text:
How can we know which alleles are together on a chromosome?
This illustration says that if the two homozygotes pr+ pr+ vg+ vg+ and pr pr vg vg are crossed to produce a heterozygous offspring (pr+ pr vg+ vg), then:

this cross gives us exactly what we need to observe recombination: a
fly that's heterozygous for the purple and vestigial genes, in which
we know clearly which alleles are together on a single chromosome.

(My emphasis.)
Source: Khan Academy - Genetic Linkage & Mapping

I can't see the logic of this: surely if there were four chromosomes involved instead of two, wouldn't we get the same result via independent assortment?
In this scenario, the red-eyed, long-winged fly would have pr+ on chromosome 1, pr+ on chromosome 2, vg+ on chromosome 3 and vg+ on chromosome 4.
Conversely, the purple-eyed, vestigial-winged fly would have pr on chromosome 1, pr on chromosome 2, vg on chromosome 3 and vg on chromosome 4.
As the mother and father are both homozygotes (the mother for the dominant alleles and the father for the recessive alleles) the offspring couldn't fail to inherit pr+ and vg+ from the mother and pr and vg from the father, and the offspring would be the same as in the illustration.
I can't see how we can get any information as to whether genes are on the same chromosome or not from this crossing (unless we know they are on the same chromosome before we do the cross!).
I'm sure I've got my own logic wrong - can anyone enlighten me?

I think they assume that the two genes are on the same chromosome. The question is, given a situation where the individual is known to be pr+,pr and vg+,vg which of the following two configurations is the case: pr+ vg on chr1 and pr vg+ on chr2 vs pr+ vg+ on chr1 and pr vg on chr2

I'll read the full text again, and see if that assumption is implied anywhere, thanks.

With reassortment you would only get proportions of the F1 with that genotype. If the genes are on the same chromosome, then all the offspring will have the given phenotype...though it has been 20+ years since I last did basic genetics so I could easily be wrong.

(moved from comments)
We don't know from the pictured cross that the genes are linked. However, IF they are linked, we know from that cross which alleles are together on a single chromosome.
Thus, the description should have something like
", if indeed they are linked."
added to the end of
"this cross gives us exactly what we need to observe recombination: a
fly that's heterozygous for the purple and vestigial genes, in which
we know clearly which alleles are together on a single chromosome."
It's the further crosses of the F1 offspring that tell us if the genes are linked and if so, how closely. The original cross is necessary but not sufficient to determine this.

Your headline question:

How can we know which alleles are together on a chromosome?

is not quite the same as the question at the bottom of the body of your post:

how we can get any information as to whether genes are on the same chromosome or not from this crossing

These questions are different in two ways that matter: (1) the second question is asking about a single crossing, the one shown in the diagram, and (2) the second question asks about knowing if the genes are on the same chromosome or not, whereas the first asks if the genes (I presume, it says "alleles") are "together on a chromosome" (depending on how you take that phrase).
On difference (1): the single crossing in the diagram does not give information about distinguishing gene locations, but the Khan Academy page you got this from goes on to describe further crossings using the flies created in the first crossing, and those crossings can show information about gene locations.
On difference (2): I would take the genes being "together on a chromosome" to mean "linked to each other", that is close enough to each other on a single type of chromosome to tend to stay together during recombination events.  Maybe you meant "on the same chromosome", but that is, importantly, a different thing.  Recombination testing cannot tell you if genes are on the same or different chromosomes; it can only tell you if they are on the same chromosomes and are close enough together that recombination will not sort them randomly, but rather tend to sort them together.  If they are far apart, the genes will stay together or be separated by recombination with equal probability, which is the result that also happens when genes are on different chromosomes.
So, the full procedure that is described on the Khan Academy page will show how much recombination you get in the fly grand-offspring.  If you get few recombinant forms compared to the number of parental forms, then the genes are close together on the same chromosome.  If you get equal numbers of recombinant and parental forms, it indicates that is not the case, and therefore the genes are either on separate chromosomes or so far away on one chromosome that recombination has full effect and randomly separates them.

Hello. I'm aware of what the rest of the article goes on to say. However, my problem is with the statement accompanying (and printed on) the illustration:  "this cross [a double heterozygote] gives us exactly what we need to observe recombination: a fly that's heterozygous for the purple and vestigial genes, in which we know clearly which alleles are together on a single chromosome." HOW could we "clearly" know from "this cross" "which alleles are together on a single chromosome"?

@Armand Thanks for the confirmation - the penny has finally dropped - not helped to do so by the ambiguous language used in the article plus the way the genes are shown as linked for both the parents and the offspring in the illustration.

@Armand If the parents are homozygous dominant and homozygous recessive for two alleles then the F1 offspring will all be double heterozygous. Crossing this offspring with a "Tester" which is homozygous recessive will give us a mix of parental and recombinant offspring (The F2 generation). By looking at the actual numbers of parental vs recombinant offspring in the F2 generation we can determine  whether the genes are a) linked (recombinant % is low) b) *on same chromosome but far apart * (yes, if the recombinant % is high) or c) on different chromosomes altogether (if recombinant = 50%).

@Armand - would you agree with that last comment?

@Naj (b) and (c) are one category -- independent assortment means either on different chromosomes or far apart on the same chromosome. In practice, one uses a "scaffold" of linked genes/markers on every chromosome to map an unknown gene. If neighboring genes in the scaffold are all linked to their neighbors, any unknown gene will show linkage to at least one of the scaffold markers.

@Armand Got it, thanks :)


text:
Plasmid harbouring subunit S of type I R/M system
We have an assembly of a genome of a Lactobacillus species. The genome also contains a 7.5kb plasmid.
Aside from the "usual plasmid genes" the plasmid contains:
 - toxin/antitoxin system
 - Subunit S of type I R/M system (No R or M subunit)
Now, to me this seems like an interesting case. It looks like the plasmid is "exploiting" the R/M system of the host (Bacterium seems to have type I R/M system indeed).
This could have the effect that the plasmid is increasing the fitness of the host (and itself) by making the R/M system more flexible in terms of target sequences by the R/M system (Phages, etc.).
My questions are now:

Does anyone know an example of such a case. Did not find any.
Do you think it works the way I suspect.
Could this be interesting for Biotech applications since phages in diary food environment are a problem.
How would you test if this plasmid has this effect?

source: Stack Exchange

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sort: votes


text:
Identification of insect casing
Photo of specimen with a US quarter (~24 mm diameter) for size reference. Please help identify what left behind this casing. It was found in middle of the yard, approximately 25 feet from nearest tree but was near a lumber pile if that is relevant. Located in south Central Colorado. Appears to be a winged beetle of some kind

Welcome to Biology.SE. This could be a California root borer (Prionus californicus), but since the antennae are broken off I think it may be difficult to get a good id ...

Note: I'm no expert and not even from North America, so take this with a grain of salt.
I think this is a May Beetle (Phyllophaga genus) or possibly a Junebug from the widespread scarab family of beetles. The adults range in size from about 12-25 mm (0.5-1.0"). A distinguishing characteristic of the scarabs is the linear ridges along the wing-casings and the beautiful stippling of the elytra (wing casings). Unfortunately you seem to have lost the antennae, which, if they are scarabs, have an enlarged club-shaped tip. It has an exposed scutellum and straight edges to the elytra, which are also features of the May beetle/Junebug family (Melolonthinae)
The Scarab family are a common pest of grass-lands and trees world-wide, and this genus is no exception - the name literally translates as "leaf-eater" (phyllo - leaf, phaga = eater).

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text:
Identification of black-and-white striped jumping insect?
I noticed this small insect with long striped antennae and legs hanging out on my parsley. I'd be curious to find out what it is.
When I got close to take a picture of it, it suddenly leapt, like a grasshopper, landing a good 12 inches away on another plant. Its body is about 1cm long. I live in Southern California if it makes a difference.

Excellent first post, great pictures. That being said, can you give us a rough idea of size (parsley comes in many varieties). Please enjoy our [tour] and refer to the [help] for guidance as to our ways.

@ARogueAnt. he said the body was about 1 cm long.

Ah yes, I was so taken by the images I must have missed that @mgkrebbs

Lovely, certainly looks like a hopper of some sort. I would guess an instar of something

Based on body shape and size, this appears to be a nymph of an assassin bug (family: Reduviidae).
I originally was thinking some species of Zelus (see bottom of post), but the orange body and bold leg-striping makes me think this is instead an early instar nymph of some species of Pselliopus.

 Credit: B. Newton (2004); Source: Univ of Kentucky
Pselliopus barberi (the orange assassin bug) is one option.
I'm on my way out the door, so I'll come back to this next week to see if a more specific species stands out...

Note: I was originally thinking the genus Zelus was a good place to start -- though native to South/Central America, about a half dozen species are found in the US. Zelus renardii (the leaf hopper assassin bug) is one such species that has an orange-bodied, black/white-striped legged instar. It's native to semi-arid and Mediterranean climates (both found in CA), and it's not too atypical to find them on crop plants even in suburban areas. [Source]. However, the leg striping just isn't predominant  enough

I doubt that this is a reduviid larvae especially due to the missing rostrum which is prominent in reduviid bugs (compare my answer below and this answer). Best, bathyscapher

Due to the

chewing mouthparts,
the greatly developed femurs specifically adapted for jumping (what fits well with the OP's observation of jumping behaviour),
prominent compound eyes and
long, filamentous antennae

we can conclude that this specimen is an orthopteran insect larvae.
Well known members of this insect order are grasshoppers, locusts and crickets.
Orthopterans undergo incomplete metamorphosis, progressing through egg, nymph and adult stages. Nymphs often resemble adults, but lack fully developped wings and reproductive structures. As this specimen lacks wings, we can conclude it must be a larvae.
Moreover, I assume this specimen belongs to the suborder Ensifera as its antenna are longer than its body (as opposed to their sister taxon Caelifera which have antenna shorter than their body).
It's often tricky to identify species from photos, so no guarantuee on that, but a genus with similar larvae would be Scudderia, the Bush Katydids, which is present all over the US with following similarities:

the "hat" with a dark lateral line
1st antenna segment brighter than the others
1st and 2nd antenna segments roundish
remaining antenna segments long, slender and dark with white ends
black eyes
white "cheeks"
typical slender, long legs with dark and bright coloration
the fine spines and hair all over the body

Image source: Katja Schulz CC-BY-2.0

Good answer, but do you this part around the wrong way? I assume this specimen belongs to the suborder Caelifera as its antenna are shorter than the body (as opposed to their sister taxon Ensifera which have more-than-body-long antenna). The pictures from OP clearly show antennae longer than body - as do the ones in your answer.

You are totally right, bob1! Thank you for reading carefully and pointing this out, I will change it accordingly :)

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text:
Species identification: plant with pitfall trap-like structures
I found this plant in Tuscany (Italy, mediterranean climate, about 60 m above mean sea level). Photos were taken at roughly the beginning of spring after a period of drought followed by a couple days of rain. Average temperature oscillates between 7-10°C, relative humidity is around 75-80%.
Unfortunately I didn't have a ruler at hand but the plant was not very tall, I'd say about 12-15 cm (5-6 inches) at most.

Family is likely Araceae. Not familiar enough with Italian flora to know possible candidates. I may have time to dig in later, but I suppose some European users more familiar with possible candidates will be able to respond before I have time.

I think that is probably a plant in the genus Arisarum based on the almost complete covered inflorescence ("trap-like" structure). In particular, it looks most like Arisarum vulgare (common name: Friar's cowl). This plant is found throughout the Mediterranean region including Italy.
The striped structure with a "lid" isn't a trap, but instead an inflorescence (branch bearing multiple flowers — in this case a spadix with its bract being the "trap"). The inflorescences are from the plant with the rounded-arrowhead shaped leaves.
That leaf shape is characteristic of several genera in the Arum family (Araceae), but the size and very rounded tip looks most like specimens of Arisarum vulgare.
The size and early spring flowering time also fit what is described for this species.

Source: user Hectonichus on Wikimedia Commons —
License: Creative Commons Attribution-Share Alike 3.0 Unported


text:
If a HIV+ person gets COVID, will it result in more mutant virus?
High schooler here.
What is the probability of the coronavirus evolving to gain traits of HIV/any other virus from a person suffering from both ailments?
As COVID virus enters cells that are already infected by other virus, what determines which of the two virii will survive and what mechanism governs what traits surviving virus will adopt/integrate?

Welcome to Biology.SE. I’m voting to close this question because it: 1) doesn't demonstrate that you've done the expected prior research (see also the "homework policy"), and 2) asks multiple questions (the second of which is much too broad). These are both reasons for closure and downvoting. Please take the [tour] and consult the [help] starting with [ask] for details of what is expected.

Similar viral strains allow genetic transfer hence recombination. The recombined strain can be selected from the original strains by its better or worse characteristics.
This does not happen in HIV x COVID-19. They are dissimilar and none of the recombinants has been observe to exist.

There is a probability of similar viruses gaining each other's genetic traits while replicating. This is known as horizontal gene transfer. This also happens in viruses, where double infections can allow genetic material between two strains to be exchanged while replicating. As the example you mentioned, the SARS-CoV-2 (the name of the virus; COVID-19 is the name of the syndrome/disease) has evidence of horizontal gene transfer between pangolin coronaviruses (Wang, Pipes, and Nelsen, 2020). Currently, there is no evidence that horizontal gene transfer happens between HIV and SARS-CoV-2 probably because they are too dissimilar.
We have seen the "how" of these things happen. Then, "what" governs the survivability of those recombination strains? Remember, recombination is a mere game of chance, there are combinations which are poor fit and some better. For poor recombinants, its viral characteristics are poorer than its origins, hence it fails to spread. On the other hand, a "better" strain is more fit (as in Darwinian fitness) than its origins, hence it spreads quicker. It's viral characteristics, both the poor and the better, selects itself from its peers. This is the idea of natural selection.
You can check this article by Li, et. al. (2020). They explain the recombination of bat and pangolin coronavirus (which may be the genesis of SARS-CoV-2), is under further purifying selection. This causes the SARS-CoV-2 strains to show the severe and widespread viral characteristics as we see today.

This part is not a continuity of my answer, however some reflection of my perspective. Welcome to SE Biology. To better understand the answer, you can first read a good introductory biology book, such as Campbell BIOLOGY. Then, you can start delve in the articles I mentioned in the answer. If you meet a difficult part inside the explanations, we are eager to help.
I am glad you are interested in these topics as a high-schooler, and hope you continue your interest in tertiary education. I personally enter biomedicine after trying to understand a then tumor misdiagnosis when I was in HS.


text:
Identity of plant bearing a cluster of bulbous, glossy red fruits (Oak Ridges Moraine)

Location: Oak Ridges Moraine, Ontario (Durham Region)
Date: October 4, 2021
Site: Full shade; hillside; sugar bush

This isn't a flower, but the cluster of shiny berries containing the seeds of a flower. My best guess is that it is a Jack-in-the-Pulpit (Arisaema triphyllum), but it's a bit hard to tell from the two leaves, which are both decomposing and at a bad angle to tell for sure. But it's definitely in the Arum family.

Their range includes Eastern US and Ontario.
Named because the flower resembles a preacher in a covered pulpit, the flowers are tiny, and bloom on the spadix (the "Jack") of a mature female. When young, the flowers are male; when sufficiently mature, they become female and can form the berry cluster.
From the site linked above:

Berries (¼ inch across) enclosing one to several seeds, at first green, become bright red as female plants begin to wither in late summer and fall.  Berries remain attached to the dry spadix, resulting in an ovoid mass of showy berries up to 2 inches long which stay on the stem even when stem has dried.  A cluster can consist of up to 150 berries, each with 1 to 3 rounded flat-sided light tan seeds.


text:
What is the name/type/species of this insect?
Facts:

Found in a bathtub in western Washington (state) (the pacific northwest).
3/16-1/4" long, 1/8-3/16 thick.
Gray colored.
No elongated noise but two antennas.
No pets in home, older 1969 build (vented crawlspace).
Found on main floor (crawlspace underneath).

This seems like a weevil or a carpet beetle. Most interested in making sure it’s not harmful.

Hi. Species ID questions need to include a photo, size, location, and as much other information as possible. See here. If you update your post with such information, it can be reopened and you'll be able to receive an answer.

In the meantime: act fast to find your open or damaged container of stored cereal grains, pasta, or similar.

Related: https://biology.stackexchange.com/questions/69598/small-black-slow-moving-insect-showing-up-in-the-home

@theforestecologist thank you. Post updated.

This is much better, but is there any chance of getting close-ups (from multiple angles)? Borrowing a good camera with a macro lens or a phone with a better camera would make it much more likely you can get a precise answer.

@tyersome we released the insect to the wild. I'll use the suggestion on the next one!


text:
Name of This Black and White Dove
I spotted this dove in a park. It was foraging among Rock Doves, Seagulls, Ibises and a few others.
It appears similar to Pied Rock Doves, but I am not certain if this is correct.

Any idea what the name of this dove is?

It's a pied version of the Rock Pigeon (Columbia livia), aka Rock Dove. According to the Cornell Lab of Ornithology, the pied variety of Rock Pigeon is one of any color that has splotches of white on the body. I think that fits your bird very well. It's not a different species, but just one of several color varieties of Rock Pigeon.
If you are not familiar with Cornell's site and enjoy birds, their All About Birds site is very nice.

Also called Piebald (Pied for short as mentioned above.) It's a pretty common mutation among different animals. Dogs, deer, and snakes such as the ball python exhibit this trait. So yeah, your bird is still a rock dove.

 the bird above is a pigeon, local breed of pigeon in African, just like any other pigeon, it has all features a pigeon has! It was got as a result of mating a brown male pigeon with a black white colored female pigeon, All local breeds from Africa!?

Welcome to Biology.SE. You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or edit your answer accordingly.

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text:
Is it possible to have action potentials in cells lacking both dendrites and axons?
I'm reading Kandel. Chapter 3 states the following:

Because the initial segment of the axon has the highest density of voltage-sensitive Na+ channels and therefore the lowest threshold for generating an action potential, an input signal spreading passively along the cell membrane is more likely to give rise to an action potential at the initial segment than at other sites in the cell.

I know it is possible to have dendritic spikes, which is an action potential given a much stronger input to open enough Na+ channels. But can there be a different action potential, not axonic nor dendritc, given that enough Na+ channels locally open in the cell membrane?
I've seen some papers talk about "somatic action potential", but its meaning and how it works I don't understand.

All of the action potentials you are describing involve the cell membrane. Do you mean to ask whether an action potential can occur in the soma? Are you thinking of an isolated soma with axons/dendrites removed? Does an action potential that starts somewhere else and spreads to the soma count? Are you asking for biological relevance or plausible theoretical possibility? What will the answer to this question teach you about neuroscience?

I am thinking about the theoretical possibility an action potential with axons/dendrites removed.

The soma of Dorsal root ganglion (DRG) neurons can fire action potentials.

There are many other electrically excitable cells other than neurons: muscles, pancreatic islet cells and even some plant cells.


text:
What insect is this? (Switzerland)
I took these photos in June in Zurich, Switzerland. The insect struck me as fairly large; I'd say the body was probably 2-3 cm long unless my memory is playing tricks on me. It sat just like this on a paved road. When I got close to take photos, it froze completely and I could take photos for minutes without it so much as twitching. Whenever I was farther from it, it would turn and walk a bit, but it seemed in no hurry to go anywhere.

See also this post.

Ah, yes. The differences in the antennae compared to some photos I could find threw me off; turns out that just means she's female. I think that's very likely a Ctenophora ornata.


text:
What factors have led to selection for intelligence in crows and rooks?
The Corvidae family could include some of the smartest species after primates. What could be the factors that differentiate them from other species of birds that have determined their potential for intelligence? The only explanation I found mentions their "juvenile gangs" but many other birds are more social and less intelligent.

@John Comments should not be used for partial answers.

@com.prehensible Comments should not be used for partial answers.

This article posits that a lot of the reasons for primates to have evolved to be more intelligent (i.e. a costly and unpredictable environment, which requires complex thinking and problem-solving skills) could also apply to corvids.  So environmental complexity might be a potential reason for these birds to have become so smart.
As far as why other birds aren't as smart, I think it's hard to say. From an anatomical stand point, smarter birds have more densely packed neurons. It's unclear based on this article why some birds would evolve more complex brains than others, but one can assume it's out of necessity based on the environment and other factors. If a species can get by with a less complex brain, it most likely will. I hope this helps somewhat.


text:
Why are our bodies created to itch when histamine is released by our immune systems?
Why do bug bites and cuts itch when scratching them clearly doesn't help us survive? Did our early ancestors need to rely on this itching sensation, or is it just that the receptors for itches just happen to be stimulated by histamine?

I guess itching, just like pain, is a signal to the organism that some part is injured.

Answer
While itching and pain are related, research indicates that these sensations are caused by distinct nociceptors. Essentially, wounds itch because histamine is released as part of the wound healing process, and histamine activates those itch nociceptors. So perhaps the more apt question is just "why does histamine cause itching?" (See also answer to What is itching?)
As of now, we might only be able to speculate.
Educated guessing
The following are a few hypotheses:

Selecting for more specific itch nociceptors, which would incorporate some mechanism to prevent itching of wounds specifically, doesn't help influence survival enough to be useful, or would impose a cost more severe than the benefit.
Itching wounds may have caused ancestral species to remove contaminants, IE by licking them.
It could be a vestigial adaptation, a simple signal saying to the original "something happened here, do something about it!"

References

New insights into the mechanisms of itch: are pain and itch controlled by distinct mechanisms?
The accelerating effect of histamine on the cutaneous wound-healing process through the action of basic fibroblast growth factor.
Physiology and healing dynamics of chronic cutaneous wounds.
Histamine-induced itch and its relationship with pain
Histatins are the major wound-closure stimulating factors in human saliva as identified in a cell culture assay.

Now I'm all itchy.

Scratching is getting potentially poisonous or at least irritant substances out and removes lodged insects like ticks.
Removing subcutane parasites like scapies mites is not feasible without scratching yourself bloody.
I don't see how "scratching them clearly doesn't help us survive".  Behaviors and skin reactions evolved way before our modern hygiene and parasite cures.

Please support your answer with references.

Can you please add some references to your answer?

Some insects produce chemicals to induce itching in order to further spread eggs laid in the wound. Some micro-organisms do the same, a cut may be infected.
It's perfectly possible that the urge to scratch is not beneficial in all situations but simply a majority of them. This would be more than enough reason to have the impulse stick around, evolutionary speaking.
The body does not differentiate very often between externally and internally produced chemicals.
For example, I am diabetic and take insulin, a hormone related to blood sugar. It is introduced to my blood stream from without, but my body reacts to it as if my pancreas had produced it, which is what happens in healthy individuals.
In an organic system which coordinates internally via chemical signals (hormones), it is impractical for parts of the system to attempt to screen out externally introduced chemicals, such as from a bug bite.

Thanks for your effort on trying to answer the question. Can you add some external references to support the claims in your answer? We always appreciate external reference to support all answers/questions on BiologySE - thanks for your contributions!


text:
Why doesn't G-actin concentration fall once microfilament polymerization begins?

I don't really understand why the monomer concentration on this graph will stay flat when the monomer concentration is above the Cc.

What do you think might be happening? What starts to happen at the Cc? What is the definition of Cc?

Cc is defined as the critical concentration which is a measure of a solution of G actin to polymerise. What I am thinking is that if the monomer concentration is above the Cc, the polymerisation will occur and forming the actin filament. But if the polymersiation occurs, suppose the monomer will decrease and the graph for monomer should drop. Thats why I don't get why the graph for monomer will be plateau.

Notice the vertical axis is not for monomers, it's for mass.

The critical concentration is better defined as the "equilibrium concentration of the pool of unassembled subunits"1.
An analogy that might be helpful is thinking about a NaCl (table salt) solution — once you add enough salt some will start to precipitate, but the amount in solution will remain the same.
You can think of the solution as having the capacity to support a certain concentration of molecules (or ions) — below that concentration subunits will separate from the polymerized form faster than it can accumulate new subunits, above that concentration the subunits will stick together faster than they "fall off" the polymer.
For more a detailed molecular understanding of why this is so, you probably need to read up on chemical equilibria — for example Chemistry or even Khan Academy might be helpful.
Reference:
1: Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Section 18.2 — The dynamics of actin assembly. Molecular Cell Biology.


text:
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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What is the difference between a human being, a Homo sapiens, and a Neanderthal?
I know that the Neanderthals were part of the genus Homo. How do they relate to other members of the genus, such as Homo sapiens?

Homo sapiens / Homo sapiens sapiens
Human being, in the popular culture generally refers to modern humans, called either Homo sapiens or Homo sapiens sapiens. The existence of the two names will make sense when talking about the Neanderthals. In the term Homo sapiens, Homo indicates the genus and sapiens indicates the species. In the term Homo sapiens sapiens, the second sapiens refers to the subspecies.
Homo neanderthalis / Homo sapiens neanderthalis
Neanderthals (or Neandertals) is sometimes referred to as a species in the same genus (Homo) as H. sapiens and sometimes as a subspecies of H. sapiens. When considered as a different species then, they are called Homo neanderthalensis. When Neanderthals are considered as the same species as H. sapiens but different subspecies, then they are called Homo sapiens neanderthalensis and modern humans are then called Homo sapiens sapiens.
Related Post
The post How-could-humans-have-interbred-with-neanderthals-if-were-a-different-species will probably be of interest to you.


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What's this stuff that looks like white chainmail armor growing on giant kelp?
I found some giant kelp coated with a material that is white, smooth, and forms a chain-mail pattern with small black oblong lumps in between the links. It feels pretty hard but not stiff (the kelp still flexes), and can't be easily removed from the kelp skin. The leaves under the coating appear to be stunted and malformed.
This was found in the Pacific in Southern California in the late summer.

I took a photo with a low-quality microscope.

Is it a parasite?

That looks like it could be the lacy crust bryozoan (Membranipora membranacea). That bryozoan is an epiphytic animal whose native range includes the Pacific coast; it does not feed on the kelp, but can weaken and damage it when abundant 1. Whether you should call this a parasite seems somewhat definitional and is something I'll leave to an ecologist to answer.
For comparison see the following public domain image from the USGS:
 Apparently photographed by: Eugene van der Pijll
In addition to the wikipedia article, you may also find this page from the Texas Invasive Species Institute to be of interest.
References:

North, W. J. (1976). Underwater California (No. 39). University of California Press.


text:
How do you identify a mosquito's sex without letting it bite you?
Are there any reliable indicators?

male and female mosquitoes are morphologically different. You seem to have shown no effort at all. Have you even checked the wikipedia page on mosquitoes? -1

I'm voting to close this question as off-topic because OP has shown no research effort

Males and females mosquitoes are morphologically quite different.
The majority of individuals you see are females. The males are not attracted to humans and so we see them less often.
The main obvious difference is the size of the antenna. When you see the large feather-like antennas of a male, you'll have no doubt; it is a male. The male also tend to be smaller than the female but given the inter-species variation in size I wouldn't use this criterion to tell the gender especially the antenna criterion is so obvious.

You can find many more pictures if you just google mosquito male female.
Why do males have these large antennas?
The male's large antennas are for sensing the females. There is a very important sexual selection among male mosquitos for accessing a mate. Female beat their wing at another frequency than males and they therefore produce different sounds when flying. So males compete on their ability to hear and recognize female. Females are attracted to CO2 and warm bodies but males are incredibly attracted to the sound of the female. During my Bachelor degree I once played a 440Hz harmonic to male Anopheles gambiae. It is surprising how quickly they respond to this sound and fly toward the speaker.


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Given the number of individuals who have a recessive disorder, how can one calculate the probability that the disorder was inherited?
Just to be clear, this is not homework.
Suppose a biological family has five children, two of whom have a certain recessive genetic disorder that is not sex-linked. The parents themselves do not have this disorder.
I want to estimate the probability that the parents are carriers. How can I do that, short of getting this probability directly from a lab study?
This problem appears to be where Bayesian statistics can help. All I need to know is:
1) the probability of the parents being carriers, given they don't have the disorder, but 2/5 of the children do.
2) The probability of the parents being carriers
and 3) The probability of the children having the disorder.
3 I can probably find without too much effort. #2, I'm guessing, is a Hardy-Weinberg problem - I just need to find the relevant statistics for people of the parents' backgrounds. But I have no clue how to start with #1.

You should read the homework policy. You will understand why I have voted to close as homework.

Assuming...

The parents are the real biological parents (no cheating allowed!)
There is a purely dominance/recessivity relationship between the alleles and no individual can express the disorder without being homozygous for the disease causes allele
De novo mutations for the disorder are rare enough to be ignored in the calculation of this probability
Trisomy and monosomy is not involved

, then the two parents must necessarily be carrier (both of them) as long as at least one of their children express the disease.
Note, by the way that some of the above assumptions are too strict and could be partially released.

This question does not require any complicated bayesian statistics (or any statistics at all) or any use of Hardy-Weinberg rule. If a children expresses a purely recessive disease, then (s)he is necessarily aa, where a is the recessive allele and A is the dominant allele(s). It means that both parents must have at least one a. Because, no parents express the disease, both parents are necessarily Aa (or aA)

Suppose assumption #2 is untrue for this particular disorder. Then, what statistic would I want to look at?

We can reduce assumption #2 to "if no individual can express the disease without being aa". If this assumption hold it is fine, you are sure that both parents were carrier. I edited assumption #2. Other assumption can eventually be further reduced or specified.

I still don't understand. Mutations cause the alleles, and a recessive allele can only express itself if a dominant allele is not present. Thus, if we're talking Mendelian genetics, then it is biologically impossible for assumption #2 to be false. I suppose I'm getting something wrong, though, aren't I?

I don't really understand what you misunderstand! Assumption #2 says that if an individual is sick (express the disease), then this individual must be aa. We can imagine a case where there are some Aa individuals that would express the disease if they smoke a lot for example. All the assumptions are probably assumptions you wanted to make to start with.

Why dont hemophilia follow these steps? The father has no diagnosis of hemophilia and the  mother can only be a carrier yet show no symptoms of a hemophilac. The child could only be a male with no x chromesome from the father because he recieved two y's from the mother, even without any family history of hemophilia the mutation is said to be spontaneous or inherited and the new adult version where it comes out of dormancy in males of 40 years of age for the first time.

@moonman239 I think assumption two is just stating that the disease is only genetically determined and that the dominance is complete. One can not get the disease by exposure to an environmental factor for example.

@Remi.b is that a correct interpretation of two?

@rg255 yes it is correct. I guess I did not need to state these assumptions as every body make them implicitly in introductory courses to genetics and now it is confusing the OP :) I merged assumption #1 and #2 hopefully that may help.

What if the allele that causes the disorder is not purely recessive? Does such an allele exist in the human population?

Yes they exist. Often the relationship of dominace is not perfect. Some disease are even caused by dominant alleles such as Huntington's disease for example


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How does the MET gene work and what happens when the promoter region gets mutated?
I am doing research on inherited risk of Autism Spectrum Disorders(ASD) due to common Copy Number Variants(CNVs) One of the mutations is the 'CC' variant of Rs1858830 in the promoter region of the MET gene. (http://www.snpedia.com/index.php/Rs1858830)
After digging a bit deeper I found that hepatocyte growth factor is a pretty ubiquitous compound in the body and it's necessary for growth/repair of many tissues, namely the liver and digestive tract. I am trying to separate the direct causal effect of the mutation itself from the effects it has on other tissue which may themselves have an effect on ASD risk.
My question comes from a study which measured reduced serum HGF levels in autistic children with this mutation. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694825/)
I am confused about the implied causal effect of the 'CC' variant on HGF levels even though it is merely the ligand for the MET gene? Please help me understand where in the gene signalling process does HGF come in, what does it do, what proteins are transcribed by the MET gene, and how this mutation effects the transcription of these proteins.

HGF is the ligand for Met, which is a membrane receptor involved in multiple transduction pathways. Gene ID 4233 we're looking at a single gene product for MET.
If we're just reading through the wikipedia page for c-Met, when HGF binds to Met, it activates the tyrosine kinase activity of Met. Met recruits Gab1, and this complex mediates interactions with Ras, P13K, ß-catenin.. not just pathways associated w/ Autism, but also associated with invasive growth cancers. An interesting note about the C allele, it's associated with decreased Met transcription. Quoting a recent article,

The present morphological and functional studies have revealed a highly novel mechanism conferred by MET receptor signaling, which we show serves a pleiotrophic role in controlling both neuronal and spine morphology, and the time course of glutamatergic synapse maturation on CA1 hippocampal neurons. Such findings are consistent with the possibility that mistimed maturation of glutamatergic synapses underlie aberrant function of neural circuits that are enriched in MET during development.

Source
So the critical results from the same study showed that when Met got knocked down or deleted, we saw maturation of neural tissue. So now, if i'm thinking about Met and HGF, your article notes that HGF is decreased in autism brains. If we (1) need HGF for Met function, and (2) ASD may be attributed to decreased Met function, and (3) the C allele decreases Met levels, we're basically looking at a system that's modulating for ASD.

Thank you very much for your thorough answer. Could you explain what you mean by "modulating for ASD"? I'm not completely sure what you meant by that, as I see two possibilities:
1.) HGF production is downregulated due to a reduced binding with MET

Basically all I was saying is the system of circumstances was pushing toward a state that would make ASD more likely. For the actual reason HGF level become reduced I'm actually not too informed!

2.)HGF is the limiting reactant in the pathways you mentioned above.
If you would like some context, I am investigating the effect of supplemental HGF in an attempt to normalize dendritic spine outgrowth and recover cognitive function in this particular mutation. I would also like to know what you think of the impact on cell growth/differentiation in  other tissue/is this an issue of merely HGF shortage or are the effects of this mutation mostly downstream of the ligand binding?

I've read through some articles where Stat3 and c-Src play a role downstream of c-Met, where they found Stat3 and c-Src in the promoter of HGF increasing HGF transcription. If it's a decrease in relative c-met levels that's heavily impacting Stat3/Src mediated HGF transcription, it could be that the actual issue is with the levels of c-Met.

One more question: The mutation itself is a change of base from a Guanine to a Cytosine. Do promoter region mutations generally mean RNA polymerase cannot fully attach itself to the promoter region resulting in reduced replication of the associated protein? When you say "decrease in c-met" do you actually mean there is less c-Met protein being produced?

I'm not sure exactly what, but either for transcription factors or for the polymerase at the promoter. Affinity is reduced for the mutated promoter, and so less transcripts are made, and less protein is actually available for the cell.


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Phosphorylation capacity of an enzyme
Let's think ProteinA can phosphorylate proteinB, proteinC and proteinD.
Condition1: All proteins are expressed and proteinA phosphorylates proteinB, proteinC and proteinD.
Condition2: Only proteinA and proteinB are expressed for that reason protein A phosphorylates only proteinB.
Which is more realistic?
1) In condition1; proteinB, proteinC and proteinD will be 3 times less phosphorylated in comparison to proteinB in condition2.
2) The proteins of both conditions will be phosphorylated same.
Cheers
Cankut

Is this a homework question?

No it is not, why?

it is a simplified version of my question which I could not find a clear answer.

I really do not understand why the people just vote for this question instead of giving a simple answer. if a person do not have any answer about a question then how he/she can vote for the question. First give an answer then be able to vote the question...

@Cankutçubuk please take the [tour] and read through the [help] to understand how this and all Stack Exchange sites work. Voting is nothing personal, it merely reflects the quality of the question or answer being voted on. In this case, the question is not in line with our homework policy, which is slightly mis-named, as it not only applies to homework but to all trivial and/or un-researched questions, especially those (like this one) that look very much like homework or exam problems. (...)

(...) If you wish to post questions such as these, please put in what research you have done to solve the question yourself, what you think the answer is or is not, and how you came to that conclusion. If you're stuck at some part, state exactly where you're stuck, and what you've come up with so far.

@MattDMo Just an additional information about my question; I am working on signal transduction and I had some difficulties to integrate phosphoproteomics and other omics data for that reason I needed some biological updated knowledge.

Don't be discouraged. At least in vitro, if there is ample chemical substrates (e.g. ATP) and protein A (i.e. kinase) remains active, the kinase will just keep phosphorylating its protein substrates (B alone or a mixture of B, C, D) until the substrates are depleted.
Thus, all substrates will be phosphorylated eventually. The contrived Condition 1 may occur only if you only supply enough ATP for A to phosphorylate one mol equivalent of its protein substrate AND A has exactly the same catalytic efficiency toward B, C, and D that are present in equal amount. Of course, any or all of B/C/D may have more than one phosphorylation sites, each of which has its own phosphorylation rate.

@SKY thank you very much for your precious answer.


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How does being afraid or nervous affect mental performance?
It's known that when somebody is not relaxed (nervous,worried....) , they can't concentrate , what exactly in being nervous is the problem?

I will try using logic, but that might only just get you on a lead:

Concentration means being focused on a specific task.
Consciously, you want to focus on a specific task, but there are other process that may want to claim ressources and that you cannot repress.
Anxiety, but also fear or worriness are symptoms that basically translate an unconscious (or conscious) proccess that requires your attention.
Therefore, two concurrent psychological process require focus from your conscious mind. Ergo, you cannot concentrate on either on them. Usually, the emotional part will win since it involves brain structure (such as the amygdala) that are specialized in shunting more evolved brain structures. That is when you are afraid of something, it is very hard to repress that feeling with logical thinking.
In psychoanalysis, Freud introduced something called as "The pleasure principle" (I hope that's a good translation). This principle is one of the few basic principles that rule human behavior. Now, anxiety is an indicator of displeasure. Your mind will try its best to settle that issue before settling anything else. That is why usually you cannot isolate anxiety.

Here's an example:
You hate spiders. You need to measure the surface of an old mannor. You've seen some spider webs. Odds are you will have much trouble to concentrate on measuring any room's surface, because one task your brain will perform for you is checking in every corner whether a spider can be seen, so you'll be able to identify a potential threath as soon as possible and react appropriatly (usually, get the hell out of there if you're really affraid of spiders.
Here's another example that doesn't use fear:
Your girlfriend texted you before an exam, and she said "We need to talk". Since you are emotionnaly bound to your girlfriend, you might get anxious: what does she want to talk about ? Your mind will begin scanning for every possibility, emphasizing on the worse ones (the ones that will disturb the "Pleasure principle" the most for instance). Now that you identified that she might break up with you, this thought will just keep popping up, even if you manage to think for a minute about the exam you should be thinking about right now.
Fact is this is a matter of autoconservation for your psychee. A breakup will certainly harm you more than a failed exam. Your brain is very smart about processing important stuff before, and any attempt from your conscious mind to shunt this will most probably fail.
By the way, there is a psychology stackoverflow. I guess you should have posted this question there.
Hope this helped !


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agglutination test using blood of the donor and the recipient
we were told that agglutination occurs when the matching antibody react with its antigen on the RBC surface (as antibody B with antigen B)....
Also when blood transfusion, Donors plasma with antibodies is diluted , so when o-donor gives blood to  B-recipient , B antibodies ( of the donor) is diluted
........
My question is in lab cross-matching test  when we put recipient's plasma(o with b antibodies for example) on the donor's RBCs (B with b antigens)..... is there agglutination, If so, how would we know the right group then?....if not ,Why not?
if the whole thing is misunderstood ,i wish to be told how it's done.

Disregarding Rh factor for a moment: when you add A-antibodies to a blood sample and agglutination occurs, this means the blood contained A-antigens (A-type). The same can be said for a sample of blood to which B-antibodies are added (B-type). If agglutination for both antibodies occurs in separate assays on the same sample of blood, it means the sample contains both A and B antigens (AB-type). If the sample is said to be O-type, this means neither A or B antigen would be present in these cells. It's safe to transfuse O-type blood into any recipient due to this fact. What you also want to watch out for, is attack on the recipients RBC's by antibodies in the donor's plasma. This can result in a hemolytic transfusion reaction (HTR), but it's noted in the following text:

Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation.

If you're in the lab doing a Coombs test, for example, you're checking to see if there are any extraneous antigens present that might results in a HTR. In a normal result, ergo there aren't any antibodies to RBC's in the sample mixture, you wont see any agglutination. This is for considerations outside of ABO antibodies, generally. If you're adding to B-type RBC's a plasma with known antibodies to B antigen, like O-type plasma, you can probably expect an event. To my knowledge, O-type plasma wouldn't be safe to give to anyone but an O-type recipient.
additional source

what i know is that o is the universal donor what i don't get is how do we know it's compatible when its plasma has the antibodies or is it not done this way at all(mixing donor's RBCs and recipient's plasma)?

O group RBC's lack antigens to either A or B antibodies, making them suitable for donation to any blood type. The recipients body wont attack the donor RBC's. The donor plasma contains antibodies to both A and B antigens, however. The assumption we're making is that out of total blood volume, donor + recipient, the amount of A/B antibody in the O group plasma will be dilute enough that there's a deleterious effect on hemolytic events involving donor anitbodies. What you wouldn't do, is give O group plasma to anyone other than an O group recipient during a plasma transfusion.

The way we find out if it's compatible, is we add A and B antibodies to separate samples of blood to determine if agglutination occurs. For O group blood, you wont see any of this. To confirm, you can back type the blood. Take the O group serum, and add either A blood cells or B blood cells to separate samples. You should see clumping in both cases (you're type AB if no clumping occurs in back typing).

is cross matching done with the blood of the donor and recipient or not ?

It's done with the serum of the recipient, and the donor's packed red blood cells.


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Protein folding, extra dimensions and bio-mathematics
One metaphor that I have found to explain how proteins fold so quickly to a native shape is that of the blind golfer.
I have made a video to illustrate this metaphor. This shows how the shape of a slope can determine precisely where individual elements will end up.
The video represents many zero-dimensional points each following its own one-dimensional path down a three-dimensional slope to end up in a two-dimensional arrangement. Or almost: the one-dimensional paths are curves in three-dimensional space, the final resting surface is not flat, and one marble sits on top of three others.) The movement takes place through the fourth dimension of time.
Proteins form three-dimensional shapes, so the "slope" that their components slide down must be in an extra dimension.
Atoms have been observed to jump through a crystal lattice, without any indication that, in travelling from their start point to their end point, they pass through the three-dimensional space that we can observe. Is it conceivable that the component parts of a protein move through an extra dimension as the protein "folds"?
There are very simple protein chains whose native folded shape is well known. Is there any data available to suggest what path the different molecules in the protein follow during the folding process? Or do they appear to "jump"?
I imagine that it would be possible to create a mathematical model in n-dimensions to describe the simplest "slope" that the protein molecules could follow as the protein collapses into its native state.
What mathematical work is currently being done in this area?

What are you asking about precisely - like now it looks too broad - there's like 100 thousand know structures. You also don't get that PES is mathematical construct - these slopes simply describe energy and there's one dimension on degree of freedom

PES = "protein expression signatures"? Sure, there are lots of things I don't get. I do understand that that "the map is not the terrain", however closely a mathematical construct appears to model reality. Precisely, I'm asking if there have been attempts to generate n-dimensional shapes which can describe the movement of individual molecules in a protein as it folds, in the same way that my video shows a 3D shape that defines the movement of a set of virtual marbles so that the end up always in the same position.

There are really two question nuclei in here. One about quantum tunneling in protein folding, and another one about free energy surfaces and trajectories on them. They're related and both interesting, but definitely distinct.

Short Answer

What mathematical work is currently being done in this area?

A... lot?
Longer Answer
The "n-dimensional slope" thing that you're talking about shows up in the modern theory of protein dynamics as the "landscapes" concept. There's no truly standardized form for the theory, so it goes by many names. Try googling folding funnel, energy landscape, probability landscape, free energy surface, etc.
adendum
Oh, and also the current consensus is that the "quantum leap"-style effects that you were talking a little bit about don't play a large role in folding, at least in the initial stages. The current thinking is that most (not all!) of the dynamics of protein folding can be modeled using classical physics. Quantum effects can't come into play until the atoms of a protein are closely smooshed together (ie after the initial "collapse" phase of protein folding has finished).

Thanks for your rapid answer. From skimming the first articles that come on a Google search for folding funnel protein, it looks as if the mathematics that is used is mostly concerned with describing the release of energy, not with the topology of the "funnel" itself. The diagrams I see look more like artist's impressions than calculated projections onto a 2D screen. Are their names of people you can suggest, who are dealing specifically with the topology of these funnels?


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Can wood frogs who have frozen and thawed remember their past lives?
Wood frogs (Rana sylvaticus) can survive being frozen for up to 7 months at temperatures as low as -16 °C. Their breathing stops, their heart stops and all signs of life disappear. (Source)
I have looked for research that shows that when these frogs thaw in spring, they retain memories from before they became frozen, but I haven't found any. Can anyone give me any insights?
Note: This research shows how butterflies can remember experiences they had as caterpillars, before their metamorphosis. Perhaps something similar can be done or has been done with wood frogs?

sweet experiment!  good luck.

Wood frogs are highly philopatric to their breeding ponds. And the fact that they return to the same pond after multiple winters, would indicate that, at the very least, they must retain at least some spatial memory after freezing.
It is worth noting that a frozen wood frog is not nearly the same scenario as a butterfly metamorphing. Butterfly metamorphosis involves complex reintegration of all bodily systems, whereas frog brains do not reform during the winter--they just cease neurological activity. Even frog metamorphosis is less complex since much of the chondocranium and brain morphology is retained from tadpole to frog.
I know it wasn't the original question, but it is relevant to note that tadpoles seem to retain their personality through metamorphosis (see Wilson & Krause, 2012; Koenig & Ousterhout, 2018), which also seems to indicate that they have neurological stability.
References:
Wilson, A. D. M., & Krause, J. (2012). Personality and metamorphosis: is behavioral variation consistent across ontogenetic niche shifts? Behavioral Ecology: Official Journal of the International Society for Behavioral Ecology, 23(6), 1316–1323.
Koenig, A. M., & Ousterhout, B. H. (2018). Behavioral syndrome persists over metamorphosis in a pond-breeding amphibian. Behavioral Ecology and Sociobiology, 72(12), 184.


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Bacterial 16S rRNA PCR amplification with universal primers
I am doing an experiment to amplify the 16S rRNA gene from bacteria present in gut contents of fish. After extracting DNA, I perform one-step PCR with universal bacterial primers (27F, 1492R) and I see a strong band of expected length (approx 1500bp). My DNA extraction readings range from 50ng/ul in some samples, to 150ng/ul in others, as measured with Nanodrop.
Does this band represent all of the 16S genes present in the sample? Thus, does this band represent 16S genes from all of the bacterial species present in the sample?
Do I need to perform a microbiome profiling PCR to differentiate and identify all of these species?
Thank you.

The band represents all of the 1500 bp sequences able to be amplified by the primers you chose - no more, no less. Amplification efficiency will likely vary between species/sequences, and while there's a decent chance that your conjecture is correct, further validation will be required to support your assumption.

Thank you MattDMo. So therefore, through DGGE or pyrosequencing of smaller hyper-variable regions of this gene, perhaps all of the different species present in a given DNA sample could be elucidated and identified?

James - yes, something along those lines would be necessary. You've amplified enough of each target (hopefully), so now you can move on to identifying and classifying the sequences it contains. Good luck!


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Cell life: division for immortality or reproduction with aging
Are the two cells that are derived from one cell, ‘twin sisters’ or a ‘mother and a daughter’?  In other words, can a cell really be divided to live an "immortal" life or is cell reproduction the reality of cell life that accounts cell age difference between two successive generations, cell aging-associated senescence in cell reproduction, and cell line survival after the death of old cells.

First of all, in eukaryotes (as far as I'm aware), older cells can be distinguished from younger cells due to telomere shortening, so there is an ageing process. HeLa cells mentioned by @Gary Chou have a more active telomerase which mitigates telomere shortening, allowing cells to continue to divide indefinitely. I think it's a very interesting question whether this immortality eliminates any sense of "older" and "younger" cells from in HeLa cell culture. I suspect not, but I am not sure on the specifics.
In general this question will depend on how an organism divides (we're going to talk single-celled organisms from now on). For example, the yeast Saccharomyces cerevisiae is a budding yeast, which means that it divides by budding a smaller cell off of the larger cell. This clearly allows for an interpretation of "mother cells" and smaller "daughter cells." Indeed, as lots of research on ageing in S. cerevisiae has shown, beyond being larger, the mother cell undergoes replicative ageing: over time the mother cell is less capable of growth and division--she gets old!
Perhaps the most interesting case of all (and maybe the one you had in mind) is when the organism divides symmetrically, like the bacteria, which undergo binary fission. For decades, as far as scientists could tell, the two cells that were the product of one bacterium dividing looked identical, and all measurements seemed to indicate that the cells were "sisters," i.e. exactly the same, both newborn. So if in the right conditions bacteria could continue to divide indefinitely, it seemed that bacteria were immortal, since each division reset the ageing clock for each bacterium.
However, a seminal study in 2005 (1) changed this view. The researchers took time-lapse microscope movies of a colony of Escherichia coli from a single cell. E. coli is rod-shaped, so when it divides it has to synthesize two new ends or poles, one for each cell, so just after division each cell has a "new pole" that was made in the process of that division and an "old pole" which had originated before. In this study Stewart et al. kept track of the old poles in the growing colony, and they defined the age of a cell as the age of its old pole. They found that older cells (i.e. cells with older poles) displayed replicative ageing, just like yeast! They grew more slowly and were less capable of dividing. This was examined rigorously by Wang et al. (2) in a "mother machine" in which bacteria were able to grow in constant nutrient conditions (by flowing fresh media across them) in dead-end channels. The cell at the dead-end of the channel always inherited the old pole, and so was a "mother" to all future cells. They found that, while a cell line was able to grow for very long periods of time completely stably, after hundreds of generations there was an increased likelihood for the cells to display signs of stress. They attributed to the accumulation of toxic factors in the mother cell over time. So even in cells dividing by binary fission, there appears to be some difference between the two cells arising from the division, depending on how old the pole that they inherit is.
These effects in bacteria are small, and require watching many generations to reveal. Even in light of these results many researchers will still call the "mother" cell the cell about to divide and the "daughter cells" the cells that result from division, implying that there is no difference between "daughters." Stewart et al. claim that on the basis of their work this conception of bacterial division must be revised, and that instead of division producing two identical daughters,

the old pole cell should be considered an aging parent repeatedly producing rejuvenated offspring.

Furthermore, they add a nice philosophical touch to their findings:

These results suggest that no life strategy is immune to the effects of aging, and therefore immortality may be either too costly or mechanistically impossible in natural organisms.

(1): Stewart EJ et al. (2005) Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division. PLoS Biol. 3(2): e45
(2): Wang P et al. (2010) Robust Growth of Escherichia coli. Curr. Biol. 20(12): 1099-1103.

Great answer, and those are the same reference papers I would have referred to. Although the Wang et al. paper suggests that there is no difference between the mother and daughter cell, and that cell death is independent of growth (and that there is not a reduction in division rate with age). The idea being that the result from Stewart et al. was due to the older cells being in the middle of the colony with fewer available nutrients.

Also the website of the Jun group (where the Wang et al. paper came from) is excellent: http://jun.ucsd.edu/ lovely videos showing the mother machine in action!

@StephUnna fair points. I didn't stress the growth-independence of cell age defects in the Wang paper enough; it is probably not accurate to use the term replicative ageing for bacteria, since the ageing effects are not manifested in problems with growth/replication. What I was referring to by "signs of stress" is the increased filamentation rate that Wang et al. observes in older cells. Though they may still grow with the same rate, there is a difference between mother and daughter cells due to accumulation of defects in old-pole cells over long times.

In term of eukaryotic cells, most of them are mortal and will indeed age (the famous telomere sequence for example). However due to mutation some cells do achieve immortality such as HeLa cell line widely used in bio research.

Could you please develop a bit your answer and include in particular the OP's question. When (for what cell types) does the analogy "twin sisters" hold and when does the analogy "mother and daughter" hold?


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Coniferous tree with alternating bunches of short needles (Toronto area)
What species of tree is this?

Location: East of Toronto, zone 6; urban
Date of photos: May 10, 2022
Diameter at breast height: ~18 inches
Height: ~30 ft

And to help you sufficiently appreciate the excellent answer below, behold — The Larch

 Short Answer
Larix laricina, commonly called Tamarack or American Larch is a deciduous conifer with short-needle-like leaves arranged in bunched fascicles in a alternating (sometimes whorled) arrangement around short stems. The tree is the only species of Larix native to the Toronto region.

 Larix laricina stem  Source: UWGB Herbarium
 Long Answer
This is a larch tree in the genus Larix.
These deciduous conifer trees characteristically have fascicles, or bunches, of short, needle-like leaves arranges in whorls around their stems. They grow in northern forests (deciduous conifer forests, boreal forests, and northern alpine forests) in temperate cold zones. (In fact, larches grow farther North than any other tree species!)
There are 3 North American Species and 9(-11) Eurasian species. Of those 12(-14) species, only 1 species, Larix laricina (Tamarack) is native to the Toronto region:

From Wikipedia:

Larix laricina (Du Roi) K. Koch – Tamarack or American larch. Parts of Alaska and throughout Canada and the northern United States from the eastern Rocky Mountains to the Atlantic shore.
Larix lyallii Parl. – Subalpine larch. Mountains of northwest United States and southwest Canada, at very high altitude.
Larix occidentalis Nutt. – Western larch. Mountains of northwest United States and southwest Canada, at lower altitudes (Pacific Northwest).

 Range map for Larix laricina. Source: Wikipedia
BONAP range maps for Larix species confirms Larix laricina as native to Toronoto, but it also suggests evidence of the European species Larix decidua as an exotic.

We can rule out Larix decidua because the bark is neither smooth nor fissured (see Wisonsin Horticulture), the twigs are not gray or yellow (see the NAS Field Guide to Trees1), and the needles are neither reaching lengths of 4 cm (see Wikipedia) nor (from my quick count from your image) achieving clusters of 30-60 needles per fascicle (see USFS).

Larix laricina, commonly called Tamarack or American Larch, then, seems like the most likely species.

Range: Canada (including Toronto ; see above)

Bark: rough and scaly (USFS)

Leaves: 2-3 cm needles (wikipedia) bunches into fascicles containing 10-20 needles (USFS).

Twigs: reddish-brown (NAS Field Guide to Trees1)

 L: Larix laricina fascicle with leaves. R: Larix laricina stem  Source: UWGB Herbarium
Your image is just a tad too blurry and my screen a tad too small to see your needle detail. A better image of the needles and an image focused on the bark would only further help to corroborate my answer.

 1. Little, E. L. (1980). National audubon society Field Guide to North American Trees: Eastern Region. Alfred A. KNopf, New York.

Thanks very much! If you click on my photos to zoom in (on a full PC computer screen), are they still to blurry? You might need to click on them a second time...to fully zoom in.


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Why do dragonflies lose all of their coloration once they die?
At 06:43 in The Secrets of Nature video Sky Hunters, The World of the Dragonfly - The Secrets of Nature the narrator says:

Scientists have been collecting dragonflies since the eighteenth century, but there’s always been a difficulty. Dragonflies quickly become deathly pale, they lose all their color. That’s why collectors have usually preferred to concentrate on butterflies...

and an image of rows and rows of uncolored dragonflies pinned to a display are show.
Question: Why do dragonflies lose all of their coloration once they die?
 click screen shots for full size

I have also seen spiders losing colors when they die.

This is probably because the color in dragon fly wing is due to chitin crystal and which is protected by some secretion over the entire wing something like cuticle upon leaves and when dragon fly dies that secreted substance upon wing washes away when not maintained resulting in shredding off of the color from wing. Sorry I can't comment (<50 reputation) so I did answer even tho im not clear with it.
Try reading this you might find something useful maybe Insect Wing
Also this journal said that while studying the wing of dragonflies they killed and kept them in lab it didnt mention that wing lost color Mechanism of the wing colouration in the dragonfly Zenithoptera lanei (Odonata: Libellulidae) and its role in intraspecific communication
So it might be possible that the video shows dragonflies after some long time maybe a week after death and body is intact because of chitin layer but wings bleached away in sun or degraded in environment.
Also wings have supply of veins so something related with continuous production might be cause of that thing too.

Dragonfly wings are usually transparent, or at most have brownish patterns.  (At least in the North American species I see flying around - the species in the link is apparently an exception.)  It's the body that is often brilliantly colored.

Oh thanks for the information :)

@jamesqf here are some bright red wings! Identify these two big, beautiful dragonflies in Taiwan?

@uhoh: Well, I did say usually :-)

@jamesqf yep! But I was so excited to see such deeply pigmented wings I had to tell somebody :-)


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Are there any known microbes capable of living in almost pure carbon dioxide?
Some bioengineering is investigated in high carbon dioxide environments. Are there any microbes like bacteria or Archaea capable of living and multiplying in such environments?

It is not speculative to ask if a microbe can live in almost pure carbon dioxide.

@DavidJonsson Thank you for the edit, it improves the question immensely. In the previous form I would have certainly agreed with Willk.

Do you mean an atmosphere of co2/nitrogen like Earth had prior to the evolution of photosynthesis?  Presumably most of the bacteria from those days would be ok with a more or less pure co2 atmosphere, at least assuming they had access to water.

This is a much better question now! I think this could be even clearer if you made the 'Title' match the 'Body'. For example getting rid of the "almost pure" (which makes it sound like you're looking for something that can live on "dry ice" or in supercritical liquid CO₂) and being more specific — for example it seems like you might be interested in anoxic (oxygen free) environments ...

Also, are you only interested in organisms that are considered to be "extremophiles"? I found references to a non-extremophile that grows under Mars-like conditions ...

These aren't technically extremophiles, but one paper identified twenty species of bacteria that grow under a low pressure, mostly CO₂ atmosphere1.
One relatively well studied species is Serratia liquefaciens (a Proteobacterium) that has been shown to grow under

low temperature (0 °C), low pressure (0.7 kPa), and anoxic, CO2-dominated atmosphere-conditions intended to simulate the near-subsurface environment of Mars2.

References:
1: Schuerger, A. C., & Nicholson, W. L. (2016). Twenty species of hypobarophilic bacteria recovered from diverse soils exhibit growth under simulated martian conditions at 0.7 kPa. Astrobiology, 16(12), 964-976.
2: Fajardo-Cavazos, P., Morrison, M. D., Miller, K. M., Schuerger, A. C., & Nicholson, W. L. (2018). Transcriptomic responses of Serratia liquefaciens cells grown under simulated Martian conditions of low temperature, low pressure, and CO 2-enriched anoxic atmosphere. Scientific reports, 8(1), 1-10.

Capnophiles (from the Greek kapnós, meaning smoke) are organisms that thrive in the presence of high concentrations of CO2.  Some of these organisms have a metabolic requirement for CO2.
Many organisms present in the cow rumen are capnophiles by necessity, as CO2 is the major gas product of rumen fermentation (66% by molarity 1 ).  One such organism is Mannheimia succiniciproducens, which was shown to thrive in a pure CO2 atmosphere when compared to pure N2 and equimolar H2:CO2.

Under N2 atmosphere, cell growth and glucose consumption rates were much lower, suggesting that M. succiniciproducens, like other capnophilic bacteria, relies on a CO2-dependent metabolism. The glycolytic flux under CO2 was four times greater than that obtained under N2.
...
When H2 was present, cell growth rate and the glycolytic flux were lower. However, the relative succinic acid flux increased by 30% under CO2-H2, and the relative formation rates of ATP and NADH were higher in the presence of H2.

Many pathogens are capnophiles, including species of Campylobacter 2, Neisseria gonorrhoeae 3, and Haemophilus influenzae 4, though ideal culture conditions for these organisms call for CO2 concentrations around 5 - 10%.

References

Hong SH, Kim JS, Lee SY, In YH, Choi SS, Rih JK, Kim CH, Jeong H, Hur CG, Kim JJ. The genome sequence of the capnophilic rumen bacterium Mannheimia succiniciproducens. Nat Biotechnol. 2004 Oct;22(10):1275-81.
Dykes GA, Moorhead SM. Survival of Campylobacter jejuni on vacuum or carbon dioxide packaged primal beef cuts stored at −1.5 °C. Food Control. 2001 Dec;12(8):553-7.
Platt DJ. Carbon dioxide requirement of Neisseria gonorrhoeae growing on a solid medium. J Clin Microbiol. 1976 Aug;4(2):129-32.
Langereis JD, Zomer A, Stunnenberg HG, Burghout P, Hermans PW. Nontypeable Haemophilus influenzae carbonic anhydrase is important for environmental and intracellular survival. J Bacteriol. 2013 Jun;195(12):2737-46.


text:
Why is the GULO pseudo gene expressed in humans?
The GULO pseudo gene is being expressed in humans according to Genecards.
Why is this still taking place after tens of millions of years since then gene lost the capacity to encode for a functional enzyme?

I suggest thinking about this from a different direction — something like: "What selection pressure is there for loss of expression of the GULO pseudogene?"
When thinking about that question note that the expression level is very low (less than 1 transcript in a million in the tissue with the highest level of expression.
In general, evolution is messy and I think your null hypothesis should be that this as a vestigial trait.
In other words, unless you can show that there is a significant cost for the low level of expression seen from this pseudogene there is nothing to explain.


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How to interpret different results from Clustal Omega and Multalin?
I have been working on aptamers, which are nucleotide sequences. They bind to various targets, in my case a particular cell surface receptor. The people associated with the project performed SELEX and they have selected sequences that have affinity for the target. My advisor believes that the sequences could share a particular binding pocket (consensus sequence).
The sequences are mostly 40 nucleotides long but some of them are shorter or longer in length. I have to aligned the sequences in an attempt to identify sequences containing a consensus site. So far I have used both Clustal Omega and Multalin, but the results from them are pretty inconsistent.
Clustal Omega Alignment:

I also aligned a few sequences using a pairwise alignment method, but I found few similar regions among the sequences.
How do I interpret these results from Clustal Omega and Multalin?

Welcome to SE Biology. Please take the Tour (we can see you haven’t) and read about asking questions here. You have explained your problem well, but seem to want us to solve it for you. However we need to know what you make of it yourself. Do you know why alignments by different programs are different? You need to read about MSA and the particular algorithms behind the ones you have used. Which one do you think has aligned the sequences better? No reading there — use your eyes. And has the better alignment found a consensus site? Again, use your own judgment and that of your advisor.

I made some edits that I hope clarify your question, but it seems to me that you might want to ask a different question — "What alignment method would work best for finding a consensus from these sequences?"

You might want to look at partial order alignment.

@tyersome Should I delete the question and ask again?

I don't think that's necessary — you can just edit your post.  However, I encourage you to follow up on @WYSIWYGs suggestion — they show signs of having significant expertise in bioinformatics!


text:
Does avocado and orange have a common ancestor?
While I'm eating my orange, I felt as if I was eating avocado. It might be genetic manipulations perhaps but it made me think if they have a common evolutionary ancestor. Is there?

Yes, they have a common ancestor just like any other living things! Here is a website that presents very accuerately the tree of life: http://tolweb.org/tree/

Actually, what I tried to ask was that if they have a relationship as humans and chimpanzees do. Should I said "close"?

Yes saying "How closely related are they?", "when lived the common ancester of.." or "when did the speciation between the two lineages occur?". But, of course I clearly understood what you meant in your question.

Here is a website that presents very accuerately the tree of life: tolweb.org/tree
Yes, they have a common ancestor just like any other living things! How closely related are they?
Both species are:

Eukaryotes (cells with a nucleus)
Archaeplastidae (plants)
Angiosperms (flowering plants)

Then, they split their way! Here is the tolweb.org page that correspond to this speciation: http://tolweb.org/Angiosperms/20646
The avocado is in the Laurales family: http://tolweb.org/Laurales/20672
The orange is in the Rutacea (sapindales, rosids, eudicots) family: http://tolweb.org/Sapindales/21051.
You can use the left arrow on the tree of these pages to come back through times and see the different speciation event that seperate both species.
While the orange is a eudicots, the avocado is part of the magnolids. The oldest fossil records of an angiosperm lived about 132MYA (see Crane et al., 2004). So the two species diverge for quite a long time! In order to give a comparison, they are as distant than humans and rabbits (it is a rough personal estimation, I don't have any reference for that!)
Note: The orange is called Citrus sinensis in latin. The species originated in China. The avocado is called Persea americana and it originated in central american (as their names indicate).
I don't know what make you feel that they are closely related. Maybe someone might say some words about their chemical compounds (and their flavour) but at first glance these two fruits taste very differently to me. Or maybe they have some remarkably similar phenotypic traits due to convergence evolution... I don't quite know about that!

As a supplement to your answer, here's link to a more user-friendly resource TimeTree: http://www.timetree.org/index.php?found_taxon_a=2711%7Corange&found_taxon_b=3435%7Cavocado&action=


text:
mixing beer with spirits, increase alcohol content?
I decided to mix beer with vodka hoping it would make me more drunk due to the alcohol content but then remembered the rest ISNT alcoholic and i cant figure out if mixing beer with vodka or other spirits would increase the alcohol content or not i would really like an answer to this as well as any health risks if there are any, thanks.

Please note that whilst health risk discussion for individual cases are outside of the scope of this site, risks associated with alcohol are well known and available from good sources online: http://www.nhs.uk/livewell/alcohol/Pages/Alcoholhome.aspx

Perhaps it's worth adding for absolute clarity that the proposed mixing will definitely increase the total alcohol consumed e.g. comparing one shot of vodka with the same shot plus a beer - obviously. The linked answer discusses the physiological effect of this mixed drink.


text:
I see various exposure limits for carbon monoxide, but what about one breath?
I see exposure limits for carbon monoxide like 50 ppm over 8 hours. This would correspond to a total inspired volume of carbon monoxide on the order of a few hundred milliliters. This exposure is supposed to be far from fatal, but I'm unsure how to think about extrapolating long term exposure limits to acute limits, thus my questions:

What are the likely consequences if I breathed in the entire 200 ml of CO in a single breath, or even an entire lungful of pure CO?
If the answers to the above end up being "you would die", is there a reasonable way to estimate the maximum volume you could acutely breath in?

"In any high level CO environment, your exhaled breath CO level will gradually rise but remain lower than the ambient level because you always absorb some of the CO you inhale as long as the level in air is higher than the level in your blood.  As soon as you stop smoking or move to a lower CO environment, you start exhaling."
So I suspect a lungful of pure CO would indeed make you feel awful, but since that wouldn't be nearly enough to replace all the oxygen bound to your haemoglobin, I imagine it wouldn't be fatal in a healthy individual, especially if you were breathing air free of CO after that one lungful.
Apparently it takes 5 hours to eliminate half of your blood CO also.

What are you quoting here? Please provide the reference. Also, it doesn’t look like this quote is really relevant to the question, since it seems to refer to specific CO-rich environments, and smoking.


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Can plants grow without photosynthesis?
Animals can survive without eating if nutrition is injected directly into their blood.
Can the equivalent be done with plants? By injecting carbohydrate rich nutrient solution, either without photosynthesis or in addition to photosynthesis.

Survive without eating: no
Survive without photosynthesis: 1. Yes, and 2. Yes-if considering only "nutritional" aspect of photosynthesis

Some parasitic plants lack photosynthesis (see the beautiful ghost plant)
Plants also grow during the night, and plants are able of respiration, which can exceed photosynthesis - and trees do so excessively when they are young and growing (learnt some time ago during an undergraduate lecture on botany)

Survive by adding carbohydrate rich nutrient solution: not sure
Survive without photosynthesis at a philosophical scale: probably not as most molecules of sugars, which we have on earth, had required photosynthesis for their generation

Very good answer! But as far as I know cellular respiration always exceeds photosynthesis. Photosynthesis, even though it does make some energy available for the plant directly, is only the process that provides glucose for respiration. The major ATP synthesis in plants also comes from cellular respiration. The difference is the carbon source. In that way, photosynthesis is analogous to animal eating as it provides the carbon source. However, the energy conversion of the carbon source then is very similar.

tsttst Yes, I am trying to imagine a way to produce food without photosynthesis on a philosophical scale. You have highlighted the other side to the problem, namely production of sugars without using plants in the first place. The reason I ask is because I am wondering if humans can survive on this planet in future without destroying most of its natural habitat for agriculture.

Hi Nick. Photosynthesis will have been required for carbon fixation and thus indirectly most present carbohydrates. Note that already now, most of the energy in ordinary plant-derived food comes indirectly from fertilizer, and not photosynthesis. (with some components of fertilizer coming indirectly from fossil oil....) . You might infer an unacceptable answer by reading the first chapter of Harari's "A Brief History of Mankind", which discusses the time before agriculture.

No, not in the long run at least. (Except for parasitic plants as I have just learned!)
Plants rely on photosynthesis to make up glucose but that is just the tip of the iceberg, there are tons of cascade reactions (also genes regulation) going on linked to the photosynthesis. Read this just to get an idea.
So, photosynthesis is so deeply linked to the metabolism of plants that replacing it with some nutrient-rich buffer will not be enough.
There are organisms that are facultative phototroph they do photosynthesis but they can live also without, they are not classified as plants, though. One example of such an organism is Chlamydomonas reinhardtii.

This is not true for all plants, as mentioned in another answer. There are parasitic plants that are incapable of photosynthesis.

True, I did not know about it.

@alec_dijinn: Thanks for editing (withdrawed the -1). As the exception of parasitic plants is there, I would not be so sure about the generality of your answer for all non-parasitc plants, though. Still a god thing to point out!


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Why do plants flower in different seasons?
I know how it is controlled (photoperiodism), but I wonder why all plants don't start to flower in spring? Is it connected with ecological niche?

This is a really big question, related to niche, evolutionary history, life history, and coevolved species (pollinators, seed dispersers etc). Among many other things.

Plants all have a strategy which takes advantage of their physological strengths and habits, and the time taken to grow fruit and seed. i.e. the first to flower have better cold resistance and can take advantage of the understory before the trees have leaves, and many, many other "strategies and physiological differences" https://en.wikipedia.org/wiki/Plant_strategies ... http://bio.rutgers.edu/~gb102/lab_13/13i2m.html

Why plants evolve to flower at various times depends on several factors. I've taken these from the book chapter Kudo 2006.
1) Climate and other abiotic conditions.
Spring, and the onset of consistent above freezing temperatures, is the first opportunity for many plants to flower, but it may not be ideal for all. For example some locations are still very dry in the spring and plants require water from rain later in the year.
Late frosts, which can damage flowers, is always a risk. Some plants can suffer the occasional frost and loss of flowers, while others hedge against this by flowering later.
2) Pollination competition.
For plants which are pollinated by animals (mainly insects), the finite amount of pollinators results in competition among plants for this resource. If all plants flowered at the same time competition would be extremely high, and no amount of animal pollinators could successfully visit every plant. Thus some plants have evolved to start flowering later in time and potentially have less competition. Note that other strategies to increase pollination from animals could also be to have larger and/or more numerous flowers.
3) Herbivory
Flowers eaten by animals are a waste of resources for the plant. For example if an insect preys heavily on flowers, and is most active during a certain part of the year, plants would evolve to flower outside of that time.
4) Seed maturation and dispersal
The ultimate purpose of flowers are to reproduce, and the timing of flowering can influence that. Plants with large fruit, such as berries, need ample time before winter to mature and this necessitates early flowering so that there is enough time for animals to disperse the fruit.
Constraints
There are many limitations to everything above, and if a plant species evolves one strategy it generally limits itself in other aspects. For example the very first plants to flower in temperate environments may have low competition for pollinators, but they also risk being damaged by late frosts. A viable strategy may be to flower throughout the spring and summer, which some plants do, but they can only grow in environments with year round resources and likely cannot produce large fruit which animals can eat and disperse. Plants which flower in late summer or autumn likely need large roots to store the water and energy to do this.

Kudo, G. (2006). Flowering phenologies of animal-pollinated plants: reproductive strategies and agents of selection. In L. D. Harder & S. C. H. Barrett (Eds.), Ecology and Evolution of Flowers (pp. 139–158).

To add a few reasons, in dry regions (e.g. Death Valley) there are ephemeral plants, which grow from seed to flower only after a rare rain.  Or in deciduous forests, understory plants grow & flower in the early spring, before the trees leaf out and block the light.


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Do lobsters demonstrate any problem solving capability?
I was watching this video where a man takes a grocery store lobster and raises it in a salt tank, the lobster exhibits curious behavior that looks like intent.  In the comments there was a claim that lobsters were intelligent animals on par with the octopi, one user claiming they could perform complex tasks related to problem solving and cooperation and that they have experienced this behavior first hand.  Looking it up I could only find a single article from peta discussion, which vaguely hints at cephalopod like intelligence.  I've not seen any supporting evidence or even discussions from reputable sources to back up anything further.
What's more is that I've looked up the neuron count for lobsters, my understanding was the smartest arthropods were things like ants and bees, and that most ocean arthropods had significantly less neurons than even ants.  I understand that you shouldn't use neurons as a proxy for intellect, and arthropods often don't have "brains", but this should apply to both lobsters and cephalopods.  In other words, using neuron counts may be applicable in comparing rough cognitive capabilities of cephalopods and arthropods, especially with several order of magnitude gaps between the two (100,000 vs 500,000,000) and because the way in which neurons are used in their body is similar.
I have huge skepticism that lobsters can demonstrate any significant problem solving capability, let along problem solving capabilities on par or comparable to cephalopods.
Are there any reputable pieces of evidence or experiments that demonstrate lobster problem solving skills?

They are curious creatures (in the can-I-eat-it-or-fight-it sense), but I doubt they have much problem-solving capacity. I seriously doubt they're as smart as cephalopods, but they probably can learn, at least a little.
They don't use a high intellect to hunt and ambush their food or to avoid predators like octopi because they largely rely on their armor and claws for defense, and they're mostly omnivorous so they'll eat plants and algae until prey wanders into their space on so they wouldn't evolve the brain for complex thinking.
I watched the video and that particular species is territorial (hence the rubber bands on their claws) so much of that intentional behavior has to do with how it maintains and protects it's territory (moving waste away from it's sleeping space to avoid attracting predators, moving the substrate around, grabbing foreign objects in it's space etc.).
I also tried to find articles on lobster intelligence, but as far as I read they don't exhibit problem solving behaviors anywhere near as complex as octopods and other cephalopods, at least not from any scientific articles that cited their sources. That doesn't mean they're not interesting though, I found this really neat article on the effects of serotonin on certain crustaceans aggressive social behaviors.
I hope that answers your question.

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