How are new people created from the DNA of an aged person. i.e. Why are we young? The question "why do we age" has been asked numerous times. But why are we young? The cells of the adult human being are an age (time>0), but how can old cells create new cells that are younger than themselves?

I.e, how are young people made from the cells of old people?

I realize that senescence, the act of a cell aging, has to do with the shortening of telomerase over time which puts a limit (the Hayflick limit) on the life of an autosomal cell. So in theory, because cells only make direct copies of themselves but the telomerase shortens with every division, each new daughter pair would be as old as the parent and would continue aging. But how come new people start senescence at time t=0?

Gametes (sperm and ovum), which fuse to form a zygote, arise from germ cells (spermatogonia and oogonia). Germ cells, like stem cells, are maintained carefully i.e the genome is preserved and transposition/recombination events are tightly controlled via different mechanisms.

So these germ cells don't have shortened telomeres. Also, during early embryonic development the future germ cells quickly migrate to an end of embryo and remain there while the rest of the body takes shape.

I'm not sure if it has been demonstrated in an article or not but once I happened to talk to Dr Wakayama (who cloned a mouse frozen for 16 years) and got to know that animals cloned by the process of Somatic Cell Nuclear Transfer have reduced lifespan. (SCNT: the nucleus of a somatic cell is transferred to an ovum and triggered to form zygote).

So, to conclude, if germ cells were not protected from mutations and deleterious recombinations, lifespan would have been reduced with every generation.


Biological Evolution outside of Earth What drives evolution forward? I heard that climate change drives species to evolve and adapt. Is there any other mechanism that is encoded in our DNA by which species can over abrupt changes, evolve and adapt?

Say for example Jupiter's moon Europa. If I find species of fishes here in Earth that could theoretically, barely survive on those oceans. If I come back in 5 million years will they look the same they did when I placed them there? or is the process of natural selection universal, and I would expect to see changes in the fishes due to their new environment which is not Earth. basically would foreign species also evolve and adapt.

You take a population of fish and put them in a new environment (another planet even). Will they evolve?

Yes they would evolve as long as they don't get extinct. It sounds very likely that they would very quickly get extinct though.

Note, however that they were already constantly evolving while being on earth whether or not their environment was stable or changing through time. Evolution is not a thing that occurs only when the environment is changing. Stabilizing selection, genetic drift and mutations affect the allele frequencies too, not only directional selection.

General comments on the post

I don't quite understand the relationship between the first paragraph and the second paragraph.

The first paragraph suggests a few misunderstanding of evolutionary processes. I recommend that you have a look at a free online introductory course of evolutionary biology such as Understanding Evolution by Berckeley University for example. Typically, if some concepts I used in the second paragraph above were unknown to you, then you definitely want to have a look at Understanding Evolution


Viruses affecting transmission capability of mosquitoes I've read about bacteria affecting the transmission capability of mosquitoes. For example:

Wolbachia suppresses dengue transmission
When mosquitoes were given antibiotics that decreased their gut microbiota diversity, they became more susceptible to malaria infection

Have there been any studies to show that the presence of certain viruses/viral diversity (rather than bacteria) has an effect on the tranmission of other viruses/pathogens?

There have been some studies looking at this, but not many. One is this study which reported an interaction between Aedes densovirus (AeDNV) and dengue virus (DENV) in Aedes albopictus: mosquitoes already infected with AeDNV were more resistant to infection with DENV, although DENV infection appeared to accelerate the replication of the existing AeDNV infection. A similar interaction was not seen with chikungunya virus (CHIKV).

In addition there are indirect interactions between pathogens of all kinds - viruses such as AeDNV which kill a high proportion of the mosquitoes they infect reduce the average survival and population density of the vector and therefore the ability of the local population to transmit disease (ref).


Can cirrhosis be caused by physical compression of the body? On a random forum, a member speculated that their cirrhosis was caused by wearing tight-fitting clothing such as a girdle or corset.  This leads me to the following question:

  Question: Can cirrhosis be caused by physical compression of the body?

The list of causes on Wikipedia does not include this.  However, this may just be because the list is incomplete.  Alternatively, it may be because physical compression is unlikely to contribute to cirrhosis.

A plausible mechanism that springs to my mind is that physical compression leads to the constriction of hepatic veins, arteries and/or their tributaries.  But I suspect the rib cage would provide significant protection against this (see below).

There is the term “corset liver”. It describes changes (“grooves”) on the liver’s surface following external compression and subsequent local atrophy, e.g. from wearing a corset for a long time. (see Dancygier: Clinical Hepatology)

A paper from the 1980s describes some abnormality in the histological findings of liver tissue of dogs after chronic abdominal compression but without providing any details in the abstract (I don’t have access to the full version). They measured an increased pressure in the Vena cava and the portal vein. (Ueyoshi, Shima: Studies on spinal braces. With special reference to the effects of increased abdominal pressure. PMID 4093227.)

A (chronic) Budd–Chiari syndrome can also cause liver necrosis and consequently cirrhosis and can be the result of venous compression from e.g. tumors.

I doubt that a comparable chronic compression is possible from wearing clothing. Corsets are still used in orthopedic conditions. I have never heard about long-term side effects on liver tissue. The explanation for cirrhosis seems unlikely to me.


What is the principle behind Microagglutination test (MAT)? Could some one please help me understand the principle behind the MAT. Also, is it only used to detect leptospira or can it be used to detect other pathogens as well? Kindly share links to papers if possible. Thanks!

Microagglutination tests for the presence of antibodies, which declare themselves by sticking their antigens together into clumps.

Leptospirosis serodiagnosis by the microscopic agglutination test.

  The microscopic agglutination test (MAT) is the gold standard for
  sero‐diagnosis of leptospirosis because of its unsurpassed diagnostic
  specificity. It uses panels of live leptospires, ideally recent
  isolates, representing the circulating serovars from the area where
  the patient became infected. A dilution series of the patient's serum
  is mixed with a suspension of live leptospires in microtiter plates.
  After incubating for about 2 hr at 30°C, results are read under the
  dark‐field microscope. The titer is the last dilution in which ≥50% of
  the leptospires have remained agglutinated

You know antibodies work by sticking to things.  If I have antibodies to a thing it is because I have been exposed to that thing, here leptospirosis.  This version of the test uses live leptospires.  If the antibodies stick to them and they clump up, the plate gets clearer.

The good thing about this is that you don't need to know anything about the antigen except it is on the germs, or anything about the antibody except it sticks to the antigen.  Also the germs are big enough to make clumps.  If you have antigens for something small that won't make noticeable clumps (for example a virus, or an individual antigen of interest) you can stick it to microscopic latex beads.  Then just as the leptospires clump up when the antibody sticks to them, the beads will clump up if there is antibody specific to the antigen you have stuck onto them.

Historically the clumping was interpreted by a human with a microscope.  You can do it with an optical density meter too.

This approach is used for lots of different diagnostic tests.  You can find them with google and "agglutination" but those links do not all explain how the test works.


How does membrane potential vary between intraceullar membranes and the cellular membrane? Question
Does each type of membrane have a different membrane potential? I'm especially interested in answers that can cite academic papers that have attempted to measure membrane potentials.
Discussion
I've asked about the composition of membranes before , and although I recieved some information, I didn't get all the information I was after. This isn't a problem with our community but rather with the field at large: the popular thinking is membranes are membranes are membranes (mostly due to the difficulties in studying membrane biophysics experimentally).
This is how wikipedia defines membrane potential:

Membrane potential (also transmembrane potential or membrane voltage)
is the difference in electric potential between the interior and the
exterior of a biological cell. - Wikipedia

This isn't strictly true. Intracellular membranes also have membrane potentials as one can imagine, and there is some unverified information regarding compartmental pH values. This is why I am interested to find out if there have been studies attempting to quantify this across the cell membrane, and across different subcellular membranes.

Yes, various intracellular membranes do have potential differences, but as you can imagine they are more difficult to measure experimentally, so in general data on this is scarce.

Summary

Mitochondrial membrane: 150mV-180mV with negativity on the matrix side. Seth et al 2011
Endoplasmic reticulum membrane: 75-95mV with negativity in the ER. Qin et al 2011, Worley et al 1994
Golgi: No notable membrane potential. Schapiro & Grinstein 2000
Lysosomal: 20mV with more negativity on the cytosolic side. Koivusalo et al 2011

Discussion

The mitochondrial membrane potential is probably the best studied case. This is the potential difference over the inner mitochondrial membrane, between the mitochondrial matrix and the intermembrane space; it is about 150mV (more negative on the matrix side). There is also a potential difference between the mitochondrial cristae (folds of the inner membrane) and the matrix which is used to drive ATP synthesis; it is probably larger than 150mV, but this is still poorly understood I think. The outer membrane is permeable (has pores) so there should be no potential difference between the intermembrane space and the cytosol.

For the endoplasmic reticulum (ER), there is little data available I think, but there are some estimates based on measurements of ion transport, which gives a value of about 75 to 95 mV (more negative inside the ER). Probably this depends a lot on the situation, as the ER is involved in regulating ion homeostasis (notably Ca2+).

For the Golgi apparatus, this study found that no potential difference vs. the cytosol, based on the movements on H+ and counterions.

Lysosomal membrane potential has been measured directly, giving values of about 20mV (more positive inside).

For the nucleus I don't know of any data, but I would assume there is no potential difference here, given that the nuclear membrane has large pores.


Identifying a spider from my childhood memory Once, as a child, I found a spider in my parents' garden. I remember catching it in a jar because I thought it looked unusual, but I never figured out what kind of spider it was and unfortunately didn't get any pictures. I've been looking for it in books and on the Internet since, based on memory, with no luck.

This was twenty years ago now, and I realize my memory of it may not be good enough to identify it now, but here's trying.

What I remember best was its abdomen, which was a dark metallic blue and sort of rectangular in shape. Its body was probably about 1.5 cm long, without the legs, and maybe 1 cm wide or a little less (I was a child, things look bigger when you're small.) It was found in a garden in the suburbs of Copenhagen, Denmark, sitting on a bed sheet drying in the sun. It left only a few strings of web, almost like a bridge, from the bottom of the jar to the lid where it had escaped during the night because the lid wasn't sealed. I never found it again or saw another spider like it.

This may be what you are searching for:

It's actually a male purseweb spider (Atypus affinis), the color fades to black, eventually.

Source: http://www.spiderzrule.com/purseweb2.htm


What is this plant which closes its leaves when touched? I came across this video on Facebook where a plant closes its leaves when touched. Unfortunately the video does not mention the name of this plant.

What's the name of this plant, and where can I see it?

It is a Mimosa pudica, a wonderful plant. According to wikipedia you can find it in the following places:

  Mimosa pudica is native to South America and Central America. It has been introduced to many other regions and is regarded as an invasive species in Tanzania, South Asia and South East Asia and many Pacific Islands. It is regarded as invasive in parts of Australia and is a declared weed in the Northern Territory, and Western Australia although not naturalized there. Control is recommended in Queensland. It has also been introduced to Nigeria, Seychelles, Mauritius and East Asia but is not regarded as invasive in those places. In the United States of America, it grows in Florida, Hawaii, Virginia, Maryland, Puerto Rico, Texas, and the Virgin Islands.

If you think that's impressive, look at this video of Dionaea muscipula the venus fly trap:

https://www.youtube.com/watch?v=O7eQKSf0LmY


Can someone identify this species from the pea family? Can someone identify this species from the pea family? The plant was photographed in Morocco in spring. The location is south of Marrakesh at the foot of the high Atlas, in a dry riverbed.

The plant appears to be Medicago arborea. Common names include moon trefoil, shrub medick, alfalfa arborea, and tree medick. It is a member of the pea family Fabiaceae. The species is characterized by the woody stems, the leaves (three), and compressed, coiled seed pods.  See further description in the links below.  It is a native of the Mediterranean basin and apparently becoming rare in nature.

http://botanyphoto.botanicalgarden.ubc.ca/2015/09/medicago-arborea/

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


Calculating CV for intra-assay ELISA Sorry if this is in the wrong thread.

I have to calculate CV for intra-assay ELISA sample OD's. My problem is that i'm finding people are using sample standard deviation in their CV formula, though from what i understand as intra-assay CV reflects variability within the same assay run that to me should be considered as a whole data set and therefore population standard deviation should be used.

Am i correct in my assumption or am i missing something?

As far as I am concerned the intra-assay CV is the average of individual CVs found in an assay.

So let's assume you have a data set of 40 samples, and for each sample you have 2 replicates (results), like the one below.

You would first calculate the mean for each sample, so in the sample above that would be: $$\frac{0.132 + 0.128}{2} = 0.130$$

Then you would calculate the standard deviation for each sample, so going back to our example above, the standard deviation for sample 1 would be as follows: $$\sigma=\sqrt{\frac{1}{2} ((0.132-0.130)^2 + (0.128 - 0.130)^2)}=\frac{1}{500}=0.002$$

Next you would calculate the Coefficient of Variation, so in our case:

$$CV = \frac{\sigma}{\bar{x}}\times100=\frac{0.002}{0.130}\times100\approx1.6%$$

Afterwards you would repeat the aforementioned procedure for each sample.

In the end you would calculate the average of all individual CVs, so: $$CV_{intra} = \frac{\sum_{i=1}^{40} CV}{40} \approx 5.2% $$

I have stolen the example from Salimetrics, I think this document explains inter-assay and intra-assay CV very nicely.

Please note: The usefulness of inter and intra-assay CVs are somewhat disputed, as this Wikipedia article mentions.


What is the significance of and biological mechanisms demonstrated in lac operon? I would appreciate it someone could explain clearly how the genes in the lac operon of E coli are activated to allow the bacteria to metabolize lactose?

The part that I really don't understand is the activation of the lac operon.  A good answer would make clear to me how the introduction or removal of lactose from the envirnment activates and deactivates the different genes there.

Also, what are the specific functions of each of the genes (lacA, lacI, lacY, lacZ).

I am in AP Biology and I will not see the light of day again if I do poorly on this test. Please help!

The lac operon in E coli is a set of four genes which work together to allow the bacterium to make use of lactose for energy. An Operon is a set of genes which are co-transcribed on a single mRNA, controlled from a common promoter.  While operons are nearly always found in bacteria, eukaryotes (and viruses that infect eukaryotes) do have some sets of genes organized into operons.

lacZ and lacY is the business end of the lac operon. They are the only 2 genes necessary for lactose usage in the cell.

lacZ codes for beta-galactosidase, an enzyme that cleaves the lactose disaccharide into D-galactose and D-glucose.  Most of know that glucose is an important source or energy via the glycolysis pathway, which is highly connected energy usage in the cell.  Galactose is readily converted by an enzyme (galactose mutarotase) into glucose, making lactose an efficient source of energy.

lacY codes for a protein found in the cell membrane called lactose permease which pumps lactose into the cell from the outside using the proton gradient inside the cell for its motive force.

The lacA gene codes for an enzyme which transfers an acetyl group to galactose, which may prevent the buildup of galactose in the cell.

The way the operon works is more important than what it does.  the lac operon was one of the first examples of transcription regulation every studied.  lacI is not in the lac operon, but it is the single gene which controls whether the operon is copied to RNA from the chromosome.  lacI is translated to the lac repressor protein (LacI), which binds to one of three sites in front of the lac operon.

lacI is a repressor gene - when it is active, it prevents the lac operon from being transcribed into RNA.  LacI is a tetramer - four copies of the protein form a complex.  LacI binds to allolactose, a derivative of lactose, when it is present in sufficient quantities, which then causes it to release itself from the chromosomal DNA, allowing transcription to occur and the lac genes may be expressed.


What does this sentence about toxemia and Clostridium tetani mean? I know that Cl tetani is not invasive and strictly localised.
I think toxemia means spread in the blood.
I am thinking this sentence

  The volume of infected tissue is small, and the disease is almost entirely a toxemia.

Cl tetani has spores.
This suggests me that these spores spread through blood.
They then open and become pathogenic in some tissues where they remain strictly locally (so small area/volume of infected tissue; I think area is better word, since the disease is not invasive) and pathogenic.

How do you understand the quoted sentence about pathogenesis of Cl tetani?

Clostridium tetani produces a protein toxin, tetanospasmin which causes the major symptom of tetanus, namely involuntary muscle spasms. C. tetani is an aerobic species, does not infect the blood, and apparently only produces toxin in anaerobic conditions.

If a pathogenic bacterium propagates through the bloodstream this condition is referred to as bacteraemia. In the case of C. tetani it is the toxin which enters the bloodstream, not the bacteria, hence toxaemia. The bacteria, being anaerobic, are inhibited from spreading through aerobic tissues.


Population genetics of pan-genome I am beginning to work in the field of human gut microbiome, and wondering how (and if) the concepts of population genetics could be applied there.

Considering the competition between the species seems straightforward, although ecological models are probably more appropriate in this case.
Considering the pan-genome of single species however seems next to impossible, as it cannot be divided into independent alleles. One could probably define a number if allels as the number of copies of a particular gene in the community. However, as it confers fitness on the whole community, it is not clear how to define selection. The notion of genetic drift also seems vague.

I will appreciate clarifications and references to relevant literature.
Update
To clarify the question:

The question is rather theoretical, motivated more by my previous work than by what I am about to do in the field of metagenomics. The latter will be analysis of shotgun sequencing data, where the focus is on identifying new species and comparing the species composition in many patients. I doubt that we will have any data permitting to study the intra-species evolution within a single patient. However, understanding how bacteria evolve to be a particular strain in a particular patient could be a plus: if members of a bacterial community with different genomes live as a group, we can't meaningfully say that some of them are more fit or less fit.
My past experience with population genetics is in the field of HIV, which for most purposes can be treated as a diploid hermaphrodite (each virion carries two copies of the genome, and the genomes are shuffled when a cell is co-infected with several virions). Thus, many basic population genetics concepts are easily applied, although the speed of evolution and the need for constant adaptation add other difficulties (motivating such approaches as fitness edge).
Finally, as was pointed in the comments, the problem is not specific to bacteria - altruism does take place in many communities, and should raise the same kinds of issues as I mentioned previously. I admit that I am not familiar with the necessary theoretical frameworks, and this can be considered a part of the question. I would guess however that most such frameworks do not account for direct gene exchange.

Update 2
A relatively recent article by Eduardo Rocha (2018) discusses the shortcomings of the neutral model (as the principal null model for modern genomics) when applied to procaryotes. This has clarified a lot for me, and I give below a short list of their points:

Mutations in bacteria cannot be treated as neutral.
Polymorphism concept is poorly defined for genomes of varying length, which requires new mathematical framework.
Promiscuity of bacteria, freely recombing and exchanging genes via the horisontal gene transfer makes it difficult to define species and apply many concepts of the traditional population genetics.
Difficulties in separating demographics and genetics (essentially, one needs a combined genetico-ecological approach).

Update 3
Inclusive fitness theory / kin theory (also here) probably fits into this context.

It is possible to perform gene-level population genetics analyses on microbiome-derived bacterial species.1,2 † However, the biology of bacteria and the nature of metagenomic sequencing data make such analyses difficult and intractable to many of the well-worked tools of population genetics. Here are some of the things you should keep in mind as you build a conceptual framework for understanding the field:
Bacterial genomes are flexible
The term "allele" connotes gene variants, and the underlying assumption of analyses involving alleles is that each (diploid) individual in a population has one or two alleles of a given gene.  When considering a bacterial population, specifically all the cells that constitute a species, some genes will not be present in all cells. For this reason, "allele" is not frequently used in discussions of complex bacterial communities.  For well-studied species like E. coli and K. pneumoniae with many complete strain genomes, plotting the number of genes found across genomes gives a characteristic U-shaped distribution.3  For a given species, this suggests that many genes are present in most strains, and many genes are present in only one or two strains.  The simple thing to do is to constrain your analysis to the gene set that you observe to appear in all ‡ individuals in a population (the core genome, to use a pangenomics term), but this likely excludes genes that are important for niche-specific fitness like virulence factors, antibiotic resistance genes, carbohydrate degradation operons, etc.  Recently, this problem has been addressed computationally by representing pangenomes as weighted graphs with genomic features at nodes 4 and by building composite reference genomes from strain genomes data encoded as reference graphs.3 #
Metagenomes are messy (but getting cleaner!)
Horizontal gene transfer is likely a frequent occurrence in microbiomes,5 confounding analyses that rely on strict inheritance. Since microbiome sequencing is often short-read, the problem of horizontal gene transfer is exacerbated by the difficulty in reliably assembling transferred genes with specific metagenome-assembled genomes.  As noted by Maximillian Press, there are several ways to address this issue. At the bench, proximity ligation sequencing can supplement traditional metagenomic assembly-by-alignment using the ground truth of physical closeness.5,6 Likewise, single-cell isolation combined with multiplexed whole-genome amplification greatly reduces complexity of assembly.7  At the computer, sequence composition (i.e. kmer content) and coverage profiles can be leveraged to associate metagenomic contigs in bins,8,9 which are like pseudo-genomes.§ If you're lucky enough to have long-read sequencing data, many of the problems associated with assembly of short reads are no longer an issue,10 with the added bonus that SMRT and nanopore sequencing produce methylation data -- unique methylation profiles can be used to infer which contigs likely belong to the same genome or to associate extragenomic contigs (e.g. plasmids) with their hosts.11,12  All of this to say that getting complete genomes from microbiome sequencing is non-trivial, but there are many techniques and tools at your disposal.
Microbiome data is relative
Much of population genetics deals in counted data -- $n$ individuals with allele $a$, $m$ individuals with allele $b$, and so on. Concerning microbiomes, the absolute abundances of individual microbes are not recoverable from sequencing alone. Microbiome data is therefore said to be compositional.  Like RNA-seq, gene or organism abundances derived from metagenomic sequencing are relative, and, importantly, many of the assumptions underlying the statistical analyses applied to absolute counts do not hold for compositional data.13,14  Thankfully, statisical tools for population-level analysis of microbiomes have been developed,15,16 though their widespread adoption has been slow.
Microbiome members are often interdependent
As hinted at in the question update, bacteria display a type of community altruism, where an individual cell with a specific gene can influence the fitness of neighboring cells that lack the gene.  For an example, see my answer to Will all bacteria become resistant against all antibiotics in the long term? concerning secreted β-lactamases.
Therefore, spatial association is an added factor when considering population dynamics of a genetically heterogeneous bacterial species.  Some methods that address cell-cell spatial proximity in microbiomes include sequencing of cryofractured fragments 17 and probe-based spectral imaging.18 Even if microbes are not spatially associated, different microbes may play complementary roles in the iterative metabolism of large carbohydrates into small metabolites.19,20
Surely, this discussion is incomplete, though I hope my answer has given you the footing you need to continue your own exploration to find the appropriate resources for your research.  For a more in-depth discussion of the points I've addressed here, see What Is Metagenomics Teaching Us, and What Is Missed?,21 particularly the sections titled Strain-Level Analyses and Ecoevolutionary Modeling.

† I recommend keeping up with the publications of Ran Blekhman, Peer Bork, and Katie Pollard.
‡ Core genome membership seldom requires that 100% of individuals represented by that genome contain the gene in question, and setting such a strict cutoff would likely exclude truly essential genes that were not found associated with a given strain due to gaps.  In practice, core genome cutoff thresholds are on the order of 90%.
# The senior author for reference 3 made a great explanatory Twitter thread.
§ Contigs and Bins and MAGs, oh my! As with any field, metagenomics has field-specific jargon. Coursera seems to have a good lecture that includes these concepts and how they relate to eachother.

References

Garud NR, Pollard KS. Population Genetics in the Human Microbiome. Trends Genet. 2020 Jan;36(1):53-67. doi: 10.1016/j.tig.2019.10.010.
Priya S, Blekhman R. Population dynamics of the human gut microbiome: change is the only constant. Genome Biol. 2019 Jul 31;20(1):150.
Colquhoun RM et al. Nucleotide-resolution bacterial pan-genomics with reference graphs. bioRxiv 2020.11.12.380378.
Gautreau G et al. PPanGGOLiN: Depicting microbial diversity via a partitioned pangenome graph. PLoS Comput Biol. 2020;16(3):e1007732.
Kent AG et al. Widespread transfer of mobile antibiotic resistance genes within individual gut microbiomes revealed through bacterial Hi-C. Nat Commun. 2020 Sep 1;11(1):4379.
Stalder T et al. Linking the resistome and plasmidome to the microbiome. ISME J. 2019 Oct;13(10):2437-2446.
Chijiiwa R et al. Single-cell genomics of uncultured bacteria reveals dietary fiber responders in the mouse gut microbiota. Microbiome 8, 5 (2020).
Alneberg J et al. Binning metagenomic contigs by coverage and composition. Nat Methods. 2014 Nov;11(11):1144-6.
Kang DD et al. MetaBAT, an efficient tool for accurately reconstructing single genomes from complex microbial communities. PeerJ. 2015 Aug 27;3:e1165.
Kolmogorov M et al. metaFlye: scalable long-read metagenome assembly using repeat graphs. Nat Methods 17, 1103–1110 (2020).
Beaulaurier J et al. Metagenomic binning and association of plasmids with bacterial host genomes using DNA methylation. Nat Biotechnol. 2018;36(1):61-69.
Tourancheau A et al. Discovering and exploiting multiple types of DNA methylation from individual bacteria and microbiome using nanopore sequencing. bioRxiv. 2020.02.18.954636.
Tsilimigras MC and Fodor AA. Compositional data analysis of the microbiome: fundamentals, tools, and challenges. Ann Epidemiol. 2016 May;26(5):330-5.
Gloor GB et al. Microbiome Datasets Are Compositional: And This Is Not Optional. Front Microbiol. 2017 Nov 15;8:2224.
Shi P et al. Regression analysis for microbiome compositional data. Ann. Appl. Stat. 10 (2016), no. 2, 1019--1040.
Kurtz ZD et al. Sparse and compositionally robust inference of microbial ecological networks. PLoS Comput Biol. 2015 May 7;11(5):e1004226.
Sheth RU et al. Spatial metagenomic characterization of microbial biogeography in the gut. Nat Biotechnol. 2019 Aug;37(8):877-883.
Shi H et al. Highly multiplexed spatial mapping of microbial communities. Nature. 2020 Dec.
Kundu P et al. Species-wide Metabolic Interaction Network for Understanding Natural Lignocellulose Digestion in Termite Gut Microbiota. Sci Rep 9, 16329 (2019).
Selber-Hnatiw S et al. Metabolic networks of the human gut microbiota. Microbiology. 2020 Feb;166(2):96-119.
New F, Brito IL. What Is Metagenomics Teaching Us, and What Is Missed? Annual Review of Microbiology. 2020 74:1, 117-135.


What gives nerves their silver colour? I always thought the silver colour specific to nerves was due to the myelin sheaths, but I've observed that unmyelinated C fibres display that same silvery appearance. Where does this colour come from? And can you distinguish myelinated from unmyelinated fibre bundles with the naked eye from their colour?

Short answer
I think the whitish color is due to the outer layer of nerve bundles: the epineurium. This surrounds all nerves, whether they contain myelinated fibers, unmyelinated fibers, or both.

Background
Nerves are bundles of axons (Fig. 1). Whether the axons are myelinated or not, the gross anatomy is similar; axons within a nerve are bundled into fascicles and surrounded by perineurium. Those fascicles are again bundled up and surrounded by epineurium. It is this epineurium that you probably are seeing and it has a whitish appearance (Fig. 2).

The surface of a nerve therefore does not contain myelin; myelin is present around individual axons and is not exposed. Hence, whether a nerve contains myelinated axons, unmyelinated ones, or both will not determine its outward appearance.

Fig. 1. Anatomy of a nerve bundle. source: EasyNoteCards

Macroscopic view of a nerve targeted for epineurial repair. source: wikipedia


Why do humans alone have the capability to have religious/spiritual experiences? What is it in our brain that makes having such experiences possible? I assume other species don't have these. Sure there are instances in the natural world where you can see individuals of the species gather around the dead one. Sometime even the alpha male in the group allows the kin/relatives of the dead individual to approach it (for whatever reason).

The kind of thing I don't see in the wild-life kingdom is an individual becoming "enlightened" or the likes.

Sure our cerebrum is highly developed and all. But "what" is it in our brain that makes it capable for humans to have such experiences?

I've read articles saying we have identified such regions in the brain. Just want to know what these structures are. Did such research establish that such structures also exist in other species too?

Its not clear that this is true.

Working with animals has been a little disconcerting over the past 50-60 years.  In the distant past, I think most evolutionary anthropologists and their like bought into the idea that humans were completely uniquely intelligent and spiritual.  But the more we try to define human sensibilities apart from other animals, the more we find its difficult to see animals as being completely incapable of human feelings and even thoughts.

I refer you to this question which describes the shift in intelligence theories over the years: Why have humans evolved conciousness?

The above reference is just to say that every definition of intelligence that is fairly broad has been overturned by animals (thumbs, socialization, tool use, self awareness, communication and language).

If you want to say 'I know we're special, but I just can't say how' you are in lots of good company... it's become pretty hard to lay down a definition that includes all human beings and excludes animals.

Lately it seems as if the definition of spiritual experience is similarly hard to define. What is your definition?  The capacity to receive and reciprocate affection or love is almost never brought up - that seems to be half of the internet.  Yet, that's a common component to many ideas of spirituality.   It was found a while ago that primates have some form of self-awareness to identify themselves as distinct from other individuals.  True this was only demonstrating that they know themselves in a mirror, but other experiments show it probably is deeper than just that.

I think the most confounding evidence is the work with animals who have been trained from infanthood to communicate to humans through sign language or symbols.  The most astounding example I know if is Koko the gorilla. She had the vocabulary of a 5 year old and the capacity to joke around, reason, and adopted pets as children including a cat called All Ball.  When All Ball who was killed by a car she mourned and remembered her adopted cat for years.  This page outlines all that, though there is a book that describes Koko's life.

  The human staff sought to discover what Koko thought about death.  So they asked, “Where do gorillas go when they die?”  Koko answered, “Comfortable / hole / goodbye.”
  They asked, “When do gorillas die?”  Koko answered, “Trouble / old.”
  They asked, “How do gorillas feel when they die:  happy, sad, afraid?”  Koko answered, “Sleep.”

So this has been taken as evidence that gorillas have a concept of their own mortality or possibly even life after death.

So what is left?  Not clear to me.  Any thoughts?

Some regions of the brain and control of electrical activity in the brain have been associated with spiritual experiences or acts like prayer and meditation.  The temporal lobe is exciting because magnetic stimulation of that region can create the sensation that there is a presence in the room with you. there appear to be many regions which are active in different instances though, which is something you might expect.

There is no evidence yet that animals do not experience similar effects in their brains, though primates have very much the same structures as we do.   Its too bad Koko has died - she might have told us.


Epistasis when interacting loci are codons within a single gene There is epistasis when the effect on the phenotype of one gene is influenced by one or more other genes (called modifiers). Is there a similar concept when the effect on the phenotype of one site within a gene is influenced by one or more other sites within the same gene?

For example: Think about an opsin (a light sensitive protein) that gets activited when hit by a wavelength of, say 500nm.  If the mutation A124S (at position 124 the aminoacid A is replaced by the amino acid S) exists, then the protein is activated when it gets hit by a wavelength of 560nm but this shift occurs only if there is a V (instead of a I) at position 95. Hope you get the idea! Are there specific words to describe such phenomena?

The Wikipedia article on epistasis has a section on epistasis within genes, which it terms intragenic complementation:

  Just as mutations in two separate genes can be non-additive if those genes interact, mutations in two codons within a gene can be non-additive. In genetics this is sometimes called intragenic complementation when one deleterious mutation can be compensated for by a second mutation within that gene.

It appears that many interesting examples of this phenomenon occur when the protein forms multimeric complexes. A multimer consisting of monomers with different mutations may function where a homogenous multimer of monomers of only one of the mutations might be inactive. See Turner et al., (1997) PNAS 94:9063-9068. The Wikipedia article mentions some examples of this under the term interallelic complementation or heterozygotic epistasis.

This reminded me of the phenomenon of protein coevolution that is currently being used to try to leverage evolutionary information to solve protein structures. When the homologous sequences of a protein are known in many different species, then a reasonable assumption is that mutations in protein residues that are in close spatial proximity will correlate, e.g. if a lysine is switched to an glutamate, then other nearby residues may mutate to accommodate the change in ambient electric charge. For more information on this effect, two very interesting papers are Hopf TA, Colwell LJ et al., (2012) Cell 149(7):1607-1621, where the sequences of a family of membrane proteins are used to predict their structure, and Skerker et al (2008) Cell 133:1043-1054, where the covariation between residues in a complex of two proteins is used to re-wire the specificity of one protein for another.


What does this “shell” belong to? I often find these, what I assume to be shells, during walks along the beach. I haven’t seen any creature or plant alive that has this feature and research attempts haven’t been successful.
There are bright reflective blue streaks along the shell and it is yellow-brown coloured and transparent. I have found these along the Northern Irish coast

I believe it's a Patella pellucida or blue-rayed limpet. They live off seaweed in deeper waters, so it's not a surprise that you wouldn't see many live ones.

Picture from an interesting article: Blue-rayed limpet holds secret for windscreen transparent displays with no internal light source


Which magnoliophyta groups are NOT pollinated by bees and why? Considering the bees as the family Apidae which families of flowering plants are definitely not pollinated by them and what could be the reasons?

-Could you say that the relationship is preserved at the family level?

(Please suppose that both groups live in the same geographic context)

Flowering plants evolved before bees, so clearly in the ~100 million years, they must have been pollinated by other methods. Some plants still retain this ancestral characteristic.

This paper shows a species Magnolia tamaulipana (Magnoliaceae) which is pollinated by beetles.


What is this plant with purple berries? This plant was seen by a friend of mine in Virginia. What is it?

It looks to me like beautyberry. Here is a link to a species page to judge for yourself. It's a very common cultivar and I've heard of people using it to control garden pests.

http://uswildflowers.com/detail.php?SName=Callicarpa%20americana

Here is an image of American Beautyberry from gardenknowhow.

It is often confused with Japanese Beautyberry which has smaller berries on stalks.


Do lower animals have instinctive behaviors? Can an organism such as C. elegans, with only 302 neurons, exhibit "instinctive or innate behavior"? If not, then at what basic minimal structure is instinct manifest?

Short answer
'Lower' organisms like C. elegans exhibit innate behaviors. In fact, unicellular organisms [without any nerve cells at all] can exhibit instinctive behaviors.

Background
Let's start by defining the central terms here, namely Behavior and Instinct:

Merriam-Webster has a general definition of Behavior:

  [A]nything that an organism does involving action and response to stimulation

And according to the Cambridge dictionary, Instinct is:

  [T]he way people or animals naturally react or behave, without having to think or learn about it.

And Merriam-Webster defines Instinct more elaborately:

  Largely inheritable and unalterable tendency of an organism to make a complex and specific response to environmental stimuli without involving reason
  Behavior that is mediated by reactions below the conscious level

Hence, C. elegans' actions are indeed instinctive behaviors.

An interesting distinction here is whether behaviors in simple organisms should be indeed called behavior, or rather be classified as [lower-order] reflexes.
According to Merriam-Webster, a Reflex is:

  [A]n automatic, often inborn response to a stimulus that typically involves a nerve impulse passing inward from a receptor to the spinal cord and then passing outward from the spinal cord to an effector (such as a muscle or gland) without reaching the level of consciousness and often without passing to the brain, such as the pain-withdrawal reflex, or the knee-jerk reflex.

This is a typical schoolbook approach-based definition of a reflex. Strictly spoken C. elegans' behaviors would not classify as reflexes according to this definition, because invertebrates do not have a spinal cord.

Nonetheless, sea anemones show protective withdrawal responses by retracting their tentacles and oral disc. Some may even detach from the substrate in response to a variety of aversive mechanical, electrical, or chemical stimuli. And earthworms show rapid withdrawal responses mediated by giant nerve fibers when subjected to unfavorable stimuli, that are in fact classified as reflexes (Smith, 1991).

Indeed, Wikipedia defines a Reflex as

  ...[A]n involuntary and
  nearly instantaneous movement in response to a stimulus. Scientific
  use of the term "reflex" refers to a behavior that is mediated via the
  reflex arc.

Thus the question then becomes what is a reflex arc? The Medical dictionary defines a Reflex arc as:

  Route followed by nerve impulses in production of a reflex act, from peripheral receptor organ through afferent nerve to central nervous system synapse and then through efferent nerve to effector organ.

Hence, in all, instinctive behavior is appropriate general terminology. When in simple organisms the behavior can be directly linked to a responseive action to a sensory stimulus, the term reflexive behavior may be a more appropriate term than instinctive behavior as far as I can see.

To push the definition of instinctive behavior even further, we can conclude from all this that single-celled organism exhibit it too, as they can show simple instinctive behaviors, such as phototaxis and chemotaxis, where they change their direction of movement in response to light and chemicals, respectively (source: Khan Academy).

Reference
- Smith, ILAR J (1991); 33(1-2): 25-31


How and when did a dedicated immune system evolve? I have recently been doing a lot of research into the interplay between the innate and adaptive immune systems in humans, and mammalian laboratory models. This has led to my reading some interesting information on the immune response in insects;

  Insects have a highly efficient immune system.  In response to a bacterial attack, their fat body (the equivalent of the liver in mammals) synthesizes a whole range of peptides with an antibacterial and antifungal effect.

This fascinated me, as the clear inference is that there are no ‘dedicated’ immune cells, but that adipose tissue has far more diverse functions that I had realized.

I have done a little more reading, and also looked at plant immune systems, which seems far more analogous to those in insects than mammals;

  Plants, unlike mammals, lack mobile defender cells and a somatic adaptive immune system. Instead, they rely on the innate immunity of each cell and on systemic signals emanating from infection sites.
  (Jones, 2006)

My questions relates to the need of an adaptive immune response in mammals. The immune systems in insects and plants - a more 'systemic' immunity due to the lack of dedicated/mobile immune cells - seems much simpler.

Given that evolution works incrementally (there are no 'jumps' - for instance, going from a non-dedicated immune system, to a dedicated immune system), I would hypothesise that organisms less distantly related to insects and plants may have tissues with duel functions (similar to insects?), but that specialize further as immune cells until gradually (down the evolutionary tree) a complex and specific immune system emerges. (This is complicated by the fact that our immune systems do have multiple roles - e.g. tissue remodelling, but I wasn't going to go into that here. Feel free in your answers if it is necessary!).

My overall curiosity can be summarized as 2 questions;

What are the possible reasons why a dedicated and immensely complex immune system evolved in some lineages of organism?
Is there any evidence of 'half-way' organisms, and about what ecological time-frame might the dedicated immune system have developed?

Immunity has probably evolved more than once as it is completely necessary for survival.  You might even argue that defenses such as antibiotics and predatory behavior are immune defenses for single celled creatures.

As you point out, plants have a different immune system than animals do.  Insects do too.  They don't have innate immune memory which many animals have, where pools of cells embody the immune response to a specific antigen.  (i.e. encode for a specific immunoglobin or a tCell Receptor variant).

I found this reference that this appears to be the collective property of jawed vertebrates.  Even so, there are many late innovations in the immune system, where reptilian and mammalian immune responses vary substantially.

Its not clear to me whether other animals have the insect system. Animals that branched off before insect lines such as radiates probably have their own way of dealing with immune response.  That's just a guess though.


How large is the range of 'same origin' when determining whether two organs are analogous or homologous? The pectoral fins of a whale and a shark. Are they analogous organs?
I was looking at this question, and I saw that the two answers defined the range of 'same origin' differently. One said that sharks and whales have the same origin as jawed animals, (therefore they are homologous) and the other said that they had different origins, namely cartilaginous fish and mammals(therefore they are analogous). Now here's the question.

How large is the range of 'same origin' when determining whether two organs are analogous or homologous? Is it as large as a Kingdom or a Phylum? Class? Order? Family? Or is there another criterion?

There is no limit: the ribosomes in your cells and the ribosomes in a palm tree are homologous structures, because both you and a palm tree inherited that structure from your last common ancestor, an unicellular eukaryote, more than 1 billion years ago.
That being said, the question in your link (and several other sources) gives an incorrect definition of homology and homoplasy (or analogy). Homology and homoplasy are not defined for "the function of the organ" or anything like that.
First, both terms apply to structures, which have a different meaning in phylogenetic systematics and evolutionary biology. A structure can be:

Morphological
Physiological
Biochemical
Comportamental (ethological)

Thus, we are not necessarily talking about organs or morphology when we define homology and homoplasy.
The difference between homology and homoplasy is very simple:

Homology: a similarity due to common ancestry.
Homoplasy: a similarity not due to common ancestry.

So, in my example using ribosomes, that similarity ("presence of 80S ribosome") regarding you and a palm tree is due to your (ours) common ancestry.
On the other hand, the thermoregulation in mammals and in birds (and probably other dinosaurs, not only birds) is an example of homoplasy, because the common ancestor of mammals and birds, an early amniote, was probably not capable of thermoregulation. Notice that here the structure is not a morphological one, but a physiological one. Another example using physiology is the pH of the blood: the pH of my blood and the pH of your blood is the same (7.4) because we inherited that feature from our common ancestor. Thus, it's a homology.
Sometimes the situation is tricky. Is the wing of a bat and the wing of a pigeon an example of homology or homoplasy? Since the common ancestor of bats and birds didn't have wings, and both bats and birds developed wings independently in their evolutionary histories, it's an case of homoplasy (analogy). What causes confusion here is that, in both cases, the wing is a modified anterior limb, and the presence of an anterior limb in bats and pigeons is an homology. The "limb" is a homology, not the "wing".
And that brings us to the case of sharks and whales. If the pectoral fin of a shark derives from the same structure that formed the anterior limb of the first sarcopterygii, then you can say (as several systematists say) that the pectoral fin of a shark and the anterior limb of a whale are homologous structures.
Summarising: given two organisms, Y and X

X and Y share a given feature;
find the last common ancestor of X and Y (it doesn't matter how long ago in the past)
did that ancestor have the feature? Did it transmit the feature to both its descendants?

If the answer to that last question is "yes", it's an homology. If "no", it's an homoplasy (analogy).


In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis? Ketogenesis pathway maps show acetoacetyl-CoA converted to HMG-CoA and only then to the first ketone body acetoacetate. Why this detour instead of directly hydrolyzing off the CoA to get there in a single step? Is it possible that some ketone bodies are made by direct conversion? The enzyme acetoacetyl-CoA hydrolase to do this job exists and can be found in rats.

I believe it is related to the fact that the enzyme HMG-CoA lyase is regulated by glucagon (activates) and insulin (inactivates). It appears that this extra step was added so the pathway can be hormonally regulated.


Does antibacterial soap work chemically? Normal soap requires scrubbing, does anti-bacterial soap require scrubbing too? Since it (I assume) works chemically, can I produce the same cleansing effect without lathering with soap and using anti-bacterial soap instead? It could save me a lot of time showering in the morning.

What the comments are trying to say might go something like this.

The antibiotic triclosan that's used in almost all 'antibacterial' products works pretty quickly - by interfering with several processes in the bacterial and fungal membrane.  It doesn't need much more than contact to work.

That being said, the longer your exposure to the antibiotic, the more thoroughly it will work.  Triclosan can penetrate the blood stream through the skin.  If you have soap suds scrubbing may or may not get the triclosan into more contact with a greater surface area as it diffuses into the skin, but probably won't affect the substantial effect it has killing surface bacteria and fungi/yeasts.

Its worth noting that the FDA doesn't recommend the use of antibacterial soap or other antibacterial products.  Soap itself is a powerful agent for killing bacteria and other microorganisms and biocides like triclosan probably encourage the emergence of antibiotic resistant strains which present a medical risk to people.


Spatial dimensions for an animal I'm reading a review paper. They say:

  The position of an object in head-centered coordinates (that is, relative to an animal's head) can be defined along three axes: the medio-lateral (radial) axis, the rostro-caudal (horizontal) axis and the dorso-central (vertical) axis.

I'm having a little bit of difficulty understanding this coordinate system as the paper doesn't provide a picture. Usually I would think of the three axis as an x-y-z coordinate system where the rat's head is the "origin" (from a mathematical standpoint), but the terminology here seems to be a bit different, so I'd like to understand from a biologist's point-of-view how these three axes are drawn relative from a rat's head.

Paper can be found here: http://www.nature.com/nrn/journal/v9/n8/full/nrn2411.html (bottom of page 602)

Wikipedia has a quite didactic article on this: https://en.wikipedia.org/wiki/Anatomical_terms_of_location#Axes

These terms are complementary with a mathematical coordinate system: if you are describing a system of axis for a cylinder, you will need to specify that (e.g.) $z$ is along its symmetry axis, here you will say that $z$ is along the rostro-caudal (or antero-posterior) axis. Also, in biology, axes do not have to be straight lines, see the neuraxis:


Are mitochondrial genes decoded in the same way as nuclear genes? Mammalian mitochondrial genomes contain only 22 tRNA-coding genes, which is an insufficient number to decode mRNAs under the standard wobble rules.

How is translation of mitochondrial mRNAs achieved with this number of tRNAs?

The possibilities that occur to me are that certain genes encode multiple tRNAs (but this appears unlikely as each gene has its own promoter) or that mitochondrial tRNAs can adopt alternative three-dimensional structures, each with a different anticodon loop and hence a different anticodon.

Answer Summary

  Translation in the mitochondria of mammals differs markedly from that
  in the cytoplasm. Although it has more similarity to translation in
  prokaryotes, it also shows significant changes from the latter. A smaller
  repertoire of tRNAs is able to translate a ‘simplified’ genetic code
  through structural alterations and base modifications that allow their anticodons
  to decode groups of synonymous codons, not possible according to the standard wobble ‘rules’.

Relationship to the eubacterial translation system

One of the pieces of evidence for the endosymbiotic theory of the origin of mitochondria was the fact that their translation machinery was more similar to that of prokaryotes than to that in the eukaryotic cytoplasm. The similarities to prokaryotes included the (smaller) size of their ribosomes, the susceptibility of their ribosomes to antibiotics specific for bacterial ribosomes, and the formylation of their initiator tRNA — fmet-tRNA.

Although in no way rebutting the endosymbiotic theory (which is widely accepted), mitochondrial translation shows several differences from that in prokaryotes. These include there being a single tRNA to decode methionine in both initiation and elongation (discussed below), the lack of leader sequences preceding the initiation codon, hence precluding a Shine & Dalgarno type of recognition by the ribosome, and additional ribosomal proteins which are thought to “provide a specialized platform for the synthesis and membrane insertion of the highly hydrophobic protein components of the respiratory chain”.

Decoding with 22 mitochondrial tRNAs

General Review: Suzuki et al. (2011) Annual Review of Genetics 45, 299–329

As the question states, mammalian mitochondria encode 22 mitochondrial tRNAs, which would be insufficient to decode mRNAs using the standard genetic code and the wobble ‘rules’ that apply to translation in the eukaryotic cytoplasm and in prokaryotes.

One way out of the dilemma would be if some of the tRNAs were encoded in the nucleus and imported into the mitochondrion in a similar manner to that of nuclear-encoded mitochondrial proteins. Although this turns out to be true for certain organisms (although the import system is different from that for proteins), and important in some cases, this is not the answer for mammalian mitochondria. Thus, as reviewed in Current Genetics (2009), the mitochondrial tRNAs encoded in the nuclear genome of H.sapiens only duplicate the 22 mitochondrial tRNAs and their anticodons. (The one exception is an extra Gln(anticodon CUG) in addition to the Gln(anticodon UUG).)

Let us look more carefully at the problem. Although there are 61 codons specifying amino acids, because of wobble, fewer than this number of tRNAs are required to decode them. The left-hand frame of the figure below shows the standard genetic code, and the minimum number of tRNAs needed to decode it using the wobble ‘rules’ shown beneath, indicated by the colour-coded rectangles.

For those not familiar with the actual pattern of wobble (summarized in my answer to another question), in elongator tRNAs the 5′-position of the anticodon has some flexibility such that a G in that position can form base pairs with U or C in the 3′-position of the codon, an inosine (I) can pair with U,C or A, but an anticodon C can only pair with a codon G. The unmodified bases A and U are rarely found in anticodons, but a variety of different chemically modified Us are found (U* in the figure) which only pair with A. Thus, the minimum number of elongator tRNAs needed would be the number of coloured rectangles — 36 — and, as there are separate species of tRNAmet for initiation and elongation, the minimum number of tRNA species is 37.

When the human mitochondrial genome was sequenced, two anomalies stood together: the limited number of tRNA genes already mentioned and (more sensationally) changes from the standard genetic code (indicated in red on the right-hand side of the figure). It was immediately realized that these changes served to rationalize the code so that all synonymous codons were in groups of four or two. If it were assumed that the decoding specificity or wobble of mitochondrial tRNAs were different, then 22 tRNAs would be sufficient using the ‘wobble’ shown beneath the right-hand frame of the figure for groups of four amino acids (dark blue) and groups of two amino acids with codons ending in A or G (red).

One further requirement was that a single tRNAmet be involved in both elongation and initiation, a requirement the fulfilment of which has already been mentioned.

What features of the tRNAs could change the wobble ‘rules’ that have been conserved between prokaryotes and eukaryotic cytoplasm? There turn out to be two types of changes. The first, and most obvious, is the fact that certain (but not all) mitochondrial tRNAs have non-canonical cloverleaf structures, the most extreme being tRNAser in which the whole D-loop is missing. The second is the post-transcriptional modification of bases in the anticodon — just as is the case for tRNAs in the cytoplasm, this can markedly affect decoding specificity.

It is not yet possible to describe the codon–anticodon interaction in mitochondrial translation in the way that this has been done in for the cytoplasm or for prokaryotes. The problem would appear to be the difficulty of obtaining sufficient pure tRNAs. Whereas it is easy enough to clone and transcribe the tRNA genes, this is insufficient without the secondary chemical modifications of the bases which is key to the structure and function of the tRNAs.


Number of MHCs in neurons I have read that neurons have proportionately less MHC molecules than other cells of the body. What is the advantage of this?

Antigen presentation by MHC will induce a cytotoxic response by the immune system, which is usually a good thing in the body since most cells can just divide and replicate again.  Neurons, however, are particularly ineffective at regenerating from such an attack, and are not easy to come by; they are also rather important!  Better not to risk it, eh?

That being said, neuronal expression of MHC is actually a pretty complex case, and this open-access article is a good start down the rabbit hole (see also here, here, and here if you have access).


Why do some organelle (like ER and Golgi complex) cannot be seen under microscope during cell division? I have recently read in a book that organelles like ER (endoplasmic reticulum) and Golgi Complex cannot be seen under a compound microscope during cell division. Why does this happen, and where do the organelles go during that time?

A cell when undergoes the process of cell division there are structures known as spindle fibres that are required to pull the chromosomes off to the poles of the cell so that it can be segregated into the cells properly while division. These spindle fibres are made of microtubules that are protein molecules constituting the cytoskeleton of a cell. Endoplasmic reticulum and Golgi apparatus are also providing a lot of support to the cells.
Also endoplasmic reticulum and Golgi apparatus are the sites where most of protein forms. While cell division these two organelles disintegrate so as to provide protein for microtubules formation, and so as to reduce support of the cell so the division of the cell is comparatively easier.
Also, during the cell division everything divides equally between the two daughter cells, so ER and Golgi bodies disintegrate so they can be equally divided into the two daughter cells.
Also, nuclear envelope is the continuation of the endoplasmic reticulum. Hence endoplasmic reticulum disintegrates with the nuclear envelope.

Here I have provided a set of possible reasons for your question.

You can refer Raven's biology for further information.


Could removing non-functional parts of coenzymes improve enzyme function? As pointed out here, many important co-enzymes (essential enzyme cofactors) such such acetyl-CoA and vitamin B12 contain nucleotide portions that do not function in the enzyme catalysis. They have been suggested to be relics of the RNA world, so it would appear to me that they are redundant. Suppose we were to remove these nucleotide portions of the co-enzymes, would that improve the working of the proteins (and perhaps our health) or wouldn’t it make any difference?

The video cited in the question is to be commended and presents a number of points relevant to questions about DNA and RNA posted here previously.

The problem with the question sems to be an incomplete understanding of the role of these coenzymes/cofactors in the function of the enzyme. (The original question implied that acetyl-CoA and vitamin B12 are the enzymes.) In contemporary protein enzymes, these non-protein cofactors are bound to the protein part of the enzyme and complement it in its function. Typically, the protein will have binding sites for the substrates (the reactants) and the coenzyme will provide the sophisticated catalysis or other essential function.

The coenzyme must obviously interact with the protein, and in a way that leaves its catalytic or functional part free to operate. This is what the nucleotide portion of the coenzyme does — in fact it is performing the same role as has been suggested it played in the RNA world, but instead of interacting with an RNA enzyme (ribozyme) by base pairing, it interacts with amino acid side-chains by a variety of weak interactions. An example of this is shown for coenzyme-B12 in the enzyme, methylmalonyl-CoA mutase (my annotations in red and brown).

To quote from the figure legend in the paper: “The lower axial ligand to the cobalt is histidine HisA610, which is in turn bound through AspA608 to LysA604. The pseudo-nucleotide tail is bound in a pocket between the sheet and the C-terminal helix.”

The situation for coenzyme-A (CoA) is slightly different, in that it is involved in the transfer of acetyl and other groups, rather than catalyis per se. However the principle is the same — there is a chemically functional portion and a nucleotide portion that binds it to the protein.

Thus, the nucleotide portion of coenzymes is not redundant and without it they could not bind to the enzyme and enable it to perform its function.


Which plants are healthy to keep in the bedroom at night? I know that there are no plants which release oxygen in the dark (Can plants produce oxygen at night (without light)?).

I also know that some plants can clean toxic agents from the air (Nasa Clean Air Study).

Are there any plants which have health-beneficial properties specifically at night, i.e. in the dark?

Assume, if you'd like, that 12 leprechauns bring the plants to your bedroom the moment you turn off the lights and place them outside your house when you turn on the lights in the morning. Can bedroom plants still be beneficial to your health in this case? If so, which ones and why?

There exist a diversity of flora you may select relative to the antigen or noxious chemical you seek to reduce.
Pursuant to the British Medical Bulletin, the critical indoor pollutants are the polycyclic aromatic hydrocarbons like furanes and benzenes, ethanal (formaldehyde) and carbon monoxide. Depending upon which gaseous or volatile compound you seek to reduce in your household, you may select Chrysanthemum morifolium for the reduction of ammonia gas, xylene and alternative respiratory irritants; Chlorophytum chomosum for formaldehyde; and Dracaena genus concerning and trichloroethylene.

If you should suffer any infestation of Penicillium mould, then it is advised that one tackle the source of the infestation directly - areas rich in cellulose and moisture.

Further information regarding is available from the following links:

9 Air-Cleaning plants that are almost impossible to kill, https://greatist.com/connect/houseplants-that-clean-air

British Medical Bulletin, https://academic.oup.com/bmb/article/68/1/209/421251


Some kind of fly, identification It has a really interesting shape. Is this a common fly ?

Edit: I found this in a relative's house. For area, I can say the  plateaus and mountainous parts of Turkey's mediterranean coast. I just saw a single one of them. It was alive. The size was like 1 cm. Never saw one before in my life. It peaked my interest so I decided to ask.

It is some sort of plume moth, Pterophoridae. I can't tell what species it is, but at least you know more about where to look! Or, hopefully, someone who knows more shows up.

There are probably better places to look, but I found this list of plume moths in Turkey on Wikipedia if you want to compare.


Open databases for copy number variations similar to TCGA The Cancer Genome Atlas(TCGA) has open data for copy number variation(CNV) from at least 10k different cancer patients. They offer two types of data, CNV data from tumor and CNV data from normal tissue samples. Is there any other open databases that offer CNV data from at least one cancer type?

The ICGC has CNV data for many different cancer types. It has many both restricted and open data sets. The DCC releases page will let you hunt through them - those that are public are easily downloaded. They also have matched expression, SNV, DNA methylation, and structural mutation data for many samples.


Question regarding stop codon I just wanted to ask that in a given RNA, If there is a start codon and no stop codon, is it still considered mRNA, I mean can it be translated to a protein ?

Yes, this is still considered mRNA. A lack of stop codon is usually due to a so-called readthrough mutation, where DNA sequence changes within the stop codon and after transcription it can no longer be recognized by release factors. But yes, ribosomes still recognize the mRNA molecule and start synthesizing abnormal proteins, usually until the ribosome stalls on the 3' end of mRNA and can neither go further nor detach. There are various mechanisms converting this "stalling signal" to a chain of intracellular reactions that lead to degradation of that protein and that abnormal RNA.

Bacteria for instance have a very curious mechanism of solving that problem, namely a tmRNA molecule that is targeted to a stalled ribosome by some specific proteins and acts as an aminoacyl-tRNA as well as mRNA template. It resumes translation, allowing addition of a peptide tag to the malformed protein, which will serve as a marker for degradation. More on that here:
https://en.wikipedia.org/wiki/Transfer-messenger_RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358797/


Can you accelerate the growth of a plant by accelerating its surroundings? I had this weird idea of making plants grow faster when I first visited an indoor nursery which used floodlights instead of sunlight. They turned on during the day and went off during night in cycles.

If the time period of the cycles are decreased, it would seem to the plants that the earth just switched to fast-motion. Will this trick the plants into growing faster?

If not the current generation, would the later generations of plants grown like this adapt to the new rhythm ?

(Given that the plant is provided with surplus nutrients to meet the new requirements.)

I would love to do the experiment myself if it would actually work!

This is not the best answer, but see that as a starter! Feel free to use my answer to build yours!

I have found a so-called professor speaking of advantages to go on a 24h light/12h dark cycle (36h cycle) to accelerate the growth of cannabis. I'm not sure of the reliability of this source.

I think the main problem we will encounter with that reduction of cycle would be the trouble with the circadian clock inside the plant. This clock is quite stable and I suspect some deregulation would happen if you desynchronize your day-night cycle with that clock.

See the effects we show on humans in the section Enforced longer cycles of
 Wikipedia or this stack question

  Researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions - both physiological, behavioral, and cognitive.


How detachment/separation works in biology? It might be a strange question, but I'm interested in the mechanics of separation/detachment during asexual reproduction, for example when an organism reproduces by budding (I don't mean cellular budding like baker's yeast). When the newly formed body is fully matured it detaches itself from the parent / original body.

It might not be caused by a specific tissue, as animals with not so differentiated bodies are (also) capable of such, but I could easily be wrong. Is this (the detachment) triggered by changes in the cell membrane? I can't really think of other explanations.

Reproductive budding and what you call 'cellular budding' are really highly related processes. Budding as a form of reproduction essentially partitions protein aggregates and damaged cellular components into the host or mother and builds fresh or 'young' cells on the opposite side of a partition. To begin understanding this look at Saccharomyces cerevisiae (budding yeast) which forms protein rings (from the septin proteins) at the membrane, around the bud neck which separates the mother and daughter cells Hartwell 1971. This ring acts a partition that in part, withholds protein aggregates and certain proteins from diffusing from the mother to the daughter. This protein ring is an example of how cells limit diffusion of proteins and cellular components to the daughter cell. Another good example that comes to mind is Linder 2007, though it is done in E Coli, not budding yeast, where mother cells maintain protein aggregates and age, while the daughter cells are given fresh components and are therefore more fresh and 'young'.

Now like you mention, imagine this process in a multicellular organism to be fundamentally the same. At some point the multicellular organism will start an outgrowth of cells, while restricting what materials are given to the daughter cells to maintain their youth. And eventually a new organism will have been created. Some of the details will be different, but the fundamental process is is quite similar. In that you start with an old cell that creates a new cell from scratch, but rather than splitting all cellular components equally between mother and daughter, the daughter cells is made in peak condition while the mother cell retains much of the cell 'junk' like protein aggregates.

Hopefully that starts to answer your question.


What are the problems in using an ssDNA or an mRNA for expression instead of using a plasmid? Let's say you want to do a gene cloning experiment. You have an empty expression vector (mRNA or DNA) and are looking to clone some gene X into it. Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?

What is the problem with handling pure mRNA nucleotides of gene X? Or even sscDNA?

What is the problem with handling pure mRNA nucleotides of gene X? Or
  even sscDNA?

Problems in directly transfecting a mRNA/ssDNA

mRNAs can be transfected into the cells and is quite frequently done. The problem with transfecting mRNAs directly is that the mRNA gets degraded soon and you will not have sustained expression. This is, however, very useful in certain cases such as creating induced pleuripotent stem cells (iPSCs) where you do not want the cells to continually express the Yamanaka factors (some of which are also oncogenes).

Also, RNAs as such are quite susceptible to degradation. It is much easier to prepare and store DNA solutions for a long time.

Similar problems arise with a ssDNA.

  Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?

One great advantage with using plasmids is that you can propagate your gene infinitely. If you were instead given a fixed amount of mRNA, then you will run out of it soon. Some vendors do practice such greedy capitalistic policies :P

When you are amplifying a DNA using PCR then cloning it has an additional advantages:

you can sequence the gene using well standardized primers (like T7)
you can make constructs that can express the gene conditionally

  You have an empty expression vector (mRNA or DNA) and are looking to
  clone some gene X into it.

You cannot easily clone something inside an RNA. You need specific RNA endonucleases. Moreover a double digestion will be disastrous in this case.

  Why vendors don't generally sell a dsDNA insert but rather provide it cloned in a plasmid

A circular dsDNA is more stable
Vendors can keep the stock of the insert for future customers without having to do PCR again
Cloned insert can be amplified via bacterial cultures to obtain very high amounts (maxi/giga preps)


Name of This Black and White Dove I spotted this dove in a park. It was foraging among Rock Doves, Seagulls, Ibises and a few others.

It appears similar to Pied Rock Doves, but I am not certain if this is correct.

Any idea what the name of this dove is?

It's a pied version of the Rock Pigeon (Columbia livia), aka Rock Dove. According to the Cornell Lab of Ornithology, the pied variety of Rock Pigeon is one of any color that has splotches of white on the body. I think that fits your bird very well. It's not a different species, but just one of several color varieties of Rock Pigeon.

If you are not familiar with Cornell's site and enjoy birds, their All About Birds site is very nice.


Prostaglandin F2-alpha production in men I am trying to find information on Prostaglandin F2-alpha, specificaly production in men. Could somebody explain how this prostaglandin is produced? What types of cells are producing it, production signaling? Any books on this subject?

As I know:

One of the most important chemical mediators are prostaglandins that in vivo act on different cell receptors and have different effects on the body. Prostaglandins are twenty-carbon lipid molecules and structurally similar to cholesterol. Prostaglandins have different types, such as F2, E2 alpha, PGI2, and so on.

A phospholipase enzyme converts phospholipids of cell membranes into arachidonic acid. The arachidonic acid within the cyclooxygenase enzyme or Cox (both type 1 and 2) can be converted to prostaglandins.

PGF2alpha has functions in uterus contraction and bronchoconstriction, so I think both uterus and lung cells produce it.

I have no special information about production of PGF2alpha in men.


How to compare Smith–Waterman algorithm implementations? Assume that you have two implementations of the Smith–Waterman algorithm (with what ever heuristic they apply to speed up) for local sequence alignment of genomic sequences.

I would like to know if one can be certain that these implementations do a good job of aligning (i.e the program has been correctly written). How do I benchmark this?

There are only two possibilities for Smith-Waterman alignment with a given cost matrix. It's either right or it's not.

Honestly, whatever you're using, it's really really unlikely that a pure Smith-Waterman implementation is wrong. It's not that complicated, really. There are a lot of heuristic improvements on Smith-Waterman, but if you're both a) sure you don't want to test them b) sure they're not being used, you can always generate lots of random sequences and align them in pairs. If any pair doesn't align with the same score in the same way, something is wrong and you should investigate further.


Extraretinal photoreception in mammals? A Finnish firm Valkee sells light-ear-plugs against thing such as jetlag. I asked a researcher in Aalto university how do they really work and he responded "why would evolution have lead to photoreceptive cells in ears?" -No direct answer. I asked a well-respected professor who said she did not know this area well enough. Now Valkee guided me to the publications such as Penetration of light into the brain of mammals (1963) and Spectral characteristics of visible radiation penetrating into the brain and stimulating extraretinal photoreceptors (1979). Related to the first one, I found this (1980) from the references:

  "It  is  now  fully  accepted that  the  perception  of  light  by  extraocular  photoreceptors  plays  a  significant  role  in  synchronizing  endogenous  rhythms  with  the  environmental  light-dark cycle  in  non-mammalian  vertebrates"

Things such as certain birds and lizards apparently have extraretinal photoreception aka photosensitive cells not in eyes (this is how I understand it). Now the publication continues

  "The  limited  number  of mammalian  species  tested  to
  date  and  the  near  exclusive  reliance  on  nocturnal  animals  leaves  open  the  possibility  of  extraocular  photoreception  in  some  adult  mammals  (Rusak  &  Zucker, 1975;  1979)."

Now according to a skeptical researcher in my university, there is only one paper supporting photosensitivity in mammals' brains: Wade et al (PNAS 85 (1988) 9322-9326 with rats. My professor in system sciences was extremely scornful when I even asked this question on a seminar course about brain -- he did not specify his reasons and pretty much labelled my thinking as inexperience. Now I am not sure whether researchers are even speaking about the same issues: too large disparities between opposing and proposing teams for the assumed effect apparently through the mechanism called "extraretinal photoreception in mammals". I am very curious.

Helper questions

  What are the mechanisms by which a led in ear would affect a mammal such as a homo sapiens? You don't get D vitamin because of no UV light. You get very-very light heat because of tosslink connection. So it cannot sense the heat as antidote against things such as SAD and jetlag. Other mechanism?
  Is the "extraretinal photoreception in mammals" just placebo or does there exist scientific proofs for it particularly with large mammals about the size of homo sapiens?
  Why would evolution have lead to extraretinal photoreception in mammals?
  Do the terms "extraretinal photoreception" and "non-eye photosensitive cells" mean the same thing? Other terms for the same thing?
  Now eyes are developed very late in cell-division with mammals. Do born-blind mammals and later-blinded mammals experience extraretinal photoreception differently? If led-light (non-UV light) has an effect on large mammals, then I expect this may be possible to see by analyzing results of mammals with different-developed visual-cortexes.
  Does this statement "Light penetrates deep brain areas, eye's receptors have developed from receptors of old CNS." by Humancharger justify the extraretinal photorecetpion?

P.s. I presupposed in this question that extraretinal photoreception is the effective mechanism by which light-in-ear would affect a mammal. It is also possible that there are other mechanisms -- I am not an expert with the terminology here, anatomically and physiologically challenging.

Its pretty well established that there are photoreceptors in cells besides the cones and rods in the retina of the eye.  Humans and most animals have four light receptor genes known (so far).  In addition to Rhodopsin - there are the short, med and long wavelength opsin genes.

While they are mostly expressed in the retina of the eye, they can be found in many other tissues as well. The first image from GeneAtlas below shows the relative amount of RNA found for short wavelength opsin in a variety of tissues - its expressed in immune and nerve cells ( cyan and forest green respectively) relatively well too.   This might imply that neurons are light reactive.  Compare that to that of medium wavelength opsin, which is primarily much more common in the retina.

This is not a psychosomatic effect.  Light receptors in the skin are known to help with seasonal affective disorder - shine a bright or blue light behind your knees.  These receptors are not connected to optical nerves, and so you don't get any image from them, but the information can affect your biochemistry anyway.

The idea of unconscious receptor inputs from other parts of the body probably applies to many sorts of receptors.  This last year there has been a great deal of interest in taste receptors which are expressed in the gut.  They can taste sweetness and other flavors a second time and register the gustatory response in the brain.  Its not a conscious input, but it registers in the brain in MRI.

Why would evolution do this?  It seems to me that this is a new way of looking at the individual life of a cell and makes a good deal of sense.  If every cell has all the genes' DNA why wouldn't a little bit of receptor expression be found in any cell which could use the information?  The conscious processes of the brain probably only take in a small fraction of the information that is sent in and there maybe hundreds of other such senses from various parts of the body to integrate, only a fraction of which we are aware of.

In addition, there are probably lots of cases where receptor signals are only used locally by cells that are sensing their local environment.  It really doesn't make sense that the individual cells must blind themselves.  Individual bacteria and fungi have scores of receptors.  It makes sense that cells that are part of an organism would have as many or more senses as well.


Breakpoint resolution for copy number variation analysis I am reading [1].
One limitation of the Read Depth approach is that "the breakpoint resolution is often poor". Which is the meaning of low-resolution breakpoint in this case?
Breakpoint is defined as the sequence breakpoint:

Examples of a structural variation include a large deletion, insertion, duplication and inversion. Each requires the DNA duplex to be broken and rejoined, and this creates a new sequence of bases at the rejoined sites, i.e. the breakpoints.
Sequencing the new breakpoint regions is a good way (perhaps the only way?) to demonstrate an inversion, which does not increase or decrease the amount of DNA.
Original sequence: 123456789
Sequence with inversion: 123765489
Breakpoint sequences are at 37 and 48

[1]: C. Alkan, B. P. Coe, and E. E. Eichler, “Genome structural variation discovery and genotyping,” Nature Publishing Group, vol. 12, no. 5, pp. 363–375, Mar. 2011.

It means that it is hard to tell the precise location on the chromosome where the structural variation event starts and finishes using only read-depth information.

Read depth is measured by counting the number of mapped reads that overlap targeted regions aka bins. These bins are typically many basepairs wide and are used to normalize coverage with respect to various parameters (e.g. GC content). Smaller bins can give better breakpoint resolution but have noisier statistics. Large bins have better statistics but can't be used to precisely call the SV boundaries.

The CNVnator paper discusses the topic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106330/


Do animals other than humans have different blood types? Humans have the ABO and Rhesus blood typing systems. I have two questions about it:

Why have we evolved these blood types?
Do other animals have different blood types as well?

The answer to this question can be found by searching the Internet.

  For some blood types, evolution and environmental selective pressures
  are clearly important for their persistence. For example, the Duffy
  blood type includes a receptor that allows certain types of malarial
  parasites to enter the red cell. Thus, in some malarial areas of
  Africa, populations with Duffy-negative blood types have a distinct
  survival advantage because absence of the Duffy antigen provides a
  measure of protection against malaria. The percentage of people
  lacking the Duffy antigen is much higher in these locations than in
  areas not endemic for malaria.

more here http://www.scientificamerican.com/article/why-do-people-have-differ/

  Animals and bacteria have cell surface antigens referred to as a blood
  type. Antigens from the human ABO blood group system are also found in
  apes and old world monkeys, which have inherited the same system.
  Other animal blood sometimes agglutinates (to varying levels of
  intensity) with human blood group reagents, but the structure of the
  blood group antigens in animals is not always identical to those
  typically found in humans. The classification of most animal blood
  groups therefore uses different blood typing systems to those used for
  classification of human blood.

more here  http://en.wikipedia.org/wiki/Blood_type_%28non-human%29


Are there differences in energy of glucose isomers? There are many isomers of glucose, including galactose and fructose. Do they have different chemical energy levels, and why? What makes galactose and fructose useful compared to glucose, and would they be more or less energy efficient at storing energy?

Basically, can isomers have more or less chemical energy than others?

The common hexoses do not differ much in energy content (meaning Gibb's energy of formation, $\Delta_f G$). But they have different structures and chemical properties. Glucose and galactose are aldehydes when present in linear form (they are tautomers), while fructose is a ketone, which gives somewhat different properties. They are also used in different macromolecules and other metabolic products. For example, galactose is a component of hemicellulose in plants, while glucose is used for glycoproteins in humans.

Glucose has evolved to be the main blood sugar in vertebrate animals, and other sugars from the diet are quickly converted into glucose. This arrangement is useful as it provides a "common currency" of carbohydrates that can be exchanged between cells of the body, and reduces the number of enzymes needed in central metabolism. The conversion of fructose and galactose into glucose has a small biochemical cost, so in this sense, these sugars afford slightly less energy to human cells than glucose. But again this is not because of an inherent difference in energy content, but rather due to how the metabolic network is structured, with glucose as a "central", preferred metabolite.

In general, though, isomers of chemical compounds can have different energy levels, because some configuration are more energetically favorable than others. The classic example is the difference between the trioses glyceraldehyde/dihydroxyacetone and their isomer lactate, which differ enough in energy to support the synthesis of 2 ATP in lower glycolysis.


What is the smallest visual unit perceptible to the human eye, like a pixel? (esp. in visual static) If you close your eyes, you can often see visual static, where individual pixel-like things are much more visible than with the more smooth, crisp images one gets with open eyes. This led me to wonder a few things:

Is there a name for this unit, like "pixel"?

What is the biological correspondent? A single rod or cone or something?

Are the individual pixel-like things making up the static noise the same underlying mechanism (and size) as the smallest perceptible units of vision one gets when actually looking at something? I suppose this is related to visual acuity. I've read that the cause of static is suspected to be excitation of neurons, but that's not what I'm asking.

Thank you.

The human eye has two types of sensors that become stimulated when wavelengths of visible light (photons) hit the pigments in these sensors. They are known as 'rods' and 'cones'. Rods detect the brightness of light, cones detect the color. There are three different cones in the human eye: red, green and blue. Each cone reacts to the corresponding waves of light. When they are stimulated due to their corresponding wavelengths, they send a signal that travels through the optic nerve to the visual cortex at the occipital lobe.
individual cones don't have different levels of stimulation and always send the same frequency, it's the lack of the stimulation of other cone types that causes certain colors to appear.
in short:

signal or photon of the appropriate wavelength I suppose.
rods for brightness, cones for color.
probably not since the cones are microscopic and tightly packed, too close and too small to see what each cone is literally receiving. The moving static you're seeing is called phosphenes and is comprised of the inherent electrical charges the retina produces both during resting state and with the eyes open. they're just easier to notice when your eyes are closed. Try covering your eyes and you may get static just like when you close your eyes.

The electrical charges get sent to the visual cortex. that's where your brain processes the image. Here's an diagram of how the rods and cones send their electrical signals to the optic nerve (the optic nerve is the [4] label).

Here's a diagram of how those signals travel to the visual cortex:


Cells created using differently aligned proteins I remember reading that scientist were making cells (I assume bacteria), that used differently oriented proteins to create a whole new class of life. Because apparently right and left aligned proteins don't interact in same way, cells made in such manner would behave similarly but couldn't be interacted with differently aligned bacteria/virus.

However I can't find any proof this story was true? I could be wrong about details. Is there a similar mechanism that would allow a whole case of twin (contain DNA, and most molecules that regular cells posses) cells that couldn't interact with existing bacteria?

The problem with this is something called the structure-function relationship. The function of a protein or enzyme is completely dependent on its structure. For example, take a look at this representation of the active site of chymotrypsin:

The side chains of D102, H57, and S195 all need to be in a perfect conformation in order for the enzyme to function properly, with the hydrogen bonds being essential. If any one of those amino acids was in the D-form, the enzyme would lose its activity completely. Having every single amino acid in the D-form wouldn't help either, as the entire protein's structure (and hence its function) would be altered.


When salivary amylase breaks down starch, are those substances tagged or destined for a particular use in the body When salivary amylase breaks down starch, are those substances identified for a particular use in the body?

Salivary amylase breaks starches brown into shorter chain of sugars. In the beginning of the small intestine, this process is continued by pancreatic amylase. Other enzymes at the surface of the intestine's lining complete the process resulting in simple sugars which absorbed into the circulatory system. Some of these sugars, if there is an excess in your diet, will be converted to fat and stored.

The rest of the sugars will ultimately be taken into cells and undergo a process termed cellular respiration. The bulk of these sugars will be broken down and used to create (recharge actually) ATP, a substance that just about any process in the cell requiring energy can use for energy. The atoms in the sugars used in this process end up as carbon dioxide, which you breath out, and water. But a certain percentage of the sugars only get partially broken down. These fragments can be used to synthesize many different substances depending on what's needed in the cell at that time.


Why pellet and resuspend E. coli for plasmid prep For maxipreps, cant you just add all the stuff that would be in P1 (RNase A, EDTA) then just add P2? Because if we pellet cells then resuspend theres got to be a reason, right? Is it slats and other stuff in the media that mess with lysis?

The reason this centrifugation/resuspension step is done has a simple reason: It concentrates the bacteria in a much smaller volume which is much easier to handle afterwards.

For a maxiprep you typically have a culture volume between 250 and 500ml, depending on the copy number of the plasmid. After centrifugation the pellet is resuspended in 10ml of Buffer P1, for lysis another 10ml of buffer P2 are added, for neutralization 10ml of P3.

Imagine doing this with 500ml culture volume - adding 500ml of each P2 and P3. This might work for a miniprep, but definitely not for larger volumes. Additionally, the centrifugation steps are carried out at high g numbers - typically something around 15.000xg. Doing this with this really high volumes is complicated and needs big centrifuges, which a lot of people are not trained anymore to operate or have available.


Why doesn't the cytosol dissolve the polar structures? we know that cytoplasm of cells are filled with water molecules and other hydrophilic molecules so my question is why the water of cytosol doesn't dissolve the ionic part of the lipid bilayer or why it doesn't dissolve the proteins and enzymes which are most polar and ionic and they still form structures,organelle and function and suspended in water?

Many cell components are not simply hydrophobic or hydrophilic, but have dual affinities. Proteins typically have structures which result in the interior of the protein being hydrophobic and the exterior, which is exposed to the water in the cytosol, being hydrophilic. Thus, differences in polarity between different regions allow proteins to be dissolved in the cytosol while still maintaining a stable structure.

Similarly, the lipid bilayer is composed of phospholipids, which can be described as "tails" of hydrophobic carbon chains connected to hydrophilic phosphate "heads". The phospholipid bilayer is organized so that the phosphate heads are on the surface of each side of the bilayer, with the carbon chains from each side of the bilayer intertwined with each other in the interior.