Why Did 6 Great Ape Species Survive But Only 1 Hominid Species? My dad asked this question when I explained some circumstances surrounding Homo sapiens survival against all odds.

We know there is only one hominid species left in the world, Homo sapiens. We also know that there are only 6 other species of great apes left: 2 species of chimpanzees, 2 species of gorillas, and 2 species of orangutans. These 7 species are the last remaining in the family Hominidae.

All the other hominids besides Homo sapiens died out tens of thousands of years ago, and we believe the reason our ancestors survived is because we were more "adaptable", meaning we were not restricted to a single environment but could survive in many others. This is the reason we later spread out all over the world, and probably why we gained "sapience" and are able to contemplate these grim circumstances.

At one point, following the eruption of the Toba volcano 70,000 years ago, there were between 1,000 and 10,000 mating pairs of Homo sapiens left, though there may have been other hominid species alive at the time. My dad asked, if the hominids faced such grueling environments and all but a few died, why did the great apes fare any better? Why are there 6 extant non-human Hominidae species left, but only 1 hominid species?

Determining why one species (or group of species survived) while others did not can be difficult to answer, but I can offer one possible explanation for the genus Homo: competition. Competition between similar species is one possibility. Consider for example gorillas or chimps. The two species of gorillas occupy different habitats so they rarely compete with each other for resources (food, water, shelter, etc.). The two species of chimpanzees have non-overlapping ranges (or minimally so) so again they do not compete for resources.

Chimps and gorillas do overlap with each other for parts of their range and even potentially use the same resources, although no competition for resources has been observed (see this primate factsheet and McNeilage 2001). The same applies for the orangutans, which lives on two different southeast Asian islands.

The genus Homo is an entirely different story. As you may know, Homo first evolved in east central Africa. The first species to leave Africa and disperse across Europe and Asia was Homo erectus. This migration out of Africa happened as early as aout 1.8 million years ago. Homo sapiens had not yet evolved. However, while H. erectus was establishing itself across Europe and Asia, populations still in Africa continued to evolve.

Modern Homo sapiens evolved in central Africa perhaps about 250-200,000 years ago and dispersed out of Africa about 100,000 years ago. Homo sapiens also dispersed across Europe and Asia. Both H. erectus and H. sapiens co-occurred across parts of their range. Some have argued (Stringer and Andrews, among others, I believe but I'll have to be at work before I can verify ths reference) that H. sapiens outcompeted H. erectus, leading to its eventual extinction by competition. They occurred together and used the same resources, so H. sapiens could have caused the extinction of H. erectus. This has been called the replacement hypothesis. The later evolving species (H. sapiens) replaced the earlier evolving H. erectus.

However, Templeton (2002) has argued that the two species interbred so the species became integrated rather replaced (if I am interpreting him correctly).  While I don't dispute the possibility of interbreeding, I am skeptical of Templeton's complete dismissal of replacement.

Complicating the picture is H. neanderthalensis. Genetic evidence published by Green et al. (2010) suggests that Neanderthals diverged from H. sapiens (in central Africa) between 800,000-500,000 years ago and also dispersed out of Africa.  They also provided evidence of interbreeding between H. sapiens and H. neanderthalensis in Europe.  Modern H. sapiens may also have outcompeted H. neanderthals.

All of this was occurring during the Pleistocene ice age. Europe was experiencing repeated bouts of extensive glaciation. Thus, it is also possible that climate change caused or contributed to the extinction of H. erectus, H. neanderthalensis, or both.

In summary, the processes that led to the extinction of other species of Homo are complex and likey interactive. Competetion among species is, in my view, well within the realm of possibility but would be extremely difficult (if not impossible) to test. Climate change is also a very likely contributing factor. There are several other hypotheses but I have tried to hit the major highlights.  The debate is certainly not settled.

McNeilage A. 2001. Diet and habitat use of two mountain gorilla groups in contrasting habitats in the Virungas. In: Robbins MM, Sicotte P, Stewart KJ, editors. Mountain gorillas: three decades of research at Karisoke. Cambridge (England): Cambridge University Press. p 265


What is this red little cocoon like creature here? I found this bug here outdoor on the wall of my backyard. I’m in California.
Red and looks like a cocoon, notice some tiny dots on its back. About 1cm.
Does anyone know what kind of insect is this? Seen it there for a few days now.
Thanks

This looks like a lady beetle pupa.  Given the appearance and your description of it's size, my guess would be of Harmonia axyridis.
Here'a link, with a picture of another pupa about half way down the page: https://edis.ifas.ufl.edu/publication/in361. This species has a diversity of colorations, both on the adults and the pupa.
Here's an example of another pupa of what is most likely the same species (from https://bugguide.net/node/view/410817/bgimage):


Can somebody be deaf to voices of some people only? The voice of females is generally of high frequency, while that of males is generally of low frequency.

Also, as we age, we gradually keep losing the ability of hearing sounds of high frequencies.

So, can such a situation occur when a person is not able to hear voices of females, or maybe of certain people, while he can hear the voices of other people? I tried searching about it, but found nothing.

Although you loose the high frequencies in your hearing with age (20kHz and below), this is highly unlikely. The frequency spectrum of our voice is pretty much limited, which is also shown by the fact the for normal telephone, the spectrum transmitted is located between 300 and 3400Hz and the spectrum band between 300 and 3000Hz is named the "voice band". See here for some details.

According to reference 1 the "voice fundamental frequency" for men is between 85 and 180Hz (depending on the reference) and for women between 165 and 255Hz. These frequencies are close enough together to rule out specific hearing of male or female voices. Furthermore the frequencies even overlap.

What happens in age-related pathological hearing loss (also termed Presbycusis) is that voices generally get muffled due to losses in the spectrum and hearing intensity. See the Wikipedia link and also reference 2 for more details.

Reference:

The frequency range of the voice fundamental in the speech of  male
and female adults
Presbycusis


How do inward rectifier potassium channels work in the heart? Apparently in cardiomyocytes, there is an inward rectifying potassium channel that operates during phase 4 of the cardiomyocyte action potential.  I have heard that despite this potassium channel being referred to as an inward rectifying channel, that in vitro the channel in fact still transports potassium from the inside to the outside of the cell.  It appears that Wikipedia seems to suggest otherwise (?).

Can someone please explain what the inward rectifier potassium channel does and its role in phase 4 of the myocyte action potential?

According to Boron's medical physiology textbook:

  "Although inward rectifying potassium channels pass current better in
  the inward than the outward direction, the membrane potential (Vm) is
  typically never more negative than Ek (equilibrium potential of potassium across the membrane). Thus,net inward K+ current does
  not occur physiologically. As a result, the activation of GIRK
  channels (G protein coupled inwardly rectifying potassium channel)
  hyperpolarizes cardiac cells by increasing K+ conductance or outward
  K+ current."


What are those huge plants / fungi on trees called? I've seen them in Scotland in August 2015:

The plants / fungi were quite high (over 2m) on the tree. They are almost circular if you view them from the top, I guess (except for the part where they are connected to the tree). I guess the diameter of them might be over 14cm.

What are they called?

Well I will agree with fileunderwater, it is a Fomes fomentarious. For more info check this: Fomes fomentarius is a tough perennial polypore that usually becomes hoof-shaped with age; it is found on standing and fallen hardwoods. Its woody upper surface develops grayish zones, and its brown pore surface features tiny round pores. When sliced open (no easy task, given its toughness) it is usually composed more of vaguely layered tubes than flesh.

Along with Piptoporus betulinus, Fomes fomentarius is one of two mushrooms that the Tyrolean Iceman was carrying around 5000 years ago. He apparently used Fomes fomentarius as tinder.

Description:

Ecology: Parasitic and saprobic on the wood of hardwoods (especially birches and beech); causing a white rot; growing alone or gregariously; perennial; fairly widely distributed in northern and north-temperate North America

Cap: Up to about 20 cm across; shell-shaped to hoof-shaped; with a dull, woody upper surface that is zoned with gray and brownish gray.

Pore Surface: Brownish; 2-5 round pores per mm; tube layers indistinct, brown, becoming stuffed with whitish material.

Stem: Absent.

Flesh: Brownish, thin, hard.


Bacterial chromatin binding data? I'm looking for data - maybe CHP^2 data that shows chromatin binding to a prokaryotic genome under some specific conditions.  Can anyone point me to a source?

A large number of prokaryotes do indeed have nucleosome-like structures.  The most well studied is H-NS in E. coli, Salmonella and some other deltaproteobacteria.  H-NS like molecules have also been found in mycoplasma (Lsr2).  One of its roles is to bind AT-rich DNA and silence transcription.  The binding is usually to suppress the expression of foreign DNA which tends to have a lower GC content than the host organism.  There is a great paper that did ChIP on ChIP with H-NS in Salmonella by Navarre et al in Science (Pubmed ID: 1676311).

As a side note H-NS does compact DNA and there is a paper by Dame et al. that demonstrates it with atomic force microscopy.


Do species ever move into new territory and then die out because of the local diseases? We usually hear that an invasive species has brought with it a disease which it itself shrugs off easily, but which then decimates the local population which has never encountered it before. It's a very common story. But it doesn't make sense to me. Surely it should be far more common for the reverse to happen? Surely a newly arriving species has to face not just one or two new things in the new environment, from one or two new individuals, but an entire environment coming at it from every direction with hundreds of viruses, bacteria and competitors it has never come across before. So how come the story is always that the invading species kills off the locals, when you would expect the invading species to have hundreds of totally new threats and strange foods to handle, would be unable to cope, and would die out?

So how come the story is always that the invading species kills off
  the locals, when you would expect the invading species to have
  hundreds of totally new threats and strange foods to handle, would be
  unable to cope, and would die out?

There is a problem of observation bias for these two scenarios.  In the first scenario a few members of an invasive species enter a new range, transmit a novel disease to the pre-existing species, which suffers a massive (easily observable) die off. In the second scenario, a few members of an invasive species enter a new range, catch a local disease, and die in short order (unobserved and unnoticed).

In other words, a few individual deaths from any cause will generally go unnoticed. Thousands or millions of deaths of deaths from a novel disease are more likely to attract attention.


Why do neurons have only one axon? I have just learnt about neurons. I wonder why neurons have only one axon. Can they transmit nerve impulses faster and more rapidly when they have more axons? Does having more axons help in coordination?

Could anyone tell me why neurons have only one axon?

Neurons generally have one axon, because of the way it sums potentials from its dendrites. Right at the axon hillock (the little area where the axon protrudes from the soma), all the potentials are summed together. Now, you have to consider that what is actually summed here is dependent on the shape of the neuron, potentials lose amplitude as they travel towards the axon hillock. If there were multiple axons protruding from different sites, they would send out different signals and compromise the computational integrity of the neuron.

Instead of having multiple axons, a neuron simply branches its axon with axon collaterals. This way, all post synaptic sites are receiving virtually the same message.


Paired-end illumina sequencing I'm tying to understand the mechanism of paired end illumina sequencing, however I dont't  understand why index primer 1 and index primer 2 are used.
paired end illumina sequencing (YouTube).

Let me begin in the sample preparation to explain you the index primers.... and let me assume please that you want to sequence amplicons like 16S. Let me further assume that you have 96 samples, which means that you have one complete PCR plate full of samples. First you prepare your samples. You are doing a amplicon PCR, clean that PCR, attach the adapters which are necessary that the sequences can bind to the glas slide and at last you are attaching indexes.
You are attaching these barcodes individually for each sample.
Looks like that image:

source: https://www.neb.com/~/media/Catalog/All-Protocols/C411AB12AFB04000BED567FC17B2A4AA/Content/PCRPlate.jpg

Let's call such indices barcodes (index = barcode). As you can see, each sample gets its own combination of a indexing primer as you are using always to primers (i7+i5) for each sample. Whats important is, is that all these primers are individuals like:

Line:
1: AAAAAT
2: AAAATT
3: AAATTT

and:
A: TTTGGG
B: TTGGGG
C: TGGGGG

(In reality these primers are longer and more complex!)

After you have done such a indexing PCR and also cleaned your PCR (get rid of the polymerase, something like this) you have to pool your samples (put them all together) before you are sequencing. And thats the point why such indexes are important. Without indexing you would have no chance to get your samples separated (=demultiplexed) again after sequencing.

When you are sequencing paired-end then you are sequencing one time forward (barcode + adapter + the sequence you want to have) and one time reverse (barcode + adapter + the sequence you want to have). One big amplicon of e.g. 500 bps gives you two sequences: the forward sequence (also called forward read) and the reverse read.

Let's call the forward read: R1
And the reverse read: R2

After sequencing you have one big pool of sequences. What you are doing first is to demultiplex your samples. As you know now you have for each samples hundreds of thousands of sequences: each consists of two Parts: The R1 read and the R2 read. What you are doing now is to separate your sequences again: You know that you used for example the indexing primers AAAATTTT and CCCCGGGG (just examples!) for your first sample. So you know that AAAATTTT belongs to the forward (R1) read and CCCCGGGG belongs to the reverse (R2) read. This means, that, when you separate all sequences which contains at the "barcoding/indexing-position" these sequences, you know that these are sequences which belong to your sample 1. For sample two you used for example the barcodes AATTAATT and CCGGCCGG and then you know again: AATTAATT belongs to the R1 read and CCGGCCGG belongs to the R2 read. Filtering that sequences out and save them in an additional file you will get your sample 2 separated. And that's why such indexes are important and that's also the reason why you always have to indexes: one is used for the forward read, and one for the reverse read.

Additionally: Why basically we have to use primers is the following: If you want to sequence an amplicon you (or at least the machine) is only able to sequence about 250 bps in each direction. When you are attaching indexes (which are in each case needed) then you are able to sequence in both directions: forward and reverse. And afterwards, when you have demultiplexed your samples you can run an assembly to put the forward and reverse reads together again.


Inbreeding vs Mutations Small populations of organisms may be exposed to the dangers of inbreeding. But if a small population manages to survive for many thousands or millions of years, would mutations eventually diversify the gene pool, rescuing the species from adverse genetic impacts?

For example, if the cheetah - a classic example of a genetic "bottleneck" - survived for a million years, would we expect the cheetahs of the future to be more diverse?

If you know of any studies that expand on this, I'd be interested in knowing about them. For example, what is the minimum number of breeding age individuals of a mammal species that would have to wash up on an isolated island to survive, and approximately how long would it be before the population is free of problems related to a lack of genetic diversity?

There are two major factors that will affect the development of diversity, given the same starting point: The mutation frequency, and the strength of selection.

Mutation frequency is unlikely to change significantly, so you're left with the strength of selection as the deciding factor for how much diversity arises and how rapidly.

"Selection" means that less-fit individuals are removed from the population, so if the selection is strong enough, you're left with the race between evolution and extinction. With a small starting population and strong selection, the most likely scenario is extinction, but the right level of selection can lead to diversity.

An oversimplified view of selection is that a population will evolve toward some Platonic ideal. If long necks give more fitness than short necks, then the population will evolve toward having longer necks. The population changes, but isn't necessarily more diverse.

But there are several modes of evolution that drive a population toward increased diversity. In theory, you could imagine that the population does better with a 50/50 mix of long and short necks than either an all-short or an all-long necked population. Examples of drives toward population diversity include positive and negative frequency-dependent selection (also known as "balancing selection"), and overdominance.

Are there any examples of bottlenecked populations where one of these drivers has led to increased diversity? Yes, there are several. The best example might be the Channel Island fox:

  The San Nicolas Island fox (Urocyon littoralis dickeyi) is genetically the most monomorphic sexually reproducing animal population yet reported and has no variation in hypervariable genetic markers.  ... foxes colonized the three northern Channel Islands (San Miguel, Santa Rosa, and Santa Cruz) ≈16,000 years ago and, subsequently, were transported by Native Americans to the three southern Channel Islands (San Nicolas, Santa Catalina, and San Clemente) 800 to 4,300 years ago ... We examine variation of five loci within the MHC of San Nicolas Island foxes and find remarkably high levels of variation. Further, we show by simulation that genetic monomorphism at neutral loci and high MHC variation could arise only through an extreme population bottleneck of <10 individuals, ≈10–20 generations ago, accompanied by unprecedented selection coefficients of >0.5 on MHC loci. These results support the importance of balancing selection as a mechanism to maintain variation in natural populations and expose the difficulty of using neutral markers as surrogates for variation in fitness-related loci.

--High MHC diversity maintained by balancing selection in an otherwise genetically monomorphic mammal

The specific question "how long would it be before the population is free of problems related to a lack of genetic diversity?" is too broad to answer with any detail, but another point to keep in mind is that the problems of inbreeding are usually less to do with loss of diversity (although that can be one problem, as the San Nicolas foxes show) and more to do with deleterious recessives emerging as homozygotes; this can be softened by various factors, including chronic low-level inbreeding before the bottleneck occurs, which "purges" out the deleterious recessives and makes the population more resistant to inbreeding. One review: Do Plant Populations Purge Their Genetic Load? Effects of Population Size and Mating History on Inbreeding Depression


How to predict the top microRNAs that bind to 3`UTR of a specific gene I would like to know whether someone could tell me

1) some of the online programs that will predict the top microRNAs that bind to 3`UTR of a specific gene (for eg-GAPDH).

I am relatively new to the field.

thanks

You'll find TargetScan quite useful. You can pick from a number of species and simply enter a gene name. It will then get the 3' UTR, show its conservation across species (binding sites in a conserved area are more likely to be active), find miRNAs that can bind to the 3'UTR, and then split those up by whether they bind to highly or poorly conserved regions. It also categorizes the hits according to various properties, like proximity to the open reading frame, in case you want to perform any sort of filtering by that.

Edit: BTW, you may want to take the target miRNAs and look at their expression in your tissue of interest. That's a good way to further narrow down their relevance.


Do large animals experience a meaningful delay when moving their most distant appendages? According to the Physics Factbook, nerve impulses travel at speeds anywhere from 1 meter per second up to around 100 meters per second. Blue whales reach up to around 30 meters long.

For a full-size blue whale, this means that a nerve impulse to move the tail muscles could take from 0.3 seconds to 30 seconds to reach the tail. While I'd imagine factors such as myelination and other adaptations function to keep this closer to the 0.3 second measure above, this is still a best case scenario, and would certainly be a noticeable delay were it a human being.

Do large organisms experience meaningful delays when moving their most distant appendages?

Yes, larger animals do experience larger delays in movement.

There have been studies of size difference vs sensorimotor delays in terrestrial mammals, https://www.ncbi.nlm.nih.gov/pubmed/30158304

That graph is for innate reflexes of a needle to the hind versus a kick-time. Perhaps no one dared to prick a blue whale.

Elephant vs shrew, heartbeat of 30 vs 1500 BPM, elephant 50 times slower than the shrew. Larger animals compensate with a better ability to predict physics and kinematics using their larger brain.

There are other kinds of movements which have more complex neural pathways that the graphs of pin-prick reflexes, that are even slower compared to size, you can study the physiology of eye to hand response in humans which varies from 120ms to 270ms for different humans.

It does have an effect on survival for example with a mongoose versus a snake, the mongoose has more versatile and faster reactions.

There are also weasel attack videos on the web.
some graphs here


Plant growing very rapidly near my house please see attached photos of a plant, that is growing rapidly near my house. All my friends failed to classify this plant. Can any botanist/biologist help to discover the species of this plant?
Thank you in advance!

It looks like a young Empress Tree (Paulownia tomentosa)

Native to China, it is an invasive species in the USA. looks beautiful when full grown however


Proteins that give color (without fluorescence) Is there proteins that have strong color, that could be seen without the need of UV and with naked eyes (with white light) - in mammalian cells?

Searching for reporter, something like GFP, but that we could see it without UV (not fluorescence).

Like chromoprotein - but it is problematic in mammalian cells because most chromoproteins need a prosthetic group.

Have a look at this paper. They have isolated a chromoprotein similar to GFP, and like the latter it does not have any prosthetic group.

This protein — asFP595 (because it was isolated from the anemone  Anemonia sulcata.), is purple coloured under white light and also exhibits a little fluorescent emission in the red region  (λmax = 595 nm).

Also have a look at these two papers:

GFP-like chromoproteins as a source of far-red fluorescent proteins
Major colour patterns of reef-building corals are due to a family of GFP-like proteins


Do birds require cilia for left/right symmetry during their embryological stages? I know that in humans ciliary dyskenisia can lead to a Situs inversus, is this also the case for birds and reptilians?

Here is a paper that talks about left-right patterning across bilateral organisms, discussing both Xenopus (frog) and chicken.

It looks like it may be hard to generalize, but the answer appears to be "yes" for Xenopus and "no" for chicken (see e.g. Figure 2, and text immediately following).

However, it looks like the question of what exactly is going on in chicken is not well understood, according to this other paper. Chickens do have lethal ciliopathy mutants homologous to mutants causing left-right defects in other organisms, but these mutants appear to have normal left-right asymmetry development in chicken.

It is also not clear that the requirement of motile cilia for left-right asymmetry is generalizable within clades though, as pigs have apparently also lost the dependence on cilia for L-R, whereas mice and humans do require cilia for L-R. It appears that pig and chicken have dispensed with cilia by the same histological mechanism (see image below, Figure 7 of first paper).

I do not know whether the mechanism has been investigated in other birds.

Hope that helps.


Can you identify this red insect? Location: Lansdowne, Uttarakhand, India

Date: 27 May 2017

Time: 5.33 pm

The insect was found walking upwards on a plastic table. It was about 3-4cm long, as far as I remember; its been a long time since I encountered it.
Spotted near a small shack in the Terai forests.

This is a nymph of a shield bug in the Tessaratomidae family, commonly called tassarotimids (or sometimes "giant shield bugs" due to typically being 1.5 - 4.5 cm long).

According to Wikipedia:

  They are mostly found in tropical Africa, Asia, and Oceania though a few species can be found in the Neotropics and Australia. There are about 240 species known

Of the subtaxa, only a few genera are even found in India:
Empysarus, Neosalica, and numerous in the subtribe Eusthenaria (e.g., Asiarcha, Aurungabada, Carpona, and Dalcantha). A key (Leston (1955)+)to this group of insects is available for purchase or institutional subscription on Wiley

Specific Taxa:

Similar to a comment under the OP's post suggests, this page appears to suggest that the nymph of a Eusthenarian called Eurostus validus (shown below) appears quite similar to the OP's specimen. However, I cannot find definitive record of E. validus being in India.

 Source: Vic wicked on Pinterest

the availability of useful information (keys, reputable websites, etc.) for this group of insects (especially for India and in English) are extremely limited, so I will just leave you here with the understanding that your insect is a tassarotimid nymph that is closely closely related to Eurostus validus, Eusthenes femoralis or some other member of the Eusthenaria.

 + Leston, D., 1955, April. A KEY TO THE GENERA OF ONCOMERINI STÅL (HETEROPTERA: PENTATOMIDAE, TESSARATOMINAE), WITH THE DESCRIPTION OF A NEW GENUS AND SPECIES FROM AUSTRALIA AND NEW SYNONYMY. In Proceedings of the Royal Entomological Society of London. Series B, Taxonomy (Vol. 24, No. 3‐4, pp. 62-68). Oxford, UK: Blackwell Publishing Ltd.


Is complete genetic linkage possible? Linkage is the tendency of genes on the same chromosome to remain together during the process of inheritance. Is it possible that two genes will remain linked generation after generation without any crossing over between them? Can anyone give an example?

Complete genetic linkage does occur in some cases.

Most of the Y chromosome (present as a single copy in males of many species) does not recombine with the X chromosome. Any genes in this non-recombining region, the "male specific Y" (which is 95% of the Y), will be "completely linked", in other words, they cannot be broken apart by recombination and are inherited as a single unit.

Non-recombining region of the Y marked as NRY from this paper.

The closer two genes are, the higher the general tendency for them to be co-inherited. When co-inheritance is non-random the genes are in linkage disequilibrium. The genetic linkage between genes is measured in centimorgans.

I'm not aware of any completely linked genes in recombining parts of the genome. By definition there is some distance between two linked genes (otherwise it's one pleiotropic gene). Therefore, if recombination is possible, then it is possible for them to become unlinked at some frequency, even if that frequency is extremely small (I could be wrong though, but scholar searches have given me nothing). There are, however, cases of very tight linkage between genes (1, 2, 3).

Note that factors other than genetic linkage can affect linkage disequilibrium.


Why is blood collected at crime scenes? I have read that mature red blood cells (MRBs)do not have DNA.  So I am curious why crime scene technicians collect blood. Is it to collect and amplify segments of white blood cells?

There's still white blood cells with DNA.

Some forensic blood tests are:

Conventional serological analysis:

Analysis of the proteins, enzymes, and antigens present in the blood, for general doctor tests: (black/white/drunk/stoned/heroin addict/polio vaccinated/hiv pos...)

Restriction Fragment Length Polymorphism (RFLP) DNA :

Direct analysis of certain DNA sequences present in the white blood cells. This method also usually requires a "large" sample size to obtain significant results.

Polymerase Chain Reaction (PCR) DNA :

Analysis of certain DNA sequences that have been copied multiple times to a detectable level.


Why is there such in interest in antibiotics against Pseudomonas? I keep finding information on anti-pseudomonal antibiotics, or information specifying the antibiotic has anti-pseudomonal activity. Is there anything peculiar to this bacterium when compared with other gram negative bacteria?

Indeed Pseudomonas is a very peculiar (and concerning) genus in clinical microbiology, specially P. aeruginosa. The reason why you keep finding emphasis on antibiotics that have pseudomonal activity is because this organism is the model of bacterial antibiotic resistance. It is often considered more deathly than other important multi-resistant bacteria such as S. aureus, Acinetobacter or Enterobacter.

P. aeruginosa is responsible for multi-resistant nosocomial diseases (a basic definition of nosocomial is an infection acquired inside a hospital) that have really high mortality rates. It is not uncommon to see hospital antibiogram results for this bacteria informing about resistance for all the commmonly used classes of antibiotics for Pseudomonas infections including 3rd and 4th generation cephalosporins, fluoroquinolones and carbapenems.

Reference: Evolution of Pseudomonas aeruginosa Antimicrobial Resistance and Fitness under Low and High Mutation Rates

There are LOADS of articles and info to read about P. aeruginosa antibiotic resistance, but I like this one since it tries to explain how the problem appeared from a genomic point of view.


gene mutation occurs on two strands of DNA or just one strand? Suppose we have one strand with 3'-AAA-5' and the other strand is 5'-TTT-3'.
So when point mutation occurs, does it happen to two strands at the same time? e.g. 3'-AAA-5' becomes 3'-AGA-5' and 5'-TTT-3' becomes 5'-TCT-3'?
Or the mutation can occur with only one strand? e.g. only 3'-AAA-5' becomes 3'-AGA-5'? but in this case, A would pair up with G.
When transcription starts, the 3'-5' strand is transcribed, if the mutation does no occur in this strand, does it mean this mutation wouldn't affect any downstream products?
Is it same for indel?

A "mutation" is a permanent alteration of the genetic composition of an individual. To obey this definition, a base change in one strand must be accompanied by a corresponding change in the opposite strand. Only in this way a mutation can be transmitted to the offspring.
The situation where only one of the strands has undergone a base change constitutes a pre-mutational DNA damage, as the double strand will show a deformation at that site. The enzymes of DNA repair mechanisms recognize and correct many such "deformations", but sometimes they do not know which was the original base, and introduce a change that become fixed in the DNA sequence.


cell specialisation and their location When we create new cells, how come they are of the 'right' type at the 'right' place?
For example, when I make a new cell on my lips, it's obviously not the same as a new one in my kidneys.

Is the differentiation done by using a different part of the DNA each cell has?
How does the mechanism of growing specific types of cells at a specific place work?

Yes differentiation is primarily about using only a portion of the genome as you pointed out. However, differentiated cells possess a kind of "memory" which enables the daughter cells to continue the usage of the same set of genes. This "memory" is enabled by epigenetic mechanisms which leave inheritable "marks" on the DNA such as methylation (I won't explain further as this would take an entire book).

About the place: each part of the body can produce cells locally (except for some tissues). For example the epithelial cells in your lips will arise from your lips. What signals the division of cells in response to a signal such as lets say injury is again a broad question. One simple mechanism is this (not an independent mode but just one aspect of a complex process): cells generally divide but stop dividing if there is no free space i.e. the cell is surrounded by other cells. This is called lateral inhibition of growth.

I would suggest that you pick up some good cell biology and molecular genetics books to understand these processes.

Cell Biology:

Molecular Biology of the Cell - Bruce Alberts et al.
Molecular Cell Biology - Lodish and Baltimore

Molecular Genetics:

Molecular Biology of the Gene - James Watson et al.
Genes - Benjamin Lewin


Why would villagers attack Orangutans? I read today in the news that villagers in Borneo were attacking refugee Orangutans. Why would they do this?

In It’s Not Just Conflict That Motivates Killing of Orangutans by Davis et al. (2013), the authors identify number of conflict and non-conflict reasons reported in the study why orangutans were killed in a certain part of Indonesia:

Conflict reasons:

pest
fear/self-defence
paid or forced to kill
orangutans interrupted logging or forestry operations

Non-conflict reasons:

traditional medicine
food
to sell or keep young as pets
hobby/sport hunting
for other trade of animals or meat
killed accidentally or opportunistically while hunting other animals

The results from this survey are depicted in this graph:

Obviously in this case they were not attacked for food. The impression I got from the article makes me think it was probably motivated by people viewing them as pests or as a threat/danger. It is almost certainly more of a social reason than a biological reason. However, in the absence of specific evidence, it is probably not helpful to speculate why this occurred.


How is bad garlic breath eliminated by swalllowing a bit of raw garlic? Please bear with me, as I am just a poor physicist.

I have learned how to make traditional pastourma  from a recipe given by my late aunt Dora, which is like pastrami except with a very strong garlic contribution and a lot of other spices. This leads, after eating, to strong garlic breath. My daughter complained of the "stink" when she was near me.

I somewhere heard that if one swallows a bit of raw garlic before eating food with strong garlic content, the breath stays fresh. I have tried it several times, and it works (my daughter the detector). It seems magical, or homoeopathic!

As a physicist, I would like to know how is this possible?

Searching the net for "how to avoid garlic breath" some references come up.

Enter Ohio State University to help. Researchers there have evidence suggesting that we can neutralize bad breath naturally before it offends those around us. According to science, here are three ways to do it.

Recommended: raw apples, lemon juice, green tea.

Green tea is very high in antioxidants called polyphenols. As with the enzymes in the apple, polyphenols cover up the odor-causing chemicals in garlic.
Sheryl Barringer, one of the study's lead researchers, said that it’s best to use the bad breath cures at the same time you’re eating garlic. So we’d recommend adding some apples to that salad with garlicky dressing or using some lemon juice in your next garlic dip. Unless you want to squeeze the citrus straight into your mouth, that is.

And in a link found there, the chemical explanation is:

According to the researchers, foods deodorize garlic breath through two mechanisms. First, enzymes in the raw foods help to destroy the odors, and then, phenolic compounds in both the raw and cooked foods destroy the volatiles. This is why raw foods were generally more effective because they contain both the enzymes and the phenolic compounds.

It must be that raw garlic taken just before eating garlicky stuff works the same way. No magic. Maybe the researchers will see this and do a proper experiment :).


How closely related are two parasites Giardia intestinalis and Trichomonas vaginalis? How closely related (from the evolutional point of view) are parasites Giardia intestinalis and Trichomonas vaginalis? Giardia genome is about 12 Mb and its major cellular proceses are rather simple. The genome of Trichomonas is approximately 160 Mb. What about its cellular processes, is it also a 'minimalist'?

Basically, Giarda is a an Excavates while Trichomonas is a Cercozoa meaning a Rhizaria (Chromealveolates in the broad sense as noticed by @har-wradim in the comments (now deleted) because Cercozoa are neither Chromista nor alveolata). Because the very basis of the tree of eukaryotes is still unresolved (eukaryotes), the most recent common ancestor of these two species is just an old eukaryote! In other words, these two species are not more closely related than are related a cat and a chestnut tree!

The links yield to Tolweb.org which shows you the phylogenetic tree and allows you to explore the relationships between organisms. Have a look to eukaryote tree especially to see the positions of the Rhizaria and Cercozoa.


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?

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).


Is genome recurrence possible like in Jupiter Ascending? I have watched Jupiter Ascending many times now and I was wondering if genome recurrence, like what happened to Jupiter Jones, is possible.

Is it possible to find two unrelated people, possibly several generations apart, that cannot be distinguished between by DNA sequencing?

Taking the example of Jupiter Ascending: in the movie Seraphi Abrasax they show the "genetic recurrence" of Jupiter Jones, which means the same sequence of DNA has repeated after several thousand years from Seraphi to Jupiter.

Various types of genetic variation exist in natural populations. One is the single-nucleotide polymorphism (SNP), which is where different nucleotides are present at the same location in the genome of different individuals in a population (with variation present in a nontrivial number of people; the threshold is usually set arbitrarily at 1%).

Even just considering SNPs and ignoring other types of variation, what you talk about would be effectively impossible.

The human genome is about 3 billion base-pairs long. Along the whole genome, according to Chen et al 2012, between two individuals there is something like 3 million SNPs. Imagine two people flipping a coin and the result is exactly the same every time, 3 million times. Now imagine instead of heads or tails, there are 4 options.

Only 1 result of the series of 3 million 1 in 4 chances is identical to the original series.

$\frac{1}{4^{3000000}}\approx\frac{1}{\infty}$ = 0

Go ahead, try it on your calculator.

Now, there are also variations that are beyond SNPs between individuals that cause much more variation between two people. These can cause even more "unprobability". Since we already require infinite people before this event is likely to happen, I think we can just call this event impossible.


Breaking a gene during recombination I just started reading about recombination frequencies of genes and related stuff, and can't find an answer to this (possibly naive) question.
Can recombination possibly "kill off" a gene ?

To be more specific, say a gene is located at position $x$ to $y$ on some chromosome.  Then, we are so unlucky that recombination decides to cut off the chromosome at location $x + (y - x)/2$, right in the middle of the gene.
So both halves will get recombined with the other halves of the gene on the homolog chromosome.  If the allele on this chromosome was different, could it result in destroying both alleles of the gene ?  Is there something that prevents this ?

Yes, you could imagine a situation where two functional alleles could produce a recombinant which was non-functional.

chromosome 1 has A and B at positions x and y - functional
chromosome 2 has C and D at positions x and y - functional
Recombination between positions x and y produces A/D and C/B versions of the gene. Either or both of these could be non-functional.

Nothing prevents this from happening, but natural selection will act on the recombinants.


How does mass spectrometry detect histone methylation? In this research paper they talk about the methylation of histone.  They use mass spectrometry to identify which peptide position is methylated. Does the number yielded by the spectrometer calculate the mass of the amino acid with and without the mass of methyl group? I wonder because I saw some introduction saying the number present the molecular mass of the molecular. I also would like to ask the mechanism of it and how you interpret this data? Thank you!

It is not simple MS, it is tandem MS. They send the sample through multiple MS and they fragment it between them. So they can get info about the molecular structure as well, not just the mass/charge of the molecule.

A quote from your article:

  MS/MS spectra of the methylated H3 protein (top down) and fragments
  upon electron transfer dissociation fragmentation. Fragments of the
  methylated H3 have a mass shift of 42 starting at C14, indicating a
  modification site at the K14 at the N terminus of the peptide.
  Normalized collision energy = 35%, activation Q = 0.250, activation
  time = 100 ms, accumulation time = 5 min.

A reference from your article:

  Frese et al., 2011 C.K. Frese, A.F. Altelaar, M.L. Hennrich, D.
  Nolting, M. Zeller, J. Griep-Raming, A.J. Heck, S. Mohammed

  Improved peptide identification by targeted fragmentation using CID,
  HCD and ETD on an LTQ-Orbitrap Velos

  J. Proteome Res., 10 (2011), pp. 2377–2388


Periodic Muscular Growth in Humans If a healthy human is at a certain muscle state and then experiences muscular atrophy solely due to disuse/lack of exercise, is it easier to gain that muscle back than if the human had never reached that certain muscle state. If so, is there a name for this effect. The reason I'm wondering is because it seems like muscle mass was definitely periodic in ancient times when food would become scarce during the winter, and that an increased ability to put back on muscle might have developed evolutionary-wise. I thought that this would fit best in biology, let me know if this isn't the case.

Disuse and lack of exercise are actually exceedingly new problems when considered on an evolutionary scale.  The bigger evolutionary pressure for the last few million years has been not starving to death, therefore not maintaining expensive muscle fibers unless they were absolutely necessary.

I haven't found any evidence of previous musculature effecting growth, but I'm going to look into it more (only some quick pubmed searches), and edit this answer.  If someone else knows more immediately, please feel free to answer.


How does the OD correlate with the number of algae cells? My research team and I are using a spectrometer to measure the OD of an algae sample. We are trying to answer the question "Is there a correlation between OD and the number of algae cells?"

What should we consider in our experiment? Is this an established technique?

As with bacterial cells, number of cell and OD are correlated. I am not a specialist, but it seems that you can use microscope to visually count number of cells, then correlate it with optical density of the solution you have. This will allow you to first establish how many cell correspond to 1 unit of OD, then use OD to estimate number of cells quicker than by counting.

Just a few details: counting of cell number is done by dropping given volume of culture on a special slide with grid, then manual counting using microscope.

If we assume that 100 cells/mL (or whatever) solution gives you OD of 1, then OD of 2 will correspond to 1000cells/mL concentration. That us due to logarithmic relationship between OD and light absorption by the cell culture.


Common genes and enzymes involved in pathogen entry into host Many microbes like Salmonella, E.coli, Legionella pneumophila etc. enter host cells via cystoskeleton remodeling of the host cell. Do all microbes follow the same path or there are any other ways for the microbe to enter the host cell. What are the most prominent and significant enzymes involved in these and what are the genes involved in the same. It's a general question as I am looking for the common genes and enzymes that most microbes employ the mechanism of cytoskeleton remodeling.

Passing through plasma membrane by remodeling host cell seems reasonable choice but actually most of pathogen use cell's normal functions like endocytosis, phagocytosis, pinocytosis etc to enter (well, indirectly you need actin remodeling for this also but pathogen is not doing it actively. ). Check this review for some 'simple' mechanism pathogen use to enter cell. As far as your question about enzymes, there are lot of common enzymes (specially manipulating kinases) which are important in these pathways.Pathogens use lot of other factors to exploit host. Cytoskeleton remodeling is indirect output of many of these signaling events. Just to put into perspective, recently hiked on social media, Ebola virus use micropinocytosis like mechanism to enter into host cell. Some other representative examples in following figure (Source :Gruenberg and Goot 2006 )


Mixed-mating plants: is the number of mixed mating plants supposed to be trivial? I am referring to Winn et al. 2011

Last sentence of the first paragraph is

  Although sampling bias against both selfing and highly outcrossing species may inflate the frequency of mixed-mating populations, the number of species reported to show mixed mating is not trivial, and calls into question the status of mixed-mating populations as transitional, and therefore the sufficiency of the theory to explain the observed distribution of mating systems in hermaphroditic species.

I do not really understand what is the logic behind the highlighted part and what is its purpose.

Is the number of mixed mating species supposed to be trivial in a case where the number is inflated (So there is a need to clarify it is non trivial)?
How does the fact that it is not trivial bring up the question below the highlighted part?

I think the main message of the quote is

"Many would have expected that mixed mating can only exist as a transitional state and thought that stable equilibriums are either pure selfing or pure mixing (or both). The observation of a non-trivial number of mixed mating populations suggest that our expectations were wrong."

The first sentence of the quote is a statistical detail of their paper and not a premise for the conclusion that there is a non-trivial number of populations that show mixed mating.

The evolution of selfing is a large topic in evolutionary biology and cannot really be summarized in a single post (even more so that many question are still open to debate). Goodwillie et al. 2005 is a review on the subject that will help you understand the work that has been done on the evolution of selfing. Very related is the evolution of hermaphrodism, dioecy and other mating systems in plants. Pannell 2002 is a very good paper on the evolution of androdioecy and the maintenance of these unexpected mating systems.


Infant tissues, organs, body parts or reflexes in an adult organism What is the phenomenon, when a normal useful tissue, organ, body part or an inborn reflex or instinct existed in the infant organism and normally should disappear or at least completely lose its function in the adult organism but it won't? Atavism and vestigiality don't seem the right terms. Is there a specific word that refers to the phenomenon?

"Remnant" is the closest term I can think of; "residual" is also used. You can find both used to describe the foramen ovale for example, which typically closes at birth (and has served its purpose at that point), but remains patent in a substantial proportion of adults, sometimes causing symptoms.
However, these terms are of course not specific for the circumstance you describe; I don't know of any that is.


How to set up a slow cooling on an AB Veriti thermal cycler? I want to incubate my sample at 50ºC and then slowly cool it down to 4ºC at a rate of 0.1ºC/s. I am using  AB Veriti thermal cycler. Does anyone know how to set up the rate of cooling? It has to do something with the ramp rate, which is given in % but I don't know how to convert this into a real rate.

If I recall correctly (from when I interned at ABI), you can't directly set this in the Veriti interface.  However, (again, I'm not 100% certain -- I couldn't find anything to confirm this after 30 minutes of googling,) the ramp rate percent refers to the percent of maximum ramp rate for the heating block.

According to the product website, the max heating block ramp rate is 5 °C/s while the max sample ramp rate is 4.25 °C/s, so you need a ramp rate between 2% and 2.4%.


What is the theoretical maximum height of a herbaceous plant stem? Foreword: I'm posting this here instead of, say, Worldbuilding, because while it is based in a speculative concept, this is a question purely of biology as we know it instead of speculative biology under non-real conditions. I would address that later and elsewhere. And sorry if this is actually more physics than biology, I have trouble pinning these things down.

I'm trying to determine what the maximum height of a non-woody plant stem can be (i.e. I don't want the tallest flowers). I think the primary issue at hand is load-bearing and resistance to bending. So I found this 1997 paper by Schulgasser and Witzum that sort of discusses what I'm looking for. It suggests that the plant's ability to resist shear forces is a matter of how bundles of fiber are arranged inside the stem and of the plant's internal pressure, which affects how much weight it can stably bear. But I'm no biologist, so the paper is difficult to penetrate. I'm sure there are other issues limiting the height of non-woody plants, like the maximum height above the ground that capillary pressure can raise water. Considering all factors, what is the theoretical maximum height of a herbaceous plant?

I've found this question, which concerns the tallest real herbaceous plant, while my question concerns the theoretical. But I would like to extend that question - are there any examples of fossil herbaceous plants that are larger than the modern banana plant, and do they run up against the theoretical maximum?

Update: I have edited the answer for a better structure and for providing reliable references.

Some of the factors that influence growth, while keeping in mind that every species has particular needs:

•   light, temperature
•   insufficient light leads to etiolation
•   water
•   amount of water and dry substances, page 185
•   water influences diameter
•   soil
•   wind
•   macronutrients
•   citokinin
•   genotype
•   heterosis
•   inbreeding
•   pinching the stem stops its growth and promotes lateral stems (I understand that you don't want to, but I list it here so that you can watch out accidents - involuntary pinching has the same effect)
•   root type
•   shelter near a fence or a wall

You might find some info as to what to consider in your calculations in this paper, although it's about trees.

Just for the purpose of knowledge, herbaceous vines like Ipomoea are also stems and they can grow longer than vertical ones. There may be more to add, but I'm only a Horticulture student, not a plant physiologist.

I strongly recommend to ask plant related questions on Gardening and Landscaping SE, a small community, but a very enthusiastic one. Also, hardly can someone become a good gardener without knowing at least the basics of plant biology and psysiology, so you have a major chance there of receiving answers in a few hours, not days.

Good luck with your project and I hope you'll return to tell us your conclusions. We will be happy to see you interdisciplinary approach.


Can crows see in ultraviolet? If so, does their plumage look different in UV? Apparently birds which appear identical to the human eye can look quite distinct under UV light. Additionally, drab looking birds might have more "spectacular" looking plumage when considering wavelengths outside of the visual spectrum.

Question: In the specific case of crows, (1) can crows see in the ultraviolet range? (2) is the plumage of crows still monochrome when considered in the UV spectrum? Is it dichromatic?

Google seems to return very little about this, although this random person claims that crows can see in UV and their plumage does not monochromatic under UV, while this article says they can not see in ultraviolet. Neither provides citations for their claims, and I am not familiar with the academic literature on this subject. Any help would be appreciated.

This question seems related inasmuch as crows seem black to the human eye. However, I know that some animals can see in UV, and am curious about whether this extends to crows.

Corvids (and raptors) are reported to not see UV Håstad et. al. 2005.

However, American crows are reported to recognize sex-specific differences in plumage that are invisible to humans Eaton 2006.

Unfortunately, I don't have access the latter paper so I don't know what the basis for that discrimination is or how to reconcile that result with those of Håstad et. al.

You might also find this well referenced blog post that summarizes these results to be of interest.


What's the use of RNA editing in kinetoplast? The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypanosoma brucei, the parasite which causes African sleeping sickness - are "encoded" in a way that the pre mRNA requiries partially heavy editing (insertion and deletion of Uridines) by the editosome (a RNA/Protein complex) until it can be translated to the correct proteins.
The information where to insert and remove Uridines is contained in small gRNA also part of the mitochondrial genome.

However this whole thing seems kind of unnecessary to me. Why did evolution not get rid of the surplus/missing Thymidines in those Genes? What's the use of this?

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.

The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

Amino-acid substitutions
ORF extension
New unique ORFs
Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.

The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a
human perspective."


Do plants take in the same amount of CO2 as they release? There are many claims in the media that trees remove more carbon dioxide form the atmosphere than they release back into the atmosphere. By what chemical pathway can this occur?
The law that matter is neither created nor destroyed surely applies as shown by the chemical pathway in the photosynthesis and respiration process.

6CO2 + 6H2O + sunlight energy.  -----> C6H12O6 + 6O2
C6H12O6 + 6O2.                  -----> 6H2O + ATP (energy) + 6CO2

Thus the SAME amount of 6CO2 taken in is released, in order for the plant to have formation of the ATP usable energy for plant tissue creation, so photosynthesis cannot happen at a  more rapid rate than respiration. If that happened, then yes, more CO2 is removed then released, but that would leave an unbalanced equation.
I am not arguing the story further down the road of tree tissue and carbon sequestration/storage.

You've made one faulty assumption: that the second reaction is occuring at the same rate as the first.  In fact, plants only burn enough glucose to fuel their activities. Much of the formed glucose is converted into storage forms like cellulose and starch.  In fact, the vast majority of a plant's carbon mass comes ultimately from CO2 which has been converted photosynthetically into carbohydrate forms. (Further reading)

Ultimately, when plants die, those carbon molecules are used as food for other species, such as animal and bacteria.  Ultimately, whether in composted plant material or fecal mater, the carbon is deposited on the ground.  So ultimately it is correct that trees & plants are removing CO2 permanently from the atmosphere.  Although some is being released to the atmosphere catabolically, more is re-absorbed for anabolic processes, and ultimately, that CO2 gets deposited on the ground in more complex carbon forms.


A question involving immunoprecipitation to identify interacting proteins? Using recombinant Flag-tagged Dcr-2 and His-tagged protein X, pull-down assays were performed to determine whether protein X and Dcr-2 interact directly. The recombinant proteins (either alone or in combination) in binding buffer (150 mM NaCl, 1 mM EDTA, 50 mM Tris pH 7.5, 1% Triton X-100) were pulled-down by Flag antibodies coupled to Sepharose beads. Following extensive washing, the proteins were eluted from the beads with SDS buffer, and duplicate sets of samples were analyzed by SDS PAGE. Samples were also taken of the proteins before they were used in the pull-down assay and these were run on the same gel (input lanes in Figure 2B). One gel was stained with Coomassie blue dye (Figure 2A), and the other was transferred to nitrocellulose for Western Blotting. The membrane was probed with a His-antibody (Figure 2B).

The question asks: Do Dcr‐2 and protein X interact directly?

My reasoning is that they DO interact directly. In Fig 2B: the intense bands on LHS shows that Dcr-2 interacts with protein X-that is bound to anti-His. In Fig 2A: the protein X interacts with the Dcr-2 bound to antibody FLAG. I feel I'm not explaining this very though...Could someone please explain their reasoning? Thank you

First: You are right with your reasoning that Protein X (X) and Dcr-2 interact directly. Lets go through the blots: In the input you check for the proteins loaded into the setting and stain unspecifically with Coomassie.
This part of the blot shows you no unspecific input, and both proteins of interest present. This also shows that Dcr-2 is much bigger than X which allows an easy identification of band patterns.

In the eluate you will only see proteins which are bound directly in the reaction or which interact with bound proteins. Dcr-2 is Flag-tagged so it will directly bind to the beads and can be eluated from them. This is shown in the coomassie part of the blot. Dcr-2 alone binds and can be eluated, while X alone does not bind and therefore gives no signal. Dcr-2 and X together give two bands, sind Dcr-2 binds to the beads and X is interacting with Dcr-2.

This binding is also shown with the anti-His antibody which only recognizes Protein X. The protein shows up in the input where X is added. It also shows up in the elution lane (where Dcr-2 is also present) showing that X is an interaction partner for Dcr-2.


Prokaryote or just a small worm In the following photos can be seen a thread-like (almost like longkou vermicelli) things. At first I was convinced that it was cyanobacteria, however a classmate said it look more like a little worm, and other person said it look like it was probably nothing (nor prokaryote nor worm). I can't find a way to settle what it is, how can I know?

Zoom 40x

This is from another sample

EDIT:
Could the first one be lyngbya? I found this website and the second to last picture kind of looks like what it is in my picture:

And also could my second picture depict nostoc bacteria?

This would be a suggestion rather than a precise answer.

Your sample being pond water a highly probable candidate of the first two photographs would be Euglena sp., though the red eyespot is not visible.

They are freshwater Excavates   and according to Washington State Lake Protection Association a common pollution-tolerant genus in Washington water bodies.

Another picture reference: A website


How many transmissions does it normally take for a neuron to reach threshold for action potential? This video illustrates and explains how the dendrite connections being activated causes the neuron to be polarized until it reaches "threshold", and firing. My question is how many times might a neuron's dendrites need to receive "fires" from other neurons in order to reach threshold. I think I understand that it isn't a binary matter, so I realize the answer isn't going to be 5 or 5,000 but a general range.

As a related question, how long does it take for polarization to wear off if additional transmissions don't come in, and if the polarization does wear off, is this wear-off mechanic important to the neural system? Is wearing off a significant aspect of the neural process, in other words?

How many action potential are needed to cause an action potential in the postsynaptic neuron depends on the strength of the synapse(s) involved. It's not possible to answer this question in general.

It is not just the number of action potentials received but also the firing pattern in which they arrive and the location of the synapse(s) on the dendrites/soma (proximal/distal, on a spine or not, on which kind of spine,...) of the postsynaptic neuron.

However, for some neurons it is possible to trigger an action potential in a postsynaptic neuron with a single action potential. But in this case it is very probable that multiple synapses were involved between the two neurons (example paper).

To your second question: the time until polarization wears off is called the time constant tau of a neuron. It is a property that varies from neuron to neuron and is one of the things that can be measured when recording from a neuron. It is one of the many factors that affects how incoming action potentials are translated into a neuron's output firing.


Genetics, sickle cell anemia Sickle cell anemia is autosomal recessive. Then Why is it an example of codominant alleles? I thought a person with sickle cell trait is heterozygous because one of his/her alleles is recessive and the other one is dominant which is not codominant.

Whether alleles are "codominant" or "recessive" or "dominant" depends on the level at which you look at it.

If you look at it from the organismal "healthy vs sick" point of view, then sickle cell anaemia is "recessive" because the individual is only sick when they have both sickle cell alleles.

If you look at it from again the organismal point of view, but this time looking at the trait as well, then you find that (if we say "A" is the anaemic allele and "N" is the normal allele) AN has a different trait (called sickle cell trait) than NN, so you could say the alleles are codominant because both the A and the N "do something" in the heterozygote.

If you look at the molecular level, again you will find that sickle cell anaemia is codominant. The gene codes for the haemoglobin beta gene. So if you have AN, then one of your alleles will be coding for the defective haemoglobin, and the other will be coding for the normal one. So you would have 2 types of haemoglobin in your blood, which means that it is "codominant."


Special visceral efferent Why are special visceral efferent nerves are named as such?

They are supplying motor impulses to muscles of pharyngeal arch, which are both skeletal(facial) and visceral(laryngeal) 1, so why only visceral in name?
Why the name special?

I tried wikipedia but didn't find any information.

Why they are special?

They are also called Branchial efferent.
They are special because they supply striated muscles derived from Branchial arches.
https://en.m.wikipedia.org/wiki/Special_visceral_efferent

Like Mandibular nerve, nerve of 1st arch supply muscles of mastication and motor nuclei of facial nerve, 2nd arch, supply facial muscles and Stylohyoid.

  Special Visceral Efferent (SVE)
  These fibres innervate certain striated muscles with a special embryological origin.
  They are referred to as the branchiomeric muscles.
  Structures that develop into gill arches in fish develop instead into various structures near or in the head and neck (muscles of the face, larynx and pharynx).
  Although these muscles are identical to normal striated muscle, neurons for branchiomeric muscles have a distinctive location in the brainstem.

..

  Why only visceral?

This term is quite ambiguous. That's why some scientists prefer term Branchial efferents. https://en.m.wikipedia.org/wiki/Special_visceral_efferent

The nerves supply striated muscles(also called skeletal, though most facial muscles have no skeletal support).

These do not supply any smooth muscle of viscera (laryngeal muscles are striated too).

But, still they are called visceral.
Well, that is because the muscles supplied are actually mostly to various viscera.
Larynx is a viscera. Pharynx and palate are viscera too. All these are supplied by 5 , 9 and 10th nerve.(Nuclei - motor nuclei of 5th, Nucleus ambiguus for 9 and 10th)
 Nerve to stapedius is muscle of middle ear, again a sensory organ.

So, the word viscera was added.

Facial muscles and sternocleidomastoid and trapezius are of course not supplying organs(viscera). That is why some say branchial efferent to remove ambiguity.
Branchial efferent represents muscles derived from branchial/pharyngeal arches. That's what is important about these nuclei.


What is the difference between a graded potential and an action potential? I was under the impression the only signals neurons send using changes in membrane potential are action potentials. But my biology professor showed us diagrams of graded potentials and action potentials and to me they looked very similar.

What is the difference between a graded potential and an action potential?

Short answer
An action potential is a binary all-or-nothing event, while a graded potential is an analog signal.

Background
Action potentials, once initiated, are basically all-or-nothing events. Amplitudes may admittedly be variable, but basically it is the spike rate that is relevant to the neural code (Gerstner et al., 1997).

In contrast, graded potentials code information mainly by amplitude. A notable example of the significance of graded potentials is the function of the inner hair cells in the cochlea (the inner ear). The mechanoreceptors on the hair cells open when deflected in one direction, while they close in the other. This is important, as that property depolarizes the cell on one phase of an input sinusoid, while it hyperpolarizes the cell in the subsequent phase. Also, stronger (louder) input increases the response, while softer stimulu generate less response (Fig. 1). In the auditory nerve this graded potential is translated into spike rates (Fig. 2). Basically the hair-cell and auditory nerve system is an analogue-to-digital converter.

Fig. 1. Cochlear microphonic: a graded potential that increases amplitude with increasing loudness. Source: Juaristi & Martínez-Conde, 2014

Fig. 2. In the auditory nerve amplitude is coded as action potential (spike) rates, low frequencies as burst-repetition rate. Source: NY University

References
- Gerstner et al., PNAS (1997); 94(24): 12740–1
- Juaristi & Martínez-Conde, Acta Otorrinolaringol Española (2014); 65(04)


If senescent cells are removed by the immune system, how can they contribute to ageing? It is said that senescent cells, also called zombie cells, can cause biological ageing.  These senescent cells are also killed by immune cells. It does not make sense as to how they cause ageing if they are removed?

In an healthy individual, senescent cells are likely removed by the immune system.  However, as we age, our immune system becomes impaired and may no longer be able to kill senescent cells.  Senescent cells can then accumulate and promote age-related diseases.


Any examples of life forms on Earth that could have survived on Mars or Moon? Do we know of any living forms on Earth that could continue to live on Mars?

Yes, research studies that were conducted have found that methanogens (microorganisms) are able to survive in conditions similar to Mars (reference). Another study conducted has also concluded that some lichen and cyanobacteria is also capable of survival.  Surprisingly, they were also found to be active (reference).

There is speculation now on whether organisms from earth have been accidentally transported to Mars on the Mars Curiosity Rover which would be funny or a cause of concern, depending on how you look at it (reference).


Chromosome 2 alternate explanation - apes gaining a set of chromosomes? I'm preparing for a debate (just between friends) on evolution (I'm in support), and one of the points I plan to bring up is the Chromosome 2 evidence.  I'm now trying to predict their potential rebuttals.  The common statement I've seen is that since the apes have 48 chromosomes and humans have 46, then there are two possibilities: either we "lost" a chromosome, which would be fatal, or there was fusion.  This, I believe, was an actual prediction prior to the answer of Chromosome 2 being identified.  But couldn't there have been a third possibility - that the apes gained a pair of chromosomes, perhaps thru splitting of some kind?  This seems reasonable to me due to the other claim that we didn't evolve from apes but that we share a common ancestor, and so the ape lineage could have acquired the extra chromosome after the split.  (Note I'm a total biology noob, so if this doesn't even make sense, then please tell me.)  I understand that this isn't the way it turned out, that Chr 2 looks exactly as we would expect from fusion, but prior to this discovery, couldn't the apes gaining a chromosome have been a possible reason?  TIA.

I guess part of the question is...what exactly are you bring up Chromosome 2 as evidence of, exactly?  It's evidence of that chromosomal rearrangements are possible, but that isn't terribly helpful to you, so I'm not sure why you are bringing it up.

I think the fusion is a rebuttal to a claim that the disparate # of chromosome is a problem for the claims of common ancestry between humans and other apes, but if they don't mention it, I'm not sure why you would need to use that particular fact.

Have you consulted talkorigin's 29 evidences of macroevolution?  Lots of good stuff there.

http://www.talkorigins.org/faqs/comdesc/


Please explain what a gene isoform is in lay terms? I am a physicist by training, however I am now doing computational biology research. I know what genes, DNA, proteins, enzymes, introns and exons are.  I sort of understand how DNA is used to create RNA, which is used by ribosomes to manufacture proteins.  That is the extent of my biology and genetics knowledge.

So, could someone explain what a gene isoform is in lay terms?  There is a related question here and wikipedia has an explanation.  However, there is a significant jargon barrier for me.

Gene isoforms are all the different RNAs that can be synthesised from a single gene. You may be referring to splice variants, which are systems of getting different mRNAs from the same sequence using different combinations of introns and exons.

(source: riken.jp)

Translating your wikipedia article:
Gene isoforms are the different RNA products obtainable from a gene that can vary on the place where the translation starts (protein synthesis), that have different sequences in the coding region (thus giving different proteins, sometimes with different functions) or by having different untranslated regions, UTR (the overhangs of the sequence that are not translated in the mRNA). This last difference, the UTR, normally gives rise to different stability within the cell as UTR secondary structures usually control the speed of degradation of an RNA.

Hope it helps


Unknown plant, please help me identify it Years ago I was into keeping tropical fruit trees/bushes indoors. One of them didn't do well under my care so I planted it outside to enjoy the final year before European winter gets it. It somehow survived, barely. Each year it did better though so 5-6 years later it's full of edible fruit. I don't know what it is. Can somebody identify it?

It appears to be a cultivar of Jujube (Ziziphus zizyphus) also known as Chinese date - https://en.wikipedia.org/wiki/Jujube
This is based on JimN's correct observation. I looked at a few dozen images of Ziziphus Zizyphus - both fruit and leaves. They appear to be identical. The fruit tastes as described. The fruiting progression matches the description in Wikipedia.


Does a phenotype include the presence of a recessive gene I am trying to understand what exactly a phenotype is to try and understand a genetics database. (Ie I don't really know very much about genetics at all)

I've been reading through wikipedia on what a phenotype is and from what I can gather it is an observable trait which may be impacted by a specific gene.

What I would like to know is if you were looking for the presence of a phenotype such as red hair, would characteristics like not red hair and carrier of red hair also be phenotypes?

For example the following table is named Phenotype,

+------+------------------+
| Code |   Description    |
+------+------------------+
| RR   | Red Hair         | this makes sense with my understanding of phenotype
| RN   | Red Hair Carrier | this doesnt
| NR   | Red Hair Carrier | this doesnt
| NN   | No Red Hair      | this doesnt
+------+------------------+

The whole code column looks like it represents a gene not a phenotype

I agree with one of Alan's comments when he says:

"I think this comes down to whether you include being a carrier of a genetic "condition" a part of your phenotype. It's almost a question of semantics"

To expand on this, I would say there are two major definitions of phenotype, and both are employed by geneticists depending on the context.  Definition one is a bit more naive, and I tend to use it when teaching or trying to explain phenotype to a layman: anything you can observe is a phenotype.  Under this definition, having red hair is a phenotype, not having red hair (or, more directly, having black, brown, blonde, etc. hair) is a phenotype, but carrying the recessive gene for red hair is not a phenotype.  I can observe without checking your genome that you do or don't have red hair, I cannot tell without checking your genome that you have one copy of the recessive gene for red hair.

Definition two is more complete, and I tend to use it more in a lab research setting: anything that is the OUTCOME of a genotype can be defined as a phenotype.  Again, red hair and not red hair (meaning brown, black, blonde, etc) are outcomes defined by the genotype.  However, depending on the context (let's say I'm interested in understanding heritable potential and not the color of hair) I'd say that the phenotypes would be 1) the ability to pass on red hair to progeny (outcomes of genotypes RR, RN, RN in your example), and 2) lack of ability to pass on red hair to progeny (outcome of genotype NN in your example).  In both cases, the phenotype is the outcome of the underlying genes, I just have to make sure I frame my scientific context appropriately.


Are dogs affected by dwarfism? My husband and I noticed a dog today that looked like a smaller version of a purebred Border Collie, although it didn't appear to be a puppy. It made us wonder if other animal species experience dwarfism.

Are dogs known to display a dwarfism gene?

The short answer is yes, other animals can experience dwarfism, including dogs, although it may not be what you are expecting.  Dogs are apparently particularly susceptible but they often are a special case.  We've so heavily bred dogs for whatever traits we desire, so now entire breeds are affected by dwarfism, such as dachshunds and corgis.

The reality is that dwarfism is a mosaic, with many types, and shouldn't be classified under one umbrella.  You're probably mainly thinking of Achondroplasia, which is just one of many causes.  You may also be aware of Hypothyroidism.  Not every case looks like others, so in animals it may not be what you except.  Other animals are susceptible, such as the sheep mentioned in the above articles, and horses, which are also a long-time target of selected breeding.


Why do our eyes close when we sleep? Why do our eyes close when we sleep? Is it to relax our eye muscles? How can it be explained from an evolutionary point of view?

Our eyelids close when we sleep probably for the obvious reason that it prevents the sclera and cornea from drying out, becoming accidentally scratched (such as blowing dust) and allowing oxygen diffusion from the inside of the eyelid (to the sclera and cornea). Fragile corneas are a requirement for our vision. Thick corneas are much less fragile but then attenuates more light.

From terdon:

1) blinking requires muscle movement which sort of defeats the purpose of resting

2) closed eyelids offer much better protection than periodic blinking

3) if you can blink, you have eyelids.


Index of ecological niche overlap What is the Pianka's Index?

How does it work?
How can one calculate this index?
How often is it used?
In what context do people usually use it?
Can one infer any statistical significance with this index?

Pianka's index of niche overlap is defined in his papers from 1973 and 1974, as:

$O_{kl}=\dfrac{\sum_i^n{p_{il} p_{ik}}}{\sqrt{\sum_i^n{p_{il}^2} \sum_i^n{p_{ik}^2}}}$

where $O_{kl}$ is the resource overlap between species $k$ and $l$, and since the index is symmetric $O_{kj} = O_{lk}$. $p_{ib}$ represents the proportion of resource $i$ that is used by species $b$. The index is a modification of one presented in MacArthur & Levins (1967).

As apparent from the formula, the only thing you need to calculate the index are estimates of resource use from the resources that both species depend on. The tricky part can be to determine how you calculate proportianal use of all resources.

I haven't used the index myself, and cannot really say anything about how common it is. I have seen references to it though. Pianka (1973) use it to study overlap between lizard species, and how the distribution of niche overlaps differ between habitat types. I haven't seen any statistical tests on it, but you should be able to use resampling or bootstrap to determine the uncertainty in the index.


Feeding behavior of organisms that prey on microorganisms Is there a specific term for organisms that feed on micro-organisms?

Use "-vore" and "-vorous" suffix [L. -vorus devouring, eating (cf. vorāre to devour].

For example: bacteriovores, algaevores, and planktivores.

Note: "Microorganism" is an unfortunate, albeit popular (viz. "microbiology") term. How small is "micro"? So small that one needs a microscope to see it? And what kind of microscope: "light" or "electron"? i would drop the term "microorganism" altogether. One can use "bacteria, "archaea," "chromists," "protists," . . .


How can epigenetic changes be erased if they are inherited? I’m a little bit confused about DNA methlyation reprogramming and about the nature of an epigenetic phenomenon. According to Wikipedia:

  After fertilization the paternal and maternal genomes are once again demethylated and remethylated (except for differentially methylated regions associated with imprinted genes). This reprogramming is likely required for totipotency of the newly formed embryo and erasure of acquired epigenetic changes.

I don't understand how something can be thought to be both heritable and erasable. Any help would be greatly appreciated.

I have done a presentation in epigenetics and the main topic was imprinting.
This paper will answer all your questions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941233/
I am adding some glimpses from this  paper here
Mammals are diploid organisms whose cells possess two
matched sets of chromosomes, one inherited from the mother
and one from the father. Thus, mammals have two copies of
every gene. Normally both the maternal and paternal copy of
each gene has the same potential to be active in any cell.
Genomic imprinting is an epigenetic mechanism that changes
this potential because it restricts the expression of a gene to
one of the two parental chromosomes. It is a phenomenon
displayed by only a few hundred of the approximately 25,000
genes in our genome, the majority being expressed equally
when inherited from either parent. Genomic imprinting affects
both male and female offspring and is, therefore, a consequence
of parental inheritance, not of sex. As an example of
what is meant by this, an imprinted gene that is active on a
maternally inherited chromosome will be active on the maternal
chromosome and silent on the paternal chromosome in
all males and females.

Hope this help and please ask if you do not understand the paper.Thank you


What animal produces male gametes by mitosis? The following question came up in my biology examination but I could not answer it:

  "What animal produces male gametes by mitosis?"

I know that some plants produce their gametes by mitosis in the gametophytes, but found no references to any animals doing so.

In organisms which have haploid males (such as honeybees), there is a variation of meiosis during spermatogenesis. The meiosis-I is abortive i.e. the chromosomal events such as crossover and separation of homologous chromosomes, do not happen. However, some cytological changes do happen which is described by Sharma et al (1961) as "simulation of the normal meiosis I". This is followed by meiosis II (which is mechanistically same as mitosis). So, basically there is no halving of the number of chromosomes and the gametes are also haploid.

So, as far as I can guess, the question in your exam sheet probably refers to spermatogenesis in Hymenopteran haploid males.

Reference:
Sharma, G. P., Brij L. Gupta, and C. G. Kumbkarni. "CYTOLOGY OF SPERMATOGENESIS IN THE HONEY‐BEE, APIS INDICA (F.)." Journal of the Royal Microscopical Society 79.4 (1961): 337-351.


Antibiotic resistance I have a biological puzzle that's been perplexing me for years.  Can you review my logic and tell me where I'm wrong or if I'm on to something.

As I understand it, most, if not all genetic engineering uses a marker gene to identify transformed bacteria.  This marker gene was/is usually an antibiotic resistance gene so the transformed bacteria will be the only ones that can grow on an antibiotic laced culture medium.

So, every (most) GMO will contain a copy of a bacterial antibiotic resistance gene.

Also, I believe that bacteria are able to spontaneously aquire DNA from their environment and / or other bacteria.

So, is it a fair question to ask if the unnatural proliferation of antibiotic resistance genes in the wild due to the commercial propagation of GMOs might be at least partially responsible for the increase in multiply resistant organisms that we are seeing?

Has anyone, for example, mashed up GMO matter, added non antibiotic resistant bacteria, grown the mix up overnight, added the antibiotic used as a marker in the GMO, incubated for a few days and then seen if any bacteria survived?

As I understand it, most, if not all genetic engineering uses a marker
  gene to identify transformed bacteria. This marker gene was/is usually
  an antibiotic resistance gene so the transformed bacteria will be the
  only ones that can grow on an antibiotic laced culture medium

Most but color markers (which gives the host cell a color that can be used for selection) are also used. More complicated selectable-counter selectable markers are also used (ie  HyTK gene). A counter selectable marker is a marker that kills a cells when it is present. A selectable-counter selectable marker is a hybrid marker that allows you to both select for cells with the marker using one selection agent and kill the same cell with a second selection agent.

  So, every (most) GMO will contain a copy of a bacterial antibiotic
  resistance gene.

Well not quite. GMO ie Genetic modified organism, includes both prokaryotes (bacteria) and eukaryotes (plants, animals, and yeast). The promoters which drives gene activity in prokaryotes and eukaryotes are different. So a eukaryote markers do not work in prokaryotes and vise versa.

Furthermore, genetic modification of eukaryotes is difficult. Hence modified viruses are often used. These viruses are made in such a way that their genome has been replace by desired DNA playload. And as the payload size is limited, often time any unnecessary DNA is also removed, like prokaryotic markers which have no function in a eukaryotic host.

Lastly due to public pressure, there has been a push towards cleaning up after genetic engineering work in GMOs that are to be marketed to the public (GMO crops). So things such a selection markers are removed (either by use of counter selectable markers followed homologous recombination or site specific recombinases).

  So, is it a fair question to ask if the unnatural proliferation of
  antibiotic resistance genes in the wild due to the commercial
  propagation of GMOs might be at least partially responsible for the
  increase in multiply resistant organisms that we are seeing?

Given the wide spread use of antibiotic in animal husbandry and by the public general, and move toward removing selection markers in commercial GMOs, I do not think GMOs are the cause of the increase in MR bacteria.

A more likely cause would simply be because we are using so much antibiotics and thus there is a selection pressure to aquire multiple resistance. Remember all our antibiotics resistance genes and most of our antibiotics were acquired from nature.

  Has anyone, for example, mashed up GMO matter, added non antibiotic
  resistant bacteria, grown the mix up overnight, added the antibiotic
  used as a marker in the GMO, incubated for a few days and then seen if
  any bacteria survived?

Yes, lots of times around the world to varying degrees of sucess. I have personally spent time doing this and so have my labmates. It will work if you prepare good quality DNA that has not been degraded by endonucleases, the bacteria are very transformable (ie the bacteria has been treated to take up DNA easily), electroporation is use (to force the DNA into the cell) and you have prokaryotic marker. A eukaryotic marker, is a marker that works in an animal cells will not work in bacteria. So you have to engineer your GMO animal to carry both a eukaryotic and prokaryotic marker.


How can a YAC be screened against a cDNA library and a cosmid library of genomic DNA to find a gene? I am reading fw2.2: A Quantitative Trait Locus Key to the Evolution of Tomato Fruit Size (doi: 10.1126/science.289.5476.85).

The authors are trying to find the gene that makes tomatoes bigger. As far as I understand, previous research had narrowed it down to "something" in the region of the genome called fw2.2. They are trying to determine the actual genetic elements responsible (which turns out to be a gene similar to human HRAS).

Supposedly, the big-fruit allele is recessive and the small-fruit allele is dominant.

They say (in section Genetic complementation with fw2.2) that:

They got a YAC containing the fw2.2.
They "screened a cDNA library" with the YAC to find transcripts that were potentially relevant. (How?)
They "screened a cosmid library" of genomic fragments to find the stretch of genome that the cosmid came from. (How?)

It is unclear to me how steps 2 and 3 work. Can someone explain how you can take a YAC, cDNA library and cosmid library to find the gene inside the region responsible for your trait, as these researchers describe?

The YAC contains a segment of chromosomal DNA. By using it as a probe they could screen the cDNA library to find cDNAs derived from that genomic region. This would be done by plaque or colony hybridisation. The cDNA clones thus identified represent the "candidate genes" .

The last step is a little unclear. Clearly they are identifying cosmid clones that map to the segment of interest, but they could be using either the YAC or relevant cDNA clones (could be pooled for this step depending upon their aim) as probes. My guess is that they used individual cDNA clones to find corresponding cosmid fragments so that they could home in on the regions encoding the identified cDNAs.


Protein degeneration/excretion in cell If I inject a dose of GFP or some other types of protein into a long-living human cell like brain neuron cell. Will these proteins being degenerated or excreted over time?

This paper gives a half-life of 26 hours for wild-type GFP expressed in mouse cells.


What do trans-fats do when in human body? Trans fats cause health problems, especially to the heart.  https://en.wikipedia.org/wiki/Trans_fat#Health_risks

My guess is that all effects happen because trans-fats are inherently toxic as the body never evolved to process them. But then L-glucose has no harmful effects, even if it cannot be digested.

So how are trans-fats processed in the body differently, and where does all the harm happen?

In Ascherio & Willen (1997) it is mentioned that, and I quote:

  [...] Trans fatty acids increase plasma concentrations of low-density lipoprotein (LDL)
  cholesterol and reduce concentrations of high-density lipoprotein (HDL) cholesterol relative to the parent natural fat. [...] [T]rans fatty acids increased the plasma ratio of total to HDL cholesterol nearly twofold compared with saturated fats. On the basis of these metabolic effects and the known relation of blood lipid concentrations to risk of coronary artery disease, we estimate conservatively that 30 000 premature deaths/y in the United States are attributable to consumption of trans fatty acids.

The US Heart Foundation explains in more layman's terms the same principles:

  Trans fat is a type of unsaturated fat that behaves like a saturated fat because of its chemical structure. It increases our risk of heart disease by increasing the “bad” LDL cholesterol, while also lowering the “good” HDL cholesterol in our blood.

And from the Better Health Channel Australia we learn why LDL is 'bad':

  Too much cholesterol circulating within LDL in our bloodstream leads to fatty deposits developing in the arteries. This causes the vessels to narrow and they can eventually become blocked. This can lead to heart disease and stroke.

Reference
Ascherio & Willen, Am J Clin Nutr 1997;66(suppl):1006S-lOS.


Circadian Clock During a Flight I am interested in knowing how our Circadian Clock responds (and if there are resultant changes) when we travel across Time Zones?

UPDATE 24th April

I am reopening this question as the statement in the answer "When you travel to different time zones, your circadian clock will be off" has further confused me. If it's the case, then I am looking to get a better explanation than that (with solid references). Thanks

When you travel to different time zones, your circadian clock will be off (incorrect). The reason your circadian clock will be off is because your body has adapted to the time zone you are from. When you enter a new time zone, your circadian clock will still be functioning on the old the time zone. If the time zone difference is $\pm 12$ hours, this is a huge adjustment.

However, your body takes inputs from the environment. That is, you may see it is day light when your body is under the impression it is evening. Your circadian clock is controlled by your master clock located in the hypothalamus. As you take in these external inputs that counter your circadian clock, a group of nerve cells called the suprachiasmagic nucleus will slowly make the master clock adjustment [1]. This resetting can take a few days.

NIH Jet Lag Prevention Guideline

Additionally, there has been a bit of research on exercise reducing jet lag. In a study, researchers test outdoor exercise with flight crew members and found that the group that exercised outdoors had a hastened re synchronization of their circadian clock [2].

Another interesting article is Jet Lag in Athletes.


How do we know how long hermit crabs live in the wild? This article states that hermit crabs in the wild are extremely difficult to track because they constantly change shells and even gender.  Later in the article, they say that hermit crabs can live 4 decades in the wild.  How can they know this if they can't follow a single crab for an extended period of time?

Hermit crabs increase in size over time and this is used to provide a minimum estimate for their age1.

You may also find this article interesting.

Reference:
SantAnna, Bruno Sampaio, Christofoletti, Ronaldo Adriano, Zangrande, Cilene Mariane, & Reigada, Alvaro Luis Diogo. (2008). Growth of the hermit crab Clibanarius vittatus (Bosc, 1802) (Crustacea, Anomura, Diogenidae) at São Vicente, São Paulo, Brazil. Brazilian Archives of Biology and Technology, 51(3), 547-550. https://dx.doi.org/10.1590/S1516-89132008000300014