What are the universal laws of Nature concerning animals' behaviour?

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

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

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

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

Selfishness and altruism

In order to have natural selection, you need:

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

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

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

Because of relatedness (Hamilton's law)

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

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

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

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

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

UPDATE (in reaction to your comment)

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

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

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

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

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

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


Name two reasons why it is impossible to determine a gene's nucleotide sequence from the amino acid sequence of the polypeptide

I can think of at least 3 reasons in addition to the one you gave:

1: As mentioned in the comments, RNA splicing takes place on most messenger RNA encoding proteins in eukaryotes. Sections of the mRNA may be spliced out, therefore multiple mRNAs with different codon sequence can encode the same gene.

2: Translation is a stateful process, since it depends on the frame of the codon. Therefore, a gene with the sequence GGATGATGATGTAA will encode the same protein as a gene with the sequence ATGATGATGTAA, due to the start codon shifting the frame of translation downwards.

3: Genes contain untranslated regions in regions before the start and after the stop codon. These nucleotides cannot be predicted from protein sequence, but are generally important in regulating protein expression.


What is the difference between infected and infectious in epidemiology?

(The document you link to says "see Chap. 1 for distinction between infected and infectious individuals", but I'll assume you don't have access to that - I certainly don't.)

Infected individuals have been infected by a pathogen.
Infectious individuals have the potential to transmit a pathogen to
others.

Note that the definition given for "infected" in the source you link to is actually wrong: hosts may have a subclinical infection, in which case they are not "now sick with it".


If I put a cup over a spider, and leave it there for a day, will the spider survive?

To answer the first part of your question: it is extremely unlikely that the spider will die or be weakened after just one day.

Wolf spiders (Lycosids) are all predators. Due to variations in prey populations, and low efficiency of consumption at higher trophic levels, they are subject to inconsistent and unpredictable food supply (Greenstone and Bennett, 1980). They are very well adapted to this lifestyle and consequently, long periods of starvation often yield no behavioural changes (Persons, 1999). It is highly unlikely that the spider will die after just one day: Anderson, (1974) observed no changes in activity after starving Lycosa lenta (a species of wolf spider) for 30 days; and Tanaka and Ito, (1982) observed Pardosa astrigera (another species of wolf spider) living for up to 54 days of starvation. Age and sex of the spider are more likely to affect its behaviour and performance than food or oxygen availability (Persons, 1999).

As for oxygen consumption, Greenstone and Bennett, (1980) measure an oxygen consumption of 100µL/hr for wolf spiders. Assuming that your cup is of the size of the unit of volume of the same name, the cup (~0.237L), a small calculation (see figure) shows that there will be enough oxygen for the spider to survive for over 98 days. The oxygen concentration within the cup may decrease as it is used by the spider, however this is likely to have a minimal effect as a cup placed on a surface is unlikely to be hermetically sealed.

In short, oxygen availability is unlikely to have an effect on the spider before other limitations (such as food) are reached. However neither of these effects are likely to cause behavioural changes during the first month.

References

Anderson, J.F., 1974. Responses to Starvation in the Spiders Lycosa Lenta Hentz and Filistata Hibernalis (Hentz). Ecology, 55(3), pp.576-585.
Greenstone, M.H. & Bennett, A.F., 1980. Foraging Strategy and Metabolic Rate in Spiders. Ecology, 61(5), pp.1255-1259.
Persons, M.H., 1999. Hunger effects on foraging responses to perceptual cues in immature and adult wolf spiders (Lycosidae). Animal Behaviour, 57(1), pp.81-88.
Tanaka, K. & Itô, Y., 1982. Decrease in respiratory rate in a wolf spider,Pardosa astrigera (L. Koch), under starvation. Researches on Population Ecology, 24(2), pp.360-374.


How does the body repair extracellular damage caused by glucose?

The Wikipedia article on "Advanced Glycation Endproducts" (or AGE) is quite nice and in this case especially the section on "Clearance", which also contains a few references.
In short the AGE which are inside of cells are taken up by the lysosome and then broken down until AGE-amino acids are left. These are secreted into the blood stream and excreted with the urine. Bigger extracellular AGE which cannot pass through the cell membrane are taken up by special receptors first and then processed, here macrophages and Kupffer cells are included. An involvement of the liver is also discussed.

The following articles are also interesting:

Advanced glycation end-products: a review
The biology of the receptor for advanced glycation end products and
its ligands
Pathogenic effects of advanced glycosylation: biochemical, biologic,
and clinical implications for diabetes and aging.


If you are looking for variations in a gene, there are a few databases you an consult.

You can of course use the usual genome browsers, search for your gene and then select the variations listed. For ADRB2 this looks like this on Ensembl. If you plan to retrieve and compare data from different genomes/genes, I really recommend learning how to use Biomart, as this is a very powerful tool.

Then you can use specific databases or search engines, which only target SNP's. Examples would be: DBSnp and SPSmart (which queries different databases).


Is there any system how genes are spread across chromosomes?

To a first approximation, it is "not too awful" to state that genes are randomly spread. In a more detailed view, it is a little more complex.

Homochromatin vs heterochromatin

Genes are not evenly spread within chromosomes. Typically, gene density is lower at the centromeres.

Supergenes

From wikipedia > Supergenes

  A supergene is a group of neighbouring genes on a chromosome which are inherited together because of close genetic linkage and are functionally related in an evolutionary sense, although they are rarely co-regulated genetically

To my understanding, such supergene may come to existence via chromosomal rearrangements or via repeated proximal gene duplication.

Supergene and synteny

From Wikipedia > synteny

  In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species. Today, however, biologists usually refer to synteny as the conservation of blocks of order within two sets of chromosomes that are being compared with each other. This concept can also be referred to as shared synteny.

A classical example of supergene with highly conserved synteny among vertebrates is the case of Hox Genes (Amores et al., 1998).

Sexual chromosome

A sexual chromosome is some kind of a massive supergene! Consider, for example, the mammalian case.

Consider a locus that affects sex determination (SD) such as the SRY gene (coding for TDF) in mammals for example. Any male-beneficial, female-detrimental genes would gain at becoming closely linked to this SD gene. Over time, hence genes rearrange and recombination is reduced (mainly through chromosomal inversions if I am not mistaken). As recombination is reduced, deleterious mutations can accumulate through Muller's ratchet and eventually pieces of chromosomes are being lost to get rid of these deleterious mutations. This is how a Y chromosome (to consider the mammalian case, a W chromosome in birds) evolve to become so small compared to the X chromosome (or Z chromosome in birds).

Other Y-like chromosomes

Other massive supergenes can lead to Y-like chromosomes. For example, Wang et al. (2013) report a Y-like social chromosome in fire ants.

Additional source of information on the evolution of sexual chromosome

The post Do males of all sexual species have Y chromosomes? might be of interest to you. Charlesworth (1991) and Charlesworth et al. (2005) might also be a good reads.


What is different between the pigment of giraffes and the pigment of flowers?

Pigmentation in most animals which is between black, brown, red, yellow and which is made up by the mixture of two pigments: Eumelanin (yellow to red) and Pheomelanin (black to brown). The ratio between these two makes a color. These are pigmental colors which are made by a special kind of cells in the skin, in mammals they are called melanocytes (and I will only look into mammals here, as this is already complicated enough). Additionally there are other colors, especially in fish and insects iridescent color play an important role.

This pigmentation is made by a cascade of enzymes from the oxidation and polymerization of the amino acid tyrosinase. So there are no minerals involved in the process. See here for more details.

For the pattern: As far as I know the literature, these pattern by x-inactivation are only present in cats. Here one of the enyzmes which is important for the generation of the dark pigment is encoded on the x-chromosome of the animals. Gene defects on this chromosome then lead to pigmentory defects.

Pigmentation patterns can be explained by a model which was formulated by Alan Turing and which is called "Reaction Diffusion Model". You can find an interesting article about this in reference 1.

Basically two different morphogens (different pigment cells) influence each other with positive and negative signals. If these signals would occur independently, than only relative incomplex two-dimensional colorations would be possible. See the figure from reference 2:

References:

How the zebra got its stripes, with Alan Turing
Reaction-Diffusion Model as a Framework for Understanding Biological
Pattern Formation


You've done a pretty decent job of answering your own question, but there are a few things that can be elaborated on.

The general convention is to use the mitochondrial Cytochrome C Oxidase 1 (COI) gene for barcoding animals and chloroplast genes (rbcL, matK, and trnH-psbA) for plants. The three biggest reasons for selecting these genes are 1) their ubiquity; 2) the presence of many copies per cell, so it's easier to PCR amplify the sequences; and 3) mitochondrial and plastid DNA has a much higher mutation rate than nuclear DNA, making it possible to uniquely barcode very closely related organisms. This method is incredibly sensitive, reliable, and easy. The original DNA barcoding publication can be found at doi: 10.1098/rspb.2002.2218

Thanks to the efforts of consortia like CBOL, BOLD and iBOL, there are now many millions of reference sequences databased, covering pretty much any multicellular organism you are ever likely to encounter (assuming you don't work on a deep-seq sub or something).

As you say in your post, there are significant limitations to using qPCR to identify species. You have to know beforehand what it is you are looking for, and you are left with a simple yes-no. This is not to say there is no place at all for qPCR in the species identification game, however. The method is very fast, and in cases where you are only interested in detecting a single species or small number of species, it's much more convenient than getting the DNA sequenced (for example, during quality control in a meat processing plant, doi: 10.1080/02652030701584041).


It is a beetle of the genus Eudicella.
There are several species and some look quite similar, they are from tropical Africa.


Converting unit/mg or unit/ml into ng/ml, or vice-versa

There is no archaism in measuring enzyme amounts in units. Unit definition for SOD and a protocol can be found here (from Sigma): https://www.safcglobal.com/technical-documents/protocols/biology/enzymatic-assay-of-superoxide-dismutase.html :

"One unit will inhibit the rate of reduction of cytochrome c by 50% in a coupled system, using xanthine and xanthine oxidase ..."

I don't think, there is a good way to convert ng's to units, since one measures either mass or enzymatic activity, and the correlation between them is not always consistent. Units should be much more reliable in terms of comparisons with other studies, if you are not considering your enzyme as, e.g., a nutritious substance.


Can we dilute PureExpress Cell Free Mix to increase number of reactions?

The PURExpress system from NEB is incredibly expensive, for this reason I have avoided it all costs during my experiments with cell-free systems.
This is the paper I've used to create my own cheaper cell-free systems while also discussing reasons why using the NEB PURExpress system is not recommended:
https://pubs.acs.org/doi/10.1021/acssynbio.8b00427

"Although NEB provides a few different formulations of
the PURE system, the commercial system can’t be customized or optimized by the user, and the precise formulation of the commercial PURE system is not publicly available."

This might answer your question as to why I would not dilute the PURExpress system since the precise formulation is not publicly known. Thus, we can hypothesize what would work at various concentrations, but at the end of the day it is unknown what they specifically use in this reaction and how one could optimize it for their own purposes. It would take some trial and error if you really wanted to dilute/change the formulation.

"Our method co-cultures and induces all 36 protein producing E. coli clones in a single flask followed by a single Ni-NTA purification."

This is the method I personally use and it can be time intensive, however the payoff is the cost and ability to optimize your system for your specific experiment.

"The PURE system consists of several different components [7], that can be separated into three main categories: proteins (transcription, translation, and energy regeneration),ribosomes, and small molecule components (salts, buffers, NTPs, creatine phospate, and folinic acid)

If you were to go down the dilution route, I would suggest reaching out to NEB before hand to receive consultation for the purposes of your experiment and any consumables you may need to also purchase. This quote from the paper shows how your system has many considerations for consumables you may need to further research to maximize the expression of certain proteins. As for how this affects the reaction time, dilution shouldn't affect time, it will however affect the amount of product you get out of your reaction.


Does the term "upper extremity" include hands?

As far as I know, and the same is written on Farlex Free Dictionary, the upper extremity or superior limb includes:

the shoulder girdle
the arm
the forearm
the hand

Again, on this Dartmouth Medical School page, the upper limb bones are described and the article includes the bones of the hand.

So, anatomically speaking, the upper limb includes the hand.


Aside from the actual microbial cells themselves, biofilms are a slime matrix made of a variety of substances, including DNA, lipids, proteins, and other signaling molecules, but the major component is something called extracellular polymeric substance (EPS), also known as exopolysaccharides.

Succinoglycan from Sinorhizobium meliloti

These are high molecular weight extracellular (exo) polymers (poly) of sugars (saccharides) linked together into long linear or branched chains, which can be modified by moieties such as phosphate, sulfate, acetate, and succinate. As the biofilm forms (below), channels can form in the EPS to facilitate nutrient uptake and distribution, hydration, and inter-cellular signaling such as quorum sensing. Biofilms are often composed of multiple species of microorganisms, from bacteria and archaea to fungi and algae, with the social (and physical) structure dependent on the species that compose it.


It is a Coleopteran insect (Beetle order) in the Ground beetle (Carabidae) family. Based on the elytra (protective wings) and the dark first antennal segment, it looks like Carabus granulatus. C. cancellatus is very similar, but has reddish first antennal segments. I don't think there are any other similar species in the Czech republic, but don't know the fauna there well. Overall, Carabus has many species and several are native to Eurasia and can be a size of 2 inches.

https://en.wikipedia.org/wiki/Beetle#Wings

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

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

https://www.insecte.org/forum/viewtopic.php?t=160369


What are the methods for infering genetic interactions?

BioGRID is an interaction database, and they catalogue interactions by (among other things) the class of experiment that discovered them. See http://wiki.thebiogrid.org/doku.php/experimental_systems#genetic_interactions

Other than that, you should look at recent reviews and publications, but you will easily get lost unless you figure out some important particulars, like:

What species? Yeast, worm, human, cell line?
What sort of interaction? Synthetic lethality? Complicated, fancy epistasis?
How much? Genome-wide? 2-3 genes?


Can methylisothiazolinone/methylchloroisothiazolinone (MI/MCI) behave as bacteriostatic in low concentrations?

Yes, MI/MCI can behave as a bacteriostatic at low concentrations.

Check out table 1 in this paper: The Mechanism of Action of Isothiazolone Biocides. For a bunch of different isothiazolones (including the two you're interested in, though they call them MIT/CMIT instead of MI/MCI) it gives the Minimum Inhibitory Concentration (the concentration at which the isothiazolone acts as a microbiostatic) and the Minimum Biocidal Concentration (the concentration at which the isothiazolone acts as a biocide)*.

It's my understanding that basically everything that can act as a bacteriocide can also act as a bacteriostatic at a lower concentration. At low concentrations bacteriocides will kill some cells while leaving others alive in a stochastic (ie random) fashion. At some concentration this stochastic killing will balance out with the natural growth rate of the bacteria, and so thus act as a bacteriostatic.

*It should be noted that the paper lists these values for isothiazolone activity against yeasts, but the results would likely follow the same trends for isothiazolone activity against bacteria, since "CMIT/MIT has broad spectrum efficacy versus bacteria, algae, and fungi" (from the above cited paper).


What ways are there to determine how big genera are?

Bearing in mind that the information is bound to be incomplete (as is the list of existing species), you could use the NCBI taxonomy database. For example, checking the page for the Drosophila genus will give you an idea of its size.

For more precise numbers, you can download the taxdump.tar.gz file from NCBI's FTP server (link), extract it and run the script below on the file nodes.dmp (a dump of the database info).

#!/usr/bin/perl
use strict;
use warnings;
use Getopt::Std;
my (%opts,%children,%ranks);
getopts('t:',\%opts) || do { print STDERR "Invalid option"; exit(1); };

my $taxid=$opts{t}||die "Need a taxid: -t\n";

sub getchildren{
    my $p=shift; ## The taxid of interest
        my $found=0; ## will be 0 unless we find a new kid
    ## For each child of this taxid
    foreach my $kid (keys%{$children{$p}}){
     ## Get the kid's kids
     foreach my $gkid (keys%{$children{$kid}}){
         ## If this one hasn't been seen before
         unless (defined($children{$p}{$gkid})) {
      ## Add it to the list of this taxid's children
      $children{$p}{$gkid}++;
      ## We found a new one, we need to test again.
      $found=1;
         }
     }
        }
        ## If we found a new one, run again
        getchildren($p) if $found==1;
    }
    while (<>) {
        ## Remove trailing newlines
        chomp;
        ## Parse the current line
        my ($name,$parent,$rank,$rest)=split(/\s*\|\s*/);
        ## Save the current taxid as a child of its parent
        $children{$parent}{$name}++;
        ## Save its rank (species, genus, order etc)
        $ranks{$name}=$rank;
}

## Recursively get all children of this taxid
getchildren($taxid);

# Count only species as children
my @kids=grep($ranks{$_} eq "species", keys(%{$children{$taxid}}));

# Print out the results
printf "Genus %s has %s members\n", $taxid, scalar(@kids);

Assuming you are on or have access to a *nix environment, save that file as genus.pl and run it on the nodes.dmp, giving the taxid of your genus of interest:

perl genus.pl -t 9257 nodes.dmp

The output of the above example (Ornithorhynchus) is:

$ perl genus.pl -t 9257 nodes.dmp
Genus 9257 has 1 members

If we try on Drosophila, we get:

$ perl genus.pl -t 7215 nodes.dmp
Genus 7215 has 738 members

This is realy not the most efficient way to do it (far better to do this in the script itself but I don't have the time to implement that now), but if you don't mind waiting, this will give you the numbers for all genera:

for i in $(grep -w genus nodes.dmp | awk '{print $1}'); do
        perl genus.pl -t $i nodes.dmp;
done


I think it might be a species of Fritillary. Below is a picture of a Marsh Fritillary.

Marsh fritillary. Source: Butterfly Conservation.org

I do not think it is a woolly bear or giant leopard moth, just because the hairs seems too sparse for a woolly bear and it lacks the distinct red striping of the giant leopard moth caterpillar. It does not seem to be arctiinae to me.


Can anyone identify what type of bug this is?

From a rummage around Google images for "black and red striped bugs", your insect looks a bit like:

Mylabris syriaca

Hycleus ornatus, although yours has different antennae.


What causes cells to inactivate one X-chromosome?

Even a male cell can count the number of X chromosomes. (Lee et al. 1996; Cell 86: 83-84)

When X inactivation is getting started the two chromosomes "kiss" - a process that lasts for a couple of hours (first shown by Jeannie Lee in 1996). The physical contact between two X chromosomes is over a small fraction of the chromosome but it's essential for triggering inactivation. (Xu et al. 2006: Science 311: 1149-52)

If it doesn't happen then the X chromosome assumes it's alone which would mean that Xist never gets switched on and inactivation never happens (a key stage in chromosome counting).

  Chromosome counting is a process in which cells determine somehow
  their intrinsic chromosome number(s). The best-studied cellular
  mechanism that involves chromosome counting is 'chromosome-kissing'
  and X-chromosome inactivation (XCI) mechanism. It is necessary for the
  well-known dosage compensation between the genders in mammals to
  balance the number of active X-chromosomes (Xa) with regard to diploid
  set of autosomes. At the onset of XCI, two X-chromosomes are coming in
  close proximity and pair physically by a specific segment denominated
  X-pairing region (Xpr) that involves the SLC16A2 gene.

Take a look at Xist and Tsix. Some more papers worth taking a look at:
Xist regulation and function eXplored
Mechanism of regulation of ‘chromosome kissing’ induced by Fob1 and its physiological significance


Why do sea mammals die on land, and drown on sea?

Mammals use lungs as their respiratory system. These animals in the process of evolution left land and started to live in the water, they developed organs that are used to swim. The shape of body also changed to reduce the resistance of water. In spite of all this they didn't developed gills.

Lungs can help in respiration only in air. So the mammals have to come above water in order to take air. You correctly have noticed that these animals die if they can't reach air, i.e. they die of drowning.

But one thing I want to mention is that they don't need to reach land in order to take breath. They just need to swim up to the surface of water for this purpose.

Anyway, I think you got the point. Feel free to ask if you have further confusion on this topic. I shall explain more if needed.


What's the difference between CREs and DHSs?

Cis-regulatory elements are simply DNA regions upstream or downstream of a gene that can affect its expression (basically they have to be in the same chromosome).

DNAse-I hypersensitive sites (DHS) are regions of chromatin that get digested during the DNAse treatment because they are exposed i.e. not protected by a protein (complex). The protein complex can either be a nucleosome or a transcription factor. It should be noted that a DNA region can be DNAse insensitive also because of its conformation.

Usually the cis-regulatory elements exert their effects by serving as a binding site for a transcription factors (or chromatin remodellers). If the proteins bind at these sites then these regions would be protected from DNAse digestion thereby making them not-DHS. However, it is known that DNA elements can act in trans as well (see papers on 3C- chromosome conformation capture, and its variants). Moreover, whether a site is protected from DNAse or not does not tell anything about its function.


Was mammal body better suited for some type of the marine environment than the body of fish?

By asking So how did they succeed in the competition with fish? you are making the false assumption that they had somehow to succeed at some form of competition. What lead you to this false assumption is I think either of the following two mistakes..

A misunderstanding of the principle of competitive exclusion.
A false assumption about the existing overlap between marine mammals ecological niche and fishes ecological niches

Competitive exclusion

The principle of competitive exclusion states that two species occupying exactly the same ecological niche cannot stably coexist. One must either become extinct or shifts its ecological niche (process that is known as character displacement).

A consequence of the above is that if two species have ecological niches that partially overlap, they can still stably co-exist.

Ecological niche of marine mammals

There are two independent lineages of mammals that evolve marine life (cetacea and sirenia). I don't know which one you have in mind when asking the question and a sensitive complete answer would depend on the lineage of interest. However, in any case, there is such a diversity of ecological niches in fishes that it is hard to really fully address the question.

Marine mammals occupy different ecological niches. There is no question of whether one has an advantage over the other as the species do not compete for the same ressources.

A typically important reason for why marine mammals and most fishes occupy different ecological niches relate to their size differences. Simply put, mammals to be quite big! For example a orca eat fishes (and other things) that had few predators before. There is therefore not much competition involved.

Just to reiterate... in your comment you say so the main advantage was the size?. Size was one of the biggest reason why they would be able to occupy previously unoccupied ecological niches. But it is not an advantage toward competition with fishes as you seem to be thinking as there probably little competition.


Quoting a great biologist Peter Medawar :

  It is by no means difficult to imagine a genetic endowment which can
  favor young animals only at the expense of their elders; or rather at
  their own expense when they, themselves, grow old. A gene or
  combination of genes that promotes this state of affairs will, under
  certain numerically definable conditions, spread throughout a
  population simply because the younger animals it favors have, as a
  group, a relatively large contribution to make to the ancestry of the
  future population.

From Why We Get Sick :

  Imagine that there is a gene that changes calcium metabolism so that
  bone heals faster, but the same gene also causes slow and steady
  calcium deposition in the arteries. Such a gene might well be selected
  for, because many individuals will benefit from its advantages in
  youth, while few will live long enough to experience the disadvantage
  of arterial disease in old age. Even if the gene caused everyone to
  die by age 100, it would still spread if it offered even minor
  benefits in youth. This argument does not depend on the prior
  existence of senescence. Other causes of death—accidents, pneumonia,
  and all the rest—are sufficient to reduce the population at older
  ages. Nor does the theory depend, like Haldane’s, on cessation of
  reproduction.

The message I am trying to get across is that - As organisms are like vehicles which carry DNA and DNA just "madly" wants to replicate itself and pass itself from generation to generation, Natural Selection will favour those traits that maximise reproductive success. These may be traits that provide maximum benefit in youth but cause gradual damage and lead to senescence and death.

You could also think like this - Every machine has wear and tear and must be thrown away after it is irreparable. Same is with our body, it is the most beautiful machine in the world but it is also subject to the same wear and tear.

Also there is the end replication problem. See telomeres if you dont know what I am talking about. There is a limit to number of times a cell can divide.

So all in all I would say that there is a biological limit - a certain age up to which a person may live.


What is Protein Expression Level?
This was the original title of the post, which I edited myself because I regard the answer as trivial, but the question as more substantial. To deal with the trivial first:

‘Level’ is not a scientific unit, and can only be used unambiguously
as a scientific term in its English sense in relation to liquids, e.g. “The level of mercury in the thermometer had
fallen.”, “The land is 10 metres above sea level.”
It is used by some people in informal speech or writing to indicate an
undefined quantitation, and because of its very ambiguity is to be
strongly discouraged in scientific communication.

So neither I nor anyone else can say what ‘protein expression level’ is without finding out what the originator of the phrase intended (if indeed he knew) in any individual instance: quantity or concentration of protein, or the rate of its synthesis.
Quantitation
Let us consider some general aspects of a cellular molecule that may require quantitation: Amount, Rate of Synthesis, Rate of Degradation and, where relevant, Biological Activity.
The quantitation of molecules at its most basic is the number species,  or, more practically, their total mass (grams), where possible related to their molecular mass (i.e. moles). The rate of their synthesis or degradation is expressed in terms of the change of their amount in unit time.
In order to compare different systems a reference is needed for the quantitation. This may be per unit volume, per cell, per g cellular protein, per g DNA etc. (However for comparison of similar systems or within one system the reference is often omitted.)
The biological activity of molecules only has meaning if the molecules are, indeed, biologically active (e.g. enzymes). It is expressed in units related to that activity.
Examples of Quantitation for Proteins
The actual units used in quantitation are determined by how one is able to measure the parameter of interest.
Relative amount of protein: You might detect a protein by the intensity of staining of a band on a gel, or by the extent of precipitation using a corresponding antibody. These would have to be calibrated against standards in order to convert raw experimental measurements to g or mole protein. Typical units of relative amount are g/g total protein, g/g DNA.
Rate of synthesis or degradation of protein. You might detect the synthesis of protein by the rate of incorporation of radioactive amino acids into non-radioactive protein, and the rate of degradation by the liberation of radioactive amino acids from pre-labelled protein. Typical units of synthesis would be mg amino acid incorporated per min per mg total protein. (This can be converted to molecules synthesized or degraded per minute, if necessary.)
‘Protein Activity’: The use of this term is not recommended. In chemical terms the activity of a molecule is a measure of its “effective concentration”, and in relation to proteins would only be the concern of biophysicists and the like. Other biologists would associate the term with the biological activity a protein such as an enzyme might have, but as many proteins are structural the term ‘activity’ cannot be applied to proteins generally. Where it is of interest it would be quantified in terms of the nature of the activity, e.g. an enzyme is quantified in units related to the amount of substrate converted to product in a given time.

Quantitation of Gene Expression using Oligonucleotide Microarrays
The two extremes in quantifying gene expression are the detailed study of the expression of one particular gene encoding a protein for which information and tools are available; and general study of the expression of many genes using modern methods that allow the study of many molecules simultaneously. Such methods included mass spectrometry (for small metabolites), two-dimensional gel electrophoresis (for proteins) and microarrays or RNAseq (for mRNA). In general in the latter case one would examine the effect of some agent or condition on the whole spectrum of gene expression.
Let us examine microarray technology as that is the main concern of the poster.

Microarray technology measures the relative amounts of mRNA.

The methodology involves amplifying a mixture mRNA species by reverse transcription to cDNAs, which are labelling with a fluorescent dye. The cDNA is hybridized to immobilized oligonucleotides based on the sequences of the genes in the organism, and the strength of the fluorescence signal is assumed to be proportional to the amount of individual mRNA species in the sample. However the data supplied to the user is the relative image intensity within the experiment, rather than units that allow one to calculate the actual amount of mRNA.
How does these relative amounts of mRNA relate to gene expression?

The relative amounts of mRNA are a relative measure of the rate of synthesis of proteins (3 in dig.), if one assumes that the rate of synthesis of each protein is similarly proportional to the amount of its mRNA (a in dig.) which would be limiting. This is a reasonable assumption in most cases given mRNA is degraded more rapidly than protein. (They are not a measure of the amount of protein — b in dig.)

The relative amounts of mRNA cannot be taken as a measure of the rate of transcription of a mRNA from its gene (1 in dig.) because of the relatively greater effect of mRNA degradation (2 in dig.) on the steady state concentration of mRNAs, and the fact that different mRNAs have different half-lives.

Postscript for the Poster
I have tried to make this answer general, to be of use to more people. As the poster is not a biologist she may still have difficulty in understanding the background to the biological experiments that generated the data she is analysing.
The biological system of interest is gene expression, which encompasses the whole series of events from transcription of genes to mRNA and their translation into protein. The background to this is that there are some genes that are (almost) always expressed, irrespective of physiological circumstances because they are needed to maintain the structure and everyday functions of the cell. This is termed constitutive expression, examples being expression of the genes for cytoskeletal actins or ribosomal proteins. Other genes are expressed (‘switched on’) only when needed (and may be termed inducible). The question here would appear to be whether the genes for the enzymes involved in DNA repair are expressed all the time (constitutively) to deal with normal ‘wear and tear’ of DNA, or whether their expression only occurs in response to some insult knwn to damage DNA, such as gamma irradiation.
As I mentioned, as an experimental scientist, one approach that can be adopted here is to look at the expression of one or two well characterized proteins that are known to be involved in DNA repair. However, there may be proteins involved in this process that you are unaware of, so the modern methods of looking at the expression of all the genes in an organism (if the DNA sequence is known) — oligonucleotide microarrays or, better, RNASeq. These methods measure relative quantities of mRNA in a cell. This is not a proxy for amount of protein or rate of  its synthesis (the term ‘protein activity’ is meaningless and is not and should not be used), it is what it is, but is also a reflection of the expression of the genes that encode the mRNAs. No expression, no mRNA.
You can think of the microarray and RNASeq approaches as a fishing expeditions. If you find mRNAs that are only present after the cell receives a stimulus or an insult, expression of the mRNA has occurred (whether or not the amounts are directly proportional to the rate of synthesis). If the mRNA is synthesised you can assume it is translated into the protein it encodes. In the case of gamma irradiation you might assume any mRNA that shows a large increase in quantity encodes a protein that involved in protecting the cell from the radiation. This will be of scientific interest, especially if it is not what one anticipated.


Species Identification: Bulbous root on plant, Southern California, USA

This is an Asparagus species, and the root bulbs are storage organs. Unfortunately, I can't identify the species. There are 219 accepted species currently in TPL. I presume this is an ornamental plant. As far as I can see, the species is not recorded as naturalized in California.


The answer to the first part of your question is that we don't take the initial 10% of a progress curve (velocity vs time) as a measure of activity, but we measure the initial rate of the reaction.  We do this by drawing a tangent at the origin.

It is merely a 'rule of thumb' that progress curves are practically linear provided that not more than 10% of substrate has been used up. If there is significant slowing down before 10% is used up - and there may be if the substrate concentration is way below Km value - then it is not valid to draw a line through the points: we must draw the tangent to the curve. That is, it is not acceptable to take the average rate during the first 10% of the progress curve.

For this reason it is desirable to use as sensitive a method as possible when measuring an enzymic rate, and to never rely on a single time point (as is common in radioactive assays) without sufficient controls to justify that it it is the initial rate, and not the average rate (or something else) that is being measured.

The reason we measure initial rates is that is makes things simpler on two fronts.

Firstly, the decrease in rate with time of an enzymic reaction may be due to many factors: product may be inhibiting the reaction, the reverse reaction may become important, the enzyme or substrate may be unstable. It is only during the initial rate period that conditions are accurately known, and such  effects may be legitimately ignored. It was Michaelis and Menten that first realized the importance of measuring initial rates, and of the great simplification principle that ensued, in enzyme kinetics. (see Cornish-Bowden, 2004).

Secondly, the rate laws themselves are greatly simplified.  Provided that eo << So (the initial enzyme concentration is very much less than the initial substrate concentration), we may take the So as being equal to the substrate concentration and 'plug in' this value into our rate law (such as the Michaelis-Menten equation), and ignore the effect of time on the value of S.  In addtion, we can set all product terms to zero. This can greatly simplify things.

For example, the rate law for a reversible single-substrate mechanism (see here) is the following:

$$ v = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S\ -{{V_{max}^r}\over{K_{m}^p}}\ P }\over{1 + {{S}\over{K_{m}^s}} + {{P}\over{K_{m}^p}}}}\ \ \ \ \ (1)$$

This one is not as complicated as it looks: we have just defined a Km and Vmax for the forward and reverse directions. But let's set product to zero:

$$ v_i = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S_o\ }\over{1 + {{S_o}\over{K_{m}^s}} }}\ \ \ \ \ = \ \ \ {{V_{max}^f S_o}\over{{K_{m}^s} + S_o}}\ \ \ \ (2)$$

We now obtain the familiar Michaelis-Menten Equation (where $v_i$ is the intial velocity).

The second part of your question is more fundamental. I'll take it to mean the following. Why does an enzymic reaction not follow second-order kinetics at all substrate concentrations? Why doesn't doubling the substrate always double the rate (as is often the case in chemical kinetics)? A. J. Brown in 1902 suggested that the reason for this is the formation of an enzyme-substrate complex and that at sufficiently high substrate concentration all the enzyme would exist in such a complex and the enzyme would become 'saturated'. The formation of an enzyme-substrate complex, of course,  is now a cornerstone of enzyme kinetics. One of the early key pieces of evidence for an enzyme-substrate complex was the observation that an enzyme is much more heat-stable in the presence of its substrate than in its absence.

Finally, it is probably worth pointing out that some enzyme operate way below Km values and at 'physiological' concentration of substrates do obey (to all intents and purposes) second-order kinetics. Catalase, for example, has a Km for hydrogen peroxide of about 1 Molar (Ogura, 1955), and one assumes that physiological concentrations never reach this level. (We need to be a little careful about catalase, however: it is one of the few enzymes that is inactivated by substrate).

A great reference on enzyme assays is the following:

Principles of enzyme assay and kinetic studies by K. F. Tipton in Enzyme Assays: A practical approach

For an introduction to enzyme kinetics, and the early history of enzymology, I like the following:

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press, London.


Why do some trees in California have dead brown leaves but also new green leaves?

Whether trees are deciduous or evergreen, their leaves don't last forever; they need to be replaced at intervals.  The process of photosynthesis depletes the chlorophyll in the leaves, so that needs to be replaced and this is a significant metabolic cost to the tree.  Therefore, whenever a tree is experiencing metabolic stress, it will slow down the chlorophyll replacement, and let the leaves die to save energy. It's metabolically cheaper to simply let the leaves die -- after removing the most precious nutrients -- and then regrow new leaves as needed, than to keep repairing the leaves that aren't needed because the tree is resting for other reasons.

In temperate areas, where there are well-defined seasons, this typically happens in the fall, and deciduous trees let their leaves die all at once in the fall.  In tropical or subtropical regions, where trees could photosynthesize all year, leaves may drop all year round (as with evergreen trees, like conifers, in temperate regions).  Often, though, their leaves will reflect metabolic stresses on the tree, such as drought.

(The Wikipedia article on "Deciduous" makes the point that this can be very localized, related to very local environmental differences that could only affect a single tree.)

Much of California is a subtropical region, and it has been experiencing severe drought for some time, so it wouldn't be surprising for a tree to have reached a point where its leaves have all had their chlorophyll removed.  On the other hand, as the El Nino event of 2015 increases, rainfall in California is returning, so it would also not be surprising for a tree to have recovered from drought enough to start making new leaves.

If your question is why the old leaves didn't fall off before the new ones started to regrow, it is probably simply a matter of timing.  The tree doesn't really "care" if the leaves fall or not, so long as they're not using up its resources, so there's no reason to force them off.  The new water supply may have arrived fairly shortly after the degree of drought that caused the tree to shut down the leaves.


Since porphyria is not one disease but many, I suppose that with "acute porphyria" you mean acute intermittent porphyria. The reason of the disease is an autosomal dominant mutation on the enzyme porphobilinogen deaminase, an enzyme that converts porphobilinogen to hydroxymethylbilane by a deamination reaction.

Now the heme is produced in many steps, and the enzyme above is important in the early steps of heme synthesis. In persons with porphyria, these heme precursors accumulate, causing toxicity. In acute porphyria the symptoms are mostly from the central nervous system. The figure under shows the steps of the biosynthesis of heme, and as you see at the upper right corner, defect in the enzyme porphobilinogen deaminase (PBG-deaminase) results in accumulation of porphobilinogen.

Glucose and other carbohydrates can help suppress disease activity, are given by vein or by mouth, and are part of initial treatment. Intravenous heme, however, is both more specific and effective than glucose and should be started if the patient’s symptoms fail to improve within 36 hours.http://www.porphyriafoundation.com/about-porphyria/types-of-porphyria/AIP [2015-05-02]

More about carbohydrates and the suppression of symptoms in porphyria http://www.porphyriafoundation.com/about-porphyria/diet-and-nutrition/the-glucose-effect-in-acute-porphyria [2015-05-02].


Can two denatured DNA strands reassociate?

Yes, heating the DNA above 94°C for some length of time will melt, or denature, dsDNA into two ssDNA strands. Upon cooling, the complementary strands will come back to anneal. The degree and completeness of annealing, or association, is dependent on a number of factors including the rate of cooling and structural properties of the DNA itself (%GC content, secondary structure). I would not expect that the majority of ssDNA strands will completely anneal to a single, complementary dsDNA strand. What is more likely is that the DNA mix will look more like spaghetti with one strand partly annealed to two other strands. When performing PCR, the primers are designed to be specific, and added in excess, so that you bias the odds of annealing to favour a primer:ssDNA association. If this weren't the case, we could not possibly have efficient PCR amplification.


Where can I find a file listing the genetic differences in humans?

Have you tried poking around the 1000 genomes project?

Try this link

ftp://ftp.1000genomes.ebi.ac.uk/vol1/ftp/pilot_data/release/2010_07/exon/snps/


Why doesn't oligodendrocyte produce neurilemma

This statement is made in contrasting oligodendrocytes with Schwann cells. Both of these cell types are glial cells involved in myelination of neurons, but their morphology (shape) is different.

Oligodendrocytes in the CNS "reach out" with extended processes that then envelope axons as a myelin sheath. You could imagine an octopus reaching out arms that then loop around a stick. Like an octopus, they have multiple arms, and each arm can cover a different axon. The nucleus and other cellular machinery is located in the 'head' of the octopus.

Schwann cells in the PNS instead wrap around a single axon. You can think of them more like a fried egg, wrapped around a stick. The egg white is the myelination, the yolk is the nucleus. The outermost wrap is where all the other machinery of the cell is, and this area is called the neurilemma.

The actual presence/absence of the neurilemma isn't that important for the function of myelination, it's just a different shape of the cells.


What counts as a 'breach of the skin' for infections(like rabies) that spread via wounds?

I believe that your books refer to 'broken' not necessarily meaning broken to the naked eye, but as in any broken epidermis.

The outer layer of your skin that protects you against infection is the epidermis. It's a water-tight layer mostly composed of keratinocytes joined together by adherens junctions. Logically, even if you can't see a breach in your skin (epidermis), there may still be one. While the chance of getting an infection from a non-visible break is less than the chance of infection from a visible scratch, it's still possible.


Why does this karyotype start numbering at 11?

Why does the band numbering start at 11? When I count other things I usually start with the number one.

It does start with the number one!

What is happening here is clearly a small confusion. Looking at the centromere in this idiogram of chromosome 12 you can see two number 11, as you stated in your question, one above and one below the centromere:

An idiogram of a Giemsa-stained chromosome 12. © 1994 David Adler, University of Washington. All rights reserved.

However, those two 11 below and above the centromere are not, in fact, an 11 (eleven): they are just two number 1 together, 1-1 or one-one.

According to Nature (2017):

  This particular idiogram depicts the pattern of Giemsa staining at a fairly low resolution (i.e., it produces about 400 total bands in a karyotype, which is just above the threshold that is clinically useful). At this resolution, the long q arm of chromosome 12 can be subdivided into two main regions, which are designated 12q1 and 12q2. Region 12q1 can be further subdivided into five subregions, designated 12q11 through 12q15, each of which corresponds to a band detected by Giemsa staining. Orally, these subdivisions are referred to as "12q one-one" through "12q one-five" (not as "12q eleven" through "12q fifteen"). The more distal 12q2 region can be subdivided into subregions 12q21 through 12q24. In addition, subregion 12q24 can be further subdivided into regions 12q24.1 through 12q24.3, even at this relatively low resolution.. (emphasis mine)

Thus, those two 11 you see above and below the centromere are (or should be), respectively, 12p1-1 and 12q1-1 (remember that this is the chromosome 12).

The confusion here, therefore, is due to:

The omission of a 12p or a 12q before all those numbers.
The omission of some separator, like an hyphen or a comma, between those numbers.

A detailed PDF from the International System for Cytogenetic Nomenclature (ISCN) can be found here.

Bonus: In case you want to know, that number 850 in the top of the idiogram refers to the number of bands:

  At this higher level of resolution, approximately 850 bands can be distinguished in a karyotype

Source: Nature.com. (2017). Chromosome Mapping: Idiograms | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/chromosome-mapping-idiograms-302 [Accessed 23 May 2017].


Valid comparison of gene expression between several genes in several cell lines

This is not an easy task, as there are many factors which you have to take in account. First there are intra-essay differences as slightly different conditions for each set of probes for the repetitions. Then, there are inter-assay differences, as differences in the array slides and so on, this paper ("Analysis of microarray gene expression data") goes into more details.

This articles might be helpful as well:

Multiple-laboratory comparison of microarray platforms
Increasing consistency of disease biomarker prediction across
datasets.
The curse of normalization.
Microarray probe expression measures, data normalization and
statistical validation.

What you could also do is go over the Researchgate, I think there are more people around with a lot of experience in this field.


Why does air from the nasal cavity not go into the oesophagus?

Swallowing food requires muscle strength to force the food down the oesophagus, which is a soft tube that collapses when empty, simply because the body is very crowded (space-efficient) and empty spaces collapse unless forced open. Only when you swallow, the oesophageal muscles force space to be made for food coming through.

In contrast, the trachea and bronchi are covered in almost-circular or C-shaped cartilage which holds them open and stable for air to flow through. You can see it here: http://en.wikipedia.org/wiki/Bronchi.

Concluding, air does not enter the oesophagus because it is always closed. Additionally, when the chest expands for breathing, the lungs expand and create suction down the trachea and not into the stomach (simply because this is where they connect).

The exception of course is if air is trapped in the swallowing motion with (or without) food. In this case it will enter the oesophagus and cause you to burp.


Examining antibody - target interactions in PyMOL

Multiple structures may be read into a given session using the following for each pdb:
File -> Open

In the narrative below, the reference antibody has the name AAA and the second antibody has the name BBB. The heavy and light chains have pdb chain IDs A and B, respectively. Adjust those as needed.
Whole molecule overlay
Make visible the reference and the moving molecules.
From the menu item next to the BBB molecule name (right panel), select:
A -> align -> to molecule (*/CA) -> Object: AAA

Antibody's variable domain overlay
I think it may be more helpful to align the variable domains than the whole antibodies or Fabs. Typing the following on the command line is a temporarily adequate way to align proteins:
align BBB and chain A+B and res 1:109, AAA and chain A+BL and res 1:109


Great find!
I'm pretty certain that is actually a Prairie Kingsnake (Lampropeltis calligaster - likely the subspecies L. c. calligaster).  The biggest indicator to me are the two alternating rows of dark spots on sides, with some blotches fusing.  They are distributed all over Missouri, although pretty rarely seen due to their microhabitat:

They tend to be fossorial, spending much of their time underground and
out of sight. As a result, there is little known about the biology and
status of these secretive snakes. Most [prairie] kingsnakes are observed
hiding under boards or other debris or crossing roads on warm
evenings.

I actually used to study herpetology in St. Louis, and we caught a few of these.  The juveniles tend to have well defined spots that fade in time, although there is some degree of polymorphism here.  Looks like yours is somewhere in between.  See pictures below for reference.
Juvenile:

Adult:

Worth mentioning these snakes are nonvenomous, and typically docile.
Photo cred: Edward Prenzler


These little creatures look a lot like White-margined Burrowing Bug or Sehirus cinctus nymphs.

Very interesting thing about the Sehirus cinctus is their brooding behavior. The female watches the eggs and even feeds the young for a few days. Have a look around. You might see it.

AFAIK they don't harm your plants.

More info:
http://polyploid.net/bugs/bugs.html
https://en.wikipedia.org/wiki/Sehirus_cinctus


How to quantitatively measure work done by a biological system?

Measuring the work done by a biological system seems pretty impossible. Imagine how many different ways one cell of your body uses energy (ATP). You can't really measure all the work done by every cell on a macro scale. Metabolic efficiency has been defined as... "health". That seems just a little ambiguous. That's why we use things like averages to determine if energy use is normal or not, such as in metabolic age.

In short, work is a more tangible term in discrete physics examples, but there is so much complicated energy use in biological systems that total systemic work can't be easily defined.


What controls the southern range of willows?

The distribution of temperate hardwood forests, as well as deserts, tundras, savannahs, and other ecosystems, is determined primarily by average climate conditions, specifically average annual temperature and precipitation. You can see how biomes are related to climate in this figure, taken from Whittaker (1975):

Temperate forests tend to be between 2.5-17°C, and between 800-2500 mm precipation. These are not exact boundaries but reflect long-term climate conditions. As climate changes, so will the distribution of the biomes.

Temperature is important in many ways.  For example, most temperate trees go dormant during the winter. This requires metabolic preparation by the tree. If the weather turns cold too fast, then the trees may be be properly prepared. Alternatively, if the weather warms to quickly the trees may not be able to come out of dormancy properly. This technical report (Coder 2011) provides more detail.

The precise mechanism that restricts the distribution of any one species would require experimental determination. As it turns out, Populus trichocarpa (black cottonwood), plus other Populus and Salix (all in the family Salicaceae) are quickly becoming model organisms for study. This should shed more light on specific distribution limitations, such as changes in soil nutrients, light intensity, or other environmental parameters. There are now regular symposia held on these model organisms. You can read an introduction to one symposium here (Tognetti et al. 2011).

As a side note: One must be careful about the mapped distributions of popular trees like willows. Many species, including Salix viminalis, have been introduced far outside their native range, including through out the eastern United States, as shown by the map you linked to. The native distribution of the species is the Palearctic (Eurasia), shown here.

Literature Cited

Coder, K.D. 2011. Trees & cold temperatures. Environmental Tolerance Series WSFNR11-12, Warnell School of Forestry and Natural Resources, University of Georgia, USA.

Tognetti, R. et al. 2011. Fifth international poplar symposium: Poplars and willows: From research to multipurpose trees for a bio-based society.

Whittaker, R.H. 1975. Communities and Ecosystems. MacMillan Publishing, New York, USA.


Mainly cell type refers to the differentiation degree to form a cell population whose characteristics are identifiable by using simple microscopy, stains or immunological methods. Examples of cell types would be T8 lymphocytes, peripheral astrocytes or hepatocytes. Cell types can be pathological too, like tumor cells.

Cell state makes references to the current physiological condition of a given cell. A given cell type can be found in different proliferation states, metabolic conditions (i.e: An adipocyte or a hepatocyte will have different metabolic profiles depending on the insulin and glucagon balance), electrophysiological state (The human oocyte rapidly changes its membrane potential once a spermatozoid has entered) or even degree of differentiation (The typical example are B lymphocytes, which can be in a "naïve" state if they haven't found an antigen, or into a mature state. Once they have matured, thay can be subdivided into cells that actively produce antibodies and cells that divide actively).

A cell function usually refers to a process that occurs inside a cell, or to the physiological function that cell type has in the whole organism. Cell functions could be metabolism, signaling, cell division, etc.; while also could be the likes of detoxification (hepatocytes), hormone production (Langerhans cells) or contraction (myocytes).


Would a person live longer, if such a person lived in a planet with lower gravity? (say, Mars)

Probably not. There's a thing called Hayflick limit, which is basically a limit of life expectancy caused by a shortening of telomeres with every cell division. And since most of our cells complete cycles more based on time (life cycle of RBC 100 days), and not due to damages to a cell, our telomeres would still shorten at the same rate. Of course the gravity could play a small part once organs have started failing, but there are many other factors that affect how long it takes for everything to completely deteriorate, and wouldn't have a big role. In fact, it could even shorten life expectancy, seeing as how our bodies are currently built to live in our current gravitational field. Without gravity, our muscles could become weak, causing other problems, which is why people at the space stations have frequent dedicated times to workout, to keep their muscles fit.


Arthropod identification request (a spider with no legs?)

This appears to be the underside of a walnut orbweaver:

These orbweaver spiders are not medically significant.
Spiders often lose their legs in wasp attacks. Some spider wasps will remove the legs and then try to bring the spider to its nest for larvae to feed on. Sometimes they drop their spider victims accidentally.
Some will simply deposit eggs into the spider and leave it there, letting the larvae grow inside the spider and feeding on it from the inside.. these ones don't usually remove the legs - they usually just paralyze the spider.
Spiders can lose their legs through various attacks, but they can also lose their legs in molting accidents... particularly if they are in the middle of a molt and then are aggressively interrupted.


Why do soap molecules not break down your skin cells when you wash your hands?

The outer most layer of the mammalian epidermis (cornified layer or stratum corneum) is composed of 15-20 layers of dead cells called corneocytes, which are basically dead keratinocytes filled with keratin intermediate filament cross-linked other proteins as well as some lipids. As keratinocytes differentiate into corneocytes (a process called cornification), the plasma membrane is replaced by what is called a conified envelope which is composed of cross-linked structural proteins and some lipids (more details in here).

Surfactants in soap do interact with components of the cornfield layer such as keratin but not in the same way they would with the lipid bilayer of a typical plasma membrane. Outcome of such interaction depends on the kind of soap as well as amount and duration of application among other factors, but even a normal soap, upon normal use on a normal skin, may cause some keratin denaturation. But the cornified layer is actually continually shed (process called desquamation) and replaced by keratinocytes that proliferate in the inner most layer of the epidermis.

You can find more details on effect of detergents on skin here and here. You can also find useful info on skin structure here and here.


Do any amphibians start their lives on land?

From wiki:

  Most amphibians lay their eggs in water and have aquatic larvae that undergo metamorphosis to become terrestrial adults

This suggests clearly that not all of them do so.

Here are a few interesting cases I could think of:

The common midwife toad carry the eggs on their back. The eggs are not necessarily submerged by water then.
To my knowledge, the Seepage salamander have terrestrial larvae but they don't feed before they reach the adult age.
The lungless salamanders has a larval stage that is within the egg. When the egg hatches, the individual that comes out is already an adult.


How valid are Koestler’s criticism of evolutionary theory?

Maybe both. Certainly his understanding of limb developement doesn't match modern understanding. The quote you provide seems to indicate that he thought the appearance of an additional digit would require a multitude of coordinated mutations. Our current understanding seems to indicate that it's all about changes in the regulation of genes. For example in fruit flies mutations in the antennapedia gene can cause antenna to grow where legs should be or visa versa. Another example is polydactyly(extra toes) in cats which be be caused by mutations to a single regulatory region.

  within a few generations, flies appear in the inbred ‘eyeless’ stock
  with eyes that are perfectly normal.

I'm not a fruit fly expert, but this seems highly dubious to me. There is a well studied eyeless mutation, but it's dominant, not recessive. Furthermore getting two copies of this mutant eyeless gene is lethal at the embryonic stage. This means that a colony of adult eyeless flys are necessarily all heterozygous. That is, they have one copy of the mutated eyeless gene, and one copy of the normal eyeless gene. By Mendel's laws, a quarter of the offspring from the completely eyeless generation are going to have two copies of the normal eyeless gene, and so will have normal eyes. I wouldn't be surprised if the flies with normal eyes outcompete the flies without eyes, so eventually the eyeless flies will disappear from the colony. I can't tell you whether Koestler has mis-characterized this gene, or is talking about some other gene all together. Citation needed.


Can canines communicate with each other using gaze direction?

It is hypothesized that the starkness of white sclera against darker colors of the pupil and iris is a unique mutation in primates that have become prevalent in human beings because it enhanced our ability to communicate with other humans and animals, including dogs, by more clearly communicating where we are looking.

However, it has not yet been established that dogs use this communication with each other, communicating more commonly with other means such as body language, head direction, vocalizations, etc. Some dogs, especially domesticated ones, do have white sclera and it is proposed that this is due to unintentional selection by humans who have a preference for such features.

What is extremely fascinating is that this 'mutation' occasionally occurs in chimpanzees and apes, too, but has not become prevalent in their respective populations.

Sources:

Secret Life of Dogs- BBC Film
Do the Eye Have It?-Academia
Common feature in domesticated dogs-CARTA
Juvenile features-NIH


How does discontinuous distribution provide evidence for evolution?

There are probably several relevant perspectives. Since you mentioned continental drift, consider a taxon (i.e. species, family, etc.) that evolved when all the continents were joined together to form the supercontinent Pangaea.

If it was a successful species that continued evolving and expanding its range, then we might expect to find its fossils - or maybe even living descendants - on multiple modern continents. In fact, dinosaurs evolved on Pangaea, and their fossils are found on every modern continent.

On the other hand, imagine a taxon that evolved after Pangaea broke up into Laurasia and Gondwanaland. If this taxon evolved in Gondwanaland, then its fossils and descendants will likely occur only on the southern continents. (Gondwanaland broke up into Africa, South America, Australia and Antarctica.)

In fact, you mentioned a good example - lungfish. On closer inspection, lungfish fossils have been discovered in North America, however. So we might guess that lungfish evolved in Pangaea but died out in the northern portion (Laurasia) for some reason.

Elephants belong to the order Proboscidea, and proboscideans were once widespread in Eurasia and North America, and they even ranged into South America for a time. The familiar mammoths and mastodons were apparently exterminated by changing climate and/or human predation. This tells us more about extinction than evolution.

But the fact that proboscidean fossils are found only in the Northern Hemisphere and South America tell us that they evolved in the Northern Hemisphere, spreading into South America only after it was connected to North America.

I'm not sure when proboscideans first evolved, but it was probably long after Pangaea broke up. However, North America and Eurasia have connected and reconnected at various times, making it possible for species to migrate between the two continents. The most famous link is the Bering Land Bridge, which existed during the last "ice age" (Pleistocene).

At any rate, elephants today survive only in the tropics, which, like the sea, are a sort of refuge for "living fossils."

There are a number of taxonomic groups - living and extinct - that are found only in the Northern Hemisphere, only in the Southern Hemisphere, or only on particular continents that are evidence of both evolution and changing environments (including climate change and continental drift).


In what range do humans generally interpret sound best?

I work on voice recognition too. Yes, very brilliant query about sound perception that I can clarify and not answer completely. Most of the text belongs to DSP SE forum, i.e. Voice rec, MFCC, filter, BP, audio processing. You may have confused the readers except for the image and the final paragraph.

I had to rephrase it to clarify it to myself:

Why are humans unable to hear pitches on a straight maths scale, they hear logarithmically? We hear according to a mystery ratio called MEL distribution, a well studied summary of many subjects perception of pitch, averaged to:

0.01% Humans have Perfect pitch, 95% are relative pitch, and 5% are tone deaf. MEL varies by the type of listener. Tone deafness is hereditary, ( info about biology and brain structurehere) and the rest of humans probably follow a gradual distribution of poor to good pitch differentiation, and they also hear amplitudes differently.

As you can see from the wiki page, there is no explanation for MEL theory, it's either neurological, a soundwave energy balance, or because of the ear anatomy.

To answer the title question, your graph shows humans have a continuous response to frequency spacings through all their perceived sound. However volume tests show amplitude sensitivity peaks at about 3kHz, which you can see on inaccurate amplitude perception and equal loudness contour graph.

MEL studies of Steinberg are stagnant since Volksmann, same as Donald D Greenwood suggested in 2009, they overgeneralize and the field needs to be developed a lot further under a different study name than MEL scale, which isn't english.

Why can they hear voice well under 1000Hz?

At least 1/2 of the sound energy of voice occurs below 1000Hz, same reason bass requires a lot of energy.

So humans can hear sub 1000Hz sounds from further away, but the more sound data you have the clearer the voice is, and computer should use nearly all of possible human voice frequencies to measure formants and N/M consonants to best accuracy. Sub 1000Hz may contain enough vowel subharmonic frequency bands at different spacings to represnt the vowels of sound basically, but it is less clear and realistic if the voice is filtered at 1000Hz, the subharmonics of AEIOU go multiple octaves above middle C male/female voicebox peak, near 440Hz.

The sub 1000Hz components are generated by the voice box, which changes tone at a slow rate, whereas the 2000-3000Hz sounds, i.e. Frictives, S,F, and N aspirated P, k, don't require very as complex sound processing to interpret (for digital sound filter processing)

The 625-1000Hz pivot component of the equation doesnt appear less straight under 1000Hz if the graph is from a parametric frequency view.

To resolve your query, Biologists would want to know:

1/Structure of the ear as a reason for sound perception imbalance
2/Child learning and adult learning of complex pitch tasks
3/Brain structures used in pitch recognition
4/Evolution of ears and psychoacoustics, reason for a hearing peak at 3k which is the same as rustling leaves
5/Physics energy and mathematical reason for MEL distribution (ask on DSP SE)

As a Voice rec researcher, you should think outside of the box. Computers don't hear like humans. Frictives like F and S have peaks around 3000-4000HZ, they are the highest and easiest to recognize and similar in all accents. Formants from vowels can peak from 400 to 500HZ roughly in men and women, at 700hz for children.

Vowels are vague and vary by accent are are the least precise element in voice-rec. That's why voice recognition hinges a lot on formants and accents which have energy peaks below 1000HZ, and timbral graphs which change wildly wether it's AEIOU sounds.

As a side not for voice-rec,
English is tougher to recognize than French because of the stress time, swingy nature and the 2-3-4 vowels per syllable, and perhaps that's why French have lost the wild traditional accents faster (I know I speak both since I was 0). Voice rec of French and other syllable time languages is easier.

I don't know why MEL is used at all in voice-rec filters. Perhaps because people use the same intonations as they hear from MEL, so the PC must know too, else because the programmers don't know enough about real sound physics, and have implemented it as a rough power-balancing graph for filter results? else some other physics reason. Other power-related filter shapes should work fine, as DSP SE if this has a known physical basis of if it uses human psychoacoustics for digital audio inaccurately:
mel-frequency cepstrum (MFC) is a representation of the short-term power spectrum of a sound, based on a linear cosine transform of a log power spectrum on a nonlinear mel.

Humans don't need perfect pitch for anything except music. Relative pitch, we nearly all have ok, and it makes sense because biologically relevant sounds, animal calls, physical signals of water, trees, voices, add together to make a continuous freqency spectrum that we have to measure all the frequencies by a similar rating of importance to interpret best. Voice contains lots of micro-expression subtones that represent clear psychological states that humans benefit to hear, and rustling leaves and other sounds all should biologically benefit from a high relative pitch clarity.


What would be the impact of depositing limestone in the oceans (to reverse acidification) on ocean life forms and biodiversity?

To simplify, acidification of oceans is due to excess anthropogenic carbon dioxide CO2:

  H2O + CO2 → H2CO3 → H+ + HCO3-

Seawater is naturally saturated with another base, carbonate ion (CO32-) that acts like an "antacid" to neutralize the H+, forming more bicarbonate.

  CO32- + H+ → HCO3-

You want to alkalinize the ocean by dumping CaCO3. That sounds pretty good, and not only would it add more buffer (and decrease acidification) but it would also help the sea creatures which use dissolved Ca2+ and CO32- to make shells of calcium carbonate CaCO3. (The other effect of excess CO2 is the leaching of CaCO3 from shells and corals or other marine organisms:

  CaCO3 + H+ → HCO3- + Ca2+

The limestone mined today is used for gravel, in concrete, road surfacing, foundation support beneath weight-bearing structures, the boulder faces of earthen dams, Portland cement (N.B. the burning of limestone in the cement-making process liberates CO2 gas), Aglime (pulverized limestone) and quicklime (process liberates CO2 gas) which are both soil stabilizers, hydrated lime used to filter potable water supplies and to treat solid and liquid waste and in processing petroleum. These are only the major uses of limestone.

The average annual limestone production in Missouri (the largest deposit of limestone in the world) is about 89 million short tons/year. The cement industry alone is a MAJOR producer of CO2. Producing a ton of cement requires 4.7 million BTU of energy (some of which will release CO2), equivalent to about 400 pounds of coal, and generates nearly a ton of CO2.

So, in addition to the CO2 produced by the use of limestone in everyday life, you want to mine it and dump it into the sea. Unfortunately, even finely ground limestone (remember all that CO2 it takes to mine and crush it) is poorly soluble in water (pH 7.0). It does increase with acid, but still is very slow. Also, it sinks. The worst acidification of the ocean is in surface waters.

Some estimates suggest that close to 100 million tons of limestone are mined globally each year. (It's probably much more than that; see Missouri alone.) You want to mine, crush (to between 40µm - 10µm!!), and deliver an additional 4 Gt/yr of limestone, even though in the paper you cite, that amount per year would not help:

  Extraordinary additional measures (adding 4 Gt limestone/yr to the ocean for > 200 years) provides a modest additional benefit (additional to cutting CO2 emissions.)

Why? What difference would knowing the effect on biodiversity be when just procuring, processing and delivering the stuff would generate more CO2 than it could possibly buffer, and would have a minimal effect anyway?


OK, I don't know how I did it but I misread your question as being why all the non-mammalian Synapsids went extinct. I answered your question at the end, but I'm leaving the rest as-is until I figure out how to rewrite it (it was rather too much work to delete).

According to The Wikipedia page for Synapsids, the answer really depends on the Synapsis since there are quite a gap between the start of the Synapsid clade and the appearance of Cynodonts.

The first big "culling" of Synapsids (i.e. the extinction of all groups except one clade that led to mammals - Therapsids in this case) seems to occurred over the Permian era. Some groups went extinct in the early Permian but most groups went extinct at various points during the Middle Permian. No clear reason is given for these various extinctions (though the page for Dinocephalia suggests "disease, sudden climatic change, or other factors of environmental stress may have brought about their end"... which basically covers all possible extinction reasons so that's helpful); it's probably various reasons specific to each. Most species do go extinct after all.

Among Therapsids, the only clade that survived the Middle Permian, most seem to have been wiped out in the Permian-Triassic extinction, the largest extinction event in Earth's history, of which only three Therapsid clades survived: Therocephalians, which went extinct soon after, Dicynodonts, which were extinct by the Early Cretaceous, and Cynodonts. Aside from the usual environmental factors, a reason for the extinction of those two clades could have been competition from the then-ascendant Dinosaurs, and Cynodonts themselves.

As for when the last non-mammal Synapsid when extinct, it appears to have been a member of the Tritylodonts, which survived into the Cretaceous (and arguably having a representative after the K/Pg extinction, emphasis on "arguably"). Mind you these are very close cousins to Mammals indeed:

  Tritylodontids ("three knob teeth", named after the shape of animal's teeth) were small to medium-sized, highly specialized and extremely mammal-like cynodonts, bearing several mammalian hallmarks like erect limbs, endothermy and lactation. They were the last known family of the non-mammalian synapsids.


Where can I find mutation datasets for cancer?

As I'm sure you're aware, there is no complete centralised database for cancer gene mutations. The most comprehensive database is the TGCA as you've already mentioned. That doesn't mean that other data isn't out there.

A broad option that might fit your needs is to query OMIM hosted by NCBI. You can search "cancer" or something more specific and then select the dbSNP tab and it will return a list of gene locations of mutations that match the query.

For a more specific search, COSMIC hosted by SANGER allows downloads of the "cancer genes" in fasta format, and various other downloads with other information are available. It's manually curated which is always a bonus, however this does mean that it's limited to just a few genes. There is also BIC. This is specifically focussed on genes related to breast cancer and is hosted by NHGRI. Again, an account is required for the download and it is limited to genes affecting breast cancers.


There is no such option. You can perform the alignment and filter the hits later. However, I wonder why you really need that. Lower E-value indicates lower chance of an alignment randomly picked from a database, to have a given score.


Drake's Law. What is the genome-wide mutation rate and what are the estimates?

There are so many things that are implied in this paper, not explicitly said.

The mutation rate here detected seems to be the emergence of chain-terminating (CT) mutations, which truncate protein coding genes, usually just one gene in a bacterium or phage, which would be possible to observe from inspecting a plate to see which colonies die or survive.

This is only a specific kind of mutation, but Drake assumes that its frequency is related to the overall mutation rate.  Which is probably fine.  Mutations we infer from this work arise spontaneously from a similar mechanism in all organisms.  This is just ionizing radiation for the most part.  So at a first glance we still believe this.  That there are no specific mechanisms for mutation.  Since this is usually ionizing radiation we would expect that the rate would go up when there's more radiation around and it most certainly does.

There are lots of reasons that animals and humans would have a smaller rate.  Drake is including in the paper the involvement of DNA repair mechanisms in the experiment as they are intrinsic to the survival of the yeast and bacterial cases and the phage may also enjoy the benefit thereof.

In some organisms there is a lot more DNA repair possible.  So that would mitigate the mutation rate in some cases like Deinococcus radiodurans.

Metazoans and diploid organisms which undergo meiosis for sexual reproduction have other methods for reducing the number of mutations they pass on.  Meiosis and recombination will allow the removal of many mutations by competition in gametes.  Since there are two copies of each chromosome, mutations are constantly being competed against their unmutated versions as gametes.  Then eukaryotes have their own repair enzymes and conditions.  Then lastly recombining into diploids, they also show mutations less often.

For these reasons and others, the mutation rate being even across the genome does not mean that that the mutations accumulate evenly.  Mutations still tend to accumulate in regions where positive selection is operational.  Here is an excerpt from a recent genomic comparison of five strains of rice:

  Despite strong purifying selective pressures on most Oryza genes, we documented a large number of positively selected genes, especially those genes involved in flower development, reproduction, and resistance-related processes. These diversifying genes are expected to have played key roles in adaptations to their ecological niches in Asia, South America, Africa and Australia.


How do I tell whether a mass spectrum was made with ESI or MALDI?

I am not an expert in this topic but from what I have heard ESI generates multiply charged ions but MALDI usually does't. It is possible to find multiply charged species in the spectrum.


What percent of your blood can you lose before you need a transfusion

Typically transfusions are indicated for hemoglobin < 7 g/dL (for adults normally: 12-15 grams per deciliter [1]) or < 8-10 g/dL if there is cardiac disease where diminished oxygen carrying capacity cannot be compensated by increased cardiac output.

The answer above is theoretical because there is no accurate way to measure blood loss in the clinical setting - it's usually a mess.

The most useful parameter to assess intravascular volume in the immediate term is blood pressure. Again, the actual number is variable but a 30% drop from baseline in the acute setting is bad.

Another less acute indicator of hypovolemia is urine output (normal is .5-1 ml/kg body weight/hr, dropping below ~35 ml/hr therefore is an indicator of hypovolemia.)[2] Hypovolemia is often corrected with sterile saline fluid and adding packed red blood cells only as needed to keep hemoglobin in the above required range, unless someone is actively bleeding (trauma, bleeding ulcer, etc.) in which case "whole blood" (or packed red blood cells, fresh-frozen plasma and platelets) is given.[3]

[1] McPherson: Henry's Clinical Diagnosis and Management by Laboratory Methods, 22nd ed.
[2] Oliguria &  Volume Depletion
[3] Fluid Resuscitation and Volume Assessment


Do scars generally continue to undergo beneficial changes after maturation?

The collagen that holds together scar tissue is continuously degraded and replaced. (Plastic and Reconstructive Surgery, 1976) If collagen synthesis slows down, due to scurvy for example, old wounds can in theory reopen. Historic records of sea voyages contain descriptions of long-healed wounds opening back up in scurvy victims, and these cases are cited authoritatively in some papers (e.g. Annals NYAS 1961), but it is difficult to test experimentally.
I would describe this more as 'maintenance' of the scar, rather than as 'continuous healing', but it may be of interest to you.


Where does DNA fit on the Chomsky hierarchy?

In truth DNA doesn't fit in the Chomsky hierarchy at all. DNA isn't a language, it is a complex molecule in a complex chemical environment. The fact that in many situations we can usefully abstract the structure of DNA as a string of four symbols should not obscure the underlying complexity. There is a simple code that describes the aminos acids encoded by triples of nucleotides, and some elements of a "grammar" in the structure of genes if you squint (start codons, stop codons, introns, and exons). But much of the function of DNA is stochastic and driven by the biophysics of the binding of RNA and protein molecules to DNA.


How does the drug MBC effect the depolymerization of microtubules in eukaryotic cells?

Carbendazim inhibits microtubule polymerization by directly binding to tubulin, preventing subunits from interacting. Therefore, mytotic spindle malforms and potentially causes aneuploidy in affected cells. Mechanisms of resistance are often shown to be changes in membrane permeability to the compound.

CARBENDAZIM (addendum)


The difference is referring to the directionality of gene flow.

We talk about genetic introgression when there is some gene flow from one population (say, population A) to the other (say, population B). We would say that population A introgresses into population B. If gene flow goes both ways, then the two populations A and B are admixing.

From Wikipedia > introgression

  Introgression, also known as introgressive hybridization, in genetics is the movement of a gene (gene flow) from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species.

From Wikipedia > Admixture

  Genetic admixture occurs when two or more previously isolated and genetically differentiated populations begin interbreeding.


How can a continuous RNA be transcribed in the lac operon?

RNA Pol doesn't worry about stop codons.  Transcription termination can occur through the formation of a hairpin in the new RNA sequence, or through the action of Rho proteins.  A lot of the time prokaryotes have polycistronic mRNAs, that is, mRNAs with multiple protein coding regions.  The stop codons are detected during translation, so you will often have all three lac proteins being translated at once off of the same mRNA.

Here's a nice section on transcription termination, or look up Rho-independent or Rho-dependent transcription termination for more info.


Could Cyanobacteria farms help dilute pollutants in the atmosphere

You have various questions here.

  If I understand correctly, roughly ~2.8 billion years ago cyanobacteria started pumping large amounts of oxygen into the atmosphere.

The great oxygenation event was not an instantaneous process and represents a change from one equilibrium (low oxygen) to another (20% oxygen). This abundance of oxygen and organic carbon means that there is "niche" for organisms that burn up pre-existing organic carbon and use oxygen as terminal electron accept. Fermenting organisms use the organic carbon as a feedstock, but don't have oxygen so the use highly reduced organic molecules as terminal electron acceptors (less energetic), making mixed acids (sweat bacteria) or ethanol (yeast).

  Using modern industrial processes could this be emulated by making cyanobacteria farms to help slow down the climate problem?

Cyanobacteria and other aerobic phototrophs convert carbon dioxide to oxygen and organic carbon they can use to make biomass. So if you had enough of these you'd need to get rid of the biomass. Responsible forestry for housing actually ticks this box (cf. vs. a mature forest, which is nearly at equilibrium where the biomass gets consumed by other organisms, else you'd had a faster growing topsoil).

  I also read somewhere that someone was able to genetically (or through other means) turn off the ability of a specific bacteria to reproduce causing it to produce a byproduct much more efficiently. Could this also help these "farms"?

It is a grand challenge of synthetic biology to stop growth. It is really hard to do as "cheat" (i.e. variant that can grow faster) will dominate. Biofuel research suffers from this as the fatty acid biosynthesis pathway is highly expensive energetically and cheats eventually win despite the most complicated safeguards.

  Alternatively could we genetically strip the bacteria of all other functions other than procreating and photosynthesis? Making this bacteria live in a "bubble" would mean it wouldn't need a lot of defense mechanisms. This could make a single purpose bacteria that would be super efficient at doing this single task.

The carbon will be a problem, so you'd need to make biomass or some value added compound.

Three additional points:

Green biotech

There are many "green biotech" companies out there and there is an increasing number of green chemistry awards going to biocatalysis (enzymes for a reaction) and in some cases synthetic biology processes (whole enginereered organisms for a product or intermediate). But the former field is slow at growing because it needs to compete against a century of homo/heterocatalyis (normal chemistry), while the latter needs a lot more technological innovation to improve the production chassis (e.g. cheats, slow reactions, iron-sulfur cluster over-expression and electron balance are common issues: hydrogenase is a classically cited example of a hard target with great potential).

Note that most green biotech uncouple the process and use the biomass from regular algae or plants to feed their engineered organisms, as it is easier and there are less containment issues.

Algal blooms

In the comments I mention, iron fertilisation of the oceans (a ship releasing a container size of nutrients across an oceanic crossing is make a substatial planktonic boom, which either increases fish levels or sinks and thus buries the carbon it converted into biomass). This is a curious case of huge scale and cheap algal farming. But we don't know all the details, yes we'd be turbocharging the oceans (which are barren relative to say a jungle), but we may favour toxin-releasing algae, jellyfish and imbalance fisheries and actually send to extinction others.

Bioreactor in the ISS

The Internation space station splits water to make oxygen, dumps all carbon waste outside (CO2 and ...) and has water and food shipped up. This is odd as you'd expect they would be the first to use algae to scrub CO2! However, things are changing: they are trialing an algal bioreactor, which on a larger scale will result in a near-closed loop system. However, there are many engineering and some biological issues that need to be faced.


Why do my tomatoes start to rot on the same fruit part?

Mold spores float around everywhere in the air, in your home and on farms. They are also likely found on the surfaces of farm equipment used for harvesting (shears, knives, etc.). Grey mold can infect tomato leaves and stems where there are lesions, such as those introduced when harvesting fruit, when cutting the fruit off at the stem. This could happen wherever such spores can find ingress between the farm, produce distributors, the market, and your home.

Cite: https://content.ces.ncsu.edu/botrytis-gray-mold-of-tomato


How do birds influence brood sex ratios?

On a more general level it is possible for parents to influence sex-ratio of broods in a number of ways, and there are other reasons why a brood might have a sex ratio distortion. The paper I've been reading this morning is about side-blotched lizards doing just this. I'll give a quick basic answer just from the top of my head and hopefully someone can give some specific examples in birds.

Bias in gamete production

Assuming XY chromosome systems where the males are heterogametic (XY, females XX) the male can influence the brood sex ratio by producing more or less Y-bearing sperm. Sperm carrying an X-chromosome will always produce daughters and sperm carrying a Y- will always produce sons. The opposite would be true for ZZ/ZW where female gamete type determines the sex, they could only produce Z eggs, therefore only having sons.

Female cryptic sperm choice

A fairly modern idea is that females can selectively fertilise eggs with sperm based on the DNA they carry, this could include whether the sperm is Y- or X-bearing. This idea is thought to explain how females produce daughters from small sires and sons from large sires in the paper I mentioned at the start.

Meiotic drive and sex ratio distorters

Meiotic drive elements may be responsible for sex-ratio distortion in broods. Just like the biased sperm production this can alter the sex-ratio at the gamete level. Genetic effects mean that fewer offspring of one sex than the other are produced. Here is one example where suppressors of the distorter have evolved in the autosomes.

Direct selection by the parents

In the paper you mention above, and with most studies, it is possible that the parents are selecting which offspring to raise after they hatch (or as an egg - it may be possible to determine sex at that point) and if females are more costly to raise and conditions are poor, they may kill/neglect the female offspring early on.

Within brood competition

If one sex is stronger as a chick it possible that the broods could become sex biased in certain conditions which consistently favour one over the other.

Consequence of environmental strain

Similarly to the last two points, if conditions are poor it may be harder for one sex to reach maturity than the other which would result in sex-bias. This is the conclusion the authors in your paper seem to come to.

Environmental effects

As with some reptiles, environment can determine the sex of the offspring. For example, incubation temperature in turtles has a considerable effect on offspring sex ratio. Given how close birds and reptiles are in evolutionary time, and the importance of active incubation in birds, I don't see that it's impossible for the parent to vary some kind of environmental factor in order to bias sex-ratio.

There are certainly more potential mechanisms and some of these ideas are fairly new in evolutionary biology research so there are many unanswered questions. I hope I will have time to find some bird specific examples later.