Rethinking junk DNA

Yeah, nothing changes really. The same people use "junk DNA" as examples of apparent "non-functional" parts. Massive argument from ignorance and the same people KNOW it is a provisional label...
 
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How times have changed. Parts provisionally labeled as junk now take center stage.

RNAs Taking Center Stage
ScienceDaily (Sep. 10, 2009) — RNAs, serving as a mere intermediary between DNA and proteins, were long regarded as a poor relation by researchers, attracting little interest. However, following the discovery of small RNAs known as microRNAs, they have increasingly been moving into the limelight. MicroRNAs bind to messenger RNA (mRNA), thereby regulating the translation of genes into proteins.
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Recently, various studies have shown that the production of microRNAs is tightly controlled, but their subsequent fate was not clear. It was assumed that mature microRNAs remained stable in the cell for days, and that their possible functions were therefore restricted: a microRNA persisting for a relatively long period cannot be involved in any processes in the cell requiring rapid adaptation.

Regulated regulators

The study carried out by Helge Grosshans, a Research Group Leader at the Friedrich Miescher Institute, has now finally shifted attention away from DNA, spotlighting the key role played by microRNAs in the theater of cellular processes. As Grosshans and his team report in the current issue of the renowned journal Nature, they discovered a mechanism for active degradation of microRNAs and showed that this mechanism is itself regulated.

Explaining his findings, Grosshans says: “What was formerly conceived of as a direct, straightforward pathway is gradually turning out to be a dense network of regulatory mechanisms: genes are not simply translated into proteins via mRNA. MicroRNAs control the translation of mRNAs into proteins, and proteins in turn regulate the microRNAs at various levels.”

In addition, the FMI researchers showed in the nematode Caenorhabditis elegans that, via regulation of degradation, it is possible to influence microRNA activity. This means that microRNAs may, after all, be involved in the regulation of rapidly occurring processes.

Targeted degradation of disease-causing RNAs

But the findings are also relevant in another respect. As microRNAs have been implicated in the development of diseases, efforts to date have focused on replacing disease-causing microRNAs with other microRNAs, or inactivating them with the aid of complementary RNA strands. Unfortunately, it is extremely difficult to deliver RNAs to target cells for therapeutic purposes. Accordingly, the prospects of success for these novel treatment approaches have been uncertain. In his study, however, Grosshans identified a protein that specifically degrades microRNAs. If it now proves possible to specifically activate or inhibit this protein and its partners, that could provide an approach which is closer to classical and well-established forms of therapy.

Grosshans comments: “We now assume that a large number of human genes are regulated by microRNAs, so the regulatory mechanism we’ve discovered has a great potential to significantly influence numerous processes in human cells."

The meteoric rise of microRNAs

MicroRNAs are short, single-stranded RNA molecules which interact with mRNAs in a sequence-dependent manner. They thus inhibit translation of mRNAs into proteins. MicroRNAs were first described in 1993 in the nematode Caenorhabditis elegans. They were subsequently also shown to play an important role in regulating development processes and in pathogenesis in higher organisms. The findings of recent years and now also Helge Grosshans’s study have shifted attention away from DNA toward RNAs, which are taking center stage. The term “microRNA” was only introduced in 2001.
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Want to provisionally label things as "junk"? In fact, give me one part of you that you want to provisionally label as junk... try and be scientific.
 
Provisionally labelled as 'Junk' DNA May Prove Invaluable In Quest For Gene Therapies

ScienceDaily (Sep. 21, 2009) — Scientists have identified how a protein enables sections of so-called junk DNA to be cut and pasted within genetic code – a finding which could speed development of gene therapies.
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The study by researchers at the University of Edinburgh sheds light on the process, known as DNA transposition, in which shifted genes have a significant effect on the behaviour of neighbouring genes. In the human genome, rearrangement of antibody genes can enable the immune system to target infection more effectively.

The research identifies how the enzyme is able to cut out a section of DNA and reinsert it elsewhere in the genome. The study, published in the journal Cell, was funded by the Wellcome Trust and the Medical Research Council.

The cut-and-paste property of shifted DNA is now being used to develop tools for scientific research and medical applications. Learning more about transposition could help scientists understand how to control the process and speed the development of gene therapies – which introduce into cells genes with beneficial properties that, for example, can fight hereditary diseases or cancer.

Junk DNA, which accounts for almost half of the human genome, was originally believed to have no purpose. However, it is now emerging that movement of junk DNA, in a cut-and-paste mechanism, can lead to beneficial changes in cells.

Dr Julia Richardson of the University's School of Biological Sciences, who led the study, said: "By forming a picture of the enzyme that causes DNA to shift, and discovering how this works, we understand more about how these proteins could be adapted and controlled. This may one day enable genes to be pasted into cells exactly where they are needed – which could be of enormous benefit in developing gene therapies."
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Seemingly misplaced DNA acts as lenses
Nocturnal mammals orient nucleic material in retinal cells to focus light
Mice and cats don’t usually agree, but both animals have the same bright idea about night vision. Cats, rats, mice and other nocturnal mammals arrange DNA in some eye cells to form miniature lenses that help focus light, a new study shows.

Scientists at the Ludwig-Maximilians University Munich in Germany and colleagues discovered the unusual DNA arrangement while investigating the function of several genes in the rod cells of mouse eyes, says Boris Joffe, one of the authors of the new study, which appears in the April 17 Cell. Rod cells are light-gathering cells in the retina of the eye. They operate under low-light conditions, while cone cells perform the light-gathering duty when it is bright.

Usually active genes are located in the part of the DNA that is at the center of a cell’s nucleus. There, the genes have easy access to the cellular machinery that rewrites instructions encoded in the DNA into RNA. Inactive DNA is pushed to the periphery of the nucleus, where it is out of the way.
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But rod cells in the mouse retina shove active genes to the outside of the nucleus, the researchers found. The center of the nucleus is instead occupied by densely-packed inactive DNA called heterochromatin. Mice put this type of DNA front and center in their rod cells.

“Everything that must be inside is outside, and everything that should be outside is inside,” Joffe says. “It was an absolutely heretic finding.”

Why the cells take on the unusual conformation was at first a mystery. “We checked one explanation after another and none of them worked, so we were forced to think of something completely unusual,” Joffe says.
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The DNA with this unusal conformation is known as "R bands" or repetitive sequences related to human Alu sequences. Was provisionally labelled as "junk". Luckily science moves on.

The team decided to examine retinas from other species to see if mice are the only creatures with the unusual DNA conformation in rod cells. After examining a dozen different species of mammals, the researchers noticed a pattern. Nocturnal animals, including cats, rats, deer, opossum, rabbits and ferrets, had the inside-out arrangement in rod cells, but animals that are active during the day had the conventional DNA arrangement with heterochromatin to the outside of the nucleus.

But the researchers still did not know why a nocturnal lifestyle would be associated with the inverted DNA arrangement in the rod cells. The team consulted Jochen Guck, a biophysicist at the University of Cambridge in England, to find the answer.

“It was very obvious to me that the nuclei could only be lenses,” Guck says.

Placing dense heterochromatin in the center of the nucleus raises the refractivity index — the degree to which the material decreases the speed of light traveling through it. The photons travel faster through the loosely packed DNA containing active genes, called euchromatin, and slower through the dense heterochromatin. Slowing down the photons creates a lens to focus light in the center of the cell.

Rod cells form columns in the retina of nocturnal animals, so that many little lenses are stacked on top of each other. The DNA lenses form a chain that acts a bit like fiber-optic cables, Guck suggests. He performed a computer simulation that shows that light would be channeled along the columns of rod cells with the inverted configuration, but cells with the conventional DNA arrangement would scatter light instead.

This is the first time scientists have discovered DNA acting as a lens in photoreceptor cells, says Gregory Acland, a veterinary ophthalmologist at Cornell University. “It’s one of those things that once someone has pointed it out, you think, ‘oh, that’s interesting,’ ” he says. But arranging components of retina cells to reduce light scattering certainly isn’t new, Acland says. For instance, birds, lizards and fish use oil droplets in cone photoreceptor cells to funnel light, he says.

Photoreceptors do channel light, but until now that function was known to occur mostly in cone cells. This may be the first evidence for light-funneling in rods, says Trevor Lamb, a vision scientist at the Australian National University in Canberra. But nocturnal animals have so many rod cells, and so few photons hit the retina at night that it isn’t clear whether funneling light through the cells would actually improve night vision, he says.

Inverted nuclei may be a remnant from mammals’ ancestors, which were likely nocturnal animals. The inverted configuration of the nucleus may make it harder for the cell to transcribe DNA into RNA because the transcription machinery must be spread around to mom-and-pop shops located on the outskirts of the nucleus instead of concentrated in factories in the center, Joffe speculates. Species that are active in the daytime have jettisoned the inverted structure; for them, the light-focusing advantages don’t outweigh the disadvantage of inefficient transcription, he says.

“As soon as it is not necessary, good-bye inverted pattern,” Joffe says.
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DNA stains reveal that the nuclei of rod cells (top left) from a mouse’s retina have a different arrangement of DNA than ganglion cells (bottom left) or skin cells (right). Blue and red colors show where densely-packed inactive DNA called heterochromatin is located; green shows where active DNA is located. In most cells, heterochromatin is pushed to the outer edges of the nucleus. But rod cells in nocturnal mammals have heterochromatin concentrated in the center, where it acts like a lens to focus light, perhaps enhancing night vision, a new study reports.

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A computer simulation shows that light would scatter in rod cells with a conventional DNA arrangement (left). But rod cells with an inverted configuration recently discovered by scientists could channel light more effectively (right).

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Scientists recently discovered that nocturnal mammals concentrate inactive DNA, called heterochromatin (blue and red), in one or two spots in the center of the nucleus in rod cells. In animals that are active during the day, rod cells have a DNA arrangement like that of other cells in the body, with active DNA (green) at the center of the nucleus.​

Guess that provisional label was wrong...
 
Isn't history fun:
The amount of DNA in organisms, is more than is strictly necessary for building them: a large fraction of the DNA is never translated into protein. From the point of view of the individual organism this seems paradoxical. If the ‘purpose’ of DNA is to supervise the building of bodies, it is surprising to find a large quantity of DNA which does no such thing. Biologists are racking their brains trying to think what useful task this apparently surplus DNA is doing. But from the point of view of the selfish genes themselves, there is no paradox. The true ‘purpose’ of DNA is to survive, no more and no less. The simplest way to explain the surplus DNA is to suppose that it is a parasite, or at best a harmless but useless passenger, hitching a ride in the survival machines created by the other DNA.
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Guess this selfish gene idea about parasitic DNA tagging along needs a bit of revision... or perhaps scrapping altogether since it actually contributes to the well being, evolution, survival and construction of the organism. Nice "selfish" parasite that :confused:.

No, because, in any case, most of the capacity of the genome of any animal is not used to store useful information. There are many nonfunctional pseudogenes (see below) and lots of repetitive nonsense, useful for forensic detectives but not translated into protein in the living cells.
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Oh contraire, this repetitive nonsense... useful for acting like lenses, focusing light, making organisms see better...
 
Oh, but I have (4½ of them). And you need to stop talking to people that are on your ignore list and then complain if those people respond to you. Bit stupid don't you think?
 
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alloytoo said:
My pleasure, oh and for your information Phrony didn't answer the question.

But I guess that didn't surprise you?
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You are still wondering how many papers have been published on DNA since 1972? That was an actual question? Addressed at me? ROFL man, that sounded like the musings of a 5 year-old incapable of using the internet.
Stop trolling and actually contribute to a science thread for a change. Your trolling is getting boring chap.
 
Phronesis said:
You are still wondering how many papers have been published on DNA since 1972? That was an actual question? Addressed at me? ROFL man, that sounded like the musings of a 5 year-old incapable of using the internet.
Stop trolling and actually contribute to a science thread for a change. Your trolling is getting boring chap.
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Oh sorry, perhaps I should have phrased it directly, I forgot your poor command of the english language, not to mention poor manners and perchant for disgusting imagery.

How many papers have been published on DNA since 1972?
 
alloytoo said:
My pleasure, oh and for your information Phrony didn't answer the question.

But I guess that didn't surprise you?
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I can only read what he writes if someone quotes him... but no.. I expect that from him which is why he is on my ignore list.

Hope you get your answers.
 
Oh look, more trolling. Here is a tip. Contributing to a thread means actually posting material that is relevant. Here is another tip. Go to pubmed and search the word DNA. Any kid with internet can do old chap, why you can't is beyond me...

Your answer: 1039311 articles poppes up (increases monthly). Since 1972? Probably less than 1039311 articles. Do you want an exact answer?
My turn to ask dumbass questions. Do you understand that reductionism is not used to detect things?
 
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