text:
Where do the Ca ions that causes neurotransmitter release from synaptic bouton, come from?
I hope the information you share will help clarify the following doubts and gaps in my knowledge:

Where do the Calcium ions in the influx (which then triggers the neurotransmitter vesicles) come from?
Are they traveling all the way from the ER of the neuron in the soma?
Are they stored locally within the neuron somewhere around the synaptic bouton?
Are they coming from outside the neuron cell?

And if you have some extra knowledge to dish out then:

Is it channels or pumps that cause this influx of calcium ions?
If these are channels then are they ligand-gated, voltage-gated or made more permeable via some other mechanism?

Thank you for reading :)

Short answer
Neurotransmitter release is triggered by an influx of calcium ions from the extracellular space into the cytosol through voltage-gated calcium channels in the plasma membrane.
Long answer
Typical synaptic vesicle release is triggered by calcium influx through T-type calcium channels. These are voltage-sensitive channels in the plasma membrane; calcium flows through these channels from the extracellular space and is bound by synaptotagmin, a type/family of proteins associated with the vesicle fusion machinery (the SNAP/SNARE complex) to trigger (or, more precisely, to increase probability of) vesicle release.
Like just about every important class of proteins, these channels can be regulated by various mechanisms: gene expression, trafficking/colocalization, subunit composition, phosphorylation, etc. See the Iftinca & Zamponi review.
Calcium from internal stores, released by various mechanisms (calcium-induced, IP3-induced, can also be important to neuron plasticity and homeostasis but does not need to travel from the soma (ER extends throughout the cell). In some special cases, these internal calcium stores can be involved in release (see for example Babai et al 2010), but this example is from in photoreceptors in the retina which use a different release mechanism than typical neurons (they don't fire spikes, they have graded potentials and graded release probability, etc). Internal stores can also influence spontaneous release probability and may modulate release probability (see for example the review by Collin et al) but are not the primary "trigger" for release.
For more on the basic synaptic machinery, I'd recommend any edition (though of course recent is always best) of the textbook "Neuroscience" by Purves and coauthors.

Babai, N., Morgans, C. W., & Thoreson, W. B. (2010). Calcium-induced calcium release contributes to synaptic release from mouse rod photoreceptors. Neuroscience, 165(4), 1447-1456.
Collin, T., Marty, A., & Llano, I. (2005). Presynaptic calcium stores and synaptic transmission. Current opinion in neurobiology, 15(3), 275-281.
Iftinca, M. C., & Zamponi, G. W. (2009). Regulation of neuronal T-type calcium channels. Trends in pharmacological sciences, 30(1), 32-40.
Dale Purves, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, Richard D. Mooney, Michael L. Platt, Leonard E. White. (eds) (2018). Neuroscience. New York: Oxford University Press.

I can't thank you enough ... thank you! I had been using the molecular biology of the cell 6th edition by alberts and coauthors but I'll look into investing in "Neuroscience" by Purves as well.

@pulkitsinghal Principles of Neural Science (Kandel) is another good textbook (the content will overlap a lot with Purves, so I'd recommend either/or rather than both).


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Glucose 6-phosphate dehydrogenase: reaction mechanism
I have searched the internet for the reaction mechanism of G6PD but couldn't find it, so I am asking whether anyone here knows its mechanism and whether they could recommend some sources that give detailed info about enzyme mechanisms generally.
I would be grateful for this because it seems difficult to find enzyme mechanisms on the internet.

How did you search the Internet? As the Internet contains sites for all the journals in which enzyme mechanisms are published, it seems more likely that your search strategy needs improvement or that you don’t have access to the journals. Did you search PDB and work with the source papers? Have you bibliographic software (eg Endnote) that allows you to search PubMed? Did you try Google scholar?   Did you follow the links in the section of the Wikipedia article on the enzyme’s structure? “But I couldn’t find it” is insufficient to demonstrate that you tried to research the topic yourself.

@David actually I searched in Wikipedia and other journals (like springer ,pub med and even PDB), but I just find info about the enzyme structure and the complications of its deficiency but I never found its mechanism .

But one of the main points of determing structure is to throw light on the function, especially the mechanism, by identifying residues at the catalytic centre where the substrates bind. I can help you but to conform to the ethos of this site I need to know if this is some sort of "homework" question, and if not why are you asking as you don't appear to appreciate the relevance of structure? Oh, and as a new user to the site, please finish reading the Tour — we can see you lack the "badge" for doing so.

@David I am not a student in biochemistry as my major subject, I study medicine and in my college we don't have to know mechanism, it is some sort of individual effort from me (not homework) to better understand biochemistry and because I am hobbyist of biochemistry, I understand acid base catalysis and other simple mechanism but I don't have enough information to be able to confirm that I can predict mechanism from active site structure and that's why I asked here to see how experts can predict and know the mechanism of catalysis and that's why I also asked for good sources on this topic

@David I am really thankful to you and I would be more thankful if you recommended some good source :books or websites (if you could also mention the source from which you get the info in your answer, I would appreciate it a lot) and thanks in advance

Disclaimer
I am not an enzymologist and this answer is based on work published in 1998, and the latest paper I consulted was 2000. Hence I cannot exclude the possibility that more recent work has modified the model shown here.
General Approaches
The general approach to elucidating the mechanism of action of enzymes has been as follows.
Historically, and before a structure is (or was) available:

Hypotheses of possible types of mechanisms would be made on the basis of the known mechanisms of non-enzymic chemical reactions.
Experiments with inhibitors might suggest what class of residues of the enzyme might participate in the reaction.
Experiments would be performed to get indirect evidence for the residues involved, e.g. by examining the effect of pH in relation to the pKa.

More recently, with structure determination less difficult and more common:

The structure would be determined and an attempt to identify the active site made on the basis of the position of a bound pseudo-substrate or inhibitor.
Residues near the substrate that might participate in the reaction would, thus, be identified.
A hypothesis of the role of these residues would be made in relation to the known chemistry (as in historical 2, above).
Experiments would be performed to test the participation of the residues — often by modifying them — and their proposed role.

Proposed Mechanism for Glucose 6-phosphate dehydrogenase
The structure of glucose 6-phosphate dehydrogenase (G6PD) was published in 1994 by Rowland et al. in Structure 2:1073-1087. To test their hypothesis of the mechanism, Cosgrove and coworkers constructed performed site-directed mutagenesis on G6PD and determined the structure of the mutated protein. On the basis of this they published a paper in Biochemistry 1998 37:2759–67 in which they proposed the reaction mechanism shown below.

The Nδ1 atom of His-240 is hydrogen bonded to the Oδ1 atom of Asp-177, forming a catalytic dyad. The Nε2 of His-240 is poised to act as a general base by abstracting a proton from the C1-OH of G6P, allowing transfer of the C1-hydride to the C4 position of the nicotinamide ring of NAD(P)+.
They summarize this as follows:

“The results support a mechanism in which His-240 acts as the general
  base that abstracts the proton from the C1-hydroxyl group of glucose
  6-phosphate, and the carboxylate group of Asp-177 stabilizes the
  positive charge that forms on His-240 in the transition state. The
  results also confirm the postulated role of His-178 in binding the
  phosphate moiety of glucose 6-phosphate.”

Suggested reading and search approach
The classic text on enzyme mechanism is Alan Fersht’s Enzyme Structure and Mechanism published in 1984. This is clearly based on a limited range of enzymes, so its importance is not in finding the mechanism for a particular enzyme, but for understanding the principles involved. (You can pick up a second-hand copy very cheaply). Fersht has a more recent (2017) book in the same area — Structure and Mechanism in Protein Science but this is much more expensive. You can view the contents on Amazon.
Other suggestions are welcomed as comments.
My approach to searching for an answer here is worth mentioning as the question indicates the poster failed in his attempt. First I just did a Google search “reaction mechanism, glucose 6-phosphate dehydrogenase”. This wasn’t very useful, but alerted me to the fact that Google was prioritizing pages related to G6PD deficiency, a clinical condition on which much had been written. To avoid this I decided to focus specifically on structure, assuming that some of the papers would be proposing mechanisms. I tried three of the following four approaches (while idly waiting for a computer program to run).

Google search on “glucose 6-phosphate dehydrogenase, structure”. This did not appear to give me a direct hit, but brought up the three other sources I went on to try.
The Wikipedia entry on glucose 6-phosphate dehydrogenase. Half way down the page is a section on structure with a diagram of the substrate binding site, so I knew I was on track. The references on this page were not very useful, but the diagram indicated the structure was PDB 2BHL.
The Google search also brought up a Protopedia page, which I actually looked for directly. At first I was disappointed by the lack of information other than the structure, but the third of three references was a Cosgrove paper from 2000 which contained the words “catalytic diad” in its title. I went for that, and it led me back to their 1998 paper.
I could have tried the Protein Data Bank and searched for 2BHL (or just for the enzyme). 2BHL would have led me to a later paper in Acta Crystallographica, which does mention the 2000 Cosgrove paper in its introduction.

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What are the implications/predictions of the selfish gene theory?
Are there any testable predictions or implications of the selfish gene theory? Or it is just interesting interpretation of the observations/experimental data? If this theory is not falsifiable and doesn't generate any predictions, how can it be helpful anyway?

The Selfish Gene theory "can be defined as the idea that the gene is the ultimate beneficiary of selection".   Argren, in Selfish genetic elements and the gene’s-eye view of evolution lays out the history of the theory and the arguments for and against it.
The theory is almost certainly correct; and it's almost certainly incomplete. The theory is testable.  It predicts, for example, that there will be genes whose sole function is to self-propagate.  Those genes can't confer much fitness disadvantage to their host or they will quickly be weeded out of the population; and they don't necessarily need to confer a fitness advantage. But to the extent that different individuals have different versions of the same genes, the versions that convey a fitness advantage are likely to win the evolutionary competition.
There are, of course parasitic genes like transposons which impose a cost by requiring the host to adapt to their presence.  As long as the host is able to adapt without losing too much fitness, the parasitic genes can ride along for free.
The Selfish Gene theory provides useful insights, but it is incomplete, because combinations of genes,  arrangements of genes, and even genetic diversity within a population can provide a fitness advantage or disadvantage. Even genes are subject to "group selection", where gene A can provide a disadvantage unless gene B is also present, in which case A and B together provide an advantage. This leads to selective pressure to link the two, e.g., by placing them close together on one chromosome, which is analogous to a cooperative relationship between the genes that provides a mutual fitness advantage.

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Significance of the resequencing of the chimpanzee genome
Introductory remark: I am not a biologist, but a somewhat knowledgeable layperson.
I have been told that sequencing of chimpanzee DNA until recently has been done almost exclusively using human DNA as a “template” to help piece together short DNA sequences. The similarity that emerges to human DNA could then perhaps be somewhat misleading, as the structure of human DNA affects the end result obtained for chimpanzees.
However, recently (2018) a new study was performed in which the assembled DNA fragments from various apes were assembled completely separately from human DNA, giving a better estimate of the similarities and differences between the DNA of humans, chimpanzees and other apes (Kronenberg et al. Science vol 360 issue 6393, eaar6343).
What new information has emerged and to what extent does it alter previous results?

Welcome to Biology.SE! Please edit to include complete references to reliable sources for the assertions you are making. I'm also pretty sure that "shotgun sequencing" is integral to modern methods for generating whole genome sequences. I think the question you are trying to ask is really about genome assembly methods. If so it would help to clarify your post. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

@tyersome I've done that for him. I'll answer the question later if nobody else does.

Many thanks, @David. I had this from a panel discussion from a creationist only. even though my source was bad (and in Swedish) it tickled my curiosity. I was not even sure if there was any merit at all to the assertion.

I've added an answer and edited your question. The distinction wasn't whole genome v. shotgun — both sequences were whole genome — but method of assembly of the fragments.

The effect of re-sequencing the great ape genomes (orangutan as well as chimpanzee) without the use of a human genome as a guide to assembly has in general been to correct mistakes and improve the ape genome sequences so that they can be compared better with the human genome.
As far as I am aware, it appears that in a broad sense the same genes are present in humans and great apes, i.e. each will have a similar (orthologous) gene for, e.g. insulin, trypsin, keratin, generally at the same position on the chromosome. As the species are different these differences are thought to come from differences in these orthologous genes or in the regions of the genome that control their expression as RNA and then protein. The differences could also affect their activity, where they are expressed in the body or whether different variants occur (by differential splicing of transcripts).
So with improved and independent genome sequences it was possible to identify a greater number of variants in these orthogonal genes.
The focus of this work was on genes that are expressed in brain cells, because a key feature that distinguishes man from the great apes is brain size. The interest was in genes that were found in separate experiments to have significantly different expression when glial or neuronal cells of human or non-human species were compared. The authors report mutational variation in 252 genes with such differences in glial cells and 123 in neuronal cells.
To quote the discussion:

These improved genomes yield a comprehensive view of intermediate-size
  structural variation among apes. As we focused on SVs (structural
  variants) that potentially disrupt genes or regulatory sequences, we
  began to address potential functional effect. Differential gene
  expression, especially in cortical radial glia, has been hypothesized
  to be a critical effector of brain size and a likely selective target
  of human brain evolution. Nearly 41% of the genes down-regulated in
  human radial glia, when compared to chimpanzee radial glial analogs
  from cerebral organoids, associate with an fhSV (fixed human-specific
  structural variants) and most often as a deletion or a retroposon
  insertion. These findings are consistent with the “less-is-more”
  hypothesis, which argues that the loss of functional elements
  underlies critical aspects of human evolution.

So, they haven’t found what makes us human yet, but have laid the foundations for studies that may at least find out why we have bigger brains.


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Induction of disease
In the paper they are infection WT and IL-22-/- mice with C rodentium on some occasions they use oral infection, on others they use IV and on some they use a bacteremia model. Can anyone please clarify why they may have done this?

Please provide a link to the paper you are referring to. Have you any ideas why they have done this? Any suggestions? You may be right or wrong and that way we can explain it, rather than provide answers without a context for you. Typically this may be done out of experimental limitations (time of onset, stage of disease, strength of induction, or age of animal, etc.), or to show that a treatment efficacy holds independent of the method of induction, since the methods are not created equal, i.e. multiple lines of evidence are stronger than a single kind of attempt.

Welcome to Biology.SE! In addition to following the suggestions from @SPr, please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. ——— In particular, your title should give a better sense of what you are asking. In addition, please improve your posts clarity — the grammar and lack of punctuation make parsing your first sentence difficult (e.g. I'm guessing infection should have been infecting). Finally it is best to spell out the bacterial genus and define abbreviations like IV. Thanks!


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Was there a time in Earth's history when some animal life existed on land but humans could not have breathed?
I understand that higher oxygen content allowed insects and arachnids to grow much larger than today and I wonder if this additional oxygen would have been toxic or unhealthy for modern humans?

Why humans? We are just a moderately large bipedal mammal.

because i am human.

There isn't evidence that the worldwide air has ever been toxic compared to today since animals came to land 530+ million years ago.
At some times in history, there has been lots of mercury vapor and perhaps other poisons in the atmosphere, for example recent research indicates that the late dinosaurs had at least 10 times as much environmental mercury from the Deccan traps eruptions which give most of southern india it's current geology. That said, the air would have been breathable, but some apex predators would have had mercury poisoning from their diets. Imprecise studies have found mercury levels in sediment go up to 1000 ppb for hundreds of years, compared to perhaps 100 ppb as they are today... other studies may find that there were higher mercury spikes, up to 30 times those of today perhaps. https://www.researchgate.net/figure/Temporal-correlation-of-mercury-records-with-other-indicators-of-Large-Igneous-Province_fig15_328051765
For oxygen, ever since the first insects emerged on land 530 million years ago, the oxygen levels have been safe for humans. https://en.wikipedia.org/wiki/Timeline_of_the_evolutionary_history_of_life


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Primitive streak being only present in caudal half of embryo affecting gastrulation?
It is my understanding that in gastrulation epiblast cells migrate to the primitive streak where they start to form the three germ layers; does this mean that gastrulation only occurs at the caudal half of the developing embryo

What organism are you asking about? 2. Where are you getting the idea that the primitive streak is only in the caudal half? 3. What do you understand gastrulation to mean?

Humans. It came up in one of my lecture notes and in my understanding gastrulation is the formation of the three germ layers (ectoderm, mesoderm, endoderm) from the epiblast

It would help a little in answering your question to know more about what organisms you are interested in, or the specific source that you are referencing, with e.g. the relevant quote.
For example, the primitive streak is specific to amniotes: avians, mammals, and reptiles. In other common model organisms such as flies or amphibians gastrulation happens differently.
Another thing to keep in mind is that gastrulation is a very large and structurally distending process, so it can't be really said to happen "only on one end" of the embryo. The whole embryo is going through gastrulation. We can however talk about the placement of certain gross morphological structures on the embryo. But really each cell is affected by gastrulation, whether it's immediately obvious under a microscope or not.
Looking at the Amniote section of the wiki page on gastrulation, it appears that the main morphological changes in gastrulation do occur on the caudal side - for amniotes.
However, in Drosophila, gastrulation involves the formation of an approximately homologous structure called the ventral furrow, which is obviously on the ventral side, extending most of the anterior-posterior axis. However the invagination event does actually happen on the dorsal/caudal side.
So, it's complicated, and it depends a lot on which organism you're talking about.
Update following response
Humans are amniotes, they follow more or less the normal amniote path in gastrulation according to the wiki link above.
An important note missing in my previous answer above is that gastrulation itself defines bilateral symmetry in embryos; prior to this establishment animal-vegetal is the only obvious axis. So we are kind of defining the rostral-caudal axis according to the formation of such structures as the primitive streak, which are formed during gastrulation.
So it's a little circular to say that gastrulation happens on caudal end only; as gastrulation includes the step that establishes the rostral-caudal axis. Without gastrulation that axis just doesn't exist.
Again, gastrulation is a process that happens to the entire embryo. It doesn't just happen in one area. Structures such as the primitive streak are just obvious clues that the process is happening. It might be proper to say that the primitive streak begins forming caudally (I don't know of exceptions, though I'm not an expert), but it would not be proper to say that gastrulation is a caudal process.

Hi thanks for the answer I meant in humans

@FazalSyed see update.

Your point that gastrulation defines the axes is a good one. I would also note that the organizing node and primitive streak are not "in the caudal half" as the OP says. They move, which is a key point. Specifically, they move in a rostrocaudal direction (or craniocaudal if you prefer), the axis is established based on that movement. Early cells that pass through the streak form more rostral structures. Later cells form more caudal structures.

I think the Wikipedia article has confused the OP with poor word choice when it says the primitive streak forms "toward the caudal or posterior end." It doesn't form at the caudal end. It moves towards that end as gastrulation proceeds


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Evolution of hunting behavior of parasitoid wasps
Wasps in the genus Pepsis lay their eggs in a specific region on a species of tarantula and their larvae eat the tarantula organs in a specific sequence to keep it alive as long as possible.
How could this process have evolved, considering that a mistake at any stage results in death?
This is the description of the egg laying behaviour:
Upon finding a tarantula, the wasp locks its mandibles onto a foreleg and brings its stinger into position so as to paralyze it.
During this process, the tarantula tries unsuccessfully to dislodge the wasp, but the wasp ultimately locates the right part of the tarantula in which to insert its stinger.
Upon inserting it, the wasp injects a venom that paralyzes the tarantula. Note that the tarantula is ten times the weight of the wasp, so the wasp takes very big risk in trying to attack such a tarantula.
The wasp then drags the tarantula into a hole that it has already dug. It pulls the tarantula down into the  hole, attaches its egg to a specific part of the tarantula's body and then covers up the hole so that predators won't find it.
When the egg hatches, the larva eats the organs of the tarantula in a specific sequence so as to keep the tarantula alive for several weeks. Eating in the wrong sequence results in the death of the tarantula, and its subsequent putrefaction, which means the death of the wasp larva.
When the larva successfully eats in the right sequence, it is able to obtain enough nourishment to prepare for metamorphosis, ultimately resulting in a full-grown wasp, which then exits the hole and becomes a predatory wasp.
These wasps are solitary, which means there are no conspecifics to teach the new wasp how to do all this.
Thus, the entire behavioral program described above must be encoded in the wasp's genome.
The description above is based on:
Punzo, F. (2005). Experience affects hunting behavior of the wasp, Pepsis mildei Stål (Hymenoptera: Pompilidae). Entomologica Americana, 113(3), 222-229.
Petrunkevitch, A. (1952). The spider and the wasp. Scientific American, 187(2), 20-23.

Please use paragraphs to make text legible to people, especially with complicated phrases. The question could be only 2-3 lines. It's a bit like AI. Evolution is usually about gradual change, so the wasp has always followed a path which has given it good survival rates. The behaviors become complex over time, from simpler to more complex.

Welcome to Biology.SE! This is an interesting question, but I suspect very hard to answer in just a few paragraphs. We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources) or even answer your own question. For example, I found several freely available review articles on this subject by searching using your title. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@com.prehensible and tyersome thank you for editing my question.

While it doesn't directly address this particular example, you should find this related question and answer to be of interest. In general, complex behaviors (and structures) evolve over very long periods of time as improvements on simpler behaviors. A look at related wasps with simpler "lifestyles" should help you understand how such an "optimized" (note it is probably sloppier than you think) behavioral program can evolve.

@com.prehensible Please show me how you can simplify this behavior.

The common ancestor is thought to have laid eggs on or in wood grubs 247 million years ago. Since then they have evolved into as many as 500,000 species, mostly with a specifif host species. The wasps have had that many generations to make the jump from one type of insect to another, from larvae to crickets to spiders, and they can lay 100ds of eggs. The specifics are very complicated, i don't know, here are some docs:  https://www.annualreviews.org/doi/10.1146/annurev.ento.51.110104.151029 and https://www.sciencedirect.com/science/article/abs/pii/S0065308X03540027?via%3Dihub

Context is everything. Lets start by working back to front.

larvae eat the tarantula organs in a specific sequence to keep it
  alive as long as possible.

Most of the time if the larva eat the organs in the wrong order they don't die, they just end up with less food. It is pretty easy to see how this could evolve to be better, larva that eat in the correct sequence end up with more food thus have an advantage, larva that eat in hte absolute wrong sequence don't survive.

on a [specific] species of tarantula

Again easy many wasps are not as picky they will lay their eggs in/on a wide variety of hosts, but specialization is favored a lot in evolution as it helps your lineage exploit a resource better and better, you only have to deal with the defenses of a single species as opposed to many different ones which might have mutually exclusive solutions.

lay their eggs in a specific region.

again failing to do this does not necessarily mean their larva die, it just means they are worse off becasue they don't get to eat as much. Again easy to see how this evolves, a wasp that picks its target end up with more well fed offspring. Many don't even lay their eggs inside the host but outside and let them eat the host from the outside in, this is what this species does.

Upon finding a tarantula, the wasp locks its mandibles onto a foreleg and brings its stinger into position so as to paralyze it.

Again not every parasitic wasp does this many don't paralyse their host, but they jab them with the ovipositor relying in brute force to injure, paralyse, or kill the host. Others just lay their eggs on them and fly away. Others simply kill the host jam it in a hole and lay their eggs on it. But wasps that paralyse the host are less likely to get attacked. but even if they kill the host instead the larva still get a meal. hunting always tends to be risky, but as long as the reward outweighs the risk it can evolve. Additionally many wasps do not target adults but larva and eggs that can't fight back. venomous Stinging is actually fairly rare in wasps occuring only in the ones that attack the most dangerous hosts. Of course once a wasp lineage gets good ant not killing its host then there is little reason for the larva to be able to eat more putrid remains of the host, as such adaptations are costly so you can see how after they stop killing the prey the larva might lose the ability to keep eating dead hosts.

The wasp then drags the tarantula into a hole that it has already dug.

Again not every species does this, some just lay their eggs on a host, without doing anything else, but this carries more risk of your larva getting dislodged or injured, but insects are not people if there is a parasite on their back there is not a lot they can do about it.

These wasps are solitary, which means there are no conspecifics to
  teach the new wasp how to do all this. Thus, the entire behavioral
  program described above must be encoded in the wasp's genome.

Even your own source disagrees with this, it shows wasps get better at subduing the host the more often they do it, laying eggs in NOT a once in lifetime thing they may do it many many times, so not being perfect can still work.
Once you see the huge variety in parasitic wasp behavior it is much easier to the step by step sequence that can happen to get to each one. You are not even at the most extreme, there are wasps that go even further, like having viral mutualists, larva that can't poop so as not to contaminate a host they live inside, and even leaving chemical markers to keep other wasps from laying eggs in/on the same host. Parasitic wasps are rather well studied I invite you to look more into them, they are really good models of evolution.

parasitoid wasp evolution:
Started radiating about 127 million years ago, at the same time as Gymnosperms (flowering plants). Today they represent 10-20% of all insect species.
They have accompanied the other insect species in their diversification since that time, and often undergo co-speciation... When a host species divides into different types, the wasp species divides too.
Species that lay inside living insects are thought to be derived from wasps that lay eggs on or in other insect's eggs or pupae. Endoparasitoids have evolved from ectoparasitoids independently in different hymenopteran lineages.
Some species also lay microeggs on leaves near a larvae, and when the host eats the leaf and the egg, it develops inside them.
They have both a sting and an ovipositor, which permits different species a variety of specialized and opportunistic behaviours to lay on or inside eggs, and to inject genes and venoms which inject into the host to modulate host immunity, metabolism and development. Up to 70 different venom proteins have been found in a single wasp species.
Parasitoids can also inject substances like polydnaviruses (PDVs), virus-like particles (VLPs), ovarian fluids and teratocytes.
This kindof reflects the complex evolution of the Pepsis species described... The different components of venoms and behaviours came as little changes over 100ds of millions of years, and the specialization on a single species of tarantula kindof gives the wasp exclusivity from intra clade competition.
Digging a hole to put the spider in does seem overly complex. apparently, it must have first learnt to pull the animal into a hidden recess... Afterwards it started to scratch and clear the recess, and that foraging movement eventually turned into excavation of a pit prior to dragging the prey.
here's one of the most readable references: https://www.nature.com/articles/srep19604


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what is the princlple of using DMS (Dimethylsulphate) for structural analysis of rRNA?
I want to check the secondary structure of rRNA (PTC) in a particular position by using DMS footprinting. I have deleted the modified nucleotide (m5c) which is present in the PTC and it helps in the ribosomal structural stability. I am interested to know after the deletion of the modified nucleotide.
I am using DMS treated RNA with primer extension. I don't understand the basic principle of DMS reacting on RNA. can you please explain me.
I used this article for reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701642/

Here is a good explanation of the theory and chemistry behind DMS footprinting, from chapter 11 of Probing RNA structure within living cells :

In vivo chemical probing assay using dimethyl sulfate (DMS). (A) DMS methylates the N1 atom of adenosines and the N3 atom of cytosines. Both of these positions are located on the Watson–Crick face of the respective nucleotides. (B) Scheme of a structured RNA interacting with a protein ligand to exemplify residues accessible to DMS modification. (C) Mapping the modified positions by reverse transcription. The enzyme terminates the extension due to steric hindrance by the bulky methyl group at the Watson–Crick face of A and Cs. (D) The pool of cDNAs is separated on a standard denaturing gel. A and C denote the sequencing lanes, which are essential to map the modified positions. In addition, an RT control, which is prepared from RNA extracted from untreated cells, is essential to determine any natural stops of the RT (lane -). Comparison of the RT control lane with the cDNA pool created from DMS-modified RNA (lane +) reveals sites of modification. Note that the band resulting from a DMS modification migrates one nucleotide faster than the corresponding band in the sequencing lane, because the ddNTP is incorporated into the nascent cDNA, while the methyl group results in a stop one residue prior to the modification.

My take -- DMS adds a methyl group at the hydrogen-bonding face of exposed A and C bases. As and Cs protected by either proteins or base-pairing interactions are not methylated.  Methylated bases inhibit reverse transcriptase, resulting in a truncated DNA product that can be visualized on a gel.  Comparison to an untreated control allows for inference of which As and Cs of the RNA sequence are exposed and which are protected, from which the native RNA conformation can be inferred (or the possibilities greatly constrained).

Yeah..you are right but if you check in the literature apart from A and C other nucleotides also modified. It gives information about solvent exposure and
unusual chemical environment. These two factors enhance the methylation. http://ribonode.ucsc.edu/Pubs/Wells_etal00.pdf                                                                  https://www.nature.com/articles/s41598-018-30383-z


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Can convergent evolution be used to explain similarity of genome of low and high Species e g. gorilla and human?
Example: 1) molecule Rhodopsin in halobacteria for producing energy from light. 2) molecule Rhodopsin for vision in human. These are said to be of different lineages and their high similarity are due to convergent evolution. Obviously then over long lapses of geologic and pre-geologic time, as the saying goes, things may be evolving to a best or most efficient at least in the particular case. So I'm wondering, much is made of the similarities of genomes of high  and low Species to "prove" man is descended from the lower species. But could not the acceptable concept of convergent evolution, in general, be used to explain the similarity of say the genome of an ape and that of a human?

For each of 20,000 genes arranged in the same way?

there are no higher or lower species, gorilla have several advantages over humans, like a much higher genetic diversity.

Because there are usually many different possible molecules that can perform nearly identical functions, it is possible but unlikely that two independent evolutionary lineages will end up with exactly the same molecule to perform the same function.  If molecule A1 and A2 perform the function FA in lineages 1 and 2 respectively, and molecules B1 and B2 perform the function FB in lineages 1 and 2 respectively; and if the probability that A1 is identical to A2 is PA, and the probability that B1 is identical to B2 is PB, then the probability that both lineages use the same molecules respectively to perform function FA and FB is (PA)(PB): the product of the two probabilities.
Let's say the probability PA is 0.01 and the probability PB is also 0.01.  Then the probability that the two lineages will have identical molecules respectively for each of the two functions is (PA)(PB) = 0.0001.  Go through the same exercise for just ten such functions, and the result is the product of all ten probabilities: (PA)(PB)(PC)...(PJ) = $10^{-20}$, a VERY small number.  So the likelihood of convergent evolution occurring on the molecular scale over a significant portion of the genome is negligible.
On the level of phenotype, though, convergent evolution is much more likely.  Different molecules and different development trajectories can produce phenotypic structures that perform closely similar functions and can even resemble each other closely.  Consider for example the wings of bats, birds, and insects.  The phenotypes can be similar, but at the genomic level there is very little similarity.
The conclusion to be drawn is that IF there is close genomic similarity between two lineages over more than a few genetic loci, then the lineages are closely related and diverged from a common ancestor.

The probability you calculate over prolonged lapse of time T is extremely small. But the probability that the genome resulted from evolution from an  abiotic state is probably as small.

@user56930 not it's really not, convergent evolution has to be probabilistic at the genetic level, while genome complexity is a much simpler directional selection, the latter can take advantage of reinforcement effects like muller's ratchet and normal natural selection.

@user56930 — This answer was an honest response to your question as to whether convergent evolution could explain the relationship between man and e.g. chimpanzees. Your question said nothing whatsoever about the abiogenesis, nor does this answer. It is thus quite unjustified to use the comment section of his answer, not to query it, but to introduce the topic of the probability of abiogenesis. I suggest you withdraw your comment.

No.  First, the idea of "lower" and "higher" species is one of those "not even wrong" beliefs that we are burdened with for reasons better not discussed here.  An ape, or a monkey or starfish, is no better or worse suited to its environment than a human.  And we do have a good bit of evidence, such as the fossil record, connecting apes & humans independently of the genomic evidence.  (Much of which was known decades before the discovery of DNA.)
@S. McGrew's answer discusses the statistical likelihood of similar genomes coming about as a result of convergent evolution. But let's approach the question from the other direction, and look at a couple of examples of actual convergent evolution.
First, the ichthyosaurs https://en.wikipedia.org/wiki/Ichthyosaur and the cetaceans https://en.wikipedia.org/wiki/Cetacea  Shaped by the pressures of their marine environment, they look enough alike that a casual observer might have trouble deciding which group a particular species belonged to. Yet one group are reptiles, the other mammals, separated by hundreds of millions of years from their last common ancestor.  Their bodily form is similar, but their genomes are very different.
Another, and even more widely separated, example are the hummingbirds https://en.wikipedia.org/wiki/Hummingbird and the hummingbird moths https://www.fs.fed.us/wildflowers/pollinators/pollinator-of-the-month/hummingbird_moth.shtml They look enough alike that they're hard for the casual observer to distinguish, they occupy the same habitat (I see both in my summer garden), feed in much the same way - yet one's a bird, the other an insect.  Again, the similarities of appearance & behavior are the result of evolutionary pressures acting on very different genomes.
There are many other examples of convergent evolution.  In most cases, if not all, the similarities have come to be as the result of similar environmental pressures acting on genomes, NOT as the result of genomes evolving to be nearly similar.  That is, if you compared the genomes of two such convergent species, they would have no more in common than two non-convergent species from the same groups.

You are getting confused by terms.
there is a difference between convergent evolution at the genetic level and the functional level.
Rhodopsin is a group of similar protein molecules with similar structure some of which have a similar function. It is not a single identical molecule. Humans and halobacteria do not have the same rhodopsin molecule nor rhodopsin genes.
The rhodopsin molecular structure may be similar but it is not the same AND the genetics and process of its production are drastically different. halobacteria and animals have very very different rhodopsin genes, and even in animals rhodopsins genes var a great deal, but vary in a predictable pattern which mirrors their evolutionary relationships.
This is convergent evolution at a functional level, stumbling across similar configurations that produce similar results, even if the coding for that structure is drastically different. think of the similarities between insect and hummingbird wings. These are not similar genetics but similar molecules or structures.
Convergent evolution at the genetic level is extremely rare and is mostly due to the law of large number than anything else. They are always small similarities in the middle of vast seas of difference. the equivalent of two books by two different authors happening to contain the same sentence even if the entire rest of the book is different. And even then it tends to only occur in closely related species where enough of the genetics are similar that the chances of getting the same mutation twice is statistically possible.
sources: https://pubs.acs.org/doi/abs/10.1021/bi00136a001
https://pubs.acs.org/doi/pdf/10.1021/bi00128a002
https://www.sciencedirect.com/science/article/abs/pii/037811199500458I
https://www.sciencedirect.com/science/article/abs/pii/S0966842X06002307


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Non-Salticidae with °oo° Eye Arrangements
Since childhood, I've always thought of the °oo° pattern of four frontmost eyes as iconic for spiders (note: the pattern does not account for any additional eyes or lack thereof further to the sides or back; also, title font seems to make the °'s relatively smaller than the main text's font does - this was not intentional). And yet taking a look at a couple of eye-based family identification tables, it seems that the above pattern is the go-to sign of a jumping spider.
Is this pattern unique to salticidae, or are there other groups of spiders with the four foremost eyes matching such a pattern (either four equal-sized eyes, or the secondary ones slightly smaller)? If the latter, what groups sport a similar look?

It is pretty much unique to salticidae, although I did find some similar eye arrangements in sicariids and scytodids.
Salticidae:

Sicariidae:

Scytodidae:

Image source


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Physiology of hyperpolarization
In my textbook, it is stated that after the closure of potassium voltage-gated channels and during hyperpolarization, potassium leakage channels allow potassium influx passively and this returns the cell to its normal polarised state. I don't understand why will potassium ions enter the cell against its electrochemical gradient ?
My textbook quote :

during Hyperpolarizatio: The Leakage K+ Channels tend to drive the membrane potential from hyperpolarized state to the resting state as they drive K+ ions inward

@BryanKrause and then comes another question if the stable membrane potential is for example -90 MV and potassium gated channels open why would potassium ions disrupt their original equilibrium (increase the inside negative charge) and move outside the cell more than before.

Which textbook is it? I think that phrase is completely wrong.

@BPinto  I think the phrase is correct and if it's wrong then what drives the membrane from hyperpolarization to normal resting membrane potential

When you`re in the hyperpolarized phase, the resting potential is closer to the K+ reversal potential.  When the voltage dependent K+ channels close the membrane permeability to potassium decreases and thus the resting potential shifts to more depolarized. @BrianKrrause answer should make it clear now

@BPinto thank you this answer made every clear

I don't get to say this on very many occasions with questions like this...
Your textbook is wrong.
A typical potassium reversal potential in a cell is ~-90 mV. Hyperpolarization through voltage-gated potassium channels can never go more negative than that reversal potential.
An experimenter with access to the cell through a patch clamp electrode could possibly set the voltage more negative than potassium reversal, in which case indeed, potassium would flow against it's concentration gradient into the cell due to the electrical potential. It is not possible to reach those very negative potentials using potassium channels alone.
For a typical cell, the resting membrane potential is more like -70 mV. This resting potential is due to the "leak conductance", which does include potassium but also includes other ions. The ratio of sodium to potassium permeability is typically around 1:20; potassium dominates but you can't just ignore the other ions. A more accurate replacement statement for your textbook would be:

The leakage conductances tend to drive the membrane potential from hyperpolarized state to the resting state as the net positive flow of ions is inward.

Even at rest, you will always find a slow potassium leak out of the cell. The reason that the cell is at equilibrium at rest is because this leak out of the cell is perfectly balanced by net positive charge flowing in to the cell; this is mostly sodium but can be other ions like calcium as well (note also that that chloride leaving the cell is also a net positive charge in).
Some of the sodium leak current is through specific sodium leak channels, but co-transporters that use the sodium concentration gradient also contribute.

Ren, D. (2011). Sodium leak channels in neuronal excitability and rhythmic behaviors. Neuron, 72(6), 899-911.

@Byran Krause what I understood from your answer is that due to the specific limited number of K+ channels (and not only the electrochemical gradient) the efflux of K+ ions is limited to a certain number and after increasing the conductance of membrane to K+ (causing hyperpolarization) ,the membrane conductance to K+ returns to normal slowing down its efflux .So, what causes the return from hyperpolarization to polarization is the normal flow of other cations with their electrochemical gradient (Na+) and the slowed down efflux of potassium not as was written by the influx of K+. Right?

@mohamed First think of each ion's reversal potential and the membrane voltage. Every ion will travel according to its own reversal potential. If potassium's reversal potential is -90mV, it will always be flowing out of the cell if the membrane is more positive than -90mV, and flowing in if the cell is more negative than -90mV. The rate of flow depends on the difference from -90mV. If the reversal potential for sodium is +60mV, it will always be flowing into the cell if the cell is more negative than +60mV. The membrane potential you actually observe, then, depends on a ratio of conductances.

and that's why the book is wrong K+ never enters the cells  and the  cell's membrane potential shifts towards sodium's potential stoping hyperpolarization ,but then the number of sodium inside the cell increases relative to before the action potential, so here comes the Na+-K+ in returning the original number of potassium ions inside the cell and expelling and excess sodium.


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lifespan of Nautilus compared to other cephalopods
Most cephalopods live uncharacteristically short lifes compared to other creatures of their size and intelligence. The octopuses with the longest lifespan for example, the giant pacific octopus, only live for up to 5 years.
This is quite long for cephalopods already, as some of them only live for as little as half a year.
The reason for this short lifespan is not aging itself (meaning loss of information in the epigenome and similar effects), but their reproduction. The maturation of their reproductive organs results in the deactivation of their degestive glands, so they basically starve themselves to death.
When the reproductive glands of an octopus are removed, their lifespan increases greatly.
Nautilus are an exception to this low lifespan of cephalopods. They live to be over 20 years old.
Why do nautilus live so long and is it possible to grow other cephalopods with similar lifespans by introducing nautilus genes?

Queen conch can grow to be over a foot long and can live for as long as 30 years. some species have been known to live to 40 or more. It's difficult to see if the nautilus has average or max lifespan of 20 years.

On a basic level, the difference in lifespan is due to the fact that the nautilus has a vastly different reproduction strategy from other living cephalopods.  While most other cephalopods exhibit a rather extreme form of r-Strategy reproduction, the nautilus is, relatively speaking, a K-Strategist.  To explain, r-Strategy is when a species produces many offspring, but puts relatively little investment into each one under the expectation that most will die.  K-Strategy, on the other hand, produces relatively few offspring, but put much greater investment into each one.
As you stated, in most cephalopods, sexual maturity triggers a shutdown of the digestive tract, as they put all their energy into reproduction, during which one spawning episode will result in hundreds or thousands of eggs.  After fertilizing the eggs for males, and for females after laying those eggs (allowing for a delay of a relatively short incubation period in some species, including most or all varieties of octopus), the adults die, having produced enough young to guarantee the next generation.  This lifestyle of a single massive reproduction event before dying is called semelparity.
However, with nautiluses, each mating results in only about a dozen eggs.  These eggs are much larger than the eggs of any other cephalopod, have a considerably longer incubation perios, and by extension, the hatchlings start out larger and better-developed.  However, technically, nautiluses aren't true K-Strategists, like humans or whales, which have only one offspring at a time and put a massive amount of investment into that offspring.  Instead, they are more like cats or dogs, Median Strategists, who fall somewhere between the extremes.  While for r-Strategists like other cephalopods, semelparity can produce enough young to ensure the survival of the species, this is not the case for Median or K-Strategists.  Instead, they must reproduce multiple times over the course of their life, a strategy called iteroparity.
While in all cephalopods, the gonads are destroyed by the process of reproduction, in nautilus females, the gonads regenerate after spawning, allowing them to mate again the next year.
It should also be noted that despite this, the nautilus spends a relatively small portion of its life sexually mature.  It takes roughly fifteen years for a nautilus to reach breeding age.
While my knowledge of genetic engineering is pretty much limited to what appears in the news, based on this information, it seems like to lengthen the lifespan of other cephalopods to be on par with that of a nautilus, you'd have to completely change the way they reproduce and the rate at which they mature, which I tend to suspect is beyond our current abilities.


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Is Urea excretion a shared ancestral trait of amphibians and mammals relative to synapomorphic Uric Acid excretion in living reptiles?
Is the ancestral condition of prehistoric amphibians and early amniotes urea excretion? Would it follow then that the lineage leading to living reptiles went on to evolve uric acid excretion as a derived trait? Therefore urea excretion is a shared plesiomorphy of living amphibians and living mammals relative to a synapopmorphy of uric excretion in living reptiles?

There are reptiles that also use urea, and mammals that excrete uric acid.  it is likely that urea is the ancestral condition (compared to uric acid) as it occurs in adult amphibians and some fish. But ammonia is even more ancestral than that, occurring in young amphibians and most fish. It is likely uric acid developed alongside terrestrial eggs, as every egg laying amniote (including monotremes) uses uric acid at least during the embryonic stages. Uric acid is more metabolically costly so there is some incentive to switch to urea if you can, although there is a counter factor as urea requires significantly more water. so it comes down to which a group can afford more water or calories. It is notable that the few reptile to witch use urea only switch during their adult stage. It is possible to do both a few desert mammals produce uric acid and urea at the same time, producing more uric acid when water stressed.


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Is sex a spectrum?
At the moment I'm especially interested in the question of whether biological sex is really a spectrum. Unfortunately I could not find any good answers on the Internet. Therefore I hope that some of you might be able to present the current state of science here and whether it is already generally accepted in biological science that sex is a spectrum.
What I am confused about here is for something to be a spectrum it must have some some sort of distribution along a parametrised scales. For example, it would be daft to think height to be binary even though there are tall people and short people. Tall and short are relative; height is defined by a continuous factor, length, measured (for example in cm) from foot to head. There is no such parameter that can be used to show that male and female are relative in the way that tall and short are. There is no scale. What I thought is that it relies on the binary to classify gonads as either male or female. So, people with disorders of sex development are still either male or female due to the presence of gonads (which define sex) if I understood correctly. There are only two gonad types since this is the fundamental feature of what sex is. I hope someone can correct me here, if this is wrong.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Sex-determination system and Sexual differentiation in humans might be informative for you and are as good a place to start as any. Read up a bit more on the topic, and then please come back to [edit] your post about what you've learned and by adding a specific biological question about something you still don't understand. Thanks

@theforestecologist So, I edited the question and added from what I understood to be a spectrum. I hope, you can help me out there.

As requested, the assumption in your edit is wrong :p. See the links in my previous comment. Hope this helps.

@theforestecologist I did read those articles already. It didn't really help me though, since they also have not mentioned exactly what sex on a spectrum means. Could you help me out here and explain what exactly is wrong in my edit? This is from what I understood so far.

Also, I am not quite sure why this question was downvoted. :/ It's a fair and crucial question and I hoped that someone could clarify it or at least give a glimpse into what current studies or science says. Just linking to wikipedia articles is not really that much of an helpful answer.

biological sex is based on presence/absence of sex chromosomes and not on anatomical gonads as you mention. Within a species, there is no spectrum (though, there are variations based on chromosomal disorders/abnormalities).

It was downvoted because it doesn't follow the guidelines for writing good questions on our website (specifically, see here). I've already described to you in my first comment what improvements you need to make to have the question receive upvotes and to receive the most helpful answer. your question is currently written in a hypothetical inquisitive manner, whereas we require prior demonstrated research to be explicitly stated in a question. Please take our [tour] to learn more. Thanks

@theforestecologist But wouldn't these variations essentially be on a spectrum then? Why would it be a "chromosomal disorder" for example being a hermaphrodite and not just another sex on the spectrum?

See Chromosome Abnormalities Fact Sheet for a review of chromosomal abnormalities.

To get an idea about the spectrum as it relates to genital development check out the Quigley_scale and the related links on that page. Also note that while hermaphrodism (defined by having both male and female genitalia) does occur in some animals (e.g. slugs) it does not occur in humans.

You're comparing apples to houses. Some things occur on a spectrum (e.g. height or intelligence) because it is multifactorial (genetics, hormone expression, nutrition/genetics, nutrition, environment, opportunity, etc., each factor contributing something) and some things do not (you are either a chromosomal male or a chromosomal female) excluding uncommon genetic abnormalities. @theforestecologist has given you the answer, and Wikipedia is actually a good resource to start at a basic level.

@anongoodnurse I don't believe the OP asked about chromosomal sex. Maybe different medical schools teach this differently, but I was taught that the karyotype is not adequate for defining biological sex.

For what it’s worth, I don’t think your question deserves as much grief as it has gotten. The only critique I’d make is that you should not conflate sex with gender.

@canadianer Just saying, that's not really a fair and reasonable critique since I specifically wrote: "biological gender". So, there has been no conflation between the term sex and gender. But thanks anyway for your input.

This Q/A might be interesting: Whats the difference between male and female

@DeNovosupportsGoFundMonica - The OP specified "biological sex". That is the correct answer to "biological sex." I think you read (as we are wont to do these days) too much into "sex". To quote the OP: "There are only two gonad types since this is the fundamental feature of what sex is." Without defining sex as gender but as "biological", I answered what I thought the OP was asking. N.B. Gender is not necessarily sex. It's all about definitions, wic the OP has not accurately specified.

I, too, commented assuming that the OP had conflated "sex" and "gender" and chose to respond as though the OP simply was referring to biological sex. If that is the case (i.e., if the OP did conflate the two), then (as @anongoodnurse suggests above), we mustn't complicate the biology with conflated social constructs, and we need to emphasize the strictly biological aspect of this question. Which is what I have tried to do.

However, since the OP has suggested in their comment that they intentionally used "biological gender" (gender normally referring to "social and cultural differences rather than biological ones" (Definition 1 here), then I would suggest that either the OP needs to define what they specifically mean by "biological gender" or otherwise this question is off-topic b/c it is not about biology.

@anongoodnurse as i was taught, karyotype is not sufficient for determining biological sex. I mean those terms precisely. Gender is a behavioral category, and not at all what this question or my comment were about. Biological sex is a (complex) question of physical phenotype that depends on a great deal more than the simple presence or absence of a Y chromosome on karyotype.

What is "biological gender"?

@BryanKrause - Exactly. Definitions matter, and the OP provided none. I think, though, you can differentiate between a simple definition of biological sex (female, male, neuter, hermaphrodite, etc.) and phychological/emotional gender.

@DeNovosupportsGoFundMonica - Feel free to tell me your definition of "biological sex." I am not too old to learn. And since I have no dog in this race (not trying to push or support my particular views/biases), I'm open to learning more.

Your question uses the word I very much... sci pubs and research dont communicate journalistically about themselves.

@anongoodnurse as I understand it, "biological sex" = reproductive phenotype, which is determined by the (variable) expression of a heterogeneous set of genes on multiple chromosomes, including autosomes.

@anongoodnurse I'd say whether reproductive phenotype is binary or not depends more on philosophy, politics, and whether you're a lumper or splitter.

Possible duplicate https://biology.stackexchange.com/questions/17327/does-any-animal-species-have-two-sexes-and-more-genders

related question https://biology.stackexchange.com/questions/52149/how-is-trangender-female-different-from-normal-female-biologically

Isn’t that rainbow logo confusing you?

Is the question only referring to the human species or the general case? This is a bit muddled, both in the Q and some comments (and the current answers).

@BryanKrause Biological gender is sex (and I even wrote it above in brackets. It's absolutely clear what I meant with biological gender). Fairly obvious.

@Tetragrammaton it is absolutely not clear because there is no such thing as "biological gender". As has been made clear multiple times in responses you've received, "gender" (regardless of adjectives you associate with it) is NOT a biological concept. As such, "biological gender" is meaningless and demonstrates a lack of understanding of terminology. Put differently, You cannot equate "sex" and "biological gender" because the latter phrase doesn't make sense. I highly suggest you [edit] your post to remove all mention of "gender" since it is at-best unclear and at worst off-topic.

Scientists Fred P. Thieme and William J. Schull of the University of Michigan wrote about sexing a skeleton in 1957: “Sex, unlike most phenotypic features in which man varies, is not continuously variable but is expressed in a clear bimodal distribution.” The same is true for chromosomes, sex organs and testosterone.

"Variability in size or composition of gonads, genital morphology, chromosomes and/or hormonal physiology"

Specere in latin means to look, that's why it's used for the color spectrum. The rainbow is often used to represent gender-identity to represent the amorphous nature of the mind.

The distribution of fitness effects for genetic mutations of whole genomes and individual genes is frequently found to be a bimodal distribution with most mutations being either neutral or lethal with relatively few having intermediate effect.
Through the process of meiosis and fertilization (with rare exceptions), each individual is created with zero or one Y-chromosome. The complementary result for the X-chromosome follows, either a double or a single X. Therefore, direct sex differences are usually binary in expression, although the deviations in more complex biological processes produce a range of exceptions, resulting in a bimodal graph.
Gender does means biological sex in the context you use.
https://en.wikipedia.org/wiki/Gender

I'd avoid using the term menagerie to describe intersex individuals

Mais pourquoi donc?

Because it contains the implication that intersex people are non-human animals. I'm sure that's not what you intended, but it can read that way.

this really has nothing to do with the question, as the linked article is discussing sex not gender.

@John the OP seems to be misusing the term gender. The edit clarifies the question to be about sex, not gender.

Menage, is a strictly non-zoological term that french proudly use to refer to their household, I 've never heard of a ménage d'animaux, an animal household. Sorry I copied that straight from the wiki because was ona small phone screen. https://en.wikipedia.org/wiki/Sex_differences_in_humans

@john https://en.wikipedia.org/wiki/Sex_differences_in_humans#Physiology besides, it's simple maths like 1+1 =2, if you can read a graph you can understand it john. bimodal distribution is not more complex than a bell curve, it has peaks.

I know what a bimodal distribution is and human gender is not bimodal, even if sex largely is and confusing them makes your answer straight up wrong. Its bad enough the question is using poor terms there is no excuse for an answer to.

Gender is not really an established word, John, it has almost no precedence in scientific literature other than the sense that I use, It's etymology doesn't make sense for science either. Since 1990 there has been a lot of identity hysteria which has seen a new sense attributed to gender, the one that you are militant about: https://books.google.com/ngrams/graph?content=gender&year_start=1800&year_end=2000&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cgender%3B%2Cc0#t1%3B%2Cgender%3B%2Cc0 and https://www.google.com/search?q=%22gender%22&tbm=bks&tbs=cdr:1,cd_min:1857,cd_max:1995&lr=lang_en

@com.prehensible sounds like even more reason not to use the term. Also what do weaver ants have to do with the question?

@John, No, it's fine to use the word as long as you don't claim there is a precise narrow definition for the word based on your imagination. Your claim that gender is not sex is nonsense according to the wiki page gender, if you read the first phrase of that page it puts your old tutor's quip in the bin.

@com.prehensible have you read the wiki? because the first sentence tells you it is a social construct, and the second paragraph goes on to tell you why sex and gender are not interchangeable terminology.

@DeNovo You are incorrect. I did not misue the term gender and properly differentiated it from the term sex, as can be clearly seen above in my post, if anyone dares to read it.

@com.prehensible Thank you by the way, for answering the question. So, we can conclude that sex is not binary and is in fact bimodal. That's not really on a spectrum, but it definitely means that sex is not that fixed as many falsly claim.

@Tetragrammaton It's usually not good to accept answers with so many downvotes. This answer is bad: it has a graph of a bimodal distribution that is just an illustration and has nothing to do with sex. The rest of the answer talks about sexual orientation and not sex. It then talks about morphology of ants which are not related to sex at all since all the worker ants are sterile females.

Bryan Krause, you are contradicting fact: physical gender is bimodal ... https://en.wikipedia.org/wiki/Sex_differences_in_humans#Physiology There is a list of other bimodal distributions in nature, which includes harvester ants, which are also related to chromosomes.

The answer is bad because you assert that sex is bimodal but provide no evidence to support it.

Scientists Fred P. Thieme and William J. Schull of the University of Michigan wrote about sexing a skeleton in 1957: “Sex, unlike most phenotypic features in which man varies, is not continuously variable but is expressed in a clear bimodal distribution.” Chromosomes, Gamete structure, Hip structure, they graph into two modes.

This is improved.  Are you willing to include the sources for your two figures?

was confused with the downvotes on this answer, until I looked at the edit history.  It's much better now, good job (imo, although I'm by no means an expert)

Short answer: it's messy, and probably no answer will satisfy everyone.
I'm only going to consider sex (I'm not going to mess with "gender") in humans.

It's reasonable to consider sex as multidimensional rather than one-dimensional; see the various definitions listed below. The same individual could have different karyotypic, morphological, and endocrinological "sex".
Some but not all of the definitions refer to continuous scales, i.e. if you pick one of the continuous measures below (Quigley scale, circulating testosterone level) you can probably find at least one individual in any not-too-narrow interval on that scale.
It's reasonable to say that many of the continuous measures below are bimodal, i.e. in some random sample of humans there are more people close to 1 or to 6/7 than in the 2-5 range on the Quigley scale; similarly, there would be more people in the ranges of 10-30 ng/dl or 200-500 ng/dl in their testosterone than in between.

Here are some of the possible definitions of sex, drawing on the Wikipedia article mentioned in the comments:

karyotype (chromosal type): this is discrete (XY, XX, XYY, XO, XXY, ...) but not necessarily easy to split into "male" vs "female" except on the basis of what the phenotype (morphology, endocrinology, etc.) looks like. Would "male" mean "has a Y chromosome" (XY, XYY, XXYY)? or "has only one X chromosome" (XY, XYY, X0)? Would female mean "has no Y chromosome" (X0, XX) or "has 2 X chromosomes" (XX, XXY, XXYY)? Non-standard sex karyotypes are rare: e.g X0 1 in 3000 live births, XXY [Klinefelter's syndrome] 1 in 1000 live births; XYY 1 in 1000 live births; XXYY 1 in 20,000 live births (Jarzembowski, J.A. “Sex Chromosome Abnormalities.” In Pathobiology of Human Disease, 185. Elsevier, 2014. https://doi.org/10.1016/B978-0-12-386456-7.01505-7 ; https://rarediseases.org/rare-diseases/xyy-syndrome/)

Below the level of the chromosome, there's lots of genetic and environmental variation that can change the phenotype (e.g. here)

morphology (gonads or internal/external genitalia): the Quigley scale referenced in comments above is one way to describe this variation. The Quigley scale could be used to classify phenotype in cases of

androgen insensitivity syndrome, i.e. someone with at least one Y-chromosome who doesn't respond developmentally in the typical way to androgens such as testosterone
someone with an XX karyotype and congenital adrenal hyperplasia who has become masculinized

(the section on intersex conditions in the Wikipedia article on sexual differentiation links to these among others)

(these are cartoons of external genitalia, in case that's not obvious)
Intermediate morphology can occur in the gonads as well as in the genitalia or internal organs; according to MedLine Plus (US National Library of Medicine), people with "true gonadal intersex" have "[both] ovarian and testicular tissue ... in the same gonad (an ovotestis), or the person might have 1 ovary and 1 testis".

endocrinology (levels of various circulating hormones): researchers most typically consider testosterone (e.g. in this article). This article reports on total serum testosterone in a US health survey. The distribution is indeed bimodal (there's a peak around 10-30 ng/dL for women and 250-600 ng/dL for men), but this article only reports the 10th and 90 percentiles; there could certainly be someone with a circulating testosterone level right in the middle.

So ... the answer to your specific question about being able to classify people based on gonad type is that although it's rare, people with true gonadal intersex as defined above could not be classified as either (exclusively) male or female on the basis of their gonads. Furthermore, it's not obvious which of the many criteria (karyotype, internal/external morphology, endocrinology) would be the "correct" way to define sex in a particular scenario.

You might consider adding a bullet point for anisogamy, a concept that applies across a wide range of species

But humans are completely anisogamous as far as I know - I'm not aware of any circumstances under which humans produce gametes that are anything other than eggs or sperm. Seems tangential to me.

Since anisogamy is fundamental to the biological definition of "male" and "female" (e.g., Parker et al. 1972, The origin and evolution of gamete dimorphism and the male-female phenomenon), and since the OP's question was "Is sex a spectrum?", doesn't the fact that humans are completely anisogamous provide one important answer?

First gender and sex are not the same thing; as an old teacher of mine glibly put it, "sex is plumbing, gender is clothing," and even that is a gross generalization. The problem you are running into is using imprecise terms to ask a scientific question (sex, gender, and spectrum are all imprecise terms in biology). Precision in language is important in science to avoid confusion. The more vague your terms the less precise an answer can be.
More importantly gender isn't really a biological term; it is a sociological term, in particular it is a form of social construct (like countries, currency, or social class). The closest you get in biology is mating strategy, in which case there are species with multiple alternative mating strategies, including species with more mating strategies than sexes, some that are quite drastically different.  Humans in particular have a very wide range of complex mating strategies, and of course some are more common than others.
Spectrum is also a tricky word in biology; would you call hair color a spectrum even though the distribution is non-uniform? How about handedness or ear lobe shape? They are both multimodal. Quite often in behavior there are evolutionary stable strategies that are only stable as multimodal distributions; are they spectra?
Even sex is tricky in biology. Since you have phenotypic sexes and chromosomal sexes, there are XY females in humans, as well as XX, XO, and XXX females. There are people with neither testes nor ovaries (both are gonads BTW), and humans with both testes and ovaries. So you end up with quite a variety of "sexes". Then you have things like chimerism in which an individual is really two individual cell lines fused together; even the term "individual human" can get tricky if you look close enough because biology is messy and doesn't respect our generalized human categories.
https://www.ncbi.nlm.nih.gov/books/NBK10943/
https://www.who.int/genomics/gender/en/index1.html

Gender is a corruption of the term "gender-identity", which is also "sex-identity", genre in french means "type" and gendre means spouse, so it's a contradiction if you know the etymology.  https://en.wikipedia.org/wiki/Gender#History_of_the_concept https://books.google.com/ngrams/graph?content=gender+identity%2Cgender&year_start=1800&year_end=1990&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cgender%20identity%3B%2Cc0%3B.t1%3B%2Cgender%3B%2Cc0#t1%3B%2Cgender%20identity%3B%2Cc0%3B.t1%3B%2Cgender%3B%2Cc0

Just a small reminder: Again (and I don't like repeating myself in that matter for the third time) I never said that gender and sex are the same thing, nor did I ever claim so. @John

@Tetragrammaton biological gender isn't a thing, even "biological sex" is not a single thing.  I have have answered the question given, if this is not what you wanted to know then do some research and ask a new question with correct terminology.

@John Again, correct terminology was given. It's written in the question above. I wrote: "biological gender (or sex)". Thus, there's no need to ask a new question. But thanks for your input.

@Tetragrammaton and As I said, biological sex can mean several different things and biological gender is meaningless.

I don't think a random variable has to have a continuous or discrete uniform distribution in order to be a spectrum. Not that the uniformity isn't important, and could be quantified with information entropy.

@LifeInTheTrees Thank you. At least someone here who pays attention.


text:
Isn't it an evolutionary disadvantage to have a single organ perform so many essential functions?
This is in reference to the human liver, responsible for not only the production of bile, but also the filtration of blood, metabolization of drugs, detoxification and so on. Liver failure is often synonymous with death. So how exactly did the liver come to perform so many essential functions, with no backup whatsoever?

While the liver is vital, I don't know why you consider it more of an evolutionary failure than many other organs. One would die without a working heart (heart failure), kidney, gastrointestinal tract, brain, lungs, etc. Maybe you can clarify your question a bit. Also, metabolism of drugs/detoxification are basically the same thing, and filtration of blood also occurs in the spleen (its major function). Thanks.

The brain performs many essential functions, although it's more like a "division of labour" type of grouping, like in a factory where everything happens in specific rooms... we could have many small livers and brains and gonads all around the body, although evolution has decided to group everything together pretty much since the early bilateral animals. What is weird is that the skeletomuscular components of arthropods and vertebrates are totally symmetrical, and the rest is totally assymetrical.

Yes, but splitting it up into multiple organs is also a disadvantage, becasue you have to grow and upkeep said organs. every solution has its pros and cons that have to balanced.  Most of evolution is lesser of two evils compromises, kluges, or "good enough" solutions.


text:
The primary source for Erich von Holst research for minnow forebrain and shoaling
I am trying to find the primary source of information about the experiments of Eric von Holst, mentioned by Konrad Lorenz in the book “Das sogenannte Böse: Zur Naturgeschichte der Aggression”/“On Aggression”. The essence of the experiment is widely known and retold in many tertiary sources.
Quoting from a secondary source: under the chapter “Die anonyme Schar”/“Anonymity of the flock” from Konrad Lorenz.
"Ein Fisch, der, aus welchen Gründen immer, in bestimmter Richtung
zu schwimmen beginnt, kann ja nicht umhin, in Bälde aus dem
Schwarm heraus ins freie Wasser zu geraten und gleichzeitig damit
unter den Einfluß aller jener Reize, die ihn in den Schwarm
zurückzuziehen trachten.
...
Man kann ganz kribbelig werden, wenn man diesem Treiben
zusieht, und man kann nicht umhin, an der Demokratie zu zweifeln
und Vorteile in der Rechtspolitik zu sehen.
...
Er [Erich von Holst] operierte einem einzelnen
Fischchen dieser Art das Vorderhirn weg, und in diesem stecken,
wenigstens bei diesen Fischen, alle Reaktionen des Schwarmzu-
sammenhaltes.
...
Das operierte Tier war eben durch seinen Defekt eindeutig zum Führer geworden.
"
"A fish which begins, for any reason, to swim in a certain direction cannot avoid leaving the school and thus finding itself in an isolated position. Here it falls under the influence of all those stimuli calculated to draw it back into the school.
...
Watching these indecisive actions one almost begins to lose faith in democracy and to see the advantage of authoritarian politics.
...
Erich von Holst removed from a common minnow the forebrain which, in this species, is the site of all shoaling reactions. The pithed minnow sees, eats and swims like a normal fish, its only aberrant behaviour property being that it does not mind if it leaves the shoal unaccompanied by other fish.
...
By virtue of his deficiency the brainless animal had become the dictator!"
The many-hour search for the words "elritze vorderhirn schwarm erich holst"/"minnow forebrain shoaling erich holst" gives only biographies and obituaries of Eric von Holst and secondary/tertiary / damn knows what sources.
Could it be that with all due respect to Konrad Lorenz it was a false quote or a stretch? Did anyone dig up primary sources?

Not my field, but I found a bibliography of von Holst here. This lists a series of articles between 1934 and 1939, mainly published in Pflügers Archiv, on various aspects of the movement of the goldfish backbone and things affecting it, but (as far as I can see as a non-native German reader) nothing involving surgery or group behaviour. After this time his publications seem to involve mainly insects and birds. If you have any difficulty getting access to the papers, let me know.


text:
Could anyone please identify this Indian bug?
Photographed by a friend recently in central India. next to Panna Tiger Reserve.

Welcome to Biology.SE! Please edit your post to add an estimate for the size of this insect as that can be a helpful clue for identifications. ——— You may also want to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

While I can't help with a specific identification, it looks to me to be some sort of immature true bug whose wings are still coming in.  That may help narrow down the possibilities.

Unfortunately I did not see it and there is only this one photo. Such amazing markings caught my eye. Was thinking assassin but could find no exact image. Thanks for trying.

@Joanna if you think my answer is right please select it as the answer. Also,@cowrie try narrowing down the species with the geographic location too, helps a lot:)

@Joanna please mark my answer as verified if you find it accurate

The species from the photo is almost definitely a Catamiarus brevipennis.

The bulged and striped abdomen
The non-striped legs
The unique pattern on the wings
The antenna thick at the beginning and becomes thinner towards the end.
The protonum also has a unique granular structure unique to Catamiarus brevipennis.

Source : India Biodiversity Portal

I suspect this is a hemipteran, an assasin bug. I think this because of the shape of the legs, the reduced elytra and the bulgy eyes. If you had a picture from the side which would show the profile of the mouthparts, and if they happened to be protruding in the shape of a stylet, i'd be more confident that it is a type of assasin bug. Its definitely trying to mimic some other insect - hope this helps!


text:
Why is an antibiotic-resistance gene required during transformation of recombinant plasmid?
In my biology textbook, it said that in transformation, the recombinant plasmid containing an antibiotic-resistance gene act as a 'selective marker'. That means that plasmid in transformed bacteria must have taken up the gene of interest and is able to grow in an antibiotic culture medium.
However, will there be a chance that the plasmid doesn't contain the gene of interest but only the resistance gene? How can those plasmids be identified and removed? And how can the resistance gene act as a 'selective marker'?
Thank you very much.

What research have you done to answer this question yourself? Have you even searched past questions on this site? This general topic comes up repeatedly. Please read the Help on asking a good question.

Suppose I pass out notes at your school. Some notes are coupons for a tanning salon.  A few say "You are the chosen.  Wear a green ribbon in your hair tomorrow.  This note is your ticket to the awesome concert".
The next day you wonder who will be coming to the concert.  You look for people with the green ribbon.  That means they got the concert ticket.
Your plasmid has a gene of interest and a marker.  The marker is antibiotic resistance.  If you got it, then you fail to die when the antibiotics come.  If you fail to die that means you have the gene of interest too.  Antibiotic resistance is a marker for having got the plasmid, just like green ribbon is a marker for having got the concert ticket.
To get the ticket but not notification about the ribbon, or ribbon without ticket the note must have been torn or damaged.  To get a plasmid with gene of interest but not antibiotic resistance means the plasmid must have been damaged.  If the plasmids were good when you added them there is not much time for them to have been damaged by random events.  It could definitely happen but odds of that happening increase with time, and in the short term odds are against a damaged plasmid or a torn note.


text:
Why do individuals vary in the number of SNPs for a given gene ( e.g. FOXO3A )?
Individual #1, sequenced by 23andMe and then inputed into Promethease for SNP data has the following SNP output:
1) rs1935949(C;T)
2) rs2802292(G;T)
3) rs13217795(C;T)
4) rs13220810(C;T)
5) rs2764264(C;T)
6) rs9400239(C;T)
7) rs2153960(C;T)
8) rs2802288(A;G)
Thus individual #1 has eight reported SNPs.
Individual 2 also is sequenced by 23andMe and then inputed into Promethease for SNP data has the following SNP output:
1) rs2802292(T;T)
2) rs2764264(T;T)
Therefore individual #1 has eight reported SNPs for the FOXO3A gene and individual #2 has only two reported SNPs.
Since SNPs represent single nucleotide polymorphisms in the sequence, why does individual #2 only have two SNPs recorded rather than all eight?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Why are there more brown-eyed people than blue-eyed people in Britain? Consider. It is the gene that exhibits polymorphism in the population, not the genome of an individual. The statement that someone has so many SNPs is incorrect. He has so many occurrences of the less common variant of a site that exhibits single nucleotide polymorphism. So your question is really why do individuals differ. I imagine you can suggest reasons for that.

Thank you for the welcome:I think my confusion is based on visualizing SNPs as single base pair substitution in the gene:
I thought SNPs can vary by basepair but not in total number - here 8 vs 2.  In the example rs2802292 is possessed by both individuals but with #1 carrying (G;T), and #2 carrying ( T;T) SNPs for rs2802292 which makes sense.
But, some rs #’s are only in person #1, such as rs1935949 (C;T).   So person #2 can have (C;C), (T;C), (C;T), or (T;T).  However #2 has no listing at all for rs1935949.  How can it be that no SNP of any type is present at location rs1935949? Thanks!

So, if I'm understanding correctly your question is why you aren't getting SNP information for all the variable positions? That seems like something to ask 23andMe about. IIRC they don't actually sequence DNA and so, due to the technology they use, I suspect that for some locations they may not obtain information.

Perhaps they don’t report an SNP if your base is the same as their reference genome.

Yes tyersome, my question is why we aren't getting SNP information for all the variable positions ( eight variable positions for individual #1 from the original example whereas only two from individual #2).  Your hypothesis does not appear to fit the situation however since individual #1 which has more variations reported also used 23andMe at the same time, so this does not appear to be a 23andMe issue?  Other ideas?
Canadianer - I am not clear this is the case since for other alleles ( besides FOXO3A we are discussing), 23andMe has reproted all (4) possible allele combinations at each SNP.

Not necessarily — for example, failures to detect information at a SNP could be due to an individual having an unusual sequence that the 23andMe technology can't "see" ...

Interesting point tyersome.  My understanding is that SNPs by definition correspond to only single nuceleotide substitutions as opposed to larger sequences ( ie those affecting >=1% of population).   Given that is the case it seems what the technology would only need to detect single nucleotide combination variants - (C;C), (T;C), (C;T), and (T;T) at that SNP locus.  The gene chip can detect any of those diploid combinations, so why would it be unable to detect which one of those 4 possibilities is present at that locus.

What do you think would happen if there was small insertion immediately adjacent to a SNP? How about a deletion of the region containing a SNP? I suspect uncharacterized or rare polymorphisms nearby might also interfere with binding to the chip. What happens if they expect C or T and you have G? I also don't think you can rule out technical problems at any level (e.g. a damaged/defective patch on the chip, dust in the detector, or software errors ...).

They have been sequenced several times via multiple companies & whole exome, so it sounds like it is on of the former suggestions you made in your last post.  As of 2015 it looks like there were at least 15 reported FOXO3A SNPs reported: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326903/   ...... It seems that having a deletion or non C/T nucleotide is far more likely to lead to reduced function than increased function ( being a rarity it is less likely selected for)......How unusual is it then for individual #1 to have only 8 and individual #2 to have only two of thoese 15 FOXO3A SNPs?


text:
What software do I need to read-write cas9? and .dna files?
I am still a complete beginner to crispr and I am still trying to learn what it is and how to actually use it. I now realise that you have to order the crispr components after you have actually designed them yourself in software that lets you design and alter the components.
Am I correct so far?
I am wondering if anyone could help me find which software I should use to design and or alter .dna files . Preferably free and open-source software. Are there any good tutorials for someone who wants to get more into crispr?

You have a long journey ahead. This guy spent about 4 years to learn what he is doing here.
He is using Snapgene software

Thank you! :) The site doesn´t allow me to upvote because I have a to low reputation but know that I am really thankful! :)

I use Snapgene for my work the interface is nice, but with the free version you can't edit files to insert/delete bases.


text:
Is there a balance or feedback between O₂ and CO₂ in the atmosphere?
Is there, globally, a balance of the concentrations of oxygen and carbon dioxide  in the atmosphere?
Plants convert CO₂ to O₂,
and with the concentration of O₂, the tendency of plants to oxidize to CO₂ increases. That is, plants burn better with more oxygen.
Based on this there may be a feedback of increasing CO₂ concentration to increasing O₂ concentration back to increasing CO₂.
This feedback requires that plant growth increases with increasing CO₂ concentration.
Otherwise there would be only a limit to the oxygen concentration as at some concentration of O₂, even a wet rainforest burns explosively.
Does a feedback loop like that exist?

Actually no.  Even if there were a feedback loop, CO2 concentrations are only a few hundred parts per million.  Convert all the CO2 to O2, and you change the percentage of O2 in the atmospere by less than 1%.  Also, ~78% of the atmosphere is nitrogen.

Yes, increase in CO₂ concentration increases the rate of photosynthesis in plants. The rate of photosynthesis is linealy proportinal to CO₂ concentration in range up to 225ppm  and  slowly increases range 225-650ppm.[Limiting Factors in Photosynthesis, Plant Physiol. (1984) 75, 82-86] (Now CO2 concentration is about 400ppm).
You can read more in Educational article on Nature journal website or in
More scientific review on the topic.

Not generally true in nature.  The rate of photosynthesis is almost always limited by factors such as the availablility of sunlight, water, and soil nutrients.  It's only when all those other factors are in sufficient supply (which probably happens only in the lab) that CO2 concentration becomes a factor.  And since atmospheric CO2 hasn't been below 280 ppm for at least 10,000 years, rates below that level are hardly relevant to modern conditions.


text:
Why is it so important to avoid infection of lacerations to the scalp?
There is supposedly something unique with regards to infections of the scalp, although I cannot remember, perhaps it was to do with the CSF and its build up? I have scoured the internet for hours but have not found an answer.

Sounds more like a question for SE Medical Sciences or whatever it is called.

No, there is noting unique to scalp lacerations (I've repaired literally hundreds of them) except that they bleed a lot more than the usual laceration. Probably because of that, there's a very low rate of scalp laceration infection. CSF is inside the cranium, not in any contact with the scalp.

@anongoodnurse i have found an answer to this question. It is to do with deep lacerations of the scalp specifically though.

The deepest lacerations of the scalp go through the galea and exposes the skull. No lacerations of the skull make contact with the CSF.

Deep lacerations of the scalp that penetrate the fourth layer (area of loose connective tissue) have an increased risk of infection. This is because pus and blood spread easily within it. This can easily pass into the cranial cavity along the emissary veins Therefore, infection can spread from the scalp to the meninges and could lead to meningitis.

Sources for this?

This does not sound right to me. Deep lacerations - the deepest go through the galea - are far from uncommon, and while they are less common than the average skull laceration, I've seen and treated very many. I've never seen an infected scalp wound. Again, scalp wounds are less likely to get infected than other wounds due to very high vascularity. (https://www.ncbi.nlm.nih.gov/books/NBK541038/) While I think this answer is theoretically possible, I assume - as I have never seen it - that it is rare (not that I haven't seen rare things...)

Sorry for the very late reply, but this was answered by my anatomy professor on a worksheet we had to do. Now that you have mentioned the galea, I will email him to ask whether this was a more theoretical question simply for students to see conenction between scalp layers, or if it has clinical relevance, and I'll post an update soon.