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Will carpenter bee larvae die if trapped or find a way to bore out?
I had a carpenter bee problem last year, beginning with the awful sounds the larvae make! The exterminators couldn’t find the bore holes (they were/are inside a gap between top of the foundation and sub floor of what was once a garage).  I eventually hired a contractor, who removed the vinyl siding, and discovered a straight line drill hole up the plywood!  He replaced plywood and insulation, saw no other evidence (except two dead bees), and sealed up the gap. It’s now spring, and I am hearing them once again.  My fear is that there is a gallery in a floor joist. If there ARE larvae and they ARE there, will they eventually just emerge into that now sealed up gap and die, or bore their way through where it was sealed or, worse yet ~ my floor?  Thank you.


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Does mitochondrial eve have to exist?
Suppose we took all living humans and found the set of their mothers, mothers' mothers, etc. and then traced down as far as possible. Is there a logical reason that this tree has to converge to one 'mitochondrial eve'?

Yes; she wouldn't necessarily have to be of the same species, but "mitochondrial Eve" must exist. The proof is pretty simple if you assume no one has more than one mother and that some mothers share a mother (and some other reasonable biological assumptions like the finite number of offspring).
Consider all living maternal lineages at any slice of time. This would effectively be a slice of all mothers, let's call it Generation N. In turn, these mothers all have mothers. We can call this Generation N-1. Not all women who have children in this generation are included: N-1 only contains mothers of the Generation N mothers. Generation N-1 must then be smaller than Generation N, because no mother has more than one mother. In practice, it's likely much smaller, since any mother who has more than one daughter who herself becomes a mother reduces the total possible by 1 more. You can recursively go through maternal generations N-2, N-3, etc this way and will find that every successive generation gets smaller. Eventually it will converge to 1 person, and that's your "Eve".
You can think about it similarly in the opposite direction, and find that as you go forward, extant maternal lineages can disappear but once a lineage disappears it cannot come back.
See also the Galton-Watson process.
A lot of "mothers" the same age as mitochondrial Eve have descendants today (in fact, they are likely to be either ancestors of everyone or ancestors of no one), but those lineages did not pass maternally. See also https://en.wikipedia.org/wiki/Pedigree_collapse

well what if at some stage none of the mothers are sisters, for every generation until the beginning of life

This isn't so far fetched. What you're asking for N is that for all living people, in the set of all mothers there is at least some who are sisters. Then for N-1 you are asking for the set of all matrilineal grandmas there is at least some who are sisters, then the same for great great grandmas etc. Remember we are starting with 7.5 B mothers though.

what's to say that if we go all the way down, we don't find multiple sources for life

Brian. I’m sorry but you need to improve this answer, because I happen not to know about this and cannot understand your answer, despite a background education in molecular biology. If it is better answered by a text, close it as homework. Otherwise I need some sort of diagram and a comparison of alternatives (I presume the poster has an alternative in mind, but he does not state it clearly.)

@David I don't think any molecular biology is necessary here, just a recognition that each prior maternal generation must be smaller (or equal) in size. Of course molecular biology is useful in estimating just how long ago that common maternal ancestor would be, but that's not really what the question asked about.

@ggmate "what if at some stage none of the mothers are sisters, for every generation until the beginning of life" - there is no biological basis for this organization. It would require every mother to have at least one daughter, otherwise the population as a whole is still decreasing and so the number of unique maternal generations is decreasing. This can happen rarely, but there is no process to enforce it in every pairing across a population over history.

Hmm not sure I quite understand. If we take the set of all matrilineal great^n grandmas of living offspring. Why is it likely for a large number of them to be sisters?

@ggmate It's not just that a large number are likely to be sisters (though in practice they are, because not everyone lives long enough to have children and many live long enough to have multiple children), it's that the number of unique matrilineal lines with continuity to the future can only decrease as you go back in history, never increase.

But the only way they can decrease is by being sisters right?

@ggmate Yes, which you must see is quite common, right?

I can see it for early generations but it’s not so clear why for going back many many generations

@ggmate Does it help if you realize that the further back you go, the more childbearing women of that generation have no maternal lineage offspring in the future/present generation? There is nothing conceptually different about going back 1 generation and going back 100, except that you start with fewer and fewer "candidates" to be the mitochondrial Eve.

it's still  if you think of it from the perspective that you're telling me that out of 7.5 billion mothers, and maternal grandmothers, great grandmothers etc of living people. they all end up being sisters. Even if on average every mother has 2 sisters who is a mother, you have to divide by 3 = 2+1. but the average number of sisters who are grandmothers is lower, maybe 1.5. At every generation this probability gets smaller and smaller. until it gets close to 0, at which point there might be 10 000 offspring and very few being related no matter how far back you go

it's not trivial that the reducing power is non negligible, from a mathematical perspective. Unless you specify details about the type of growth that is occurring with humans?

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Methanol and brain damage -- special affinity for optic nerve or just really toxic?
Methanol is known for causing blindness. One explanation I have read is that the optic nerve is especially active and so methanol will be preferentially taken up by the cells there which then die.
But I assume methanol is also bad for neurons concerned with, for example, memory and cognition. But is this wrong? Could it be that methanol for some reason tends to cause temporary or permanent blindness but is no more toxic to other neurons than ethanol is?

Methanol toxicity is relatively rare and comparatively little is known about its etiology. I found a correspondence published in the journal Nature in 2004, it seems to a good review of the literature, given that I could not find a recent review on the topic. Please take a look, especially at the sources that the following paragraph cites:

Methanol is particularly toxic to the optic nerve, leading to acute
blindness. Based on a histopathological study, the retrolaminar optic
nerve myelin sheath seems to be selectively vulnerable to methanol
poisoning due to its anatomical structure. In the acute phase, the
hyperaemia and swelling of the optic disc has a papilloedema-like
appearance. The axoplasmic flow stasis at the nerve head and
alteration of the myelin sheath in the retrolaminar nerve segment were
demonstrated in experiments using rhesus monkeys. The pathogenesis is
presumed to be histotoxic anoxia in a vascular watershed area, which
is the result of direct inhibition of cytochrome oxidase by formic
acid. Additionally, the increasing pressure following oedema in the
visual pathway might further aggravate the deterioration due to
ischaemic changes. Therefore, effective methods to treat the oedema
might be important, such as the use of intravenous steroids and
diuretics. The mechanism of subsequent optic atrophy in patients with
methanol poisoning is still unknown, it was suggested to be due to
progressive demyelination. The distinct glaucomatous-like cupping of
the optic disc suggests extensive loss of retina ganglion cells, which
has been thought to result from retrograde degeneration of optic nerve
axons.

It seems that in our best understanding, the optic-specificity of the action of methanol seems to be due to the nature of the myelin sheath that insulates the optic nerve.

Thanks, interesting. But methanol I would guess is still not good for the brain overall, perhaps the same or perhaps worse than grain alcohol for areas concerned with memory, etc.

What makes you think it only affects the eyes? Paraphrasing Wikipedia, upon ingestion, symptoms include decreased levels of consciousness, impaired (or loss of) coordination, vomiting, abdominal pain, smelly breath, kidney failure, and (alas!) blindness or vision loss. That doesn't sound to me like it only affects the retina.

@S Pr: I did not say only eyes but basically I am trying to understand two things: why it seems to be especially bad for the optic nerve and whether it is more toxic in general than ethanol.

@releseabe Methanol is at least an order of magnitude more toxic than ethanol. The treatment for methanol toxicity used to be IV ethanol in an attempt to displace the methanol. I know of no cases of blindness following profound intoxication; death occurs before anyone reports blindness.

@anongoodnurse: Never heard of intravenous ethanol as treatment, very interesting.

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Is it possible to use PCR to test for Machado-Joseph disease?
Machado–Joseph disease (MJD) is a rare inherited neuromuscular disease that is caused by a mutation in the gene ATXN3. The protein encoded by this gene contains "CAG" repeats in the coding region, and the expansion of these repeats from the normal 12-44 to 52-86 is the most common cause of the disease.
It is well known that amplification of repetitive DNA by PCR is prone to errors, mainly caused by misalignment/slippage of the polymerase during the elongation phase.
Does anyone know if there exists a specialized PCR protocol or polymerase that could accurately amplify the repetitive region of ATXN3 such that one could then use gel electrophoresis or Sanger sequencing to approximate the number of CAG repeats?

This paper describes an allele-specific PCR protocol to detect CAG repeat expansion in MJD patients:
Maciel P, Costa MDC, Ferro A, et al. Improvement in the Molecular Diagnosis of Machado-Joseph Disease. Arch Neurol. 2001;58(11):1821–1827.


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Can the metatranscriptomics replace the approach of functional metatranscriptomics/functional metagenomics?
While metatranscriptomics reveals information about the expression of genes and their functions too, Functional metatranscriptomics (https://www.nature.com/articles/ismej201167) allows the characterization of genes expressed by different eukaryotic microorganisms. My question is can we use both of those techniques? I couldn't find out if they will bring the same results or each one of them will give its own.

Hi Noor, and welcome to Biology.SE.  I'm assuming functional metatranscriptomics involves isolation of RNA, reverse transcription, and then cloning of cDNAs into a model organism?  Your question would be better received if you provided links to studies that exemplify the methods you're comparing. Perhaps this and this?

Yes, perfect example, I wonder can metatranscriptomics, just the total RNA-sequencing replace that approach?

I would consider these to be complementary approaches. They don't really provide the same information, or even the same kind of information.
A big challenge with sequence-based genomics and transcriptomics is that they rely on sequence homology for functional annotations. In other words, they only provide indirect information about gene function, which can be incorrect or, in many cases, completely absent (this is why you often see annotations like "hypothetical protein xxx" in genomics papers). So what can happen is, you may identify a great number of genes with no functional annotation, so you have no basis for determining what they are doing, or worse, they are incorrectly annotated and you publish misleading reports. This is especially challenging in complex and diverse environments like soil.
The advantage of the functional approach is that you don't have to rely on sequence homology for functional annotation, since you're characterizing the phenotype directly. The disadvantage is that you can only fined the specific functions you are looking for. To bring it back the example you linked, if you're only screening for dipeptide transporters, you would not be able identify anything that doesn't directly influence that phenotype.
So, it really depends on what information your are after in your study. If you wanted to completely replace the functional genomics approach with sequencing approaches, it would only work if your genes of interest already have reliable functional annotations and if your sequencing depth is sufficient to identify them. That said, sequences from a functional study like the one you shared could be used to inform your sequencing approach, or to mine existing metagenomic or metatranscriptomic datasets for genes with share homology. Heck, if you only have a few target genes and they have some well conserved regions, you could probably come up with an acceptable RT-PCR approach too.

Here is my understanding of the terms you present.
Metatranscriptomics refers to RNA-seq of a mixed microbial community or environmental sample. This is a general approach to characterize the gene expression of all organisms in a sample, and will rely on alignment of transcripts to existing genomes or metagenomes for which genes have been called and annotated.
Functional metatranscriptomics refers to the process of isolating RNA, reverse transcribing the RNA to make a cDNA library, and cloning that library into a model host to assess cDNA-encoded functions. This is a method that allows for identification of transcripts that encode a specific function in cases where the organism(s) that produced those transcripts are not genetically tractable. In the ISME paper you link, cDNAs were cloned into a yeast strain lacking dipeptide transporters in order to look for environmental genes that complement the knocked-out functions.

My question is can we use both of those techniques?

These are two techniques that differ in the type and scope of data produced, and their utility in application will depend on the scientific questions you want to answer.


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Can anyone tell me what species this baby bird this is?
Can anyone tell me what species this baby bird this is? He or she is less than two weeks old. Fell out of nest. He is doing well. I live in Sacramento Ca, Thank you.

Looks like possibly a baby starling to me

whatever it is, it probably needs feeding in the same instructions as a baby blackbird or a starling, i.e. every few hours, hard work.


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Beetle (?) on Acacia (Senegalia) greggii?
I was working on my botany skills and took a photo of Acacia (Senegalia) greggii.  When I reviewed the photos, I saw a beetle (I think it's a bettle) that I had not noticed in the field.  I'd say its body is about 2 cm long.  This plant was growing in a dry wash in Phoenix Arizona USA, and the flowers on the plant were just maturing.  Observed around 9 am and the temperature was about 75-80 F. What species is this insect?

Looks to me like the Longhorn beetle (Schizax senex), possibly a female, but it is hard to judge the length of the antennae. This beetle has long antennae (hence the longhorn name), with the male having antennae that are nearly twice as long as the female. S. senex is the only species of the genus.
They are hirsute with a pale margin to the wing cases. The species was described in 1873 by LeConte, with the description being rather wonderful (in my opinion):

Niger opacicus, pube breve minus subtili cinerea vestitus, prothorace fortus, elytrus subtilius punctatus, his marginae suturali laterali apicali et scutello fulvo-pubescentibus

My very rough translation - better Latin scholars please fix:

Black opaque, hair short with subtle grey arrangement, prothorax strong, wing cases with subtle dots, and the join margins and edges pointed and scutes fawn-coloured and very hairy.

Note that I found this with a very quick google of "beetles arizona" and scanning through the linked arizonensis beetles page, which was at the top of the links provided by google. I am not from the USA or in the USA, so please anyone with a better identification, feel free to chime in.

Looks like a very good match, thanks!


text:
What is this bug living on the plaster in my home?
It's a small larva looking creature that pops out of a volcanoe-esque hole in the bathroom. SE United States.

Sort of looks like a barnacle... but could be the start of a wasp nest if it is on a ceiling. Can you comment on whether it is submerged in water or what sort of surface it is adhered to?

It's on typical drywall on the wall in my home.

Opening is about a mm big.

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Direction of translation/transcription
Perhaps it would not be wrong to say that "translation/transcription goes in the direction of 3' to 5'" or "in the direction of 5' to 3'";that's because these statements are ambiguous, not specifying "XX's".
However, I am confused.
So I would like to clarify by clarifying the "XX's".
My Question;

Are the following understanding correct?

(1) Transcription;
In the case of transcription, the RNA polymerase moves in the 3'→5' direction of the template strand of genome DNA, and the ribonucleotide attaches to the 3' side of the mRNA during synthesis, am I right?
(2) Translation;
In the case of translation, the ribosome moves (relatively) in the 5'→3' direction of the mRNA, and the amino acids are attached to the C-terminal side of the polypeptide, am I right?
(3) Overall;
The genetic code is "the sequence of the complementary strand of genomic DNA read in the 5'→3' direction, with T replaced by U". For example, if the sequence of the complementary strand of the genomic DNA is "5'-ATGTTT...termination codon-3'", the corresponding sequence of the mRNA is "5'-AUGUUU...termination codon-3'", which is "N-terminal - methionine - phenylalanine ...C-terminal" sequence.

The genetic code is a cypher: ATG=Met, UUU=Phe etc and nothing else. See the Wikipedia entry. I am sure the direction of transcription and translation are illustrated in the answers to other questions on this site. Please check. If not try Wikipedia or Berg online at NCBI bookshelf. Happy reading!

AUG, to be consistent  with UUU. The genetic code is a table of mRNA codon / amino acid equivalents, so U. However because one is usually doing conceptual translations of DNA in genomic sequences then one talks about ATG and TTT.

What I want to focus on is the direction of enzymes and synthesis.


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Why is decomposition process much slower for poisoned insects?
I have always noticed that the pest roaches killed by roach spray start to break down much more slowly than a roach that was stomped or attack by a lizard. In those cases the roach's body attracts ants within an hour or two, and they leave the wings and antennas after a couple of hours or so.
But when I kill a roach with spray, there's no ants or flies. The antennas break after 24 hours but the body stays intact for at least a week, provided that the roach is kept in a clean and dry place but has access to air.
So, if there's no maggots or attracted insects because of the poison, the only decomposition happening is from the bacteria/protozoa inside the roach's body? And the cellular death? Absolutely nothing intruding from the outside?

You're wondering why if you kill an insect with an insecticide spray, why other insects don't attack the body for food?

@mgkrebbs No. I was wondering what's happening inside the body and in microscopic level because in non-poisonous cases ants or maggots do the job quickly in front of our eyes. Also, most poisoned roaches go to dustbin before I can get my hands on them, but right now I have a specimen lying on my floor for 7 days straight, visibly unaffected from outside.

Features of a rotting insect carcass
What you see after an insect dies is its chitinous exoskeleton. It is a tough biomaterial that takes time to decompose, given its structure, and few microbes can digest it, let alone as quickly as soft tissue. It's a little bit like human bones. The insect's inner soft parts will degrade quickly, just as with any dead, soft tissue. However, what remains looks intact, because the outer cuticle is resistant to deformation; it keeps its shape!
Exoskeleton decomposition by insects
Ants are known to, and can and will break exoskeletons into pieces and carry it away in parts. They are ubiquitous and exist everywhere, so it's no surprise you see them doing this job all over the place. Flies and worms and mites may also feed on the softer parts and on the yeast or microbes that flourish in the decomposing tissue. It is also possible that some insects lay their eggs into the carcass, which would in some cases be a rich source of nutrition for the young insects, when they are in their larval stages (what you may confuse for worms).
Poison deters exoskeleton decomposition by other insects
If you introduce poison into the mix, obviously the roach carcass with be contaminated and its exoskeleton will remain relatively less likely to be touched by other insects, since it remains noxious to them. The effect on micro-organisms would be less pronounced, but that depends entirely on the contents, concentration, volatility and weatherablity of the insecticide that was used.


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

The variant which caused the Spanish flu is still circulating today.

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

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

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

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

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

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

Lovely answer, but what is the "Pest"? Did you possibly mean Yersinia pestis (the Black Death aka. the Plague and apparently also as the Pestilence)?

@tyersome Yes, you are right. I edited my answer.

Great answer. I'd add that we can't definitively identify many historical illnesses, even those in well recorded history because medicine, diagnostics and even language has changed, so things that were recorded as an illness a few hundred years ago might have been ascribed to "humors", but we now know as a virus. There's also different diseases being lumped together into one name or vice versa. Also, there are lots of unknowns - what caused "dancing mania"? Could it have been an illness?

The 1890 "Russian Flu" pandemic is now believed to have been caused by one of the common cold Coronaviruses, HCoV-OC43. At the time of historical pandemics, there was no way to identify the infectious agent, though. So connecting the pandemic to the virus is based on descriptions of symptoms, and patterns of which demographic groups were most affected; as well as genetic analysis to estimate when the virus jumped from animals to humans.

Accounting for expected mutation rates and working backwards, they calculated that the jump into humans occurred around 1890.

That date isn't the only thing linking OC43 with Russian flu. Many patients of that pandemic had pronounced symptoms affecting their central nervous system. Today, although mostly associated with mild colds, OC43 is also known to infect nervous tissue.

It's likely that all of the common cold Coronaviruses caused pandemics when they first started infecting humans. For the others, that happened much longer ago than OC43, so the historical record is less detailed, and there is more uncertainty in the genetic analysis.
In fact, it's possible that many or even all of the viruses that currently circulate among humans without problems were much less benign when they first emerged.
Another example is the outbreak of severe symptoms from Zika infections in the Americas when the virus arrived there, after circulating in humans for (at least) decades in Africa with only mild symptoms:

In the outbreaks reported up to 2013, most of the infected patients were asymptomatic and only 20% of them had mild symptoms such as fever, arthralgia, maculopapular rash, and conjunctivitis.

So it's suspected that many "harmless" viruses were worse when they first emerged into humans, but with the tools that are currently available, there is no way to establish definitively whether any particular virus caused major pathogenic outbreaks in the past.


text:
Why do OX5034 GM mosquitos require the presence of tetracycline to survive? What does the drug do in this case?
I'm confused. Debug Fresno; why are the released mosquitos said to be sterile? from 2017 addresses male mosquitos released with a bacteria that will affect fertility of females after mating. They are not genetically modified.
CNN's 2021 article First-ever US release of genetically modified mosquitoes begins in Florida Keys describes release of Oxitec's OX5034 GM mosquito Aedes aegypti. Curiously, these can be kept viable for reproduction when maintained in an environment that includes tetracyline, an antibiotic.
Question: Without the bacterial infection, is it just a coincidence that the GM strain needs an antibiotic to survive? What does the tetracycline do in this case? Why was this drug chosen?
Potentially helpful resources:

https://www.oxitec.com/en/our-technology
https://endmalaria.org/sites/default/files/Enca%20Martin-Rendon.pdf

I think that those mosquitos predated this particular lethality mutation.  So it's what they had on hand to work with. That just so happens to be a means to control the population of all of their mosquitoes.

A good explanation can be found at http://hackaday.com/2021/05/03/genetically-modified-mosquitos-biohacking-for-disease-prevention/

The other answers are correct and on the right track, but I will expand on them with the specific mechanism for these mosquitos. The following paper discusses the engineering behind strain OX513A upon which the OX5034 strain is based:
Phuc HK et al. 2007. Late-acting dominant lethal genetic systems and mosquito control. BMC Biol 5:11
Oxitec mosquitos carry a transgenic construct containing two genes. One encodes for a fluorescent marker, DsRed2, for identifying genetically modified mosquitos and the other encodes a protein called tTAV:

The tTAV gene is under the control of a minimal hsp70 promoter flanked immediately upstream by a tetO site. The tTAV protein is a transcriptional activator that binds tetO and enhances expression. What that means in this construct is that expression of the tTAV gene creates more tTAV protein which binds to tetO which leads to more tTAV expression, etc. This is the positive feedback mechanism mentioned in the above image. Importantly, however, the tTAV protein can bind tetracycline and, when complexed, can no longer bind tetO and therefore cannot drive its own expression. In other words, in the presence of tetracycline, there will be minimal tTAV expression.
tTAV overexpression is lethal during development. Although the exact mechanism of lethality isn’t entirely clear, there are some leading hypotheses:
Knudsen KE et al. 2020. Genetic Variation and Potential for Resistance Development to the tTA Overexpression Lethal System in Insects. G3 10(4): 1271–1281

tTA overexpression is thought to cause lethality due to “transcriptional squelching,” that is a general interference in gene expression (Gong et al. 2005). Consistent with this hypothesis, some genes identified by the GWAS were involved in gene silencing (Su(var)2-HP2) (Shaffer et al. 2002; Shaffer et al. 2006), chromatin binding (mamo) (Hira et al. 2013), chromatin remodeling (Hira) (Loppin et al. 2000) and alternative splicing (bru1)(Spletter et al. 2015), which could all influence the level of tTA expression. Other candidate genes were involved in defense response (PGRP-LC, Lmpt)(Jin et al. 2008), the septate junction (cora) (Tepass et al. 2001) and apoptosis (out) (Coffman 2003); all of which are systems that could potentially impact survival. Four genes; eff, tey, CG32085 and CG13085, encode proteins that are predicted to participate in protein ubiquitination and degradation (Thurmond et al. 2018; Gramates et al. 2017). For example, the Eff protein is a E2 ubiquitin-conjugating enzyme (Chen et al. 2009). It has been suggested that overexpression of the tTA protein could cause lethality due to interference with ubiquitin-dependent proteolysis (Gong et al. 2005) as ubiquitination of VP16 is required for activity and also signals destruction (Salghetti et al. 2001).

To summarize, tTAV is a transcriptional activator and, in Oxitec mosquitos, it regulates its own expression in a positive feedback loop: tTAV protein binding to its response element tetO leads to more tTAV gene expression which leads to more tTAV protein. This overexpression of tTAV is lethal during development. However, tTAV can also bind tetracycline and, when it does, it can no longer bind tetO. In the presence of tetracycline, there is no positive feedback loop and and only basal, non-lethal amounts of tTAV are expressed.

Image from the Oxitec website.

yikes! Thank you for this profoundly specific and thorough answer! :-)

@uhoh You’re welcome!

Very nice answer!

@tyersome Thanks!

They don't go into any detail on the sites you link to and I don't have time to look into patents, but from the context it sounds like they may be using a tetracycline repressible promoter. This is often referred to as a Tet-Off promoter.
The core elements of these promoters were discovered in the bacterium Escherichia coli1 and several variations have been developed. These types of promoters work in organisms from bacteria to yeast to mammals1-3.
References
1: Gossen, M., & Bujard, H. (1992). Tight control of gene expression in mammalian cells by tetracycline-responsive promoters. Proceedings of the National Academy of Sciences, 89(12), 5547-5551.
2: Baron, U., & Bujard, H. (2000). Tet repressor-based system for regulated gene expression in eukaryotic cells: principles and advances. Methods in enzymology, 327, 401-421.
3: Orth, P., Schnappinger, D., Hillen, W., Saenger, W., & Hinrichs, W. (2000). Structural basis of gene regulation by the tetracycline inducible Tet repressor–operator system. Nature structural biology, 7(3), 215-219.

Yes this certainly sounds likely, thanks!


text:
Is sonic hedgehog a gene or a protein or both?
Is sonic hedgehog a gene or a protein or both?
I think sonic hedgehog is okay as a name for a chemical.
Having said that, I am a little bit concerned about the way sonic hedgehog seems to mean the protein and the gene that codes for it, which is likely to cause confusion.
"Sonic hedgehog is a protein encoded for by the SHH gene." says en.wikipedia.org/wiki/… which later says: "Two of these genes—i.e., desert hedgehog and Indian hedgehog—were named for species of hedgehogs, while sonic hedgehog was named after Sonic the Hedgehog, the protagonist character of the eponymous video game franchise. The gene was named as such by Robert Riddle, who was a postdoctoral fellow at the Tabin Lab, after his wife Betsy Wilder came home with a gaming magazine containing an advert for the Sonic the Hedgehog video game"
The New York Times: "A Gene Named Sonic". The New York Times. 1994-01-11.

SHH gene stands for Sonic Hedgehog Signaling Molecule. This gene "codes" for the protein Sonic hedgehog protein. Normally genes and the proteins they code for have similar names. It can be confusing if you only use the abbreviation.
https://www.genecards.org/cgi-bin/carddisp.pl?gene=SHH#:~:text=SHH%20(Sonic%20Hedgehog%20Signaling%20Molecule,Solitary%20Median%20Maxillary%20Central%20Incisor.
BTW: I am unsure why people downvote your question. It's totally valid. Don't get demotivated because some people think they are too smart.

Your confusion is warranted! The formatting rules for gene and protein nomenclature differ between model organisms. Even within a species, naming conventions may be inconsistently applied across the literature.
In Homo sapiens, the sonic hedgehog gene SHH (note italicization) encodes the sonic hedgehog protein SHH (or Shh protein, as on Uniprot). Human gene nomenclature is standardized by the HGNC.
As in humans, Drosophila gene and protein names are distinguished by different italicization; per FlyBase:

Protein product names and symbols should not be italicized in printed text. Where feasible, proteins that are named for the gene should be further distinguished by capitalizing the initial letter of the gene symbol or name. For example, the protein product(s) of the hh (hedgehog) gene could be correctly denoted as Hh or Hedgehog; the protein product(s) of the RpL38 (Ribosomal protein L38) gene could be correctly denoted as RpL38 or Ribosomal protein L38; and the the protein product(s) of the AGO1 (Argonaute-1) gene could be correctly denoted as AGO1 or Argonaute-1.

I’m partial to the naming conventions in Saccharomyces, where gene encodes PROTEIN (e.g. mpk1 and MPK1).
For both eukaryotic and prokaryotic microorganisms, the ASM Molecular and Cellular Biology submission guide for authors is a good resource for genetic nomenclature conventions.

Thanks for saying my confusion is warranted. But your answer doesn't mention 'sonic hedgehog'.

I've updated my answer to clarify that the human sonic hedgehog gene symbol is SHH, and the human sonic hedgehog protein symbol is SHH. Indeed, both the gene and the protein are named "sonic hedgehog".

So a hedgehog is a gene and a Hedgehog is a protein?

The first line on Wikipedia states "Sonic hedgehog is a protein encoded for by the SHH gene." Which part of it do you have trouble with? I'm genuinely curious.

@SPr The trouble is that this is only one opinion, that is contradicted by the NYT. Also, why is it 'hedgehog' and not 'Hedgehog' as stated by FlyBase?


text:
To which ungulate species does this tooth remainder belong?
Found on the beach in Çanakkale, Turkey.

I have found a lot of these, but this is the first one that has parts like long teeth. My other findings have sometimes 4, sometimes 6 tubes. Very solid, stone-like objects. Is this from a marine animal or is it a non-living formation, I wonder.
Below image is for scale in centimeters.

View from top and bottom

Other similar findings without teeth-like parts

Additional images:

Thanks. As I thought from just the side photo in your original post, it looks like a molar of some ungulate. I don't know anything definitive but I'll try to look into it a bit more for you. (you will find other similar photos on our site -- so do a search if you haven't already)

Thank you. Interesting, I always find these things on the beach. I did not figure out the reason. I'm waiting for your further explanations.

Whales, dolphins, seals, etc. are marine ungulates. When they die, they are fed upon and what's not edible/eaten/disintegrated sometimes makes it to shore. Your specimens are lovely. The best I ever found was a seal molar. One.

I have 30 - 40 items like these, but I am still not sure that there is marine remnants in them. I checked seal and dolphin molar after your comment, but they are very different than mine. You are lucky.

@anongoodnurse right you are about the marine ungulates. However, just cetaceans (e.g., whales and dolphins) are of the Ungulata clade. Seals are order Carnivora and are not considered part of Ungulata. However, all ungulates and the extant members of Carnivora are lumped together in the larger Ferungulata clade.

@turin I'm in the throes of final exam season at my university with much grading to do -- I'm unlikely to explore this topic further for the time being. I hope someone else can help you narrow further!

@theforestecologist no problem. Good luck with your exams.

Its definitely not a marine mammal, just based on size and general configuration.
those convoluted ever growing teeth are pretty diagnostic of non-cetacean ungulates.
Just based on the pattern I would say bovidae, but that does not narrow it down much in turkey, the H shaped central portion is fairly diagnostic of bovidae. However you have several antelope species not to mention domesticated animals that each would fit that category.
I suggest changing the title to ask for ungulate tooth identification. You need someone specialized in mammalian teeth to narrow it down to species. if you can add more shots of the tooth crown (the complex ends like those below) that is the part most useful for identification. See the examples below. The more you have the better.

Source

Thank you @John. I will change the title as you suggested and add more tooth crown images.

I have added new images. Just for your information.

Sheep or goats teeth.
As it was found at the edge of water and may be from drowning, I would predict that it is much more likely to be from a sheep, as goats are so very much safer around water.

Image from:
"Enamel hypoplasia in molars of sheep and goats, and its relationship to the pattern of tooth crown growth"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403278/
But really I know because I was a farmboy.

A pic from the top is better than one from the side, a side shot is not very diagnostic in mammals.

I think he's basically right, because: which animal has been cooked in 20,000 BBQ's over the years on beaches in Turkey? sheep an goats. statistically, its 20 times more likely to be a sheep than another common ungulid because of the meshoui type tradition.


text:
Is there any data on Neanderthal admixture in Western European Hunter Gatherers?
If there is any data, was the rate of admixture higher than today? Like WEHG brought the component in? Or was the amount maybe lower, like other groups like Early European Farmers or Yamnaya brought the admixture? Or was it evenly distributed?

tldr; Neanderthal ancestry is roughly equally the same between the groups you mentioned.
It's almost certain that the major pulse of Neanderthal admixture into non-Africans occurred very soon after the primary out of Africa event (here I am referring to the out of Africa migration which contributed towards most of the ancestry of all non-Africans today - of course there were other out of Africa migrations which were effective dead ends).
This is well established from a) looking at the size distribution of Neanderthal fragments in the human genome (ref, ref) and b) the fact admixture occurred around 232–430 generations before the 45kya year old UstIshim individual was alive. So most lines of evidence suggest this admixture took place between 50-60kya.
This is much earlier than the diversification of West Eurasian populations into groups like Yamnaya, Anatolian farmers and Western Hunter Gatherers. Therefore, there is no reason to expect any one of these ancestral groups would have had higher amounts of Neanderthal ancestry than any others, since the admixture event occurred into the common ancestor of all these populations.
Indeed, from Haak 2014:

The ancient individuals had indistinguishable levels of Neanderthal
ancestry when compared to each other (∼2%) and to present-day
Eurasians (Supplementary Information section 6)

There are some ancient individuals such as Oase1 who carried substantially more Neanderthal ancestry than modern day samples (in fact this individual has very recent Neanderthal relative), but that they didn't contribute anything towards the ancestry of later groups.
Btw I know a lot of these reference are old - I will add some more recent estimates later, but they don't change the overall picture.


text:
Sex of fern gametophytes
The following image is from Campbell Biology, 12th edition

It says, "Each gametophyte develops sperm-producing organs called antheridia and egg-producing organs called archegonia". This seems to suggest gametophytes are either always hermaphrodites or most of the times hermaphrodites.
I have done a little bit of searching and now am convinced that they are not always hermaphrodites.

"Most ferns, on the other hand, are homosporous; they produce a single
type of spore. After germination, each fern spore has the potential to
develop into a male, female, or hermaphrodite gametophyte."

https://science.sciencemag.org/content/346/6208/423.summary#:~:text=Most%20ferns%2C%20on%20the%20other,%2C%20female%2C%20or%20hermaphrodite%20gametophyte.
Are they most of the time hermaphrodites? How common are unisexual gametophytes?

Your image has text (top) that reads "most fern species produce a single type of spore that develops into a bisexual photosynthetic gametophyte." So right in that source, you know already that no one is claiming that they are always bisexual (by which they seem to mean hermaphrodites), and a statement that they are both hermaphrodites. I do not see any conflict between the textbook and the quote, and the textbook at least seems to think that they are mostly hermaphrodites. Generally, making  statements with the word "always" is a bad idea in biology.

@MaximilianPress There is a contradiction.
a) Most fern species are hermaphrodite
b) Most fern species have the potential to become  a male, female or a hermaphrodite.
a) and b) are potentially contradictory.
My question was about the ratio. what is Male:Female:Hermaphrodite gametophytes? The answer will depend of the species ofcourse. So can be a complicated. But It can be easy too, for example Overwhelming majorities of gametophytes may be hermaphrodite

I do not see that your statements (a) and (b) are contradictory. Obviously the implication is that unisexual gametophytes are relatively rare, as you suggest. I am not a fern biologist so I don't know about relative proportions, but measurements of these proportions have been done in at least some species, e.g. https://www.jstor.org/stable/23728097?seq=1, which do show slight majorities of bisexual gametophytes in the lab and in the field.


text:
Do some vascular tissue cells have chloroplast?
Vascular tissue includes xylem, phloem, parenchyma, and cambium cells. Does photosynthesis occur in some vascular tissue cells? Do some of them have chloroplast?
Vascular tissues are made up of xylem and phloem, each of which are complex tissues (having more than one cell type). So some of their parenchyma cells may have chloroplasts.
The bundle-sheath cells are the photosynthetic cells arranged into a tightly packed sheath around the vein of a leaf. It forms a protective covering on leaf vein, and consist of one or more cell layers, usually parenchyma.
I am not sure whether these two "parenchyma"s are the same or not.
Are the bundle sheath cells vascular tissue cells?

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

@MattDMo ok, I added something :)


text:
What is this tiny bug
I have seen these on my floor several times now that spring has arrived and temps have started to go up. It is silvery in color, appears to have a hard and segmented shell, it kind of reminds me of a lobster. They are very small, the dark line in the picture is the grout between two tiles on my floor for scale. I am guessing it is about three quarters of a centimeter in length. I am in Utah.

This is a silverfish (Leipisma genus, the most common being Leipisma saccharinum). They are extremely common pests world-wide, eating a range of plant-based materials, particularly those made of cellulose - such as any pieces of paper you have lying around - books, book bindings/glues and cardboard. They will also eat things like cotton, silk, crumbs, dead insects (including other silverfish) and lots of other things too.
Unfortunately if you have seen one, you have many more around. Call a pest-control expert.

Well, I mean, maybe it depends on the climate or something (I'm in the UK) but we've been finding silverfish in our house occasionally for years and there's never been any problem.  Never observed any sign of books being nibbled or anything.


text:
What kind of animals are these little creatures?
I have 3 tanks. 1 with my fishes and 2 other are technical.
The smallest one is 0.5l and I'm using it as trash bin where I put dead plants and algae from main aquarium and it has sand from the see at the bottom. For more than 5 monthes it was full of algae and no alive creatures. Now it has many live black dots that are very fast moving and now the tank is very clean.
Second technical was planned to used for daphnia (didn't get it yet). It has 5l volume now. In the bottom it has simple ground and rasied Glossotigma eletinoides from the seeds. Also it has many algae (including Spirogyra).
Two tanks are closed tightly.
I have a some questions about it:

What kind of animals are these?
Can I move black dots to the other tank to have it clean from algae?
Are these creatures safe for me?
Are these creatures safe for my fishes?

I recorded video, it has 3 parts (1 tank, 1 tank in zoom, 2 tank in zoom):
https://youtu.be/3jbqPiAcKOc

Update:

Tank 1. This animal is hard to catch

Tank 2. In water I see only one type and on the stick I got 2 different animals. The left one looks like one of the species of daphnia.

Update 2:
I think I found what I have in the tank 1. It is some sort of Ostracod (seed shrimp), because I saw whiskers and slit in the shell

Welcome. It's best practice to include (an) inline pictures of the critter at hand. External links are discouraged and I am personally quite hesitant to click on them (spam, phishing etc)

Welcome to Bio.SE! Two recommendations to ensure a better response (to follow up form the previous comment): 1. Use a site like ezgif.com to convert a few seconds of your video to a gif to include the gif as an inline photo in this post. 2) Is there any way to get more magnified images? -- the resolution on these videos make an accurate ID tenuous at best.

Looks like in the first picture it could be Pleidae or some Helotrephidae, or not?)

Also I dropped fruit twig inside 1st tank and these creatures occupied it fully.

Yep, these are definitely ostracods. Some are predators, but their small size and preference for that plant stalk suggests that they are detritivores. In that case adding them to your fish tank will be beneficial, as they will clean the water by feeding on suspended particles, and serve as a source of food for smaller fish and animals, much like copepods or daphnia would.


text:
What is the role of a chemotroph in an ecosystem?
Chemotrophs are bacteria that synthesize ATP based on favorable REDOX reactions. This solves the problem as to how they can survive. But what exactly is their function in an ecosystem? For example, can they provide nutrients for algae?
I want to know if we can cultivate chemotrophic bacteria to provide nutrients for plants. This way, we could grow them in a place like Mars where the soil is made of a lot of inorganic material. I was especially interested in algae because some species can provide a lot of nutrients humans need.

The problem is that just any old inorganic material won't work.  You need materials such that the chemotrophs can cause them to undergo an exothermic reaction and harvest the energy from the reaction to support their life processes.  In a sense, they're not that much different from animals: it's just that the food they eat doesn't come from plants via photosynthesis.

Chemotrophs are usually found in extreme environments where they can be the source of all energy for the ecosystem also called the primary producers. Deep-sea hydrothermal vents are a great example of a chemotroph primary producer and support the growth of large eukaryotes like the tubeworms (Below). The chemotrophs supporting life at the vents can oxidize Sulfur to create ATP.

But chemotrophs don't just have an impact on these small ecosystems, they are actually responsible for earth-scale geochemistry affecting all life. (Cool paper on that here). The reason why chemotrophic bacteria are usually not found in "normal" environments with algae is simply competition. A heterotroph using hydrocarbons will occupy a niche faster and more efficiently than any chemotrophic bacteria.
You are definitely right on the Mars soil question, where chemotrophic bacteria could be used to fix carbon or nitrogen and solubilize nutrients for future plants on mars. But maybe some cool chemotrophs are already living there!

Just to shore up this vocab a bit, all organisms that rely on chemical energy (as opposed to photonic energy) are chemotrophs. This includes essentially all non-photosynthetic organisms, not just extremophiles. Chemoautotrophs can use carbon dioxide as their only carbon source and are rightly considered primary producers, but they aren't really limited to extreme environments either. Most are oxidizers of reduced inorganic compounds like ammonia, dihydrogen, and various compounds of iron and/or sulfur (also making them lithotrophs, as opposed to organotrophs).


text:
Is the kinase domain of a protein kinase the same as the catalytic domain?
I am learning about protein kinases and I have read that the protein kinase domain is a structurally conserved protein domain containing the catalytic function of protein kinases. I am wondering whether the kinase domain is equivalent to the catalytic domain (the domain that contains the active site) of an enzyme? Any insights are appreciated.

What is a catalytic domain?
Catalysis is the acceleration of a rate of a chemical reaction.
The catalyst is the molecule responsible for catalysis.
A catalytic site is the exact place or region on the catalyst (e.g. enzyme or compound) that is resonsible for catalysis. These are the active sites on enzymes, for example.
A domain is a part of a protein - it may include a site, or it can also refer to the site itself, depending on the context. One can say catalytic domain to mean the exact part of the enzyme that performs the catalysis.
What is a kinase?
Kinases are enzymes that catalyze the transfer of a phosphate group. It's a specific biochemical reaction. In other words, they phosphorylate other molecules with the help of phosphate donor molecules (such as ATP). One part of the kinase is responsible for the catalysis of its phosphorylation reaction, and this part is called the kinase domain. It is, of course, a catalytic domain. More precisely, it is designated a kinase domain.

So, as you can see, now you should understand the following statements:

All kinase domains are catalytic domains. (Kinase enzymes catalyze phosphorylation!)
Not all catalytic domains are kinase domains. (Phosphorylation is not the only kind of catalysis!)


text:
Inheritance simulator not working properly
I created a python program to simulate inheritance (a simplified version of it) to better understand how it works. A person is represented by a class that contains a chromosome property, a method for reproducing with another person, a method for generating gametes (through recombination), and a method for calculating how similar a person is to another person (by comparing the chromosomes).
The problem with my program is that cousins are not as similar to each other as they are supposed to be. My program says that 2 cousins about 75% similar when they should be 12.5% similar. I don't understand why this is. I think it could be down to 2 things

My similarity function is wrong.
The way I am representing a chromosome is wrong.

Here is the code:
    import random

    CHROMOSONE_LENGTH = 1000
    NCHROMOSONES = 22

    class Person:
        def __init__(self, chromosones = None):
            self.chromosones = chromosones
            if  chromosones is None:
                self.chromosones = []
                for i in range(NCHROMOSONES):
                    self.chromosones.append ((self.get_random_dna(),self.get_random_dna()))

        def get_random_dna(self):
            #return [random.random() for x in range(CHROMOSONE_LENGTH)]
            return [random.choice(["0","1"]) for x in range(CHROMOSONE_LENGTH)]

        def get_gamete_meiosis(self):
            gamete = []
            for i in range(len(self.chromosones)):
                gamete.append([])
                for a,b in zip(self.chromosones[i][0],self.chromosones[i][1]):
                    gamete[i].append(random.choice([a,b]))
            return gamete

        def reproduce(self,mate):
            chromosones = []
            my_gamete = self.get_gamete_meiosis()
            mate_gamete = mate.get_gamete_meiosis()
            for i in range(NCHROMOSONES):
                chromosones.append((my_gamete[i],mate_gamete[i]))
            return Person(chromosones)

        def get_similarity(self,other):
            sim = 0
            for s,o in zip(self.chromosones,other.chromosones):
                for a,b,c,d in zip(s[0],s[1],o[0],o[1]):
                    if a == c or a == d:
                        sim += 0.5
                    if b == c or b == d:
                       sim += 0.5

            return sim/(CHROMOSONE_LENGTH*NCHROMOSONES)

    grandmother = Person()
    grandfather = Person()
    child1 = grandfather.reproduce(grandmother)
    child2 = grandfather.reproduce(grandmother)
    grandchild1 = child1.reproduce(Person())
    grandchild2 = child2.reproduce(Person())
    # Should be 12.5%
    print(grandchild1.get_similarity(grandchild2))

A chromosome is represented by an array of 2-tuples. Each tuple represents a chromosome pair. The number of pairs is set by the NCHROMOSONES variable. There are 22 pairs in the above code.
The actual genetic data is represented by an array of 0s and 1s. The number of 0s and 1s in a chromosome is set by the CHROMOSONE_LENGTH variable.
The similarity function takes two people and compares them at each position of each chromosome. If the two people have the same number at a given position, then it adds 0.5 to the sim variable. It then averages this across all positions. The reason I add 0.5 is because two people can either be 0%, 50% or 100% identical at a given position on a chromosome. 0% occurs when neither pair is identical, 50% occurs when 1 pair identical, and 100% occurs when both pairs are identical.
I noticed that as I use more symbols than just 0 and 1 to represent genetic data, the similarity actually approaches 12.5%. But I don't understand why this should be.
So my basic questions are:

Is my way of calculating the similarity correct.
Why can't I use just 0 and 1 to represent genetic data?

There are a couple of things going on here, I think. Let's start with simple conditional probability:
import random

sim1 = [random.choice([0, 1]) for x in range(1000)]
sim2 = [random.choice([0, 1]) for x in range(1000)]
for locus in range(1000):
   if sim1[locus] ==sim2[locus]:
     match+=1
print(match)
# prints 492

In other words, even two completely independent samples from [0,1] with uniform probability are expected to match about half of the time (492 / 1000 ~ 50%).
So you are correct, the problem lies in your fashion of encoding the data. When you are talking about "similarity", what I think you mean is "identical by descent". This is distinct from "identical by state", meaning what actual alleles you have.
Two individuals can be identical by state at a large number of loci without any significantly close family relationship, if they are members of a population without a lot of common alleles. This is close to what we mean when we say that humans are all 99.9% identical to each other- this is because most of the positions in the genome have very little variation. So, if you choose two people who have no common ancestors in the last 1000 generations, they will still be identical by state for >99% of their loci. This is the real lesson that your simulation is showing you, I think!!
If you want to show identity by descent, you will have to choose a different encoding. Using e.g. nucleotides will still run into the problem that very frequently the nucleotides will be identical by state in unrelated individuals, whereas what you actually care about is "did this allele originate from the exact same ancestor". So you want some way of guaranteeing (or nearly so) that every ancestor contributes a distinctive, unique allele that you can always distinguish. For example, the following code will produce a "unique" identifier that could be used for each founder individual (e.g. every time you call Person():
import uuid
unique_id = uuid.uuid4()

So really, what your Person.get_random_dna() method should do is something like this (minimal modification to your code):
        def get_random_dna(self):
            unique_id = uuid.uuid4()
            return [unique_id for x in range(CHROMOSONE_LENGTH)]

You may need to fix something else as well, I have not actually run this.

What would be the equivalent of my 0s and 1s for actual dna? Would it be a,t,c and g? So that means I should only need 4 symbols? Excuse my ignorance, but I don't know much about this.

@user1235598399 It depends a bit on what your application is, but the nucleotide symbols won't fix this- they will merely change the error to one in which the probability distribution is somewhat different. If I am correct and your goal is to understand "identity by descent", then you might consider coming up with a unique hash for each "founder" individual and using that as the signifier for its genotypes. I'll update answer to reflect this.


text:
Please identify this bone found on the beach
I've found it on the beach in Çanakkale, Turkey. Width 7.5 cm, height 5 cm. Inner hole dimensions are 2.5 cm x 3 cm.

It's an atlas vertebra from a large herbivore, a goat, a young horse, a deer. Also know as the C1 vertebra it's probably a sheep from a mechoui party.

Thank you. Goat is most probable animal here on these beaches.

Hehe look at the moderators joke comment.... " A sheep is an animal which says 'mehehehe' and it's white and wooly"


text:
Defining "species" (Are species an emergent property or an ensemble of quantitative differences?)
Interbreeding
Defining species by the criteria of not being able to breed is problematic:

The concept loses its meaning in phylogenetic prospective, since closely related species were able to breed between themselves in past, during the speciation event (an "event" that often lasted hundreds or thousands of generations)
The definition is problematic for simpler life forms, such as bacteria exchanging genetic material, or viruses where different species from the same family may differ only quantitatively (e.g., HIV vs. SIV).

(Excellent exposition of this view on the difficulty/impossibility of defining species is presented in this answer, as well as in the answer by @SPr below.)
Emergence
On the other hand, species are not reducible to merely accumulation of genetic variation. When looked from more general prospective (e.g., here), species are an example of an emergent phenomenon (the same inability to interbreed is a qalitative rather than quantitative difference.) We thus should be able to define a critical boundary between what is the same species and not, although this boundary does not necessarily lie in time domain. Inability to interbreed is a vague definition, since it may be due to very different reasons: phisiological, genetic, assortative mating, etc.
Operational concepts
In some domains we could choose to define species based on a criteria of convenience. E.g., considering an ecological community one may define as species the organisms that cannot interbreed, but also those that do not share the same habitat. While such an operational definition may work well for practical studies, it is not unique and subject to change from one study to another.
Are species an emergent property or an ensemble of quantitative differences?
Can we give a robust definition of species/speciation? Can we define a domain of applicability of such a definition? (e.g., defining the forms of life for which species can be defined)
Background
When speaking of emergent properties, I tried to skip some techncialities that led me to this question, which is why this part of my question may appears somewhat vague. So I would like to add more details here.
Phil Anderson in his article Broken symmetry, emergent properties, dissipative structures, life: are they related? formulates emergence in mathematically rigorous terms as a kind of phase transition in a non-equilibrium system. Phase transitions are characterized by summetry breaking, i.e., appearance of a completely new property in a system. What I termed previously robustness is, in Anderson's language, called phase rigidity.
The question is thus: whether speciation is a kind of such phase transition (as claimed, e.g., in the Melamede's article, already cited earlier) OR whether it is merely incremental accumulation of changes. (However, in such a formulation question is unlikely to be answered either in physics or biology communities.)
For more context: in his article Anderson criticizes Ilya Prigogine's school on a few technical points, but it is Prigogine and his co-workers, who are at the origin of such thinking. In particular, they have multiple publications on the subject of such disspative structures, and non-equilibrum thermodynamics more generally. Many of their articles are available by googling.
Update
After some discussions in the comments: the crux of the question is whether (or tow hat extent) speciation occurs via abrupt or incremental changes.

Organisms differing by abrupt acquisitions, such as presence of a nuclear membrane or an extra chromosome, are unambiguously assigned to different species (and cannot breed or reproduce viable offspring).
On the other hand, most ambiguous cases seem to be those where the "species" differ only by a incremental changes (such as the number of nucleotide substitutions/insertions/deletions).

Ring species could be a possible test case: if the species at the beginning and the end of the ring cannot breed, do they always differ only by incremental changes? If one species differed by a number of chromosomes, it likely wouldn't be able to breed with any of the others.
Update 2
Here is a useful answer: species can be defined from many different viewpoints.

Ew "closely related species were able to breed between themselves in past", it's also the case in the present.  See for instance the development of the "coywolf" in eastern North America: https://en.wikipedia.org/wiki/Coywolf

@jamesqf sure, horse and donkey can breed, but two breeds of dogs sometimes can't. This underscores the insufficiency of this definition. But the point I was making was dufferent - if you have suggestion of more precise formulation, I am listening.

@Vadim often the difference with dogs is physical rather than "can't". Imagine a female chihuahua trying to breed with a male great dane, or vice versa. I don't think the genitalia would fit, nor would the pups in the first instance.

@bob1 physically can't :) the point is that any two nearest relatives could cross at some "point". It is the chimpansee-girilla-human problem - which of the three are closest relatives?

@Vadim my point was that they can if you take the sperm from one and use it to fertilize the other, it's just they they don't (not for lack of trying I am told) because things don't fit, or can't reach... They are definitely not separate species.
Horse and donkey can interbreed but offspring are usually sterile - mule and hinny respectively, so definite separate species. But the boundaries between other organisms aren't so clear.

@bob1: Yes, just about everyone regards dog breeds as varieties of a single species, yet the "don't fit" problems ensure that some breed pairings don't produce offspring that are viable without human assistance.  (Indeed, I've read that some show breeds like bulldogs need human assistance.)  OTOH, dogs, wolves, and coyotes are regarded as different species, yet can interbreed and produce viable offspring.

@bob1 my understanding is that horse and donkey have different number of chromosomes, whereas dogs differ by a number of point mutation (nucleotide substitutions/insertions/deletions). To retake the main theme: this is an example of abrupt vs. incremental changes. Are any known ring species more than dogs in this respect?

Another example of different species that freely interbreed are trout.  Particularly within the US Great Basin, where the drier climate after the Pleistocene created a lot of isolated stream/lake systems, which often evolved their own trout species.  Then eastern brook & rainbow trout were introduced, and freely bred with the native species, and with each other, producing viable hybrids such as the tiger trout: http://www.ndow.org/Species/Fish/Tiger_Trout/

@jamesqf by what criteria are these "species" are then judged to be different species?

@Vadim: 1) Taxonomists and people who discover (or want to have discovered) new species give them names.  In that context, see the arguments between "lumpers" (who think the minor differences between some of those species should better be called varieties) and "splitters" (who think minor differences justify calling them new species).  2) In the US, the EPA, Forest Service, various environmental groups &c who use the "splitter" side of the argument as justification for policies protecting the supposed species.

Can we give a robust definition of species?

No.

Species constantly evolve, diverge, converge, interbreed, and mix and shuffle and trade and spread genes. To draw a box at any particular point in time around a population or lineage, and to say, "all contained within are members of such-and-such species" fails to appreciate that this would only work for that particular case, and arbitrarily so; it is obviously futile to have a sound microtaxonomy that would be generalizable to all animals, or microbes, or plants, or viruses for that matter. What consensus there might be for (e.g.) beetles is a poor yardstick for judging whether two alike bacteria ought to be lumped together as a species. Also, life, genes, individuals and populations are dynamic over time, so whatever box we draw will by definition require adjustment, and you can see that this adjustment will have to be arbitrary in many respects. This is an old problem, and it is more philosophical and ever-debatable, rather than something to be settled by empirical science triumphantly. From Nicholson's 1872 A manual of zoology (two centuries ago now):

"No term is more difficult to define than "species," and on no point
are zoologists more divided than as to what should be understood by
this word."

And to echo all that has been said from Piglucci (2003) Bioessays:

"First, the species problem is not primarily an empirical one, but it
is rather fraught with philosophical questions that require — but
cannot be settled by — empirical evidence."

Which also summarizes a few major biological definitions, some of which do not align:

And also a few philosophical issues that are worth considering when discussing the species problem:

This is not to say that conventions don't exist, or that there is a lack of an operational and specific definition of a species in each respective field; however, there is no overarching definition that applies robustly, hence the answer at the top!

Also, search around on this SE for similar Q&As. I find no duplicates but some similar ones.

Thank you for the answer. It provides many useful insights. However, what I really would like to understand is when quantitative differences between two organisms transform into qualitative ones... or whether such a transformation never takes place and the differences are always quantitative.

@Vadim Can you not think of species that have qualitative differences between them? Even individuals of the same species can have qualitative differences. Maybe you have a different idea of what that means?

@BryanKrause Good point. Perhaps, it is more precise to ask what quality makes organisms belong to the same species or not. I think not being able to breed is a wrong quality, but the idea is correct: the quality is either there or not. If we can show that such a quality cannot exist, it is in itself a strong claim.

@Vadim I think SPr's answer and some other Q&A here make it pretty clear there is no single definition, and can't be one that is agreed upon.

Remi's answer here is excellent: https://biology.stackexchange.com/a/39669/27148

@BryanKrause the linked answer is indeed very complete. However, it addresses only one line of thinking - the one that I outlined in the first part of my question. And this line of thinking, it seems, is in contradiction with how we think about the emergence of life, which impliues a series of abrupt qualitative changes.

@Vadim What does "emergence of life" have to do with "species"? Who is the "we" that implies abrupt qualitative change? I think Remi's answer there makes clear that "species" is just a classification we draw for convenience when what we are really dealing with is "lineage" which can't be separated except by (relatively) arbitrary means.

@BryanKrause I cited Phil Anderson and Ilya Prigogine in my question. Although neither might have mentioned species - this specific question is based on the quoted Melamede's article, where speciation is listed as one of the abrupt transitions between the emergence of cell and the evolution of body systems.

@Vadim I can't access that article and don't see any quote from it. I'm guessing something is getting lost in the details. I would not describe speciation as "abrupt" except in special cases or using special definitions of species (or a geological meaning of "abrupt", perhaps).

@BryanKrause I suppose that it can be found for download by googling - (but I wouldn't post link for downloading copyrighted material). Anyhow, I see your point of view, and I tend to agree with it... but it still seems as a grey area to me.

@Vadim Dug a bit further and did find the article.. so, okay, this seems to me like a lot of word salad and not a lot of substance, at least with a casual glance. The author also seems to be mixing the words "species" referring to biological species and "species" in the context of "chemical species", the more generic "kind/sort", which has little relationship to the concept in biology. I wouldn't recommend taking it too seriously. In any event, I don't see any reference to anything "abrupt", if there's a particular quote that is relevant you should include it in your question.

@Vadim - check out ring species as an example of the difficulties in determining what is a species and where. The problem is that you are approaching it in a computational manner, where things have exact definitions. Species do not have exact definitions precisely for the reasons S Pr outlined. Biology is messy! An example of the difficulty is cancer research, where cell lines evolve in the lab so that results from one lab are not reproducible in another, even though both are working on the same cell line.

@bob1 I am not looking for exact universal definition of species. The point of the question is whether species a result of small incremental changes or an abrupt jump - like appearance of a cellular membrane. Depending on which corner you look from (taxonomy or abiogenesis) the answer is different (in my view).

@Vadim - both is the answer. Abrupt jumps are seen in some circumstances, incremental in others.

@Vadim You say in my view, species definition depends whether one considers it from a taxonomical vs. abiogenetic point of view. I think we would all disagree with you. Defining species has exactly the same problems regardless of whether you believe that at some point (i) life was designed to evolve, (ii) created and subsequently evolved, or (iii) evolved out of inorganic material. Evolution exists and that makes defining species boundaries arbitrary, since all life, populations and lineages are in constant flux over time. That's it. See, whether it's abrupt or not is irrelevant.

@SPr Perhaps abiogenic is too general a word for the veiw that I expressed, but I think I have described clearly enough the two contradictory viewpoints in my question. We have a good reason to belive that there is abrupt transition between being alive or not, between being cellular organism or not, between having a nucleus or not, etc. Any division in species that is not grounded in evolution is indeed arbitrary. And I don't see any problem with populations and lineages being in flux - so the species change, some disappear, some split into more species.


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Is it possible to use two forward primer and one reverse primer?
I have eGFP and the gene fragment i assembled by pcr.The next step is that i have to join my fragment fragment into 3'p end of the eGFP.I have three primers FP1 is forward primer for eGFP, FP2 has overlapping between eGFP and my fragment. RP1 is just revcom of my fragment 3 prime sequence. How can I assemble this by pcr. is it possible to mix all the three primers together with GFP and my fragment.

Well, technically yes but no. Why yes is because on paper this looks simple enough but think about the technicalities. Your FP1 and FP2 will have different TMs, meaning the temp required to make the complete fragment with FP1 and RP1 will be different than to the MP of FP2. Effectively when the temp for FP2 reaches it might cause FP1 and RP1 to detach.Or the opposite might happen, where FP1 and RP1 are attached whereas FP2 might not.
Another problem I could think of is that as the PCR is cycling, the difference will lead to random length amplifications if at all you get any. The maximum amp product you might see will be of Frag-2.
If you want to fuse such fragments, I suggest going for OE-PCR (Overlap extention PCR).
This is a highly effective method to join two pieces of DNA using PCR. the concept is similar to what you have proposed.
Look at the wiki page- https://en.wikipedia.org/wiki/Overlap_extension_polymerase_chain_reaction

This image also explains the process...

Thanks for you explanation. For Overlap extention PCR i need more primers or overhangs in the fragment right. But i don't have the overlap in my fragment instead i have it on my primer. Is it possible to do by Gibson assembly?

@Anteres I don't see what you mean by "technically yes". It is simply not possible to achieve the fused fragment by the three primers proposed by the op.

@gaspanic - correct, it can't be done by the PCR as designed. It could be done with a fairly simple blunt-ended ligation of the two products. Though in that case I would do the PCRs individually rather than in 1 tube. The OE-PCR is the correct procedure for this, or simply put it all into a GFP-vector in-frame with the GFP.  I can't think of many applications where you would need a naked GFP-GOI construct without promoters, RBS etc.

The ultimate aim is to integrate my fragment into the 3' end of the gfp plasmid. The plasmid has all the essential features. I thought i can assemble gfp and my fragment by pcr then i can incorporate into the plasmid. Is that wrong?

What do you mean by the 3' end of the gfp plasmid? Is GFP already in the plasmid, and all you need is to insert your second fragment downstream of GFP? In that case your primers FP-2 and RP-1 should be sufficient, assuming that you have appropriate restriction sites near the 3' end of GFP.

The reason why i am doing this, to preserve all the restriction site.

In order to get a good response I think you will need to post a new question clarifying what you have and what you want to achieve. The comments section is not the right place for this.


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How many times is a single strand of mRNA translated into a protein?
In other words, is the mRNA damaged or somehow "marked completed" in the translation process? Or does it pop out the other side of a ribosome ready to be translated again? If the latter, how many copies of a protein result from a single strand of mRNA?
Thank you in advance!

A relevant question, but the topic is covered in general textbooks in the section on translation. On the web try searching for polysomes and then think about what their existence implies. A search for mRNA half-life will reveal the answer: “It depends on the mRNA and the organism.”

Thank you for the pointer, @David. With your assistance, I think I was able to answer the question.

I'm answering my own question for the benefit of anyone else who might be wondering about this. (Please note that I'm just a programmer, not a biologist, but thanks to David's comment, I was able to come to what I think are some correct conclusions.)
A single mRNA strand can be translated more than once, even more than once at the same time. The polysome that David references is a group of two or more ribosomes all attached to the same mRNA strand, all working on translating it simultaneously.
I believe that it may be possible for a single mRNA strand to be translated hundreds or even thousands of times. My reasoning for this is that a virus injects one copy of its RNA into a cell, and from this one copy, new viruses are replicated until the cell bursts. This "burst size" varies by host cell and virus, but it can range from hundreds to tens of thousands or more. While there are still a lot of things I don't understand about the specific steps the RNA goes through (are there intermediary copies made from which multiple mRNA strands are produced?, etc.), it still seems to suggest that a single strand of mRNA can be translated a lot.

Note that for translation and transcription are two different things. Transcription is copying the RNA into new RNA. Translation "reads" the RNA and makes protein. Your third paragraph confuses the two. In the case of SARS-CoV-2, the RNA genome (+ sense single stranded (+ss) for this virus) is the same as a mRNA in a cell, but it is copied into a double stranded RNA and then made into a new +ss for packaging and translation. see here

Thanks for the comment, @bob1. What I meant by that remark was that I didn't know if the viral RNA was the actual thing being translated or not. Conceivably (at least to my naive mind), the "master" RNA could first be transcribed into intermediary copies which are then translated. I reasoned that this might allow thousands of copies of a virus to be replicated even though a single mRNA strand can only be translated a smaller number of times. I was trying to acknowledge the holes in my knowledge that would invalidate my earlier, simpler logic.

See the diagram in the paper that I linked. It shows that the incoming COV-2 is partially translated to produce a replication and transcription protein which forms a complex with the RNA, which then produces dsRNA and goes on to produce ssRNA for both translation and viral progeny.

@bob1, Wow, there is a lot to unpack there. Thank you for the help and pointers!

The  question asks about mRNA, but your answer seems focused on one particular viral RNA. It fails to address the differences in mRNA half-lives between species (eukaryotes v. prokaryotes) and within species. Nor does it address the mechanism of mRNA degradation. I suggest you need to do more reading if you really wish to understand the answer to the question you have asked. Have you searched this site to see if the topic has been covered previously?

@David, yes, I came to this site specifically hoping to find and answer to that question, and when I did not, I asked it myself. I am unsure what you mean when you say my answer is focused on one particular viral RNA. I refer to viral RNA only to show that it must be possible for RNA in general to be translated many times, though clearly there are many holes in my knowledge, including that I do not yet know what differences there are between viral RNA and mRNA. I have not marked this as the answer for that reason. Perhaps someone more qualified than I will be so kind as to write an answer.


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How many mRNA strands are in a single dose of the COVID-19 vaccines?
I realize there are several different mRNA vaccines. I would be happy to know the ballpark figure for any of them.
As a follow-up, is it known about what percentage of injected mRNA strands are successfully translated into proteins?

Check https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem - it seems like this question and your other recent question might suffer from this issue. What is motivating the questions you're asking here? What are you hoping to get from these numbers?

Partly it's pure curiosity. I couldn't find this information anywhere. Regarding my other question, after a night's sleep I realize mRNA must be translatable more than once, or it would not be possible for a virus to replicate more than one copy of itself. Still, what about "friendly" mRNAs? What prevents an mRNA from being translated indefinitely? I'm just curious!
But yes, you're right that I am also wondering about how the total number of spike proteins generated by an injection would compare to those encountered in a natural infection.

I think it would be better to ask one of those intended questions more directly, rather than the one you asked - that's kind of where the XY problem comes in where you are asking something that you think will get you closer to answering your intended question, rather than starting with the intended question.

Thanks, I appreciate that. But I'd also just like to know the answer to this question. For what it's worth, I think it would add value to everyone to be able to search for this specific question and find a simple answer. Maybe I'm just searching with the wrong terms, but I was not able to find it.

Well, we can work this out empirically.
We know that the average molecular mass of a base of a RNA is 339.5 g/mol.
Despite this, to calculate the approximate molecular mass of a single-stranded RNA molecule, you multiply the number of bases by 320.5 (because some bases are more common in sequences than others) and add 159 (same source). This means for a single-stranded molecule of 1000 bases, it will have a molecular mass of 320,659 g/mol. The Pfizer vaccine has a sequence of 4284 bases.
4284 * 320.5 + 159 = 1373181 g/mol.
The Pfizer vaccine has 30 ug/shot (PDF, see page 27 under "Description") or 30x10-6 grams
number of moles = mass/molar mass.
n= 30 x 10-6 grams/1373181 g/mol
n= 2.185 x 10-11
number of molecules = n (above) x Avogadro constant (6.022 x 1023)
Number of molecules = 1.316 x 1013
Now this is a ball-park figure because the RNA isn't actually RNA it has had some special additions to the uridines that make it less susceptible to immune regulation, replacing the uridines with  1-methyl-3'-pseudouridylyl (see Wikipedia link to structure above). However, I believe this alteration to the mass, will not alter the number substantially; it'll still be in the 10 trillion range.

The 30 mcg/dose in the Pfizer pdf indeed refers only to the RNA. The lipid nanoparticle etc. is counted separately. In case anyone else was wondering that.

Wow, thank you, @bob1! That is a truly tremendous number. So that would mean that, seeing as we only have 30-40 trillion cells, depending on the uptake of the mRNA into cells and the number of times each strand is translated, you could end up with more spike proteins floating around your body than your total number of cells. What an incredible surface area for your immune system to notice. Awesome!

Also, for comparison, this source (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7685332/) says that at peak infection, a person can have 1 billion to 10 billion virions in their body.

@BrianRak - The data on how much is produced is proprietary. I suspect that the 30 ug is the amount of RNA, definitely not all of that will be packaged, some will be lost to degradation (transport, preparation etc), and some proportion won't make it into cells. My experience using plasmids and liposphere preps (common in bio labs, but not the same as the Pfizer ones) is that somewhere between 30 and 90% of cells in a dish will be transfected, but it will definitely be less than that in vivo. There are too many variables to answer the second part of your question in the OP.

@BrianRak to address your second comment - in culture (ideal conditions) you get about 10^6 (1 million) - 10^7 infectious particles/ml, so these numbers seem surprisingly low to me, but I guess it will be a staged infection - not all cells getting infected at once, unlike in the lab where a whole flask of cells will infect at the same time.


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Coinfecting oncolytic viruses - first virus carrying the receptor for the second
One challenge to using oncolytic viruses as a treatment for cancer is that the viruses may cause off-target effects. I'm curious to know how useful it would be to create an oncolytic virus that has the receptor for another virus encoded into its genome (kind of like a viroreceptor)? It would probably be best if the encoded receptor is a receptor not present in humans, so maybe a receptor present on the surface of another animal's cells. If the first virus replicated to a higher degree in cancer cells than normal cells, and/or if the first virus was largely cleared from the normal cells before the second virus was administered, then it seems the cancer cells would differentially express the receptor for the second virus, and that could limit the off-target effects of the second (perhaps more potent) virus. (Of course, there are other ways of limiting off-target effects - injecting the viruses intratumorally, using viruses that the host would mount a memory response against, etc. - feel free to include these in your answer if you'd like.)
I'm sure there may be challenges in practice (one that comes to mind is whether a given first virus would have the genomic space to carry a receptor for the second, in addition to other desired genes) but I'm curious to know what people about this idea in the spirit of a thought experiment, or if you could point me to any relevant papers etc.

From the [help/dont-ask], If your motivation for asking the question is “I would like to participate in a discussion about ______”, then you should not be asking here. In addition, this is an opinion-based question (and thus off-topic) because it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where … you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise. Please see the [tour] and other [help] for details.

Short answer: No.
Longer - No. Why would you do this? - if you can get the first virus to replicate to high levels in a manner that is specific to cancer, then why not use that first virus alone rather than run the risk with two separate viruses.
Don't forget that for the virus to reach all parts of the tumour it will need some cell to cell transmission, which means that it exits the cell (possibly in a lytic manner) in the first case, so there probably isn't any need for the second virus.
The second point is that the immune system (innate and adaptive) will recognize the virus infected cells and start to clear them (that's the whole point of oncolytic therapy), probably before the second virus is administered.
Thirdly, not all cell types support viral replication efficiently. This may or may not be the case for the specific virus(es) and cancer types you target, but it is something to be considered.


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In what stage of bacterial growth can penicillin inhibit the growth of the cellular wall?
The bacterial growth has 3 main stages: lag-phase, log-phase and stationary phase. I was wondering in which one of them penicillin can inhibit the growth of the cellular wall of bacteria and why.
I was thinking that the respons would be lag and log phase, because at these points bacteria multiply the most, while in stationary phase most of the bacteria are in adult form with a well formed bacterial wall already, but I'm not quite sure.

You may be interested in the Eagle effect. (As I understand things, penicillin has no effect on gram-positive bacteria in stationary phase growth (as the bacteria are not dividing)?) From the Wikipedia article cited: "In this instance [stationary phase growth] since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity."

yes, thank you! This is very usefull.

This is a really good question that requires you to appreciate a few different details and to overcome a few implicit assumptions that you might perhaps have.

The bacterial growth stages you refer to only apply to a population of bacteria. Individual cells do not undergo these stages.
Relatedly, bacterial population growth stages are independent of the stage of bacterial cell wall growth.

You can have mature or immature bacteria at any stage of "bacterial growth", with either fully formed walls, or with none. This understanding should answer your question partially.
Here are a few more things to consider, for a more complete understanding:

Penicillins are a class of molecules, of varying efficacy and bioavailability across the body and across different kinds of walls and membranes.
Inhibiting the spread of bacteria can be achieved using two types of antibiotics... bactericidal or bacteriostatic ones. Bactericidal means the bacteria die, while bacteriostatic means their growth is slowed or stopped.
Penicillins are bactericidal agents that exert their mechanism of action by inhibition of bacterial cell wall synthesis and by inducing a bacterial autolytic effect. So even mature bacteria will die off in the later stages of outgrowth. In principle, it does not matter what growth stage the bacteria are at, the bactericidal mechanism will take place regardless.
Pencillins are more effective against Gram-positive bacteria. Gram-negative bacteria have a lipopolysaccharide and protein layer that surrounds the peptidoglygan layer of the cell wall, which acts as a barrier for the penicillin from reach its target (which is responsible for completing the synthesis of peptidoglycans, the structural component of bacterial cell wall). However, penicillin can get into Gram-negative cells, for example through channels called porins.

This is more or less very standard knowledge that is easy to look up. Wikipedia's entry on penicillin is a good place to orient yourself if you already haven't.

Penicillin is a beta lactam antibiotic that inhibits Transpeptidase enzyme ( Penicillin binding protein).
Transpeptidase is required for the cross linking of murein monomers required for cell wall synthesis.
So as Penicillin binds to Transpeptidase it does not let it involved in cross linking of murein monomers and hence cell wall synthesis can't be completed.
This is how Penicillin inhibits bacterial growth .
Now the phases ( lag ,log , stationary) you mentioned are used when a culture of bacterial colonies is grown and not used for a single bacterium .


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Can a strand not be synthesised in 5' -> 3' direction?
I've been solving some biology questions, and according to one of them ( I have the responses too) the following phrase is false:
"Both strands are always synthesised in the 5' to 3' direction."
How can this be? From what I know DNA is always read from 3' to 5', and synthesised from 5' to 3'.
When is DNA not synthesized from 5' to 3'?

What do you mean “how can that be?”?  That’s the way it is. Deoxy-ribose is not symmetrical. Enzymes have substrate specificity. And plasmids have no bearing on the matter. Search for Berg on NCBI Bookshelf, and read the section on DNA synthesis. Pay careful attention to the chemistry.

I have looked trough the book you have recommended me, and it still did not give me the response I needed.  According to this book "At a replication fork, both strands are synthesized in a 5′ → 3′ direction.". Which I agree with, my question was why according to my book, it says that it is false that strands are always synthesized like that. Unless, it was referring to the direction of growth, in which case the lagging strand grows in the 3' to 5' direction, but it doesn't because my book uses the word "synthesized" not "grow". This is where my confusion comes from.

Am I right in thinking your concern is as follows? All known DNA polymerases add NTPs to the 3'-OH of the deoxy-ribose so that the direction of synthesis is 5′ → 3. In most organisms the two strands grow in both directions by a complex mechanism at the replication fork involving RNA primers and Okazaki fragments etc. However small circular genomes use a different mechanism — the rolling circle mechanism (described in Wikipedia etc.) — in which growth is just in a single direction. If so, and you still have a question about this, could you clarify what your question is.

It sounds like your guess was right and the exception is the lagging strand. The statement is phrased poorly, but it seems like they were going for the lagging strand. Either they meant for you to think that
-the lagging strand is growing 3' to 5'
or, more likely,
-the polymerase is only synthesizing on one (leading) strand at a time
While technically the book was correct, it was a trick question and phrased unfairly.
You are completely right that DNA is synthesized from 5' to 3'. I don't know of any exceptions to this, but hesitate to say anything overly definitive because there are so many rare exceptions in science. I can say with some confidence that DNA polymerase cannot ever synthesize in the 3' -> 5' direction. If you haven't already, I highly recommend checking out the Khan Academy article, Molecular mechanism of DNA replication! Nature Education also has a pretty good article on the topic, Major Molecular Events of DNA Replication.

I don’t even think the book was technically correct. It’s odd to say that DNA synthesis occurs 3’ to 5’ even if you are referring to lagging strand growth.

I agree completely, I was trying to cover all the bases since it's so unclear what the book was going for. I edited my answer so hopefully it's a little more clear though!

text books are rarely written by relevant scientists, the person who wrote the question probably did not understand it.