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РОССИЙСКОЙ ФЕДЕРАЦИИ
Государственное образовательное учреждение
высшего профессионального образования
«Пермский государственный национальный исследовательский университет»
Кафедра английского языка профессиональной коммуникации
English Reader for Students of Biology
Английский язык, пособие
Пермь
2018
Составители: Бабаджан Сергей Савельевич, Корлякова Алла Фирсовна
Английский язык. English Reader for Students of Biology. Пособие / сост. доценты С.С. Бабаджан, А.Ф. Корлякова. Перм. гос. ун-т. – Пермь, 2018. – 103 стр.
Данное пособие предназначено для студентов-ьиологов 2 курса и магистратуры.
Издается по решению методической комиссии факультета современных иностранных языков и литератур Пермского государственного университета.
Plants
Tasks
Task1 Match the words in column A with their explanations in column B
A B
1. Whim capable of working successfully; feasible
2. Mystery fine powder produced by flowers
3. Dappled very noticeable or unusual
4. Hue marked with spots or rounded patches
5. Pollen a colour or shade
6. Viable the part of a stamen that contains the pollen
7. To deter done extremely carefully
8. To vary to make someone not want to do something or continue doing it.
9. Anther a sudden desire or change of mind
10. Striking to become different or changed.
11. painstakingly something that is difficult or impossible to understand or explain
Task2 Say whether the following is true ,false or not me .
1. When scientists discovered he trout lily anthers and pollen had different colours, they could not understand their purpose.
2. Nobody has ever done research into variations in colour of some flowers’ sexual organs before.
3. When the scientists mapped all the available information about the trout lily , they immediately understood what the variations depended on.
4. Whatever they did , the pollen colours remained unchanged.
5. Their experiments proved that pollinating insects had colour vision.
6. They discovered that different insects were attracted by different colours.
7. Austen didn’t have a clue as to why insects preferred one colour to the other.
8. The answer hasn’t been found yet but the problem is sure to be solved within several months.
9. It is still unclear what makes trout lily maintain pollen colour variation.
Task3. Answer the following questions.
1. How do colours vary in the trout lily?
2. How do researchers explain this phenomenon?
3. What is the function of different petal colours?
4. How did the researchers start their experiment?
5. When all the information was mapped, what relationship did they find?
6. What experiment produced results different from all the rest?
7. How did Austen explain the insects behavior?
8. Why does the trout lily keep changing its colours?
Amazonia, tasks
Task1. Find words/ expressions meaning the following:
1. to pick out , choose;
2. to think about (something) carefully;
3. an aviary is a large cage or covered area in which birds are kept;
4. to set free;
5. a result or effect;
6. to move away from something or someone.;
7. cause or enable (a condition or situation) to continue
Task2 Say whether the following is true, false or not mentioned.
1. Some birds in a flock are always on the alert and warn the other birds whenever there is danger.
2. Scientists say it’s a wonder predators ever beat the system
3. They argue that these alarm-calling species are vital, and that conservation efforts should focus on them in the future.
4. For a long time scientists had no idea what made birds of different species flock together and why these flocks were so stable.
5. When they caught the sentinel birds and kept them away from flocks, the flocks either chose another area or disintegrated.
6. Birds occupying the canopy are at greater risk than others.
7. By acting as an alarm sounding system, the sentinel birds open up parts of the forest to other bird species that may have previously found the habitat too risky, in turn allowing species that may not o previously met to mix.
8. Scientists intend to pay more attention to the complex communications that are alarm calls.
Task3 Answer the following questions.
1. Why were biologists from San Francisco university surprised?
2. What explanations did they come up with?
3. How did they check their ideas?
4. What did the experiment show?
5. What level of the forest is the most dangerous?
6. Why is it more dangerous than the others?
7. What part ,in terms of ecology, do sentinel birds play?
The CRISPR Antidote
Scientists hacked the machinery of cellular warfare to splice genes. Now they’ve found a way to guard against it, too.
By Eric Betz| Friday, November 10, 2017
An arms race is playing out inside your body. It’s part of an invisible war that’s raged for billions of years. When viruses hunt and infect bacteria, the bacterial survivors store pieces of their vanquished foes — DNA snippets — within their genomes so that next time, they can detect and defend against the attack. In response, viruses evolve their own counterattack.
The bacteria’s natural defense system is called CRISPR-Cas9. And in 2012, biochemist Jennifer Doudna, together with French microbiologist Emmanuelle Charpentier, upended genetics with an ingenious idea. What if scientists could exploit CRISPR as a gene-editing tool? Since then, Doudna and others have hacked these cellular weapons in an effort to treat diseases and create stronger crops. Now scientists are attempting another task: avoiding unintended mutations resulting from their gene edits.
To grasp the tool’s precision, imagine the letters of a genome — G, A, T, C — typed into a stack of books dozens of stories high. A guide RNA shepherds Cas9 — which acts like a pair of DNA scissors — to the right spot, where it zooms in on just 20 letters and lets scientists change a few.
“CRISPR-Cas9 lets you find the right spot,” says Joseph Bondy-Denomy, a microbiologist at the University of California, San Francisco. “That’s a big deal.”
Indeed, a global gene editing revolution is underway. Lawyers battle over patent rights. CRISPR startups are selling stocks on the NASDAQ. And in a milestone this year, Oregon Health and Science University researchers used CRISPR to successfully correct heart disease-causing genes in human embryos. It was the first U.S. CRISPR experiment on humans.
But despite its track record, sometimes CRISPR brings unintended consequences — gene edits in undesired locations. Scientists call these “off-target effects.” Cas9’s scissors don’t always stop once the targeted cuts are made. Sometimes the scissors will roam for another day or two, cutting other sites that resemble the target but aren’t quite a perfect match.
“If left to their own devices, over time, [CRISPR proteins] might have the ability to cause trouble,” says Doudna, who is also a University of California, Berkeley, professor.
In May, a group of ophthalmologists and others sounded the alarm bells in a letter published in Nature Methods. The team used CRISPR to fix a blindness-causing gene in mice. But when they re-examined the mice, they found hundreds of unintended genetic mutations.
Doudna challenges the group’s methods and thinks that, in general, the off-target fear is overblown. Scientists knew about these mutations, and the technology is more than accurate enough for academic research purposes. The problems begin only as scientists move CRISPR into complex clinical trials.
Bondy-Denomy, the UCSF micro-biologist, appears to have found a “natural” way to combat these off-target effects. His research focuses on the arms race between bacteria and viruses, and last year, Bondy-Denomy started testing out a hunch. If bacteria defend against viruses using CRISPR, he reasoned, then viruses likely have a response to counteract it. He was right. Viruses do produce “anti-CRISPR” proteins that grab Cas9 and impair its gene-editing ability. He published his results in Cell in January 2017. “This is basically an off switch,” he says.
By summer, Doudna, Bondy-Denomy and their collaborators had used this viral counterpunch to reduce off-target effects. In Science Advances, the team detailed how they used CRISPR to make edits and then deployed anti-CRISPR to stop the Cas9 scissors from running amok.
The technique could help CRISPR move from the lab toward more therapeutic applications where absolute precision is required, Doudna says. Other teams are exploring different ways to avoid off-target effects, too. For example, the team that edited human embryos earlier this year saw no off-target effects, thanks to prep work aimed at keeping CRISPR on a shorter leash.
However, this gene-editing antidote could have another important use. Security experts, including former Director of National Intelligence James Clapper, worry that CRISPR makes things easier for would-be bioterrorists. Bondy-Denomy says if someone launched a CRISPR attack on humans or our crops, anti-CRISPR could work as an antidote. DARPA, the U.S. military research agency, liked the idea enough to give Doudna and Bondy-Denomy a grant to continue making Cas9 safer.
While Bondy-Denomy doubts CRISPR will ever be deployed in a human battle, he can at least be confident in knowing anti-CRISPR has already proven itself in the cellular arms race.
The CRISPR Antidote, tasks.
Task1. Find the equivalents of the following word combinations in the text.
1. держать на коротком поводке
2. предоставленные сами себе
3. по-видимому нашли
4. выйти из-под контроля
Task2. Find words/expressions meaning the following.
1. that cannot be seen;
2. enemy;
3. to understand;
4. the quality, condition, or fact of being exact and accurate ;
5. having started and in progress
6. the results or effects of something;
7. . a small cutting tool with two sharp blades that are screwed together;
8. to look like;
9. to question the truth, value of ideas;
10. to get out of control
Task3 Say if the following is true, false or not mentioned.
1. The bacteria that are not killed by viruses make pieces of the viruses’ DNA a part of their genome, which helps them survive another attack.
2. A French scientist came up with the idea of using the bacteria natural defence system to make changes in genes.
3. He suggested using CRISPR-Cas9 to combine genes of different species creating chimeras.
4. American researchers used CRISPR to successfully correct heart disease-causing genes in people addressing their heart problems and making heart surgery unneccasary.
5. If they are not taken care of, after a while CRISPR proteins normally mutate and cause cancer.
6. A California University scientist is of the opinion that the off-target danger is exaggerated.
7. To solve the problem scientists decided to use other bacteria with different CRISPR proteins.
8. CRISPR may prove handy for criminals.
9. The only remedy in the situation is to make people and crops immune to CRISPR proteins.
Task4. Answer the following questions.
1. What arms race does the author mean?
2. How can the bacteria natural defence system be used?
3. What difficult problem do scientists face?
4. What is the way out?
5. Has this method been put to practice? Why? Why not?
6. Why is the technique so important?
7. What are the other uses of the antidote?
Part2
Task1. Match the words in column A to the explanations in column B
A B
1. to eclipse to seem
2. to harken(hark) back to have an idea that is likely to lead to an important discovery
3. to replicate to understand
4. to be onto something to find something or someone that you have been looking for
5. derision to overshadow or surpass in importance, power, etc •
6. chase down to make an exact copy of; reproduce
7. to figure out to return to an earlier subject
8. to appear mockery , ridicule
Task2 Say whether the following is true, false or not mentioned
1. Though other laboratories were able to do the experiment and have the same results, MacConnel’s research was laughed at.
2. A Trinity College scientist does not agree with Glanzman’s hypothesis.
3. He thinks the most basic behavioural responses involve some kind of switch in the animal and there is something in the soup that Glanzman extracts that is hitting that switch."
4. The experiment was reproduced with untrained worms which after cannibalizing trained worms showed no difference in behaviour.
5. One of McConnell’s students was never given a permanent university position because his work was questioned.
6. After growing new heads the trained worms which were beheaded exhibited the same behavior as before.
7. And though memory RNA is still believed to be a myth, a recent research has confirmed that these worms’ memories do work in astoundingly bizarre ways.
8. Glazman still doubts if MacConnel hypothesis is correct, but he thinks he and his colleage had an idea that was likely to lead to an important discovery
9. The mechanism behind memory is still hard to understand , which can partly be explained by too much emphasis on synaptic strength.
10. It is not easy to do research in the memory sphere if you do not agree with accepted theories.
‘Artificial DNA Base Pair Expands Life’s Vocabulary
By Nathaniel Scharping
Scientists have taken another step towards putting two additional letters in the dictionary of life to work.
Researchers at the Scripps Institute have engineered cells to successfully transcribe a brand new artificial DNA base pair and make a never-before-seen protein with it. The breakthrough is part of an effort to expand the library of amino acids that animal cells can work with, potentially leading to the creation of compounds entirely different from those life can produce now.
The work was led by Floyd Romesberg, an associate professor of chemistry at Scripps, and adds to his 20-year effort to create synthetic DNA “letters.” DNA is currently comprised of four nucleotides, or letters: C, G, A and T—C binds to G, A binds to T. These couplings, or base pairs, comprise DNA as we know it. Romesberg and colleagues created two completely new letters, he calls them X and Y, and inserted them into a cell’s genome. Instead of four base pairs, the “semi-synthetic” cell now has six.
This drastically increases the number of codons — you can think of them as genetic “words” — and therefore, the number of things cells can make. Currently, there are 64 different triplet combinations of C-G and A-T possible. Three of those are stop codons, and many combinations are redundant, leaving our bodies with just 20 codons, or words, to make compounds with. Add in another base pair, and the number of potential words increases to 216. That more than triples the total, and the potential applications are vast.
“We will never need more codons,” he says. “We can now write more information in cells than we’d ever want to use.”
Expanding Vocabulary
In 2014, Romesberg successfully coaxed a cell to incorporate his custom X and Y base pair to its DNA, and found that it would remain there as long as he kept supplying the nucleotides. He’s now shown, in a Nature paper published Wednesday, that cells can not only hold on to the new base pairs, but they can use custom RNA sequences to transcribe codons with these new base pairs into something tangible.
Transcription is the process by which RNA copies bits of DNA and uses them to make things our bodies need. With new base pairs, the cells could make new codons, and those new genetic words held the blueprints for compounds that were previously impossible for cells to make. What’s more, the cells transcribed the new codons just as efficiently as the natural ones.
Adding the base pair to DNA demonstrated that storage was possible, he says, his latest work shows that the information can be retrieved works, and now he must show that cells can actually use the new compounds they make to do something interesting.
Romesberg provides a demonstration of this by adding in two new amino acids to a common fluorescent protein called GFP using E. coli bacteria. Bacterial cells with the extra base pair were able to produce amino acids that showed up in the flowing cells, proving that a new compound could make it from DNA to reality in a cell. The potential applications go far beyond glowing proteins, of course. Animal cells are currently only able to produce a finite set of things, limited by the number of genetic words they have to work with.
“We are making amino acids that are not normally made, cells are not capable of storing the information to make them,” Romesberg says.
This could mean new medicines, new nanomaterials, new reagents for chemical reactions. It could also eventually mean cells that can carry out functions no cell today can.
Don’t Panic
With the mention of new types of cells, thoughts of nightmare science-fiction scenarios are inevitable. Romesberg says that there are significant barriers to these cells ever making it outside the lab, however.
“One thing that’s really important to keep in mind is that we have a fail-safe built into this,” he says. “X and Y are unnatural nucleotides, [they] are not made by the cell. And this is not a “Jurassic Park” situation because these are man-made things.”
In his previous work getting cells to add the X and Y nucleotides into their DNA, he found that the cells immediately purged the base pair from the DNA as soon as he stopped giving it to them. Because these nucleotides aren’t natural, animal cells can’t manufacture them. The only way to keep them in a cell’s DNA is to keep them in the lab where they can be constantly supplied with new materials.
“They are not trivial molecules, they’re unlike anything a cell already makes,” Romesberg says. “It would have to assemble two complete new pathways out of something from which it has nothing similar to.”
For applications like creating new drugs, this would work fine because researchers could just keep giving them the supplies they need. If they escaped, however, the synthetic nucleotide would disappear from their genome.
“For a long time, people thought that the molecules of life were somehow different and privileged relative to the molecules of things that weren’t alive,” Romesberg says. “Maybe the molecules of life aren’t as special as we thought. And maybe a chemist can come in and design things that function alongside them. Maybe life is not the perfect solution, maybe life is a solution.”
‘Artificial DNA Base Pair Expands Life’s Vocabulary
Tasks
Task1. Find the following words/ expressions in the text.
1. a sudden, dramatic, and important discovery or development;
2. wholly;
3. consist of; be made up of;
4. place, fit, or push (something) into something else;
5. no longer needed or useful; superfluous;
6. to make something do something by dealing with it in a slow ,patient and careful way;
7. to get or bring (something) back from somewhere;
8. on the other side of a place or barrier ;
9. limited in size or extent;
10. finally;
11. that cannot be prevented or avoided
Task2.Say whether the following is true, false or not mentioned.
1. Scientists managed to create new proteins with the help of artificial DNA and include them into rats metabolism.
2. This experiment makes cells produce new things by increasing the number of “genetic words”
3. The number of codons (six instead of four) is enough now to write more information in cells than will ever be necessary.
4. While transcribing the cells didn’t see any difference between the natural codons and the new ones.
5. The cells constitute a “stable form of semi-synthetic life” and “lay the foundation for achieving the central goal of synthetic biology: the creation of new life forms and functions.
6. This experiment is very dangerous and can get out of control leading to the appearance of new animals.
7. Its results can be used for biological warfare helping create new microbes and viruses.
8. The scientists are sure there is not much difference between the molecules of life and the molecules of unliving things
9. The artificial X-Y base pair is formed via hydrophobic attraction between the two elements, rather than hydrogen bonding.
Task3. Answer the following questions.
1. The article mentions a breakthrough. What breakthrough is meant and why is it a breakthrough?
2. Why is the number of codons so important?
3. Can we say that the more codons the better it is? Why? Why not?
4. What’s the point of having six base pairs instead of four?
5. What experiment did Romesberg do in2014?
6. What did Romesberg prove now?
7. How can the discovery be used?
8. What prevents the new cells from escaping and the experiment from getting out of control?
9. Do you think in future this obstacle will be removed and we shall have animals with six base pairs or artificial life?
Tasks.
Task1. Match the words in column A to their explanations in column B
A B
1. insights a contiguous length of genomic sequence.
2. effort a structure composed of contigs and gaps.
3. bias to make something do something by dealing with it in a slow and careful way
4. from scratch an accurate and deep understanding
5. contiguous unchanging over a period of time, uniform , steady
6. nebulous to try very hard to do something, work
7. to distinguish to explain
8. to coax to seem
9. to account for fail to notice
10. dissimilarities from the very beginning,
11. consistent vague and not clearly defined
12. to appear a result or effect
13. to undergo to differentiate (between)
14. prone to sharing a common border; touching
15. consequence a tendency to prefer one thing to another, and to favour that thing.
16. to overlook to go through , experience
17.scaffold differences
Task2. Say if the following is true, false or not mentioned.
1. The discovery concentrates on the genetic differences which appeared when humans and apes went their own ways.
2. Scientists established that the extent of DNA sequence difference is on the order of 1.6%.
3. The existence of the differences became immediately evident once a comparative analysis of their genomes was made.
4. The latest research gives an exhaustive list of genetic variants which appeared or disappeared in different apes all of which show the differences between humans and apes genomes.
5. These differences account for different food they eat, their body structure and the way their brain was formed.
6. Scientists discovered that chimpanzees and humans shared a common ancestor only 4.6–6.2 million years ago.
7. Chimps’ smaller brain volume, which is three times less than human brain volume, may be due to differences in gene expression during brain formation in humans and chimps.
8. High resolution, comparative analysis of great ape genome assemblies helps us understand how great apes evolved.
9. Other discoveries reported in this Science paper come from an investigation into the origin of a fossil virus, similar to present day retroviruses, that is thought to be present in the genome of all African apes.
10. The retroviruses which developed from the above virus are typical of modern apes, only.
Task3. Answer the following questions.
1. Why is it so important that new, higher-quality assemblies of great ape genomes which have been generated were not based on the human reference genome?
2. How can the newly assembled genomes be used?
3. What prevented functional differences that distinguish humans from other apes from being discovered when their genomes were first compared?
4. How was the problem solved?
5. What was the purpose of creating organoids?
6. What did they reveal?
7. How do you understand a” less is more” hypothesis?
8. What happened to the genomes African great apes’ ancestors?
9. What did the changes result in?
10. How did the human genome change in the process of evolution?
11. Can we say that ape genomes are fully understood? Why? Why not?
Task4.Choose the right option.
1. . Those genes are more likely to have lost segments of DNA specifically in the human branch important in regulating their expression.
a. It is more likely that those genes are losing segments of DNA specifically in the human branch important in regulating their expression.
b. There are more chances that segments of DNA specifically in the human branch important in regulating their expression lost those genes.
c. It is more likely that those genes and segments of DNA specifically in the human branch important in regulating their expression lost each other.
d. There are greater chances that those genes lost segments of DNA specifically in the human branch important in regulating their expression
2. On the other hand, certain human genes appear to be linked to up-regulation for neural progenitors and excitatory neurons in the nervous system
a. On the other hand, certain human genes appeared from regulation for neural progenitors and excitatory neurons in the nervous system
b. It seems ,on the other hand, that certain human genes are linked to up-regulation for neural progenitors and excitatory neurons in the nervous system.
c. On the other hand, it appears that certain human genes were linked to up-regulation for neural progenitors and excitatory neurons in the nervous system
d. On the other hand, up-regulation for neural progenitors and excitatory neurons in the nervous system seem to be linked to certain human genes.
3. Modern day chimpanzees and gorillas carry hundreds of PtERV1 retroviral insertions that appear to have originated from this source that never made it into the human genome
a. Modern day chimpanzees and gorillas carry hundreds of PtERV1 retroviral insertions that it seems appeared from this source and found themselves in the human genome.
b. Modern day chimpanzees and gorillas carry hundreds of PtERV1 retroviral insertions that seem to have appeared in the human genome.
c. The human genome carries hundreds of PtERV1 retroviral insertions that appear to have originated from chimpanzees and gorillas.
d. Modern day chimpanzees and gorillas carry hundreds of PtERV1 retroviral insertions that seem to have come from this source that never made it into the human genome
Better medical knowledge
In a medical context, people are likely to be given advice and guidance about genetics by a doctor or other professional. But even with such help, people who have better genetic knowledge will benefit more and will be able to make more informed decisions about their own health, family planning, and health of their relatives. People are already confronted with offers to undergo costly genetic testing and gene-based treatments for cancer. Understanding genetics could help them avoid pursuing treatments that aren’t actually suitable in their case.
It is now possible to edit the human genome directly using a technique called CRISPR. Even though such genetic modification techniques are regulated, the relative simplicity of CRISPR means that biohackers are already using it to edit their own genomes, for example, to enhance muscle tissue or treat HIV.
Such biohacking services are very likely to be made available to buy (even if illegally). But as we know from our explanation of pleiotropy, changing one gene in a positive way could also have catastrophic unintended consequences. Even a broad understanding of this could save would-be biohackers from making a very costly and even potentially fatal mistake.
When we don’t have medical professionals to guide us, we become even more vulnerable to potential genetic misinformation. For example, Marmite recently ran an ad campaign offering a genetic test to see if you either love or hate Marmite, at a cost of £89.99. While witty and whimsical, this campaign also has several problems.
First, Marmite preference, just like any complex trait, is influenced by complex interactions between genes and environments and is far from determined at birth. At best, a test like this can only say that you are more likely to like Marmite, and it will have a great deal of error in that prediction.
Second, the ad campaign shows a young man seemingly “coming out” to his father as a Marmite lover. This apparent analogy to sexual orientation could arguably perpetuate the outdated and dangerous notion of “the gay gene”, or indeed the idea that there is any single gene for complex traits. Having a good level of genetic knowledge will enable people to better question advertising and media campaigns, and potentially save them from wasting their money.
My own research has shown that even the well-educated amongst us have poor genetic knowledge. People are not empowered to make informed decisions or to engage in fair and productive public discussions and to make their voices heard. Accurate information about genetics needs to be widely available and more routinely taught. In particular, it needs to be incorporated into the training of teachers, lawyers and health care professionals who will very soon be faced with genetic information in their day-to-day work.
This article was originally published on The Conversation. Read the original article.
‘Are We Really Prepared for the Genetic Revolution?’ Tasks
Task1. Find words/expressions meaning the following.
1. to expect or predict;
2. a particular characteristic, quality, or tendency that someone or something has;
3. the achieving of some aim;
4. very small;
5. to aim;
6. to go through, experience or be subjected to;
7. able to be used or obtained;
8. easy to attack or criticize;
9. evident;
10. to make (something) continue indefinitely
11. in accordance with the rules or standards
Task2. Say if the following is true, false or not men tioned.
1. Mapping the human genome 15 years ago changed the world.
2. The author hopes that in the next five years all genetic diseases will be eradicated.
3. It is not enough to be able to find variations in the genome to understand how they result in specific characteristics we observe.
4. Since genetic data are more and more widely used , the absence of understanding may affect our decisions badly.
5. Pleiotropy means that each gene is responsible for one or two traits.
6. By sequencing the DNA of a child at birth we can determine with almost 100% accuracy his or her future academic successes.
7. There is an erroneous opinion that genetic information is something permanent and will lead to children being streamed in terms of their DNA.
8. Changing one gene is risky and can result in dangerous side-effects
9. Even the most enthusiastic scientists are likely to disagree with providing potential crackpots the tools to interfere with the recipe of life.
10. Teachers, lawyers and doctors should be taught genetics as genetic information will soon becomed part and parcel of their work.
Task3. Answer the following questions.
1. Why didn’t mapping the human genome 15 years ago lead to a breakthrough in treating diseases?
2. What is pleiotropy?
3. What causes misunderstanding?
4. Why shouldn’t we use genetic information to stream children ,dividing them into gifted, not so gifted and plain stupid?
5. What can people gain from genetic knowledge?
6. Why is biohacking so risky?
7. What technique does it use?
8. What does CRISPR involve? ( the answer can be found in one of the previous texts)
9. Why is the concept of the gay gene outdated and dangerous?
10. How can genetic knowledge help here?
YOUR BRAIN IS SPECIAL.
So is mine. Differences arise at every level of the organ’s astonishingly intricate architecture; the human brain contains 100 billion neurons, which come in thousands of types and collectively form an estimate of more than 100 trillion interconnections. These differences, in turn, lead to variances in the ways we think, learn and behave and in our propensity for mental illness.
How does diversity in brain wiring and function arise? Variations in the genes we inherit from our parents can play a role. Yet even identical twins raised by the same parents can differ markedly in their mental functioning, behavioral traits, and risk of mental illness or neurodegenerative disease. In fact, mice bred to be genetically identical that are then handled in exactly the same way in the laboratory display differences in learning ability, fear avoidance and responses to stress even when age, gender and care are held constant. Something more has to be going on.
Certainly the experiences we have in life matter as well; they can, for instance, influence the strength of the connections between particular sets of neurons. But researchers are increasingly finding tantalizing indications that other factors are at work—for instance, processes that mutate genes or affect gene behavior early in an embryo’s development or later in life. Such phenomena include alternative splicing, in which a single gene can give rise to two or more different proteins. Proteins carry out most of the operations in cells, and thus which proteins are made in cells will affect the functioning of the tissues those cells compose. Many researchers are also exploring the role of epigenetic changes—DNA modifications that alter gene activity (increasing or decreasing the synthesis of specific proteins) without changing the information in genes.
In the past few years the two of us and our colleagues have come on especially intriguing suspects that seem to operate more in the brain than in other tissues: jumping genes. Such genes, which have been found in virtually all species, including humans, can paste copies of themselves into other parts of the genome (the full set of DNA in the nucleus) and alter the functioning of the affected cell, making it behave differently from an otherwise identical cell right next to it. Many such insertions in many different cells would be expected to yield subtle or not so subtle differences in cognitive abilities, personality traits and susceptibility to neurological problems.
Our early findings of gene jumping in the brain have led us to another question: Given that the brain’s proper functioning is essential to survival, why has evolution allowed a process that tinkers with its genetic programming to persist? Although we still do not have a definite answer, mounting evidence suggests that by inducing variability in brain cells, jumping genes may imbue organisms with the flexibility to adapt quickly to changing circumstances. Therefore, these jumping genes—or mobile elements, as they are called—may have been retained evolutionarily because, from the standpoint of promoting survival of the species, this adaptation benefit outweighs the risks.
ANCIENT INVADERS
THE IDEA THAT MOBILE ELEMENTS EXIST and move about in the genome is not new, but the recent evidence that they are so active in the brain came as a surprise. Gene jumping was first discovered in plants, even before James Watson and Francis Crick spelled out the double-helical structure of DNA in 1953. In the 1940s Barbara McClintock of Cold Spring Harbor Laboratory observed that “con-trolling elements” moved from one place to another in the genetic material of corn plants. She discovered that under stress, certain regions in the genome could migrate and turn genes on and off in their new location. The products of McClintock’s experiments were the now famous ears of corn with seeds of varying colors—a demonstration of genetic mosaicism, in which genes in a particular cell may be switched on or off in a pattern that differs from that of neighboring cells that are otherwise identical.
McClintock’s research, which at first encountered skepticism within the scientific community, eventually resulted in her receiving a Nobel Prize in 1983. In subsequent years it became clear that the phenomenon of genetic mosaicism is not restricted to plants but also occurs in many organisms, including humans.
McClintock did her work on transposons, which are mobile elements that use a cut-and-paste mechanism to move a stretch of DNA around the cell’s genome. More recent research on mobile elements in the brain had focused on retrotransposons, which employ a copy-and-paste approach to insinuate themselves into new areas of the genome. They basically replicate themselves rather than popping out of the surrounding DNA, after which the copy takes up a new position elsewhere.
Retrotransposons make up as much as half of the nucleotides, or DNA building blocks, in the human genome. In contrast, the approximately 25,000 protein-coding genes we possess make up less than 2 percent of mammalian DNA. The jumping genes are descendants of the first primitive molecular replication systems that invaded the genomes of eukaryotes (organisms having cells that contain a nucleus) long ago. A group led by Haig H. Kazazian, Jr., at the University of Pennsylvania showed in 1988 that retrotransposons, which were once thought of as nonfunctional junk DNA, were active in human tissues.
In particular, one type of retrotransposon, known as a long interspersed element 1 (L1), appears to be a key player in the human genome. It is able to hop around frequently probably because it, unlike other mobile elements in humans, encodes its own machinery for spreading copies of itself far and wide in the cellular genome. Analysis of its behavior in cells reveals that when something prompts an L1 in the nuclear genome to begin the “jumping” process, it first transcribes itself into single-stranded RNA, which then travels from the nucleus to the cytoplasm, where it serves as a template for constructing proteins specified by some parts of the L1 DNA. The proteins then form a molecular complex with the still intact RNA, and the whole complex heads back to the nucleus. There one of the proteins, an enzyme called an endonuclease, makes a nick in specific sites in the DNA. It also uses the RNA as a template for producing a double-stranded DNA copy of the original L1 retrotransposon and inserts this duplicate into the genome where the cut was made. Such reverse transcription, from RNA to DNA, is familiar to many people today as part of the way that the HIV virus gets a DNA copy of its RNA genome to take up a permanent home in the genome of the cells it infects.
Retrotransposition often fails to run its course, which produces truncated, nonfunctional copies of the original L1 DNA. Sometimes these snippets (or the whole L1 copy) have no effect on a protein-coding gene. Other times, though, they can have any of several consequences, both good and bad, for a cell’s fate. They may, for instance, drop into and thus alter the protein-coding region of a gene. This maneuver can lead to creation of a new variant of the protein that helps or harms an organism. Or this positioning may stop a given protein from being made. In other instances, the newly pasted DNA may fall outside of a coding region but act as a promoter (a switch that can turn on nearby genes) and alter the level of gene expression—the amount of protein made from the gene—with, once again, good or bad results for the cell and the organism. When LI retrotransposons end up in many places in neurons or in many cells of the brain, or both, the brain will be very different from the one that would have formed without their influence. It stands to reason that such genetic mosaicism could affect behavior, cognition and disease risk and could also help explain why one identical twin may remain disease-free when a sibling is diagnosed with schizophrenia, for example.
WHERE DOES JUMPING OCCUR?
UNTIL RECENTLY, most investigators aware of L1 retrotransposi tion assumed that it mostly took place in germ cells (ovaries or testes). Although a few clues suggested that L1 genes stay active in somatic tissues (nonsex cells) during early development or later, these clues were generally dismissed. If genes exist merely to propagate themselves, as one evolutionary theory holds, jumping genes would have little cause to remain active in somatic cells because such cells would not pass the DNA to an organism’s next generation: after all, the affected cells die when their owner does.
Better detection tools have now revealed that retrotransposons can move around somatic tissues during early development and even later in life. These events happen more often in the brain than in other tissues—a direct challenge to the longstanding dogma that the genetic codes of brain cells in adults are identical to one another and remain stable for the cells’ life.
In our lab at the Salk Institute for Biological Studies in La Jolla, Calif., for instance, we monitored gene jumping in a mouse whose cells were genetically engineered to undergo retrotransposition and fluoresce green when an L1 element inserted itself in genomes of a cell anywhere in its body. We observed glowing green cells only in germ cells and in certain brain areas, including the hippocampus (a region important to memory and attention)— which suggests that L1s may move around more in the brain than in other somatic tissues. Interestingly, the jumping was occurring in progenitor cells that give rise to hippocampal neurons.
In various organs of fully formed organisms, a small population of progenitor cells stands by, ready to divide and give rise to specialized cell types needed to replace cells that die. The hippocampus is one of two regions of the brain where neurogenesis, generation of new nerve cells, occurs. Thus, L1s appear to be active during early development when neurons are being born, but they can also move around in the adult brain in the areas where new neurons continue to be born into adulthood.
Even with the mouse experiments, more evidence was needed that retrotransposition was actually occurring in the brain. We undertook an analysis of human postmortem material that compared the number of L1 elements in brain, heart and liver tissues. We found that the brain tissue contained significantly more L1 elements in each cell nucleus than the heart or liver tissues did.
Much of the jumping had to have occurred during the brain’s development because retrotransposition requires cell division— a process that does not take place in the brain, except in two circumscribed areas—to happen after early childhood. An analysis suggested that each neural cell in humans undergoes an average of 80 L1 integration events, a rate that could well lead to a great deal of variation among cells and in the overall brain activity of different individuals.
A recent finding from researchers at the Roslin Institute near Edinburgh and their colleagues supplies further confirmation of L1 activity in the human brain. The researchers reported in 2011 in Nature that a total of 7,743 insertions of L1s in the hippocampus and caudate nucleus (which is also involved in memory) in three deceased individuals contained integrated L1 elements. (Scientific American is part of Nature Publishing Group.) That study also implied that the emerging portrait of genetic diversity in the brain will only get more complicated as this research moves forward. The Roslin team was surprised to come on about 15,000 members of a class of retrotransposons known as short interspersed elements (SINEs). The preponderant SINE, part of a group known as Alu elements, had never been encountered before in the brain.
Our findings made us wonder what might trigger L1 activity. Knowing that the hippocampus is also a site where neurogenesis transpires and that exposure to novel situations and exercise triggers neurogenesis in mice, we decided to see if exercise might be one spur to gene jumping. We found that after our transgenic mice ran on a wheel, the number of green fluorescing cells increased about twofold in the rodents’ hippocampus. Given that novelty and challenge also prompt neurogenesis, we are entertaining the possibility that a new or unfamiliar environment could be another instigator of retrotransposition.
If we are correct and L1 jumping does increase as the nervous system learns and adapts to the outside world, the finding would indicate that individual brains and the neuronal networks that make them up are constantly changing and alter with each new experience, even in genetically identical twins.
ORIGINS OF DISEASE
WE ARE CONTINUING TO EXPAND the evidence for the hypothesis that jumping genes contribute to human variation in brain processing by moving beyond just counting L1s in DNA. In our quest to link our data to real events that have either positive or detrimental effects on living people, it is sometimes easiest to pinpoint the bad outcomes that resulted from a gene that jumped, if only because the consequences are so obvious.
In November 2010 our team reported in Nature that a mutation in a gene called MeCP2 affected L1 retrotransposition in the brain. Mutations in the MeCP2 gene can induce Rett syndrome, a severe disorder of brain development that almost exclusively affects girls. The discovery that MeCP2 was mutated in patients with Rett syndrome and other mental disorders raised multiple questions about the molecular and cellular mechanisms of this disease. Our research showed that the mutation in the brains of mice and humans with Rett syndrome resulted in a significant increase in numbers of L1 insertions in their neurons—a finding that suggests that the jumping genes might account for some of the effects of the MeCP2 mutation.
L1 activity has also turned up in other disorders. An analysis of the frontal cortex regions of individuals with schizophrenia revealed increased production of mobile element sequences compared with those without the condition. Circumstantial evidence suggests that L1 elements are an important component of various brain disorders, including autism. Understanding the role of mobile elements in the development of psychiatric diseases might lead to new methods for diagnosis, treatment and prevention.
The continuing research into jumping genes in the brain could potentially challenge an entire academic discipline. Behavioral geneticists often follow groups of identical twins over long periods to control for the effects of genes and determine the environmental contributions to such disorders as schizophrenia. The new findings showing that jumping genes actively revise genomes after an embryo forms question the assumption that “identical” twins are genetically alike. Indeed, the new discoveries will make it ever harder to disentangle the relative effects of nature and nurture on our psyches.
The question remains: Why has evolution not destroyed these vestiges of ancient viruses from within our cells, given that jumping genes have a high chance of introducing potentially fatal genetic flaws? To answer the question, we should acknowledge that humans have always been under attack by viral parasites and other invaders that expand the size of our genomes with jumping DNA. The bodies of humans and our evolutionary forebears may not have been able to fully eliminate the interlopers, but they have adapted to at least coexist with the invaders by silencing them through a variety of clever mechanisms that mutate and disable them. It also appears that, in some cases, our genomes have commandeered the genetic machinery of L1 retroelements to enhance our own survival, which is one reason that cells may sometimes allow, or even encourage, L1s to jump around the genome under carefully controlled conditions.
One clue to why they persist may come from closer analysis of the finding that mice from a single genetic strain raised under highly controlled conditions vary greatly in their responses to stress. The observed behavioral differences are distributed typically in the population (picture a bell curve), a pattern that implies that the mechanisms producing this variability are random, as the sites of L1 retrotransposon insertions seem to be.
The putatively random nature of how L1s move from place to place in the genome implies that natural selection may, in effect, be rolling the dice in the hope that benefits from helpful insertions will outweigh any deleterious consequences of other insertions. And nature may be placing bets frequently on the neural progenitor cells of the hippocampus so as to maximize the possibility that at least some of the new positions will give rise to a population of adult neurons particularly well suited to the tasks the brain will confront. A somewhat similar process occurs when the DNA in immune cells rearranges itself to produce an array of antibodies, after which only the antibodies best equipped to fight off a pathogen are selected for full-scale production.
This scenario does not seem far-fetched. L1-mediated effects do not need to be large and do not have to occur in many cells to influence behavior. In rodents, a change in the firing pattern of a single neuron might be enough to make a difference.
More possible support for this idea is the discovery that the only lineage of L1 jumping elements currently active in the human genome evolved about 2.7 million years ago, after the evolutionary split from chimpanzees to bipedal humans—a time when our hominid ancestors were first beginning to adopt the use of stone tools. That finding lends credence to the notion that the L1 elements may have helped build brains that can process information about the environment rapidly and that can thus more readily meet the challenges of ever changing environmental and climatic conditions. L1 jumping genes seem to have been a collaborative partner in advancing the evolution of Homo sapiens.
Your brain is special, tasks.
Part1, p.1-2(up to ‘Retrotransposition often fails…’)
Task1. Find words/ expressions meaning the following.
1. very complicated or detailed;
2. in succession; one after the other;
3. having a quality that stimulates interest;
4. to cause to happen;
5. the action of putting something in or between;
6. (especially of a change or distinction) so delicate or precise as to be difficult to analyse or describe;
7. to make some small changes to something in an attempt to improve it or repair it;
8. to make someone or something have a quality very strongly;
9. the ability to be easily modified;
10. finally;
11. to compose;
12. not damaged in any way; complete
Task2. Say whether the following is true, false or not mentioned
1. If all the conditions are equal, mice grown in the laboratory are absolutely identical and exhibit the same behavior.
2. The actions we take during our life and our feelings and impressions, all these affect neuron connections in our brain.
3. There is growing evidence nowadays that other factors should be considered, for example, alternative splicing in which a change in one gene may result in several identical proteins.
4. Epigenetic changes modify the activation of certain genes, but not the genetic code sequence of DNA.
5. Jumping genes insert themselves into a human cell resulting in changes in its behavior.
6. Though the existence of mobile elements has been known for a long time, scientists had no idea their activity would be so intense.
7. McClintock’s research was immediately recognized by a scientific community and right after its publication she was awarded a Nobel prize.
8. A good example of reverse transcription is the HIV virus which changes the DNA of the cell it infects.
Task3. Answer the following questions.
1. What factors affect the human brain causing its diversity?
2. Why are proteins so important?
3. What new factor has recently been discovered?
4. Can we say that there are as many jumping genes in the brain as in the othewer tissues? Why? Why not?
5. How do jumping genes affect cells?
6. Why did this process develop in the course of evolution? What’s its meaning?
7. What was the main idea of McClintock’s experiments?
8. How did the scientific community react to her discovery?
9. What’s the difference between her research and more recent research on mobile elements in the human brain?
Part2, p.2- 4 (from ‘Retrotransposition often fails…’ up to ‘ Origins of disease’)
Task1. Find words/ expressions meaning the following.
1. it is obvious or logical;
2. informed about , acquainted with ;
3. to reproduce or cause to reproduce; breed;
4. to wait , be in (a state of) readiness ;
5. to deal with , engage in;
6. verification , proof;
7. mixed ,diversified;
8. to come to light, be known;
9. subjection , vulnerability ;
10. to consider as possible;
11. initiator
Task2. Say whether the following is true, false or not mentioned.
1. Truncated, nonfunctional copies of the original L1 DNA have either no effect on a protein-coding gene or affect it badly resulting in a great harm to a cell.
2. Most scientists are still sure that retransposition takes place mostly in germ cells though there is evidence to the contrary.
3. Retransposition is more typical of the brain and is a good proof that the genetic codes of brain cells of grownups differ and can change during the cell life.
4. In future experiments, the researchers will attempt to block retrotransposition at various times in development using RNA interference to look for any changes in cell behavior.
5. As the research goes on, the brain will be found to be more and more genetically diverse.
6. The researchers are sure that anew and unknown environment could also result in retransposition.
7. In a study of rodents neural stem cells, researchers discovered an up to twofold increase in the retrotransposons, which can jump around the genome.
Task3. Answer the following questions.
1. How do truncated unfunctional copies of the original L1 DNA affect a protein coding gene?
2. What is the argument against retransposition being confined to germ cells?
3. What does the fact that retransposition is more frequent in the brain mean?
4. How was it proved?
5. Where are nerve cells generated?
6. Why did human postmortem material have to be examined?
7. What did the Roslin team discover?
8. Why were they surprised?
9. What factors increased gene jumping?
10. Why is this finding so significant?
Part3, p.4-5 (from ‘Origins of disease’ up to the end )
Task1. Find words/ expressions meaning the following
1. having a harmful or damaging effect ;
2. to explain;
3. fragment , trace;
4. stop oneself from ,refrain;
5. defect;
6. differ in size, amount, degree;
7. unsystematic , unmethodical;
8. harmful;
9. improbable in nature; unlikely
10. to make something (e.g. an idea) more believable
Task2. Say whether the following is true, false or not mentioned.
1.The fact that the number of L1 insertions in mice brain Increases greatly due to the mutations in the brain of mice with Rett syndrome means that the jumping genes are surely responsible for some effects of the MeCP2 mutation.
2. The effects of L1 activity are most likely to be neutral or deleterious.
3. Because of the latest findings scientists express doubt about the genetic identity of twins, the differences being due to jumping genes.
4. There are convincing facts which prove that that L1elements are an important factor resulting in various brain disorders.
5. Sometimes the genetic mechanism of L1 retroelements increases our chances of survival which explains why L1s may jump around the genome under carefully controlled conditions.
6. In mice and rats a change in the work of a single neuron is enough to influence their behavior.
7. L1 jumping elements appear to have been a crucial factor in the origin and development of man.
Task3. . Answer the following questions.
1. How do jumping genes affect people?
2. Why is it easier to notice unfavourable effects?
3. What is Rett syndrome and what causes it?
4. Is it the only disease caused by L1 elements? Why? Why not?
5. Why is it wrong to consider twins genetically identical?
6. How does it happen that people still have traces of ancient viruses despite millions of years of evolution?
7. When did L1 jumping elements originate?
8. Are they peculiar to humans or can they be found in apes and monkeys, too? (Prove!)
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Дата: 2019-02-02, просмотров: 245.