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Why do I have 95% of chimpanzee's DNA, and only 2% of Neanderthal's DNA?
Excuse me if it is a question with a simply answer, but I don't understand these discoveries, looking a discrepancy from my unknowledge of genetics:

I have 95% of Chimapanzee's DNA,

and,

I have [only] 2% of Neanderthal's DNA.

Neanderthals should had also chimapnzee genes, so what does that 2% of  correspondency between Neanderthal and actual Homo sapiens genome exactly means?

Related: https://biology.stackexchange.com/questions/1981/how-many-genes-do-we-share-with-our-mother https://biology.stackexchange.com/questions/41974/why-are-the-genomes-of-humans-99-5-the-same https://biology.stackexchange.com/questions/61147/neanderthal-human-genetics

Some version of this question has been asked and answered several times... I thought we had a more clear canonical answer but maybe I'm just thinking of the first in my list.

Also https://biology.stackexchange.com/questions/9172/do-apes-and-humans-share-99-of-dna-or-99-of-genes-what-is-the-difference

@Bryan Krause thanks. So we share 95% of DNA with chimpanzees, but 2% of genes with Neanderthal. Genes are formed using only 5% of simple letters of DNA sequence. That's what I understand. And that 2% is what? Don't we have a bigger correspondence with Neanderthal genes than 2%? I still missunderstand it.

Can you excuse me and add a comment if closed? I have personal interest because I have asperger disorder related with neanderthal genome, and I don't undesrtand english very well (and a bit of dislexis).

This all a question of what is meant by “share % of our DNA”, which is obviously different in the two cases. My “todo” list includes writing a definitive answer to all the questions that result from loose journalistic language in this area. Alas, I have not yet found the time. Your response to @BryanKrause illustrates the confusion: you are using %DNA and %genes as if they were equivalent. They are not. And what do you mean by %genes? Not what the 2% means, I bet.

Probably iayork's answer here (also linked above): https://biology.stackexchange.com/questions/61147/neanderthal-human-genetics is the most succinct way to put it without deeper explanation.

My interest grew when I read they created micro brains with neanderthal DNA. But that's totaly out of my knowledge. Just I felt a bit more Neanderthal as asperger, after reading: "neural structure developed unusually, mirroring some of the developmental differences seen in people with autism"  http://discovermagazine.com/2019/january/ancient-brains

@Bryan Krause I contribute to marck it as duplicate. Personaly I learned the comprehension mistake I had and I learned DNA is not the same as genome. However I still don't understand what's my 2% genome correspondance with neanderthals Max Plank Institute published. I guess it takes in consider variations of N that were transmited to sapiens. It should be a result calc to determine % of ancestors we have/tax of specie mixing. Maybe I could reformulate my question but I am studing exams for a public job on gov. Maybe in some months. Ty!

@Universal_learner The 2% is referring to alleles that were A) Absent from homo sapiens at one point, B) Present in neanderthals, C) Present in present-day homo sapiens due to breeding between humans and neanderthals. It omits alleles shared in both. Also beware of the ASD/neanderthal linkage, it is not a scientifically supported theory to my knowledge.

@Bryan Krause thanks, I understand. So it is a kind of tax of intrusion of Neandertal pool, being the total pool the actual human genome (not DNA).

I find it a confusing data. That doesn't mean at all I have a 2% of Neanderthal genome neither (I have 2% of exclusive neanderthal genome). And also, I thougth my neanderthal pool as asperger/autist was very similar to other humans, that 2%, afecting in my case on nervous system (the difference); but maybe in my case is 5% who knows, I haven't sent a sample to max planck institute with my genome.


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Are there examples of animals being sexually attracted to another species more than to their own?
I just thought that from the perspective of a female domestic cat, a male bobcat probably looks like the archetype of a perfect mate. As tall, strong, muscular and mighty as it possibly gets. Clearly preferable to any of these boring male domestics.
Has anyone ever done any research on this topic, like presenting a male cat and bobcat to a female in heat and scientifically evaluating her response? (I'm not exclusively asking for cats and bobcats, but for any type of animal, and I'm just using the cat-bobcat-example to better explain the question.)

Here are a few examples. All are open to debate as to whether it answers your question.
Zoophilia in humans
When asking of example of a "species" that does something, it is easy to forget about the diversity of behaviours among individuals of that species. It raises the question of how frequent must the behaviour be in that species to accept that the species is representative of this specific behaviour. Many might be tempted to disregard humans as examples thinking that zoophilia (sexual fixation of a human on non-human animals) is very rare but the reality appears quite different.
The Kinsey reports (1953) estimated that 8% of men and 3.6% for women had sexual interaction with animals at some point in their lives. More recent studies tend to find somewhat similar results (of the order of a few percents). These numbers seem to go way higher for people living near farms. Although these numbers seem debated, the Kinsey reports (1953) estimated that 40–50% of people living near farms have had sexual interaction with animals at some point in their lives.
Given the prevalence of zoophilia, I would argue that humans could be considered an example of a species where (some) individuals are sexually attracted to individuals of another species.
Many animals have sex with about anything
In my life I have seen many dogs, rabbits and bulls attempt to have sex with inanimate objects. If a dog can be sexually aroused by a pillow (poor pillow), then I am pretty sure it can be sexually aroused by individual of another species.
Here is a picture of a moose trying to mate with a statue of a bison

Note btw that I am talking here about animal species that have a very high cognition, so below is a funny example with a beetle.
A tragic love story
In Australia, a species of Buprestidae (family of beetles) called Julodimorpha bakewelli has gone through an important decrease in population size. The blame is on people throwing their empty bottles of beers on the side of the road. Why? Males are attracted by the brown shiny color of the females and it turns out that many glass beer bottles have this same exact color. Hence, males started to spend all their time mating with beer bottles rather than with females causing a decrease in the species population size.
Sure a beer bottle in not another species but it shows how individuals of a species can be more aroused by something else than individuals of its own species (and the example is funny; the study won the IgNobel prize in 2011).
Amazon Molly
The Amazon molly is a fish species in which there is no males. All Amazon mollies are females. However, the amazon mollies need sperm to reproduce. How is it possible?
The females have to seek for sperm in a sister species in order to activate the development of the eggs. They mate with males of this sister species but don't use the genetic material of the father from the sister species (otherwise they would not be two different species). The amazon mollies are therefore only sexually aroused by individuals of another species. See Kokko et al. (2008).

Not to mention all those flowers mimicking female insects to attract pollinators...

Not just flowers some predatory insects so it as well.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Is the Amazon forest O2 and CO2 neutral?
In these days, we receive a lot of concerning news about the Amazon burning. Recently, I came across widespread claims about the production of O2   and the absorption of CO2 by the Amazon forest, something known as "carbon dioxide in, oxygen out". However, I also found claims that the Amazon ecosystem uses up all the oxygen it produces, and that it is a stable carbon sink, i.e. it acts like a carbon storage system, not as a sponge for carbon.
What are the real facts about oxygen and carbon dioxyde dynamics in the Amazon forest? I'd intuitively say that the second hypothesis is stronger, but I'd like to have a confirmation backed by some papers.

tl;dr We don't really know. A reasonable guess is that it's a weak sink, gradually turning into a source via increased drought frequency, but it's extremely hard to measure; carbon flux is highly variable both spatially and temporally (so it matters both when and where you measure), and it's difficult to make sure that you're accurately measuring all the different components of carbon flux.
Dolman and Janssen 2018 say:

Ground observations suggest that, through tree growth, the Amazon forest acts as a net carbon sink to the atmosphere (Brienen et al 2015), which is confirmed by atmospheric studies (Gatti et al 2015). However, the sink strength appears to have been declining since the 1990s and recent drought events in 2005, 2010 and 2015 might have temporarily reversed the Amazon carbon sink into a source (Feldpausch et al 2016, Gatti et al 2015)

They go on to discuss the great difficulties in constructing an accurate model of Amazonian carbon dynamics (for the purpose of predicting future source/sink relationships).
Rice et al. 2004
summary based on measuring living trees and coarse woody debris [CWD], it looks like a particular patch of forest was a small net source, but this may be a transient effect.

Amazon forests could be globally significant sinks or sources for atmospheric carbon dioxide, but carbon balance of these forests remains poorly quantified.

In other words, "it's still unclear [as of 2004], so we did another study."

We surveyed 19.75 ha along four 1‐km transects of well‐drained old‐growth upland forest in the Tapajós National Forest near Santarém, Pará, Brazil (2°51′ S, 54°58′ W) in order to assess carbon pool sizes, fluxes, and climatic controls on carbon balance.

So they took a very small sample of a particular forest type.

The gain in live wood biomass was exceeded by respiration losses from CWD [coarse woody debris], resulting in an overall estimated net loss from total aboveground biomass ...

So this particular patch of forest was a carbon source at this particular time ...

... a period of high mortality [probably] preceded the initiation of this study ... transfer of carbon between live and dead biomass pools appears to have led to substantial increases in the pool of CWD, causing the observed net carbon release.

... but that may be due mostly to a recent die-off - maybe not true over a longer time scale ...

... the hypothesized sequestration flux from CO2 fertilization ... would be comparatively small and masked for considerable periods by climate‐driven shifts in forest structure and associated carbon balance in tropical forests.

... it will probably bounce around a lot (i.e., it's not wise to extrapolate this result either in space or time).
Miller et al. 2004

We used two independent approaches, biometry and micrometeorology, to determine the net ecosystem production (NEP) of an old growth forest in Pará, Brazil. ... Biometric inventories indicated that the forest was either a source or, at most, a modest sink of carbon from 1984 to 2000 ... biometric and micrometeorological measurements in tandem provide strong evidence that the forest was not a strong, persistent carbon sink during the study interval.

and a more recent reference ...
Antonucci et al. 2018

The objective this paper was to quantify the hourly variability of CO2 fluxes in the year of the El Niño, in 2015, in a tropical rain forest in the Western Amazon ... The average daily behavior of CO2 fluxes showed higher concentrations of absorption during the day than emissions overnight, behaving as a carbon sink, corroborating the importance of the forest in assimilation of the atmospheric carbon.

references

Miller et al, "Biometric and micrometeorological measurements of tropical forest carbon balance". Ecological Applications 2004, https://doi.org/10.1890/02-6005
Rice et al., "Carbon balance and vegetation dynamics in an old-growth Amazonian forest". Ecological Applications 2004, https://doi.org/10.1890/02-6006
Antonucci et al, "CO2 fluxes in a wet tropical forest area in Western Amazon in year of El Niño". Ciência e Natura, v. 40, 2018. https://periodicos.ufsm.br/cienciaenatura/article/view/30718
Dolman and Janssen, "The enigma of the Amazonian carbon balance", Environmental Research Letters 2018. https://iopscience.iop.org/article/10.1088/1748-9326/aac78e/meta

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Need help with ImageJ thresholding
I'm trying to measure the colocalization of two proteins in a .tiff image taken with a wide-field fluorescence microscope. In ImageJ I have split the image into the two channels (red and green), and now I have to apply a threshold, however when I threshold both channels the bright areas corresponding to the cells are located in the darkest part of the histogram instead of the brightest part, as you can see in this image for the red channel:
https://www.screencast.com/t/QO2iVt0JM
Why ImageJ is assigning darker values to the cells rather than to the background? I'm having problems with this as I cannot properly select these cells for the colocalization analysis.
Anyone does have any clue? Any help would be greatly appreciated.

Check the "dark background" checkbox that is unchecked if the background is dark and you want to select the bright cells. Right now it is assuming the background is bright.

I was thinking about that too but it just inverts the colors, simply assigning white to the cells while they are still considered the darkest objects in the spectrum:
https://www.screencast.com/t/INdZ5pFLHgIn
Here instead how cells (or metal particles like in this case) should appear on an histogram:
https://www.screencast.com/t/TlFxRwsXubr

On the last picture, the particles are bright so they appear as a peak on the far right of the histogram, while the other peak on the left represents other objects in the background that have been excluded by thresholding them out. You may notice on the histogram that this left peak is inside a rectangular black frame representing the background. And as you can see the “Dark background” box is not checked.
With my image I get exactly the opposite, which is weird… and I don’t know what am I doing wrong.

@betelgeuse That's from your actual data then and can't be fixed with imageJ. Look at your histogram vs that one: it's doing the best it can do with what you gave it.


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What is this giant insect that just bounced off a second-floor glass door?
At about 11 pm, I heard a loud impact on the nearby glass door to a second-floor balcony. I thought it might be an acorn but it'd be a very unlikely angle - it'd have to be thrown from below or be a very strange ricochet.
So I looked and encountered this rather impressive creature recovering on the balcony:

Those planks are six inches wide.
I've never seen one of these before. What is it? Are those giant serrated appendages on the front mandibles or antennae?
I expect it's not as hazardous as it looks, but is there any risk of it biting people or pets?
Do they routinely launch themselves two stories into the air, or would it have crawled up and then just bounded from the balcony floor?
Location: Southern Oregon, USA.

Searching the Internet again this morning, I think I may have identified it as a California (Giant) Root-Borer Beetle (https://www.insectidentification.org/insect-description.asp?identification=California-Root-Borer-Beetle). Yes?
They fly, and are active at night.
The disturbing serrated appendages are antennae (whew!).
It looks like I have nothing to fear from it unless I or others panic at its appearance, but it or its progeny may be bad news for nearby deciduous trees.

Species ID answers should ideally be accompanied by an image confirming the species.

Prionus californicus would have been my guess due to the serrate antenna, Trichocnemis spiculatus are another large beetle without such saw-like antenna.

Species ID answers should ideally be accompanied by an image confirming the species, and some background information to show the species' distribution matches that where the critter was found according to OP, and some links to allow other users to background-read on your sources.


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Which species of bumblebee(?) is this?

I observed this beautiful insect near a forest in northern Switzerland. What is it?

To me that looks like a "hover fly" — specifically the Pellucid Fly (Volucella pellucens).
Compare with:

This species is present throughout Europe according to the wikipedia article (first link).


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I can't Identify this "bug" that seems attached to fresh cut wood
I'm a very amateur entomologist (I'm actually just an old fat hippie that loves all critters).
I don't have any chops here, but I swear I've done my due diligence and tried to figure this out. I'm asking because I'm baffled. (Leg stripes are Arachnid-ish, but thorax is completely wrong ... I just dunno...)
My girlfriend sent me a pic; she swears these things were jumping out of a seasoned firewood pile and by her words "attacking".
Location:  PA Pocono mountains, circa Kunkletown, heavily wooded area.
Now granted, there was a lot of drinking going on, it was "girls weekend out", and there was a hot tub.  I wasn't there; so I cannot actually confirm what really happened... (Of course I wish I was there, but ... nevermind)
HOWEVER - here's a pic.  You can't make this up.  Or, at least, I'm not making this up ...
What is this critter?  I think it's "insect" by the leg count I can see.  But edumicate me; this is a new one to me and I'm very intrigued.
Many thanks best!
On Edit
Perhaps some sort of "wood cricket" based on rough taxonomy of the leg configuration, and it's penchant for jumping.  Pure speculation.

I think I may have it.  gOOgle terms "giant cricket wood tiger stripes" yielded very similar critters:  So-called "Camel, Cave, or Cellar Cricket."
Order Orthoptera (Ensifera), Family Rhaphidophoridae.
Genus and Species will be next to impossible unless I can capture one, but obviously one of the North American varieties that like to hang out in damp decaying wood.
From the interwebs:


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Photosynthesis immature fruits
Do immature fruits perform photosynthesis? Yes they have chlorophyll bodies. But do they have stomata through which they can absorb carbondioxide like the green leaves? Sincerely Ulrik

Yes.  Both fruits and seeds often possess stomata as well as chloroplasts, which have been shown to be quite important in many cases for seed and fruit development.  It makes sense when you think about it.  If these vital components of the plant can make some of their own energy, rather than relying entirely on sugar reserves produced elsewhere (especially given how much sugar your average fruit has to produce), this would be a vastly more efficient system.  If you are interested in a more detailed look at fruit and seed stomata, the following paper should make for a good starting point:
https://www.jstor.org/stable/2442508?seq=1#page_scan_tab_contents
The authors of this paper conducted an in depth investigation of the structure and functions of the fruit and seed stomata present in a number of species within the Eschscholzia genus.  It's an interesting read.

Yes. I grow grapes. Next year I shall seek out two clusters of grapes. One I shall leave exposed to sunlight, the other I shall cover with alu-foil. I shall let you know the result.


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Separate DNA fragments with very different size (oligo and lambda-DNA)
I am running a ligation reaction to one of the sticky ends of lambda-DNA.
The oligo for the ligation is 25 bp (10x excess), whereas lambda-DNA is 48 kbp. I would like to recover the lambda-DNA and discard the unreacted excess oligo.
Given their vastly different molecular weights, they should be easy to separate, but I could not find a standard methodology online.
I do not want to run gel and my total sample volume is 0.5 mL. There are some filtration columns that may work, but the input volume is only 25 uL (I have 20 times that).
I don't have to get rid of all the oligo, having slightly more lambda-DNA than oligo at the end would suffice.
Which simple protocol may work in this case?

A spin column might work for your purposes since you can do multiple rounds of binding if your volume is too large to bind in a single pass, but for DNA of that size a lot will be irreversibly stuck to the column.  See for example the protocol for the Monarch® PCR & DNA Cleanup Kit.
Consequently I would recommend just doing an ethanol precipitation, which favors recovery of longer DNA molecules (see for example this protocol).

Nice answer. The Monarch stuff only seems to work for DNA up to 25 kpb (may not work for my 48 kbp). My lambda-DNA didn't seem to go trough the gel filtration column, I may take a look into that ethanol precipitation.


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Why is Chromosome 1 called Chromosome 1?
Chromosome 1 is the designation for the largest human chromosome. Humans have two copies of chromosome 1, as they do with all of the autosomes, which are the non-sex chromosomes. Chromosome 1 spans about 249 million nucleotide base pairs, which are the basic units of information for DNA. It represents about 8% of the total DNA in human cells.
Why is Chromosome 1 called Chromosome 1? Is being the largest human chromosome the only reason?

If they had started with the smallest, then what if one is found later that was missed because of its small size? If you start from the largest, that's less of a problem.

Because biologists aren't  C-language coders  :-)

@forest But it would have been much more embarrassing if they'd started with the largest and then found a larger one! (I'm looking at you, zeroth law of thermodynamics.)

@user1136 Is there some reason it's written "any body" (this is the actual title of the paper) or do I need to write a follow-up called "Can Anybody Spell?"

@user1136 Thanks -- that makes a lot of sense. I agree that it's a very good title, now that I understand it.

Chromosomes were first known about from karyograms (that's the word for chromosome pictures like these) sort of like this one (1)(2):

The scientists looking at these chromosomes didn't know much about them at first. They were discovered before anything was understood about genes, but by 1922 it was thought they were the carriers of genes. Without much understanding of the chromosomes, and certainly no understanding of what they carried, scientists needed an easy way to order and compare them. They chose a straight forward option - size - and paired them up and then lined them up biggest to smallest. Because the sex chromosomes didn't fit into this scheme of matching pairs they were left to the end.
Hence Chromosome 1 is Chromosome 1 because it is the largest autosomal chromosome.
Notes:

The actual first karyogram was of a plant, this one is of a human male.
The image above is public domain, obtained from Wikipedia, and originally made by the National Human Genome Research Institute.

This also works for chromosomes in other species, but sometimes with complications due to interspecific phylogenetics. Chromosome 2 turned out to be two smaller primate chromosomes fused, and these half-chromosomes are now called 2A and 2B. In particular, in non-human primates this has required a renaming of chromosomes, and one that isn't as simple for them as numbering by size.

@user1136: double checking, I see that it was the first observation of chromosomes that was in 1842 but Karyograms were presumably a bit later. Human chromosomes are not the easiest to see so the science advanced in other organisms earlier

Size is a difficult one to judge when chromosomes are similar sizes, and it was more difficult before staining of the bands.
Because of this, some chromosome naming systems group chromosomes into different categories of the centromere type (acrocentric, telocentric), so the largest do not always necessarily descend in order of size. Some genomes still use a sub-classification system, such as Feline (A1, A2, B1, B2), though it is a lot easier to treat chromosomes numerically in programs.

Welcome to Biology.SE! While interesting, this doesn't really answer the OP question. ——— Please take the [tour] and then consult the help pages on the standards for [answer] effectively. Thanks!


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What does basipetal succession (of flowers/leaves) mean?
The definition says that basipetal succession is the arrangement of flowers such that the older ones are present at upper side and the young flowers are arranged towards base. But in this diagram:

the oldest flower is at the base and the youngest is towards the upper side. Can anyone help me understand this?

The definition you quote is a bit misleading — what matters is where the lateral flowers are connected to the inflorescence axis, not where they are physically in space.
Thus, due to the way these cymes develop (starts with a terminal flower and then a lateral bud grows out to form anther terminal flower, etc.) they must be basipetal because the first flower to develop is the terminal flower.  In other words, for cymes the lateral buds tend to overgrow so it looks like they are above, but what really counts is where they are placed on the inflorescence axis (which is below).
You may find this explanation clearer than the one in your textbook.

In my book, it says that Helicoid and Scorpiod Cyme are examples of Cymose Inflorescence which shows basipetal succession of flowers.

Sorry, my original answer wasn't very good — I hope the edited version is more useful to you!

Thank you, I really understand this much better!

You're very welcome!


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Growth rate oscillation in the a population of non-interacting bacteria
I have come across this theoretical paper claiming that if you start a batch culture from a single E. coli cell, the exponential growth rate of the population defined as $$k = \frac1N \frac{dN}{dt}$$
could oscillate for as long as 30 to 40 generations. In this equation, $N$ is the number of cells, and $\frac{dN}{dt}$ is the rate of change of the number of cells with time.
My question is:

Have these oscillations been ever observed? This seems like a very simple experiment. Looking for references.

Edit: As mentioned in the paper, the "oscillations are hidden to the optical density measurements which provide a proxy for the total mass of the population" and not the number of cells.

The theoretical article concerns growth rates of single cells. There are many studies that model cell cycle as a non-linear oscillator (see Tyson and Novák, 2015).
However, growth rate measurements in microbiology are usually done on cell populations consisting several cells. You generally do not observe any oscillation because:

Cells are not synchronized
There can be variations in growth rate of different cells because of noise
The measurement time points are much larger than the period of oscillation

Some of these reasons are already mentioned in the paper you linked (Jafarpour, 2019).
I do see some ups and downs in the growth rate in my own data; E. coli growing in LB in a 96 well plate.

X-axis is the time in seconds; measurement was made every 15minutes. Y-axis denotes difference in OD between two consecutive measurements. The different colors are biological replicates. However, I cannot say that this is the kind of oscillation that Jafarpour talks about. It appears more like stochastic fluctuations in growth rate or measurement errors (they are also not damping by the end of growth).


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creating life in the laboratory
Originally life came about through non life but Scientists are unable to achieve this in a laboratory . Why is this ? Is it the time factor ? I believe that it took one billion years for life to evolve here on Earth did it not ?

Should this not be tagged abiogenesis rather than evolution?

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

It seems that science has moved on somewhat, and scientists have created 'living' (self-replicating) artificial bacterial cells. They built the genome
from physical materials and transplanted the engineered genome into an existing bacterial cell.  This site has a timeline of the history of the project https://www.jcvi.org/first-minimal-synthetic-bacterial-cell

So they have only built the genome and not an entire living cell ? How far away are they from creating a self replicating living organism ?

Well, they have built an entirely new self-replicating organism, but needed an empty cell to get it started.  They may not prioritise making a cell from scratch, because bacterial cells are plentiful.


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What is this African bug?
This is an arthropod I found in an apparently abandoned mongoose burrow in the Maasai Mara game reserve, Kenya:

That was the best photo I could get of it. From what I could tell, it had six legs and very long antennae, so I'm guessing it's an insect. It was vaguely orthopteran-like and had striped/banded legs with a dark dorsal side.
Does anyone have any idea what this could be? Even if the species can't be discerned, I'd appreciate knowing what clade this critter belongs to.

Based on the long legs and long antennae, I'd say you're correct that it's an orthopteran, very likely a cricket or one of its allies (i.e., suborder Ensifera).
Within this subgenus, the most likely candidate families are either the "true crickets" (Gryllidae) or "camel crickets" (Rhaphidophoridae).
Your photo is not nearly good enough to begin making more informed specific guesses. However, If I had to guess, it could possibly be a cricket in the genus Phaeophilacris, which are striped-leg crickets found in Africa.

See inaturalist for incidence of this genus in Africa.

You can see some photos of Phaeophilacris Bredoides here, with a few photos copied below:

 Source
You can read an interesting paper about communication in this genus here1

 1. Heinzel, H.G. and Dambach, M., 1987. Travelling air vortex rings as potential communication signals in a cricket. Journal of Comparative Physiology A, 160(1), pp.79-88.


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What is the name of this insect?

This insect was found in my garden in India on the evening of August 07, 2019. It's rainy season here.

it's a leafhopper. a lot of them have horns. You are supposed to state the location of your garden, if it's in america/india/UK/south africa.  https://www.google.com/search?q=horned+leafhopper&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjkn4yml_HjAhXtAmMBHe5NBDAQ_AUIECgB&biw=1972&bih=1009

Not a leafhopper but a treehopper (same order, suborder and infraorder, different family); if another is seen a side view will help (the pronotum of all treehoppers is of high value in identification, but we do need that side view to go further -- which will be done by someone else; I don't know the Indian fauna of the group).

This is a treehopper (an insect in the family Membracidae).
As Arthur J Frost mentioned in his comment above, it will be difficult to ID this specimen more specifically given the angle, lack of further info, and my personal lack of knowledge of Indian fauna.
However, you can view an at-least similar looking species by viewing Oxyrachis tarandus, which is found in India (see here and Sharma & Pati (2011)1).
You can find photos of O. tarandus here, with one copied below for reference.

 © www.NatureLoveYou.sg

 1. Sharma, A. and Pati, P.K., 2011. First report of Withania somnifera (L.) Dunal, as a new host of cowbug (Oxyrachis tarandus, Fab.) in plains of Punjab, northern India. World Applied Sciences Journal, 14(9), pp.1344-1346.


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Why are ducks more cautious than pigeons?
In my city park there are mostly two types of bird:

Mallard ducks
Rock doves (pigeons)

When I feed pigeons, they approach me very closely. Sometimes they peck the food that fell on my feet. If I hold my hand with food in the air some pigeons will land on my hand and eat.
In the same park there are Mallards, who are always very cautious and they try to maintain about 1-1.5 meters distance from me. They also run away when they see some rapid movement of mine.
Why are ducks more cautious? Why are pigeons more careless?

For goodness sake, stop feeding pigeons! Let them forage for themselves.

And I suggest also that you duck soup.

A possible reason is that pigeons in a city live there year around, while urban ducks often migrate, or their populations are refreshed by new "recruits" from wild populations ; so pigeons have more opportunity to adapt to being close to people.  Another possible reason is that pigeons are more agile than ducks on land and are more able to escape if you decide to grab one for dinner.

This could be due to the fact that mallards are wild animals, whereas, although they may appear to be, ferral pigeons/rock doves, are not. They are, as the name suggests, ferral. Meaning they were once domesticated and then their ancestors were set free and left to breed out in the wild. Therefore they may still have some ingrained trust in humans whereas mallards would not.
Edit: sorry I'm new here and didn't know that it was necessary to add sources.
https://books.google.co.uk/books?hl=en&lr=&id=whScRZEmRl4C&oi=fnd&pg=PA3&dq=info:Xm_-vES8Sv0J:scholar.google.com/&ots=eWsLsAP-9I&sig=5j0XfJ8vaEMTTEL6djwXOq4409c&redir_esc=y#v=onepage&q&f=false
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=why+pigeons+are+feral+and+not+wild&btnG=#d=gs_qabs&u=%23p%3DtgCc_1AYDyIJ

Welcome to Biology.SE! This could become a good answer, but factual answers rather than speculation are expected on this site. Consequently, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to consult the [help] pages and [meta] for additional advice on [Answer] effectively on this site. Thank you!

Thanks. I've added references now. Sorry I didn't know that it was necessary. Although I don't think the downvote was needed :(

Not my downvote! — Thank you for editing. Unfortunately neither of your links works. Your first link leads to an unavailable page (at least for me). The second appears to be a link to a google scholar search, which isn't an acceptable reference. I encourage you to pick out a few of the articles from that search that support your claims and then add them as individual references (see links above for an acceptable format). Also note that links often break over time and so formal references should always be included. Thanks!

Ahh okay, thanks for letting me know!

Maybe pigeons are smarter and recognize free lunch faster .  I once worked where thy had a 40 acre lake which attracted Canadian Geese. The geese were a nuisance ,covering walk ways with dung , etc. So the grounds keepers put 2 inflatable alligators on the lake , that kept the geese at the other end for over a week. One day , herring gills landed on the alligators , the geese came back in a matter of hours. Were the gulls smart ,recognizing inflatables , or were they dumb and not recognize danger ?


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Why is the size of the human penis not in proportion to that of the rest of the body?
According to this research
https://qph.fs.quoracdn.net/main-qimg-2ffcc3b19663af67c96ac1be8f3d6351-c
it is more likely for tall men to have large penis
but there are still many tall not having large
It is clearly not matching the size of other organs such as arms, legs, hearts, etc.
If you see a tall man you can see he has long arms, long thighs, bigger heart, etc.
similarly for short men, they have short arms , legs ,etc.
why it is not the same for penis?
why tall men may have short penis or short men may have long ones?
why the length of the penis does not match with make height similar to other organs?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — at a minimum please supply a credible source showing that human penises deviate more from their expected proportions than other parts of the human body. ——— Please also take the time to check out the [tour] and then the help pages starting with [Ask] questions on this site. Thanks!

Asymmetric is the wrong word. That would mean that one half (along the length) does not appear to be the mirror image of the other. "Male" would appear to be redundant also. You should edit your question say something like "Why is the size of the human penis not in proportion to that of the rest of the body?" (Remember the question mark.)

Why are some people more intelligent than others? Why are some people taller than others? Perhaps all theses have the same or similar answer...

@SolarMike it is definately not the same. the intelligence is not a physical thing, it is not an organ. taller people have tall arms, tall legs etc. there is a percentage of proportion that goes with these organs ( like your heart size is matching your fest size) to a certain degree is accurate. but for penis there is no theory that works, foot size is false, and penis size vary for the same tall people ( so my question again why penis size vary (biologically what causing this difference in size, why it is not same as other organs matching a percentage of the human tall))

According to genetics all phenotypical characters are inherited from both biological parents. The Y chromosome is mainly responsible for appearance of male characters and the only source of getting Y chromosome is from biological father. However other traits i.e. of height  can be inherited from either biological father or mother. Therefore if the height of mother was taller and is dominant over father's height then the child will be having the mother's height. The Y chromosome related characters would remain same and you would not observe any change in male character.  Therefore, you can not relate all physical characters with Y-chromosomal characters.

but you don't see a tall man (coz the father was tall) with short arms (coz mother was short and has short arms) all organs for tall men are tall and big that matches that tall. except for penis it is vary for the same tall people

Welcome to Biology.SE! Your answer over simplifies the genetics of both penis size and height (for evidence start here:https://en.wikipedia.org/wiki/Human_penis_size). Inclusion of references is also highly desirable. ——— Please take the [tour] and then consult the help pages on the standards for [answer] effectively. Thanks!


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Phylogenical differences with nuclear and mitochondrial DNA
This is a textbook question, I would like to verify my answers. According to the textbook it is possible to construct a phylogeny using nuclear and mitochondrial DNA and these trees to be different, I should give reasons why this might occur.
Here's two that I think might be valid
(1) Mitochondrial DNA is maternal, while nuclear DNA comes from both parents. It is possible to have a (female) hybrid C between species A and B, and if C cross with an individual with genotype (A), the offspring could show some genes from the species B. I consider this to be a phenomenon of introgression, and genic flux would be in these case shown in the nuclear DNA, but not in the mitochondrial.
(2) Mutations might occur. mtDNA has a higher mutation rate than nucDNA. If the phylogeny is constructed looking at a gene, more recent mutation could should in the mtDNA.
This is what I could think of, I would like to know if they sound acceptable, and if there are more possible reason to find different phylogenies using mtDNA and nucDNA.


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Are casein proteins in UHT milk digestable for infants or toddlers?
As a novice cheesemaker, I have read that Ultra High Temperature prosessed milk is unsuitable for cheesemaking, as casein proteins are denatured and cannot be curdled with rennet.
I have verified that claim experimentally. Although curd has formed, its quality was poor (I managed to make whey-like cheese after further heating though).
As casein is the majority of milk protein and curdling with rennet is important component of milk digestion, I started to worry if feeding UHT milk to toddlers is a good idea. (I also wonder, whether boiling milk may lead to a similar casein denaturation.)
Unfortunately, Wikipedia addresses only the cheesemaking aspect of UHT processing. I do not know whether it is possible to digest temperature-denatured casein (without proper curdling).
Moreover, after some more research I am not sure what is mechanism of milk digestion in infants: Which enzyme curdles milk in human infants?

Why are you asking specifically about infants and toddlers? They have the same enzymes as adults and they typically digest milk better than adults.

@Jan It is exactly because they typically digest milk better than adults. I want to avoid answers based on age-related enzyme production loss. I have been taught in school that our infants produce rennet while adults don't (which I am not so sure any more). For sure a lot of adults do not produce enough lactase - thus I expect there may be similar case with rennet.
Also, because a toddler is the main milk consumer in my family. ;)

Goat’s milk is easier to digest but did you mean cows milk?

UHT treatment increases the digestibility of casein.
Ultra High Temperature Treatment, but Not Pasteurization, Affects the Postprandial Kinetics of Milk Proteins in Humans (Journal of Nutrition)

Moreover, the UHT treatment of milk causes structural changes in its
  protein system. The main change is the denaturation of whey proteins
  and their interaction with casein micelles. Consequently, it was
  expected that the behavior of the UHT milk would be similar to that of
  casein micelles, as observed with native casein. However, it has been
  shown that the interaction between casein micelles and whey proteins
  is also accompanied by a large increase in number of very small,
  soluble particles resulting from the desegregation of casein micelles.
  Consequently, by weakening the interaction forces between caseins,
  heat treatment provokes both a loss of the micelle framework and the
  formation of small aggregates. Correlatively, an increase in the
  amount of nonsedimentable casein has been observed in UHT milk
  following high-speed centrifugation (33). Two effects of these changes
  on milk properties may be softer coagulation and a higher
  susceptibility to enzymatic hydrolysis due to loosening of the
  micellar structure and the presence of small aggregates that may be
  more accessible to enzymes.

In the stomach of adult or infant, gastric acid and the enzyme pepsin denaturate whey and casein proteins from either raw or heated milk Critical Reviews in Food Science and Nutrition). The denatured proteins are then nearly completely digested by the enzymes pepsin in the stomach and by trypsin, chymotrypsin and peptidases in the small intestine (Medical Libretexts.
Humans, including infants do not have the enzyme rennin (chymosin).

Rennin, also called chymosin, protein-digesting enzyme that curdles milk by transforming caseinogen into insoluble casein; it is
  found only in the fourth stomach of cud-chewing animals, such as cows.
  Its action extends the period in which milk is retained in the stomach
  of the young animal. In animals that lack rennin, milk is coagulated
  by the action of pepsin as is the case in humans. A commercial form of
  rennin, rennet, is used in manufacturing cheese and preparing
  junket (Britannica).
Chymosin is secreted in the neonatal stomach of ruminants (cattle,
  goats, camels), pigs, cats, and rats. Animals including humans,
  chimps, and horses have inactivating mutations in their chymosin gene
  and do not secrete the enzyme (vivo.colostate.edu).

There's one study that mentions the presence of chymosin in humans, but the evidence seems to be very weak as described in another Biology SE answer. Some articles, like this one mention chymosin in humans without proper references.

Does it mean that UHT processing does not affect latter cuddling in the stomach?

UHT does not affect casein, but it does affect whey protein. I'm not sure what exactly this means in regard to milk curdling in the stomach. But stomach acid and pepsin denaturate both casein and whey; this does not prevent their digestion or absorption, but it can slow it down, which can be actually a good thing, because it results in more even nutrients supply. In general, various types of heating do not slow down the digestion or absorption of nutrients. In other words, stomach acid affects milk proteins more than heating.

From what I have read so far curdling is important to prevent proteins from leaving the stomach too early. Also, from slide #22 of this presentation on UHT treatment (no further references though) I infer that denatured whey protein may disturb casein curdling.

@abukaj, at the top of my answer, I added a quote from the ScienceDirect article, which says that heating makes both casein and whey proteins more digestible, which means they are both more accessible for pepsin, which breaks them down. So, this first phase of digestion of proteins in the stomach is increased; the second phase, which occurs in the small intestine, does not seem to be increased, but in summary, the digestion time is shorter.

Hesting milk to 90°C does not count as UHT processing. The milk is not even boiled.

@abukaj, I found another source (see in the answer), specifically about the effect of UHT treatment on milk proteins. In short: UHT increases digestibility of both casein and whey proteins. If proteins are digested easier, they will leave the stomach faster, so they will quicker come into the small intestine when they will be digested further. So, in this case, faster passage of protein through the stomach does not decrease but speed up their digestion.


text:
Why do we need to grow plants to make food?
Why can't we synthesize the nutrients that we need directly from chemical reactions, from energy and simple inorganic molecules found around us? If it's hard, why not try to copy how plants do it?
I feel like growing plants is very inefficient: it is consuming a lot of energy for intermediate steps that may not be required – growing roots or inedible parts, performing reproduction, consuming soil and space, requiring constant light and irrigation... And huge amounts of energy is invested to slightly compensate for these caveats and increase productivity, while it still looks like an inefficient way of doing synthesis of nutrients and other compounds we need to eat.
Is there a reason that such resources are not directed to building processes to perform such synthesis via other – hopefully more efficient – means than growing plants/animals?
Note that I found a partial answer there, however I was not satisfied by an unexplained "photosynthesis is the only viable way to create material that can yield those nutrients".
Is photosynthesis that hard? If that so, why?
If it's so hard using organic chemistry, why cannot we simply extract/mimic the biological reactions happening in the plants to generate nutrients? (we still don't need to grow whole plants)
If we are not able to do that, what does it means about our current understanding/mastery of chemistry and biology ?

I'm voting to close this question as off-topic because it is about logistics of industrial chemically-synthesized food production.

Is there another stackexchange I could move it to?

I am not sure (perhaps [worldbuilding.se]). In any stackexchange, this would be a broad question.

Why are so many "why" questions accepted here? Everything is turning into phylosophy instead of biology. Why does everyone question everything when there is no major problem with it? Also, many nutrients, mainly sugars and sugar alcohols, are already artificially produced and they are mainly associated with - problems.

Even if we could synthesize "food" reasonably efficiently, we don't know everything that is needed for a healthy diet. 2) Growing plants provide many other services - from replenishing oxygen to soil stabilization to just being pleasant to be around.  Since you have them for all those other reasons, why not use them for food too, rather than resorting to industrial chemistry?

I'm simply curious, and I find it hard to find good answers to these questions. 1) seems to make sense ! 2) we could go back to having forests everywhere instead of fields, which seems like it would have lots of benefits

@palkeo: Plenty of things to eat in forests, and then there are grasslands.  WRT #1, you might reflect on the fact that (AFAIK, anyway) we really don't synthesize any significant amounts of organic chemicals from scratch (that is, starting with CO2, H2O, nitrates, and a few minerals, as plants do) .  Most things start from organic feedstocks, either plant-derived, or petrochemicals.

We are part of a biological system, and we evolved to be part of it. Plants are the base of that system, and the main means of capturing energy and inorganic compounds and converting them to nutrients which are bio-available, along with bacteria.  The further we move from the niche we evolved to occupy, and the further we change the environment of the rest of the system, the more likely we are to bring about our own extinction.
Edit: This answer is somewhat opinion based. We haven't finished the experiment that proves this thesis, yet.


text:
How old would seashells be if I found them 9 ft deep 30 miles from the ocean while digging a pond in North Carolina
 This is a picture of some specimens that I found while digging a pond. I'm 30 miles from the coast in Wilmington, North Carolina and dug down about nine feet past the blue clay and hit a layer of seashells.

This Wikipedia page might interest you.


text:
Why are human bones usually curved?
Is there any simple explanation as to why human bones are more curved than straight and are thicker at ends and thinner in the middle?

Can you explain what you mean by curved? Do you mean the surfaces of the bone are curved because of the greater width of the ends, or do you think the actual bone (i.e. the actual axis of the bone) is curved (one is true, the other may be an illusion, or present in disease.)

@anongoodnurse - I meant the axis.

Thanks. The anatomical axis of normal long bones is usually a straight line, but the outsides can be curved. Just clearing up terminology. Ribs are obviously curved, and quite commonly fractured as a result.  This might be rightly deleted as an answer in a comment.

The slight curve allows bone to absorb shocks better.
This curve allows the bone to act like a spring and flex a little bit. One issue as bone get older is that they become harder and, therefore, more brittle which leads to the elderly breaking bones for a fall that younger individuals just get a bruise. Young children often get stick or "splitting" breaks where the bone does not break but separates as the bone is still soft.
The ends tend to be thicker as that is where the joints are and there are forces that need to be absorbed.
Of course, if the load applied to the bone is just too much or it is a sharp shock then bones will break, but really the skeleton is nature's design for a suspension system to allow us to do what we need to do walk, run, stand, etc
This set of slides makes good reading, with things like "less ductile", "elastic behaviour" and "strength in compression" worth looking for:
Mechanics of bones by Phillipe GILLET
A quick search gave many results but of these two shown the first seems very interesting from an engineer's perspective:

shock absorbing "goo"
shock absorbtion

While I think you're right, you can improve your answer by adding literature that supports your thoughts.

@Arsak As an engineer, I wrote an answer explaining the function in layperson's terms, the OP did not ask for any formulae of how to calculate the maximum stress point or the maximum bending point for a given load. So, for the question asked I think the answer stands as sufficient. If you want to ask a question about stress calculations or whether a cylindrical structure is stronger or weaker than a solid structure you have that option.

I wasn't thinking about calculations or similar sophisticated level, rather about an introduction to biophysics for example that covers what you've written. And sorry if my comment reads like an attack, that wasn't my intention. I just know that the community prefers well referenced answers to maintain quality of the site.

While this sounds plausible, it is not correct. Long bones are not curved and they are not springs of any type. Furthermore, your sources do not support your assertions.

The two sources given are unrelated to the question asked and the answer given. Please provide appropriate references related to the specific question and answer asked, not unrelated trivia. I worry that the presence of unrelated citations appears to give an answer more credibility than it deserves - I find this worse than lack of citation and perceive it as a form of academic dishonesty.

@anongoodnurse please show me a perfectly straight bone.

Solar Mike, it is not the responsibility of the commenter to prove you wrong; it is the responsibility of the answerer to prove their answer is correct. Users are encouraged to point out wrong answers, not to argue with them.

As @BryanKrause pointed out, sources should address the question. Your added source, while long, does not discuss the axis (straight or curved?) of the bone. Again, it does not support your answer that bones are curved to provide a springlike advantage.

@anongoodnurse I did not choose it based on the length.... But words like ductile...

At this point, comments become discussion, so I will not press my point any further, Just looking for an answer based in fact, with proof if needed/challenged.

@anongoodnurse: After looking at a number of on-line pictures of human skeletons, I have to disagree.  The long bones ARE curved.  Sometimes, as with the femur & tibia, the curvature from end to end can be quite subtle, but it seems to be there. And of course there is a lengthwise curvature, with the ends being wider than the middle.

@jamesqf - The diaphyses of the long bones are not curved. Tthe anatomical axis (different from the mechanical axis) of the humerus is a straight line. I don't count the joints as curves. Joints are larger/oddly shaped because of their function. The radius/ulna, because of the rotatory function, are slightly  curved. The other long bones (tibia,  humerus, and shorter "long" bones (metacarpals/tarsals, phalanges, etc.) are not. Add all of them together, and the answer is that most bones are not curved. In any case, the answer does not support its assertions. (Bones are curved for springiness.)

@jamesqf - I don't want to promote an argument from authority, but as an ER doc, I have looked at literally many thousands of xrays over the decades, in addition to, well, studying human anatomy. I can see how someone would think they're curved. But if they are curved, there's something amiss (an old fracture, an early vitamin D deficiency, a musculoskeletal disorder, etc.)

I don't know anything about biophysics or engineering, but could someone explain why a "rigid" structure is better at absorbing shock if it's curved? If the answer is too long, a link would do.


text:
Star-like organism seen in microscope

I found this strange star-like thing while observing a slide of onion root somatic cells. I don't know that it is; I even doubt if it is an organism. It has conical arms directed  radially outwards all over it's body. It wasn't moving. If it was indeed living,  maybe I had killed it while flaming the slide. Anyway, I am interested in knowing more about this  unexpected guest of mine. Can anyone tell me what it is ?

It may be a stellate trichome from a plant.
You can find other ones by taking swabs from the onion and nearby plants.

cool images here
wiki info about trichomes


text:
Database for Macroinvertebrate Taxonomy
I compiled different data sets of invertebrate occurrences across some countries and now I want to ensure that all the taxonomic information is homogenized and correct. To this end, I am looking for a database which allows me to evaluate my date. Basically, the equivalent to what algaebase.org is for algae.
I know about gbif.org but already found some mistakes in there.

Have you sent your observations to gbif.org? Sure they would be happy to improve their database...

No, not yet but thanks for the suggestions I will consider it in the future.

So, you have the mistakes you found, why not send those now?

Because I did not keep a record. I just cross-checked algae base with gbif on some species and found different results on what is considered the expected name and what a synonym.


text:
What's the evolutionary purpose of having hearts?
According to this
New understanding of heart evolution

Humans, like other warm-blooded animals, expend a lot of energy and need a lot of oxygen. Our four-chambered hearts make this possible. It gives us an evolutionary advantage: We're able to roam, hunt and hide even in the cold of night, or the chill of winter.

But in the other hand, there are heartless JellyFish of 2.3 meters with up to 70-150 tentacles per one of each 8 lobes of up to 37 meters in lenght. Lion's mane JellyFish
Having humans spending a lot of their energies in moving limbs, even though I understand JellyFish move in another environment, I'm having a hard time believing moving our limbs spend more energy than moving 70-150 tentacles per one of each 8 lobes of up to 37 meters in lenght.
What's the evolutionary purpose of having hearts? Is it for animals with it to be able to expend more energy or is there any other reason for it?

Perhaps the currents help move those tentacles... water is approx 1000 times as dense...

Evolution has no purpose. BTW, bacteria also move and they don't even need nervous system for doing so.

Have you tried looking up the energetics of movement for vertebrates?  ——— Note also that a jelly doesn't need a heart to transport oxygen to its tissues since it is very thin and absorbs oxygen from the water.  This makes the comparison to the energetics of a jelly completely irrelevant!

There are very important advantages (not purposes) of having heart.
Animals that have heart are more agile and can be much larger than others. That is because they can move nutrients, gases and waste products faster and efficiently between parts of the body. Without heart and circulatory system, all the necessary material must be moved inside the body through diffusion which isn't efficient especially at longer distances and fast.
All of the largest animals that live and had lived on earth have heart. An animal which doesn't have heart can be large and can be very long, but will be thin to get a very large surface area which will increase the efficiency of diffusion between the body and the environment.
On terms of advantages that they provide, having a heart (and circulatory system) is better than not having one, having closed circulatory system is better than having open circulatory system.


text:
What is the kind of this wasp killing spider from UK?
I heard a wasp buzzing rigorously and when I looked at it, it was caught in a spider web. The spider was on top of the wasp. After some time, they become silent. When I exhaled gently on them, spider moved but wasp did not. Later, the wasp was dead. The spider was obviously smaller than the wasp, yet it emerged victorious.
I attached a photo of the spider. While I am not sure whether this is the one killing the wasp, this certainly lives around the event site.

It should be around 1 cm in body length, excluding the legs. It is situated in UK.

If the wasp gets trapped in the web, then the advantage goes to the spider - it’s not a direct conflict...

Can you get a clearer picture?  Or perhaps you can pick it out from something like this: https://spiderid.com/locations/united-kingdom/

Hanging upside-down in a web suggests one of several groups, but in a building structure, and in what appears to be a messy, tangled web, I think we can safely put this one down as a member of the 'cobweb spiders' - the Theridiidae.  This group includes the infamous Black Widows, and some are known to successfully take relatively large and dangerous prey.
So, your particular spider has an obvious clue - the somewhat flattened dark abdomen with a large, light-colored patch in the middle of it.  The shape suggests Steatoda, and there is only one spider that this could be:  Steatoda nobilis, one of several spiders that frequently get called "False Widows".
Here are two links and a representative photo:
https://www.naturespot.org.uk/species/steatoda-nobilis
https://www.cabi.org/isc/datasheet/119917

Oh, I should add that despite the breathless hype the tabloids like to get up to, these spiders are known to be pretty harmless to people.  On rare occasions, a bite (which is not easy to get from these shy spiders) may produce symptoms like a mild Widow bite, but the discomfort seems to pass within a day or so.

Thank you very much. Even though I couldn't photographed it well enough to show the pattern on its stomach (or whatever it is called for an arachnid), it is obviously this one.


text:
Why do death cap mushrooms not warn of their poison?
This has been puzzling me for a long time now. There is an evolutionary predilection for living things which have evolved strong defensive measures (that may not themselves be visible) to give distinct visual or audible warnings advertising these measures.
Wasps, hornets, snakes, and bees are all brightly coloured. Snakes may even have rattles to advertise their venom. These things by in large don't want to have to use their poison in a defensive capacity. Getting revenge on a predator who has mortally wounded you is a Pyrrhic victory.
These warnings are so potent that many animals without such measures will mimic these warnings in order to piggy pack on a general evolutionary bias towards an instinctive avoidance of anything that warns of being poisonous.
But take the death cap mushroom.

This innocuous fungus looks identical to completely harmless mushrooms. It has no foul smell. In fact, evidence shows that it actually has a pleasant taste! That picture above actually looks pretty tasty in my opinion.
This fungus has gone to the trouble of developing one of the most potent poisons in nature (humans have a seriously robust digestive systems by animal standards, and yet a single death cap can easily kill an adult human).
So why so secretive about its arsenal?
I know this same question about evolving poisons that are not well advertised could be applied to a large number of animals, insects, and particularly fungi, but I think the death cap is the most extreme example in both the lethality of the poison considered, and combined lack of advertising.

I collect and eat wild mushrooms and that Amanita looks very frightening to me.

Two questions need to be asked, 1) Was the mushroom's poison evolved specifically to serve as a poison, or does it serve some other function and just happens to poison humans?  (Given the long-delayed effect, this seems possible.)  2) Was the poison evolved for humans, or for some other species (insects, perhaps), which can detect warnings like odors or UV markings that humans can't?  Or a third possibility: the mushrooms are fruiting bodies.  A critter that eats them gets dusted with spores, goes somewhere else, and dies, providing a food supply for the spores.

Related https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont?noredirect=1&lq=1

Most of this type of evolutionary question are generally worthless, IMHO. You can rationalize anything post hoc and then go away with the misapprehension that you have been involved in science.
To add a few of those possible post hoc explanations (which took longer to type  out than think up):
1) The poison is only accidentally a poison.  It serves some other function in the mushroom's metabolism.  There are numerous possible examples of this.  For instance, the stalks of rhubarb are edible, while the leaves are poison; potatos are edible unless they've turned green from exposure to sunlight...
2) The poison might not be directed at humans.  The mushroom might have some warning that would be obvious to other species, for instance a smell or markings visible in UV (such as many flowers have).  We have lots of examples of poisonous plants that we grow because they're attractive to us: datura, lily of the valley, foxglove, oleander, delphinium...
3) If I'm not mistaken, mushroom poisoning takes rather a long time to kill, which argues against it being a defense.  The poison might have evolved as an aid to reproduction.  Mushrooms are the fruiting body of the fungus.  If an animal eats it, it consumes the spores.  If it dies hours or days later, it has transported those spores to a distant location, and the corpse provides nutrition for the new fungi.
However…
Doesn’t the all-white toadstool look distinctive and memorable to you? It doesn’t look remotely like the field mushrooms or other edible mushrooms I would collect. What edible fungus would you confuse it with?

The death cap is infamous for looking like safe mushrooms. For instance https://www.mushroomguru.co.za/uploads/5/5/2/1/5521125/4187215_orig.png
This is also totally safe, albeit not as tasty. https://www.wildfooduk.com/wp-content/uploads/2017/06/White-false-11.jpg
All evolutionary questions are post hoc, unless you have a couple of million years to spare to actively observe change.

@Stumbler — One of your links is broken, but I am only speaking from experience and my post hoc reasoning may be faulty. All evolutionary questions may be post hoc, but that doesn’t mean they have the same level of uncertainty. Speculating about why something is the way it is is in a different league to calculating the time of the last common ancestor of mice and rats from their DNA sequences, for example.

I'd be okay with this sort of "we can't really know" answer if you included some of the different likely competing explanations. Jamesqf's comment is a decent starting point that hits most of the basics (might not be primarily a poison, might not target humans, might not be necessarily selected to prevent predation, etc).

Bryan — Well my main point was really that the “Exterminating Angel” whiteness appeared distinctive to me and my wife (who knows more about fungi than me). I suppose it depends on where you live. But I invite @jamesqf to edit my question with his comment to improve it. That’s supposed to be acceptable, here.


text:
Are pseudogene counted as a subtype of long non-coding RNA genes?
Are pseudogenes regarded as a subtype of the genes for long non-coding RNAs?
I could not find the answer to this question in an internet search.

A note on nomenclature in modern biology
As it stands, this question seems to assume there is some legal commission, Académie française, or the like that is devoted to continually determining scientific nomenclature, and that those in the field obediently follow it. While organizations like IUPAC — The International Union of Pure and Applied Chemistry — do exist for standardization, they move very slowly, and only come out when the dust has settled (so to speak). So if I write an article about genes I can classify them as suits my purpose. I may wish to distinguish just between coding or non-coding; or between structural, informational, regulatory and junk etc. etc. Nobody is going to throw me in gaol if they disagree.
Is it scientific to classify pseudogenes in this way?
By this, I mean do the genes (for that is what we can compare) for long non-coding RNAs (ncRNAs or lncRNAs) have enough general features shared by pseudogenes that it would be useful to sub-type pseudogenes in this way. In my opinion, No. Pseudogenes are generally regarded as non-functional — remnants of unsuccessful or uncompleted gene duplication, or of reverse transcription of mature mRNAs into the germ-line DNA. In many cases they are not even transcribed.  There may not be a single function for those gene-products termed lncRNAs but in general they are transcribed and thought to have functions concerned with gene regulation. There are no structural similarities with pseudogenes, so that all the genes have in common is that they are, well, long, so to that idea I would say “So long!”
How do the genome annotators regard this?
The people that make the rules, de facto — and revise them as science advances — are the ones with the job of annotating sequenced genomes. I haven’t made a general survey of genomes, and am restricting myself to the genome of the fruit fly, Drosophila melanogaster, with which I am familiar. The distinct Biotypes for genes in the data at FlyBase are currently (2019) as follows:

ncRNA (aka lncRNA)
protein coding
pseudogene
snRNA
tRNA
rRNA
snoRNA
pre miRNA

I suspect that this is standard among the large genome databases, and it can be seen that pseudogene and ncRNA are regarded as distinct categories.
Of course, one can argue with this classification — where are the SINES and LINES and Drosophila-specific mobile elements, for example? But that just illustrates what I have written above.

Thank you @David for your comprehensive response.


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Is mating between human and non-human primates theoretically possible?
I wonder if it is theoretically achievable to produce living offspring between a human and a non-human primate. Great apes have 24 pairs of chromosomes compared to our 23, however, it is known that a mule is made from a donkey (62 chromosomes) and a horse (64  chromosomes).
Are there other reasons why this human/non-human primate hybrid can't survive?

I don't know if it is theoretically possible (I guess yes), but there have been actual experimental attempts to do so, that all failed.
https://en.wikipedia.org/wiki/Humanzee


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What renders a cytoplasm basophilic?
I know that being basophilic or acidophilic corresponds to affinity to certain dyes used in microscopy.
What i want to know is what characteristics of the cytoplasm can we infer from its basophilic property? Does it give us any idea about its different compartments relative abundance, or practical features of the cell? Can we predict how acidophilic and basophilic cells differ in their life and roles?
Thanks for help.


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Blood and hair follicles from 25 people put on the Moon; enough to regenerate a human population?
Discussion on the question Why were blood and hair follicles from 25 people put on the Moon? calls into question whether this is a stunt or might have any basis in science.
There's two parts to my question:

If somehow preserved well, do hair follicles and blood samples from a group of humans provide sufficient coverage alone to reconstruct a human population as far as the DNA content is concerned? Ignoring that you don't have an egg to put it in, is enough DNA present, or would there be key bits of DNA missing that you'd need a germ line sample in order to get? I suppose this can be asked as "can we clone people from blood and hair follicles alone?"
Would 25 individuals be enough to obtain a viable population of clones?

Background from the linked question:
The Wired.com article A Crashed Israeli Lunar Lander Spilled Tardigrades on the Moon says:

Spivack had planned to send DNA samples to the moon in future versions of the lunar library, not on this mission. But a few weeks before Spivack had to deliver the lunar library to the Israelis, however, he decided to include some DNA in the payload anyway. Ha and an engineer on Spivack’s team added a thin layer of epoxy resin between each layer of nickel, a synthetic equivalent of the fossilized tree resin that preserves ancient insects. Into the resin they tucked hair follicles and blood samples from Spivack and 24 others that he says represent a diverse genetic cross-section of human ancestry, in addition to some dehydrated tardigrades and samples from major holy sites, like the Bodhi tree in India. A few thousand extra dehydrated tardigrades were sprinkled onto tape that was attached to the lunar library.

If the 25 human samples were from diverse regions of the world, i'd bet that it would be easy to build a human population with medical supports, although the frailties may not make them viable for wild tribe life.

No, because AFAIK you can't just clone a mammal from DNA.  You need a mother from the same or a closely-related species.  Think of it as "blueprints": instructions to a factory that has a lot of highly-specialized CNC machinery.  Without having those machines (or being able to build duplicates), your CNC instructions are useless.

@jamesqf so perhaps the use of the verb "clone" in the question was misguided. There's still the question of the fraction of the genome present in hair follicle and blood being sufficient.

If you had the technology to build a human from the DNA in hair follicles, you'd probably have the technology to synthesize DNA from scratch. So instead of sending up 25 hair follicles, send up an SSD with DNA sequences from thousands of people.

@user137 a little bit like this?

If we assume for a moment that the samples could be successfully cloned, 25 individuals is probably not enough to maintain a stable human population for more than a few hundred year without experiencing severe inbreeding depression and eventual extinction.
In population biology, there's a general rule of 50/500 for minimum viable population sizes. Essentially, a minimum population of 50 is needed to prevent inbreeding depression, and 500 to stabilize genetic drift. Of course that's a generalization used in management situations, and lots of factors go into making a calculation like this with any amount of precision.
One estimate gives a minimum viable human population (for generational space travel and permanent colonization) of ~40,000 humans in order to maintain genetic diversity. But that only applies to a population carefully screened and selected to maximize the effective population size. Another suggests 160 people could be enough for a stable population, as long as they return home to mix it up with the rest of humanity every 200 years or so.

Thank you for your well-supported answer! I was worried about the samples not covering a complete genome, but didn't stop to think about this issue at all!


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Can you identify this insect (orange back, 6 legs)?

Found a couple of them in central europe on a zucchini plant (in august).
They are about a centimeter in size.
Tried looking for insect with orange back and 6 legs but no result.
[EDIT from comment]: The insect in this post looks pretty similar. There is a difference though - the one in my picture has orange legs not black ones. (maybe different stage of larvae or different species of ladybug or just random?)

There is a related question and answer here which identifies a similar creature as the larval form of a 'spotted lady bug' or beetle; and this is probably what you noticed.  Another possibility is the larval form of a burying beetle (Nicrophorus), but that's less likely.

Yeah I think you're right, that's it ... one difference though, the one on my picture has orange legs not black ones

If you find more, and they are larvae, you just have to watch what they turn into.  Right.  I'm not an expert but the related question was too obvious not to let you know about it.

It is a harlequin ladybird larvae.

This is one of the most variable species in the world, with an unusually broad range of color forms. It is native to eastern Asia, but has been artificially introduced to North America and Europe to control aphids.
I figure that Wiki is saying "it has some of the highest color variability of any wild plant or animal".

wiki: harlequin ladybird


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Why do watermelons have a rind?
Random questions come up when talking with friends - such as this one!
We were curious: what are watermelon rinds good for? So what benefits does it give the watermelon? Why did mother nature give it such protection?

I apologize if this should not be the right forum to ask such a question.

If it didn't have a rind, the water inside would easily evaporate.

Thank you for the reply, jamesqf. Also @downvoter, care to explain the downvote?...

Possibly because you have shown no effort at prior research...

@Solar Mike: I don't know if you could really do research on a question like this.  Perhaps you could look at the evolution of melons (perhaps the water-containing flesh helped the seeds to sprout in their hot native climes?), and then the results of several thousand years of selective breeding by humans.  (None of the melons we eat today are what Mother Nature gave us, any more than wheat or corn are.)  You might find this interesting: https://hyperallergic.com/226096/the-evolution-of-the-watermelon-captured-in-still-lifes/

@jamesqf So you have answered your own question : Yes you can do research on watermelons... I was guessing as for the reason for the downvote unless you missed that. PS, I was not the downvoter...

@Solar Mike: While interesting, none of that really answers the OP's question.  It's like any "why" question in evolution: you can come up with a "Just So" story, but the only real explanation is that it (and previous changes) worked, so proto-melons survived.

You have answered the question yourself: it's protection.
Melons have originated in what is today South-Eastern Africa and Western India according to this source. In a hot and rather dry climate having a watery fruit can bring an advantage to the seeds (helping them to sprout in an otherwise dry soil). At the same time, any source of water would attract animals eating the fruit. A shell would protect the seeds during the ripening process like the shell of a nut prevents it from being eaten.
On the other hand, animals eating the melon might actually be desired, since fruit eating herbivores help spreading the undigested seeds. The shell would then especially protect the watery flesh from water evaporation or predators who are not helping to distribute the seeds. A ripe melon opens up and releases the seeds from their protective shell.


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Is SCNT possible with only the nucleus of a somatic cell (rather than a whole somatic cell)?
The following figure from Life: The Science of Biology (11th edition) explains how SCNT (somatic cell nuclear transfer) was used in the cloning of Dolly:

(The original paper about cloning Dolly - Viable offspring derived from fetal and adult mammalian cells)
Note that an enucleated oocyte and a whole somatic cell were fused, i.e., the nucleus of the somatic cell wasn't isolated from the somatic cell.
Another example in which SCNT was used successfully is the cloning of the monkeys Zhong Zhong and Hua Hua. In this case, fetal fibroblasts were fused with enucleated oocytes, as explained in the paper Cloning of Macaque Monkeys by Somatic Cell Nuclear Transfer.
However, one can find various explanations and figures on the internet that explain that in SCNT, only the nucleus is transferred into an enucleated oocyte.
For example, the following figure is used in Wikipedia's SCNT page:

Though it is noted alongside the figure:

The diagram depicts the removal of the donor nucleus for schematic purposes; in practice the whole donor cell is transferred.

So my question is:
Has anyone ever successfully used SCNT while using only the nucleus of a somatic cell, without the whole somatic cell?
(My guess is "no, the nucleus alone won't do", basically because of the importance of the centrosome, along with the following quotes from the paper From Zero to Many: Control of Centriole Number in Development and Disease:

Centrioles are essential for the formation of microtubule‐derived structures, including cilia, flagella and centrosomes. [...]

  Notably, oocytes and spermatozoa lose parts of the centrosome in a complementary manner. Centrioles, but not centrosome proteins, are lost in the oocyte. On the other hand, in sperm, the PCM material is lost, but not the centriole/basal body, which is necessary for flagella formation. Fertilization brings together the basal body from the sperm, which becomes a centriole within the zygote, and the PCM from the egg.

)


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How to find which genetic pattern is responsible for structure of a cell
I studied that DNA are blueprints that describes an organism.
How do I learn more specifically about DNA regions responsible for storing structure of a cell.
By Structure of a cell I meant to ask which genes are responsible to store the 3-d structure of cell, sub units of a cell and its structure, number of layers a cell should contain and how thick it should be etc.
What I have researched to find answers: Looking at bacteriophage, it has 6 legs and they fold and lock. I did a recent study and learnt that genes are same throughout the organism and epigenitic modification turns on/off a particular gene based on the cell group it belongs to by a process called methylation. I signed up in coursera for a curriculum course, but yet to choose one.
What I am looking for: Is there a reference educational material that teaches gene in below format.

Movements of a cell always stay in this region.
Shape of the cell is defined by head region of DNA.

To put in a question, How do I learn how to map which region of gene is applicable for which characteristics of a cell?
Why am I looking for this answer: I want to build a simulator that can take in an organism's DNA and simulate its growth and cell structure. I am looking for precise sub field in genetics that will educate me for my need.
PS: Thanks for providing feedback on the question. I'll pickup asking the right questions gradually once I get a grip on the subject.

Welcome to Biology.SE!  Please clarify what you mean by structure.  Do you mean the three dimensional shape of a cell? —— It is expected that you will demonstrate that you have done research on your own before asking questions here — to do this please outline what you already know (ideally with references) about this subject. ——— Please also take the time to take the tour and then the help pages starting with How to Ask questions on this site. Thanks!

As an additional note this a very broad question about a very complex topic - even with additional clarification there will still be whole textbooks on the answer.

I am going to post an answer that is maybe not helpful for the exact goals, but which will maybe help restate the problem to be easier. As commenters noted it is super big and complex, many whole careers have been devoted to solving very small parts of this problem.
Possible problems with premise
I think that this question starts from this statement as a premise:

DNA are blueprints that describes an organism

This premise is not correct. Or rather, it is a way of explaining what DNA is doing in very simple terms. I do not think that you will be able to simulate with any precision cell structure based on DNA sequence. But at the end of the answer I suggest some things that are a little more focused that I know you can do.
More specifically, DNA is not a blueprint because DNA does not have instructions for how to build a cell. DNA is more like instructions for how to maintain and repair a cell. A manual for a car may tell you how to keep your car in good working order and how to replace every piece of the car, but it does not tell you how to build a car.
A quick example: cells are enveloped in the plasma membrane, which has as its fundamental component a bunch of phospholipids. DNA has instructions for these steps:

how to make new phospholipids
how to insert phospholipids into an existing plasma membrane

DNA does not have instructions for this step:

how to make a new plasma membrane de novo

DNA is always assuming the pre-existence of a cell. Cells won't work without DNA, but DNA is useless without an existing cell.
Some things you might be able to do

There are specific genes that are related to some cell compartments, like e.g. endoplasmic reticulum (ER). Eukaryotic cells have ER and prokaryotic cells do not. If you see genes for ER, you can guess that your cell should have ER. You would need to infer the presence of such genes, but there are existing tools that do this gene prediction from DNA sequence, e.g. https://en.wikipedia.org/wiki/List_of_gene_prediction_software
For your bacteriophage example, it seems like you are interested in macromolecular structure of a phage particle. (Note, bacteriophage are not cells). There do exist a lot of programs for predicting protein structures from protein sequence. You can often infer protein sequence from the DNA sequences of genes. Proteins are important building blocks of cells, and there is a lot of work on figuring out their structure (field is called "structural biology", loosely). I would recommend looking at some of the existing software in this field, e.g. https://www.rosettacommons.org/software.
I would recommend looking into existing cell simulators, which exist. For example: https://en.wikipedia.org/wiki/Virtual_Cell, https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005991. I am sure there are more that you will be able to find.

Hope that helps.
UPDATE
I realized afterwards that when I say that that DNA doesn't tell you how to make a cell that could be considered confusing, because cells divide to make more cells. However, The process of cell division is not making a new cell "de novo" (out of nothing)- rather it's taking an existing cell and reforming it into 2 cells.
In other words DNA does this:
1 cell --> 2 cells
But DNA does not do this:
materials of a cell --> a functional cell


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Will amylase inhibitors affect the colorigenic reaction between starch and iodine?
I'm doing an experiment for my IB bio EE involving colorimetry. I'm not experienced at all with colorimetry, so I'm having some trouble planning it. The experiment is on enzyme kinetics, and I'm testing the effect of an inhibitor on the rate of digestion of starch by alpha-amylase. Currently, my plan is just to use a starch solution with an iodine indicator, add the amylase and inhibitor and measure the change in absorbance of a certain wavelength over time with the colorimeter, however, I'm worried that when I add the amylase and the inhibitor it'll affect the colour of the solution quite a lot. Will this be an issue, and if so is there a better method I could use to control for it?
Any help would be appreciated, this is my first time actually planning an experiment and I'm finding it difficult :)

Small scale testing is part of designing bigger experiments...

Agree with @SolarMike, you could see the effect of amylase inhibitor on absorbance of starch–iodine complex before proceeding with the main experiment.

Let's work through the options.
First, the amylase could affect the color of the starch-iodine complex by direct association (rather than gradually digesting the starch).  I'd think someone would have noticed that by now, but you could test amylase + starch + iodine versus starch + iodine negative control at "time 0" to see what you think.
Next, your inhibitor could affect the color of the starch-iodine complex.  In that case, a starch + iodine negative control will look different from an inhibitor + starch + iodine negative control.
Finally, perhaps amylase binds the inhibitor in some special way that causes the whole complex to hunt out starch-iodine complex and make a strange color.  It seems unlikely, yet it's not that unlikely since depending how it works the inhibitor might manage to jam up amylase in mid-bite with the starch attached, and the protein somehow manages to mess with the wrapping of starch around iodine.  In that case you need to look at whether (amylase + inhibitor) + starch + iodine looks different from amylase + starch + iodine and/or inhibitor + starch + iodine at "time 0", then consider the color change from there.
For "time 0", you might conceivably need to extrapolate back to that time point after measuring changes after some short time intervals you can accurately measure, if the color change is rapid.

To measure your amylase activity, you will monitor the disappearance of amylase’s substrate, starch.
Starch reacts with iodine (which is yellow) to form a blue compound (Amax 620 nm). This reaction is
the basis of a colorimetric assay for amylase activity. You should be very careful about the volume of the final solutions so it won't effect your results. For example you will add inhibitor to one of them and you won't add that to the other but you should add water instead of the inhibitor so dansity won't be a problem. (final volumes should be same since starch amount at the beginning will be same) You can use some acid like HCL to stop enzyme activity so it won't change the colour and won't effect your results. After the acid stops the enzymatic reaction and the iodine
reacts with the starch to produce the blue color. Any starch that has not yet been hydrolyzed by the
 amylase will turn blue color being proportional to the amount of starch
remaining. The intensity of the blue color can be by measured by its absorbance at 620 nm. The greater the change in absorbance between a sample containing the initial
amount of starch (without enzyme) and the hydrolyzed mixture containing the enzyme, the greater the
amount of starch degraded by the enzyme, therefore the greater the activity of the enzyme being
measured. Make sure you give the enzyme enough time and heat to catalyse the reaction. Sorry for grammar errors. I hope this was helpful!
Edit:you asked if inhibitor effects the experiment. I did say it above. If you use a colorless substance to denature or inhibit the enzyme it won't effect your results. If you can't do this you may add the inhibitor after the reaction is over so it won't effect the reaction but you may eliminate possible differences in color

Welcome to [biology.se]. Please have a look at the question again: it is about whether amylase inhibitors would affect the reaction between starch and iodine in any way. Can you please [edit] your answer to address that point?


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Rubbery Orange and Fuzzy Mould From Bread
So I share a house, and my other housemates are currently away. One of them had some "plain" bread (a popular type in Scotland), complained a piece had mould on it, and so I had assumed they'd thrown the rest away before they left.
So you can imagine my bemusement when I decided I wanted some toast, opened the bread bin and was greeted by this:

You can just about see where my housemate's bread was, in the red packet on the left under the mass of orange and fuzz. The loaf in front was unopened, but the packaging was just so covered in this stuff I had to throw it away.
Now I didn't think to take any more pictures, as my priority was getting rid of this, on which I may have gone overboard (if I'd had a flamethrower I'd have used it) so there's no trace left. I only became curious later, but looking around on articles about bread mould I haven't found anything whose description seems to match what I'm seeing; in fact most are just describing the usual blue/grey mouldy patches seen on the bread itself, and none of the pictures I've found show anything that looks like this, the worst showed a piece of bread entirely blue/grey with a few millimetres of fuzz on it. Articles on orange mould seemed focused on the type that can appear on grout and such, and wasn't immediately identifiable as being the same thing.
The fuzzy parts appeared fine like concentrated spiderwebs, while the orange stuff was somewhat rubbery, or at least the bits left stuck to the plastic bread bin after I got rid of the worst of it. Also of note is that there was a lot of something, presumably spores, when I opened the bread bin, or maybe just the spider-web like stuff disintegrating; fortunately I wasn't breathing in at the time. This stuff has grown quickly as well, though I expect the mouldy bread must have been bad when my housemates left, this orange/fuzzy stuff has exploded out over only about two or three days.
Anyway, I'm curious, is this just some normal progression of the common penicillium variety, or is it something else? Is the orange the natural colour, or has it leached colour from the wasted loaf's packaging?
Apologies for being a bit imprecise, my scientific background is in computers, and the scientist part of my degree really just means I'm a programer.

Post it to Paul Stamets else another mycologist. ID'ing that type of species is pretty difficult! https://www.emlab.com/resources/sampling-guides/pcr-mold-sampling/


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What will happen if mitochondria had a structure like lysosomes?
I wanted to know an explanation how the structure of mitochondria affects its function. Therefore, how would it turn out if its structure is like the structure of lysosomes, what is going to happen?

Mitochondria are double membraned organelles with an outer membrane which is a rod-like shape, and a convoluted inner membrane (Figure 1).

Figure 1
On the other hand, a lysosome is a single-membraned vesicle containing digestive enzymes, with no internal structure. Its function is to keep these dangerous enzymes in a compartment.
The "purpose" or "role" of the mitochondria is to do cellular respiration to provide energy (as ATP) to the cell. To do this, the mitochondria have many respiratory complexes (groups of proteins which make respiration happen) embedded in their internal membrane (Figure 2). As you can see in Figure 1, this membrane is convoluted with many folds; this is to increase the surface area of the membrane to have more space for respiratory complexes.

Figure 2
Moreover, these complexes pump out H+ ions into the intermembrane space. The fact that there is this thin intermembrane space allows for a buildup of H+ concentration which is crucial for ATP production (through the action of ATPase). This process is called chemiosmosis and you can learn more about it here as a starting point. A lysosome with only one membrane does not have an "intermembrane space", so this buildup in concentration cannot happen.
If you would like to learn more about mitochondria, I would recommend reading Power, Sex, Suicide: Mitochondria and the Meaning of Life by Nick Lane.


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Where can I obtain the sequence of the E. coli ribosomal RNA precursor?
I have found separate sequences for 16S rRNA (from the small subunit) and 23S rRNA and 5S rRNA (from the large subunit). I need the full precursor rRNA sequence, which I cannot find.
However the complete annotated sequence of the E. coil genome is available:
https://www.ncbi.nlm.nih.gov/nuccore/U00096.3?report=fasta
Does changing the T to U of this sequence give me the complete rRNA sequence?

Generally most organisms have multiple copies of the genes/regions coding for ribosomal RNA (since it's needed quite a lot). Additionally these regions can be repetitive or otherwise similar to sequence or place correctly in the genome, therefore it's generally harder to find good genomic sequences for rRNA compared to other genes.
Based on your link, it seems that you are looking for the rRNA of E.coli; the GeneBank entry corresponding to the fasta file you linked contains the annotation of the full genome and has 7 entries for sets of ribosomal RNA (named rr[slf][A-H]*).
If you take any of the sequences spanning one of these regions you should get the sequence of the full precursor. However, there are things you should be aware of:

there will likely be minor sequence differences between all 7 regions
Apparently most of the e.coli rRNA operons also have tRNA genes mixed into them (these are different for all 7 operons)
replacing the genomic T with U will make the sequence look like RNA, however ribosomal RNA is often also edited post-transcriptionally, so the sequence you get may not fully match the mature rRNA sequence.

Another website that gives a better readable overlook over the rRNA operons in e.coli is this, it also contains source links & seems to match the genbank entry from what I can see.

Example on how to find rRNA region from the geneBank entry:
This is a (shortened) part of the annotation of the GeneBank entry, which shows the 'A' ribosomal genes :
gene  4035531..4037072
  /gene="rrsA"
rRNA  4035531..4037072
  /gene="rrsA"
gene  4037141..4037217
  /gene="ileT"
tRNA  4037141..4037217
  /gene="ileT"
gene  4037260..4037335
  /gene="alaT"
tRNA  4037260..4037335
  /gene="alaT"
gene  4037519..4040423
  /gene="rrlA"
rRNA  4037519..4040423
  /gene="rrlA"
gene  4040517..4040636
  /gene="rrfA"
rRNA  4040517..4040636
  /gene="rrfA"

As you can see the genes in the region/opernoccur in order rrsA, ileT, >alaT, rrlA, rrF (the fact that this is an operon can not be inferred from the GeneBank entry) and if you take the corresponding region of the fasta sequence (nucleotides/characters 4035531 to 4040636) you'll get (most of) the primary transcript sequence.
  Since promoter & terminator Sequences are not annotated in GeneBank (or any/most other genome assemblies), you can't easily get the sequence before the first and after the last gene. One  potential source for these might be the other ressource I linked, which lists some sources for terminator sites.

* This is expressing all names as regex. i.e. for rRNA operon A there are rrlA, rrsA & rrfA; same for B,C,...

@User I added an example of what I meant with that paragraph

Thank you very much, this helps to find most of the operon sequence. @User