

  Furthermore, when Morgan mated the red-eyed males of the F1 generation with their red-eyed sisters, [..]

Let's forget about the white-eyed males from above, we will just cross the red-eyed males with their sisters.

  they produced about one-quarter white-eyed males, but no white-eyed females.

By they produced about one-quarter white-eyed males what is meant is that a quarter of all individuals were white-eyed males. That is half of the males were white-eyed. The other three quarters of the individuals were red-eyed.

The males received their X chromosome from their mother only (as they can only receive the Y chromosome from their father). Half of the males have therefore received the white-eyed allele while the other half have recevied the red-eyed allele. For the females, they all received from their mother either a white-eyed allele from their mother or a red-eyed allele. As we selected only father that had red eyes in the previous step, all father carry exclusively the red-eyed allele. As a consequence, all females receive a red-eyed allele from their father. Therefore half the females are homozygous red-eyed or heterozygous. In any case, all females are red-eyed.


What is this plant ...? I would like to know what is this plant ? Does anybody have an idea ? Somebody offered it to me but there is no explanation about how to care about it...
Some purple flowers appeared, during 2-3 days. And now it seems it lacks something, but I don't really know what to do :(

Any idea ?
Thank you very much !

That is a beautiful Pink Quill, or Tillandsia cyanea. I have included two websites below about this plant, both of which include care tips.

http://home-and-gardening.info/2009/09/18/a-guide-on-growing-tillandsia/
http://houseplants.about.com/od/bromeliads/a/Bromeliads.htm


Why some parts of the human body have immune privilege? Why have the eye and CNS have immune privilege? Why does the body not develop tolerance against their tissue and instead risk their damage in case an accidental immune cell infiltration?

Wiki:

  ...in immune privileged sites, tissue grafts can survive for extended periods of time without rejection occurring

The immune privilege is happening for brain, CNS, eye, testis and the uterus. All these tissues (or structures) share that they cannot be regenerated once they get damaged by an overshooting immune reaction. Infections in the eye followed by a strong immune response often lead to the loss of the eye, in rodents loss if immune tolerance against the fetus leads to abortion.

So basically this is a protective mode for these tissues to protect them from a stong immune reaction. See the references for some more details (especially on how this works).

References:

See no evil, hear no evil, do no evil: the  lessons of immune
privilege
What is immune privilege (not)?
Immune privilege or privileged immunity?
Immune Privilege and the Philosophy of Immunology

  Each immune privileged tissue has a unique function. The eye must protect the light path and signals that stimulate the retina, and photoreceptors to preserve vision. The testis has to protect the sperm as they proceed to the epididymis where they mature. The maternal reproductive tract has to protect its eggs both before and after fertilization and thus has developed specialized mechanisms to modify the body’s response to foreign antigens. These unique challenges require different solutions and lead to unique immune privilege mechanisms. However, although microenvironment and the stromal cells that carry out the particular function may vary between tissues, and consequently the mechanisms that promote regulation may be unique to that cell or tissue, the goal is the same: limit collateral damage to preserve tissue integrity and maintain homeostasis to the extent possible, without compromising host defense.


Twins reproducing with each other ( just hypothetical) If 2 twins (look exactly the same and also the genes which control their morphology, behaviour etc. are same and present at the same locus) produce an offspring , will their offspring be exact copy of their parents ?

Sorry . I know its not moral.

Monozygotic twins won't be able to reproduce (naturally), because they are of the same sex. Dizygotic twins may or may not be of the same sex, just as regular siblings; genetically speaking, they are just siblings, not twins, so this case is out of the scope of your question.


Importance of germline and somatic genomic mutations to the purpose of treatment in cancer Is there a hierarchy in the sets of genomic mutations (somatic and germline) to the purpose of treatment in cancer?

Can they be considered at the same level in the context of targeted therapy or are there reasons to prioritise one set vs the other?

A) There isn't really a fixed hierarchy that is applicable across the board - alterations are often binned into actionable targets and non-actionable ones. In terms of customised cancer vaccine for immunotherapy (Eg - www.sciencemag.org/news/2017/04/personalized-tumor-vaccines-keep-cancer-check ) , more antigenic mutations tend to be prioritised.

B) Sometimes there are reasons to prioritise mutations over others even for small molecule targeted therapies. For example, one would want to target mutations that are clonal rather than subclonal where possible, so that the bulk of the tumour, rather than a small fraction of the cells in it, are targeted. Alternatively where one has, for example, a resistance mutation arising from prior therapy (You see this with EGFR T970M mutations) it is an indication for next generation EGFR inhibitors that specifically hit the resistant mutation.


Why is the neuronal plasma membrane more permeable to potassium ions than sodium ions? From what I understand, the greater permeability of the neuronal plasma membrane to K+ ions (which diffuse out) than Na+ ions (which diffuse in) helps to maintain the -60 mV resting membrane potential. However, I am not sure why. After all, K+ ions are larger so should the membrane not be less permeable to them? Could it be to do with the greater charge density of Na+ ions or is there another reason altogether? Does it have something to do with the 'leakiness' of ion channels?

Also, why is it that the resting potential is maintained and does not become increasingly more negative? Should it not be that because 3 Na+ ions are pumped out and 2 K+ are pumped in continuously, and more K+ ions are diffusing out than Na+ is diffusing in, that the potential is becoming increasingly negative? Is movement of other ions also involved in maintaining this potential?

The cell membrane is inherently quite impermeable to any ion, because it is made of hydrophobic fatty acids. Ions are hydrophilic because of their charge and small size. Metal ions are relatively small and, indeed, have therefore a high charge density. They gather a lot of water around them and hence, they are hydrophilic.

Therefore ions, including Na+ and K+ are transported via dedicated ion channels, which form specialized pores in the membrane. They consist of vast families with many members and a host of different characteristics. Hence, the size of the ion does not matter, because they are transported through channels.

There are indeed leaky K+ channels, but not leaky Na+ channels. And exactly this feature is the reason cells are negative on the inside, because positively charged K+ leaks from the cell.

There is just so much the Na+,K+-ATPase can do. In the end  it burns ATP to fuel each cycle to pump out Na+ and pump in K+. At a certain point it cannot transport anymore Na+ out (K+ diffuses relatively freely) because the concentration gradient of Na+ and the electrical gradient (inside negative) gets too steep.


Sample suggestions for phase contrast microscopy I am a non-bio student working on an academic paper recently and would like to have some sample preparation for phase contrast microscope.

For it to work, I imagine the sample to be:

Transparent;
Easy to obtain from daily stuffs;
Easy to slice and prepare (i.e. approachable to people untrained in bio).
Best dimension around 10 micros, and is well seen under x100.
Preferable to be seen dynamics at room temperature.

My current thoughts are:

Human: oral cheek cells, red blood smear, sperm.
Plants: onion surface cells.
Others: yeast, pond water.

Any further suggestions (especially dynamic ones)? Thanks!

Any green, soft leaf from a non-toxic plant is a good start. Cut a thin slice from the leaf (either to look at the cross-section or the surface). Try different leafs with different colors - there might be colors in the cytosol and/or in chromoplasts.

Concrete example for dynamic structures:

Elodea leafs: they consist of only two cell layers and can be looked at under the microscope without further preparation. Keep the the leaf in water and cover it with a cover slide before looking at it under the microscope and add water when it starts drying out. The green chloroplasts in the plant cells are moving around as long as the cell lives.

You might find Elodea either in a pond or in a store selling aquarium fish and the like. You can keep Elodea alive and grow it in nutritious water at a sunny place.


Is it possible for a sex chromosome to be homologous? I am following a great introductory biology course online, MITx: 7.00x on edX.

A question in the course assumes a cross between a pure-breeding male fly and a pure-breeding female fly:

  You are studying genetics in a hypothetical fly and you find a fly
  that has purple eyes. Assume that the purple eye phenotype is due to a
  mutation at a single locus. Use the notation E and e, where the upper
  case letter is used for the allele associated with the dominant
  phenotype and the lower case letter for the allele associated with the
  recessive phenotype.

  You cross a pure-breeding male fly with purple eyes to a pure-breeding
  female fly with normal eyes. All of the F1 offspring have normal eyes.
  From this experiment you determine that the purple eye phenotype is
  ______________ to the normal eye phenotype.

My question is this: how can a male fly be pure-breeding? The reason I wonder is that as far as I understand, pure-breeding implies a homozygote gene, yet the sex chromosome can not be homozygote because the Y chromosome is not homologous to the X chromosome. In other words, does it make sense to speak of homologous sex chromosomes?

How can a male fly be pure-breeding?

A fly or any organism can only be pure-breeding for a certain trait, not all traits at once. If the trait-determinant allele is found on an autosomal chromosome, this is not a problem. If it's on a sex-chromosome (chr1 in flies), it is sex-linked, and therefore cannot be pure-breeding because it may depend on the sex of the offspring whether the trait is expressed. For instance, you may have a male carrying an allele on its X chromosome; its female offspring will inherit the X, but male offspring will not (those inherit the Y chromosome), i.e. it is not pure-breeding. Male flies cannot be pure-breeding for traits determined by loci on their sex chromosomes. Similarly, you may have a heterozygous female carrying an allele on one of its X chromosomes (A/a); its female offspring will only inherit one allele, either A or a, so it is not pure-breeding either. A female fly must be homozygous for an allele on its sex chromosomes to be pure-breeding for that trait.

Male flies can be pure-breeds for traits determined by alleles on autosomes.

Also, cool and useful funfact, Drosophila sp. male flies do not experience homologous recombination during meiosis. This is called achiasmy! This is useful to know when designing complicated crosses when there is a difficulty in balancing a genotype.

  Does it make sense to speak of homologous sex chromosomes?

The X chromosomes in females (X + X) are homologous, but the male Y chromosome is not homologous to the X. They are vastly different, just like the X and Y sex chromosomes in humans.

  Pure-breeding implies a homozygote gene

Correct. Pure-breeds are allele homozygous so that all offspring, regardless of recombination, inherit the allele.


Does aneuploidy include the loss of chromosome arms? I'm wondering if the definition of aneuploidy includes loss of a chromosome arm (telosomy) or arms (ditelosomy).

I'm aware that aneuploidy normally depends on the number of discrete chromosomes (so a chromosome without an arm would be treated as one chromosome), but in the genetics course I'm taking, telosomy and ditelosomy were listed in 'types of aneuploidy'. Was this just for convenience, or does the definition include them?

To my knowledge aneuploidy regards to chromosome numerical change, not to losses within chromosomes.
Take a look at this paragraph from An Introduction to Genetic Analysis. 7th edition (Griffiths AJF, Miller JH, Suzuki DT, et al. New York: W. H. Freeman; 2000.)

  Aneuploidy is the second major category of chromosome mutations in
  which chromosome number is abnormal. An aneuploid is an individual
  organism whose chromosome number differs from the wild type by part of
  a chromosome set. Generally, the aneuploid chromosome set differs from
  wild type by only one or a small number of chromosomes. Aneuploids can
  have a chromosome number either greater or smaller than that of the
  wild type. Aneuploid nomenclature is based on the number of copies of
  the specific chromosome in the aneuploid state. For example, the
  aneuploid condition 2n − 1 is called monosomic (meaning “one
  chromosome”) because only one copy of some specific chromosome is
  present instead of the usual two found in its diploid progenitor. The
  aneuploid 2n + 1 is called trisomic,2n − 2 is nullisomic, and n + 1 is
  disomic.

This term (aneuploidy) was coined by Gunnar Täckholm in 1922, and if you want to check the original description you can just look for his original paper:

Täckholm, G. Zytologische Studien über die Gattung Rosa. Acta Hort. Berg. 7, 97–381 (in German) (1922).


Using UV to kill bacteria in shoes I see that UV-C is the best to kill bacteria generally. We are interested in using to kill off odor in shoes.

What illuminance is needed to kill most bacteria with UV-C?

Thanks!

The wavelength of UV-C most effective at provoking mutagenesis in DNA is 260 nm, which has been shown to kill Cryptosporidium parvum at doses below 10 mJ/sq cm.

http://www.ncbi.nlm.nih.gov/pubmed/12834745

In units of lux, 10^5 lux of sunlight has been shown to kill 99.9% of Aeromonas salmonicida after two hours of exposure.

http://www.sciencedirect.com/science/article/pii/S0043135499001591


Can endemic diseases be acute? Diseases can be classified as :endemic ,or pandemic,...etc.
 An endemic disease is an infectious disease which is generally or constantly found among people in a particular area.
Disease conditions are :

acute: rapid onset , severe symptoms and brief duration.
chronic:gradual onset and long duration

Can an endemic disease be acute? Or is it always chronic ??

Endemic and chronic/acute are unrelated properties of a disease. Endemic is a description of the frequency of a disease in a population or in an area. Chronic/Acute is a description of the state or course of a disease in an individual.

For example, influenza is endemic in North America: the frequency goes up and down, there's always a few people who have it, but most people don't. Periodically the influenza virus mutates, and becomes much more successful at infecting people. The frequency of the disease goes way up, and influenza becomes epidemic. However, regardless of whether the disease is endemic or epidemic, the disease processes is usually acute: it comes on suddenly, it gets worse for a few days, and then it get better (or you die).

Malaria in endemic in much of Africa and SE Asia (it's always around), but the disease can be either acute (you have fever, chills, prostration), or chronic (the parasite lives in your body, and you can be a source of the disease, you don't necessarily have obvious symptoms, but may be suffering long term damage.


What is the difference between influenza A and B viruses that causes their distinct seasonal patterns? I recently learned from an answer at health.SE* that influenza B tends to occur later in the season compared to influenza A. According to the graph in that answer, during this year’s flu season the peak for influenza B was mid-March, compared to late December for influenza A. I’m wondering why this is. What are the virological factors that account for this difference?

*Now public!

Regrettably, I don't believe we know - we don't actually know why influenza is a seasonal disease in the first place. There are a number of possible theories, discussed in this review, but none of them are compelling enough to be a definitive causal explanation

In terms of the difference between Influenza A and B, B mutates at a much lower rate, which may explain the slower rate of dramatic antigenic shifts, but that isn't enough to disrupt the seasonal cycle by a few months at most.


In DNA repair, how is it determined which strand contains the error? DNA replication is more accurate than transcription (or RNA replication) because mechanisms exist for proof-reading and repair of DNA, but not for RNA.
Consider a segment of a DNA strand, AGTC. Its complement is GACT. Now suppose its complement is mutated to TACT — the DNA repair system will replace the wrong T by G. Why isn’t A in the original strand replaced by C? How does the system determine that the first strand is correct and its complement is incorrect?

There are many types of DNA repair. Let us limit to the following three different types to answer this condition.

1. UV damage

Exposure of a cell to UV light can result in the covalent joining of two adjacent pyrimidines (usually thymines), producing a dimer. These thymine dimers prevent DNA polymerase from replicating the DNA strand beyond the site of dimer formation.

In such cases, UV-damage specific endonucleases cleave both the 5' and the 3' end of the lesion. Along, with the lesion some normal DNA is also lost as an oligonucleotide. Here modifications are being made only on one strand, the other is taken as a template (correct) and the DNA in the lost part is replaced.

The UV-damage may occur on both the strands but locally, one is affected and the other is the template (since you can't have thymine both sides)

2. Base Excision

Normal DNA bases can get deaminated spontaneously or on insult to an abnormal base (not on DNA).The abnormal base is excised by glycosylases and gap is later filled by considering the other strand the template.

3. Mismatch repair

What you are talking of in your example is not a case of deamination or UV damage but a mismatch repair. There can be errors in replication too where such a case could set in. There are specific enzymes for this repair, but discrimination is based on the degree of methylation. GATC sequences, which are found approximately once every thousand nucleotides, are methylated on the adenine residue. This methylation is not done immediately after synthesis, so the newly synthesized DNA is hemimethylated (that is, the parental strand is methylated but the daughter strand is not). The methylated parental strand is assumed to be correct, and it is the daughter strand that gets repaired.

The above said mechanism of discrimination is only in the gram negative bacteria. To quote Wikipedia,

  However, in other prokaryotes and eukaryotes, the exact mechanism is not clear. It is suspected that, in eukaryotes, newly synthesized lagging-strand DNA transiently contains nicks (before being sealed by DNA ligase) and provides a signal that directs mismatch proofreading systems to the appropriate strand. This implies that these nicks must be present in the leading strand, and evidence for this has recently been found.

There are other cases where there is damage occuring to both strands that I'd suggest for further reading.

References

Lehninger's Principles of Biochemistry, Ed. 6
Lippincott's Illustrated Reviews, Biochemistry, Ed. 5
Wikipedia. DNA mismatchrepair


Why is a magnesium ion essential for ATP activity in enzymic reactions? The Wikipedia entry on Magnesium in Biology includes the following:

  ATP (adenosine triphosphate), the main source of energy in cells, must be bound to a magnesium ion in order to be biologically active. What is called ATP is often actually Mg-ATP.

I don't understand why magnesium is essential for breaking the high energy bond in ATP?

As far as I know there are two main reasons for this:

promoting a nucleophilic attack

  In general, Mg2+ interacts with substrates through inner sphere
  coordination, stabilising anions or reactive intermediates, also
  including binding to ATP and activating the molecule to nucleophilic
  attack (wiki)

 - assists in the leaving a pyrophosphate group and may also facilitate the cleavage of the bond between the α- and β-phosphates by its electron-withdrawing effect. (source)

  wouldn't the presence of mg hinder release of phosphate?

As with all reactions this is dependent of the concentration of the molecules
involved as stated here:

  The Gibbs free energy change (ΔG) due to ATP hydrolysis depends upon
  the concentrations of the various participants in the reaction. When
  the concentrations are farther from their equilibrium values, the
  absolute value of ΔG is greater. Under “standard” conditions (i.e.
  concentrations of 1M for all reactants except water which is taken at
  its characteristic concentration of 55M) the Gibbs free energy of ATP
  hydrolysis varies from -28 to -34 kJ/mol (i.e. ≈12 kBT, BNID 101989)
  depending on the concentration of the cation Mg2+. The dependence on
  Mg ions occurs because the positively-charged magnesium ions help to
  stabilize the ATP molecule. However, in the cell the conditions are
  never even close to the standard state values. (source)


electrostatic charge of viruses, especially Coronaviruses I am searching for (and failing to find) literature about the electric charge (+/-) of viruses, specifically the Coronaviruses.  I am aware that it is a complicated issue, including interaction of pH and electrostatic charges, etc.  However, I note that electrostatic charge of various materials is investigated for barrier protection, suggesting that there are normal average or overall charges for viruses.  Can anyone comment on this?

Especially, I want to know, at neural pH, are Coronaviruses more likely to adhere to a negatively or positively charged surface?

Thanks.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213776/#!po=1.19048

  All viruses are coated with proteins and contain genetic material which can either be DNA or RNA. Since both nucleic acids have phosphodiester bonds, the genetic material provides a partial negative charge to the virus. The viral nucleic acid genomes are wrapped in proteins that can be neutral, negative, or positive in charge. Therefore, the net charge of a virus depends upon the cumulative charges of the genetic material and the protein.

So the electric charge of a virus particle depends on the constitutive parts of the virus of interest; particularly if enveloped or non-enveloped; the outward-facing heads of the phospholipid bilayer membrane of an enveloped virus will carry a negative charge.

Two references in the above paper may help with a deeper dive into the subject:

Lodish H. et al. Molecular Cell Biology (ed 4.). (W. H. Freeman, New York, 2000). (Google Scholar)
Michen B. & Graule T. Isoelectric points of viruses B. J Applied Micb. 109, 388–397 (2010). (PubMed) (Google Scholar)

I couldn't find any papers on the electrical properties of novel coronavirus specifically. But looking into SARS-CoV may be suggestive of general properties. Its envelope proteins have a positive charge that help with targeting and infecting ACE2-expressing cells (https://clarivate.com/wp-content/uploads/dlm_uploads/2020/01/CORONAVIRUS-REPORT-1.30.2020.pdf).


DNA polymerase I exonuclease activity Does DNA polymerase I in bacteria use forward or reverse exonuclease activity to remove RNA primers? One of my books says it uses 5' to 3', but another says it uses 3' to 5' exonuclease activity.

Update: I know RNase H can remove the primers, but the exonuclease activity of pol I can also remove them.

Googling your question showed that it is RNAse H that removes the RNA primer. DNA Pol I has both 3'-5' as well as 5'-3' exonuclease activity for proofreading and nick repair activities, respectively. See the wiki on Pol I