BEST IELTS Academic Reading Test 11
ACADEMIC READING TEST 11
READING PASSAGE 1
You should spend about 20 minutes on Questions 1–14, which are based on Reading Passage 1 below.
How bacteria invented gene editing
This week the UK Human Fertilisation and Embryology Authority okayed a proposal to modify human embryos through gene editing. The research, which will be carried out at the Francis Crick Institute in London, should improve our understanding of human development. It will also undoubtedly attract controversy – particularly with claims that manipulating embryonic genomes is a first step towards designer babies. Those concerns shouldn’t be ignored. After all, gene editing of the kind that will soon be undertaken at the Francis Crick Institute doesn’t occur naturally in humans or other animals.
It is, however, a lot more common in nature than you might think, and it’s been going on for a surprisingly long time – revelations that have challenged what biologists thought they knew about the way evolution works. We’re talking here about one particular gene editing technique called CRISPR-Cas, or just CRISPR. It’s relatively fast, cheap and easy to edit genes with CRISPR – factors that explain why the technique has exploded in popularity in the last few years. But CRISPR wasn’t dreamed up from scratch in a laboratory. This gene editing tool actually evolved in single-celled microbes.
CRISPR went unnoticed by biologists for decades. It was only at the tail end of the 1980s that researchers studying Escherichia coli noticed that there were some odd repetitive sequences at the end of one of the bacterial genes. Later, these sequences would be named Clustered Regularly Interspaced Short Palindromic Repeats – CRISPRs. For several years the significance of these CRISPRs was a mystery, even when researchers noticed that they were always separated from one another by equally odd ‘spacer’ gene sequences.
Then, a little over a decade ago, scientists made an important discovery. Those ‘spacer’ sequences look odd because they aren’t bacterial in origin. Many are actually snippets of DNA from viruses that are known to attack bacteria. In 2005, three research groups independently reached the same conclusion: CRISPR and its associated genetic sequences were acting as a bacterial immune system. In simple terms, this is how it works. A bacterial cell generates special proteins from genes associated with the CRISPR repeats (these are called CRISPR associated – Cas – proteins). If a virus invades the cell, these Cas proteins bind to the viral DNA and help cut out a chunk. Then, that chunk of viral DNA gets carried back to the bacterial cell’s genome where it is inserted – becoming a spacer. From now on, the bacterial cell can use the spacer to recognise that particular virus and attack it more effectively.
These findings were a revelation. Geneticists quickly realised that the CRISPR system effectively involves microbes deliberately editing their own genomes – suggesting the system could form the basis of a brand new type of genetic engineering technology. They worked out the mechanics of the CRISPR system and got it working in their lab experiments. It was a breakthrough that paved the way for this week’s announcement by the HFEA. Exactly who took the key steps to turn CRISPR into a useful genetic tool is, however, the subject of a huge controversy. Perhaps that’s inevitable – credit for developing CRISPR gene editing will probably guarantee both scientific fame and financial wealth.
Beyond these very important practical applications, though, there’s another CRISPR story. It’s the account of how the discovery of CRISPR has influenced evolutionary biology. Sometimes overlooked is the fact that it wasn’t just geneticists who were excited by CRISPR’s discovery – so too were biologists. They realised CRISPR was evidence of a completely unexpected parallel between the way humans and bacteria fight infections. We’ve known for a long time that part of our immune system “learns” about the pathogens it has seen before so it can adapt and fight infections better in future. Vertebrate animals were thought to be the only organisms with such a sophisticated adaptive immune system. In light of the discovery of CRISPR, it seemed some bacteria had their own version. In fact, it turned out that lots of bacteria have their own version. At the last count, the CRISPR adaptive immune system was estimated to be present in about 40% of bacteria. Among the other major group of single-celled microbes – the archaea – CRISPR is even more common. It’s seen in about 90% of them. If it’s that common today, CRISPR must have a history stretching back over millions – possibly even billions – of years. “It’s clearly been around for a while,” says Darren Griffin at the University of Kent.
The animal adaptive immune system, then, isn’t nearly as unique as we thought. And there’s one feature of CRISPR that makes it arguably even better than our adaptive immune system: CRISPR is heritable. When we are infected by a pathogen, our adaptive immune system learns from the experience, making our next encounter with that pathogen less of an ordeal. This is why vaccination is so effective: it involves priming us with a weakened version of a pathogen to train our adaptive immune system. Your children, though, won’t benefit from the wealth of experience locked away in your adaptive immune system. They have to experience an infection – or be vaccinated – first hand before they can learn to deal with a given pathogen.
CRISPR is different. When a microbe with CRISPR is attacked by a virus, the record of the encounter is hardwired into the microbe’s DNA as a new spacer. This is then automatically passed on when the cell divides into daughter cells, which means those daughter cells know how to fight the virus even before they’ve seen it. We don’t know for sure why the CRISPR adaptive immune system works in a way that seems, at least superficially, superior to ours. But perhaps our biological complexity is the problem, says Griffin. “In complex organisms any minor [genetic] changes cause profound effects on the organism,” he says. Microbes might be sturdy enough to constantly edit their genomes during their lives and cope with the consequences – but animals probably aren’t. The discovery of this heritable immune system was, however, a biologically astonishing one. It means that some microbes write their lifetime experiences of their environment into their genome and then pass the information to their offspring – and that is something that evolutionary biologists did not think happened.
Darwin’s theory of evolution is based on the idea that natural selection acts on the naturally occurring random variation in a population. Some organisms are better adapted to the environment than others, and more likely to survive and reproduce, but this is largely because they just happened to be born that way. But before Darwin, other scientists had suggested different mechanisms through which evolution might work. One of the most famous ideas was proposed by a French scientist called Jean-Bapteste Lamarck. He thought organisms actually changed during their life, acquiring useful new adaptations non-randomly in response to their environmental experiences. They then passed on these changes to their offspring.
People often use giraffes to illustrate Lamarck’s hypothesis. The idea is that even deep in prehistory, the giraffe’s ancestor had a penchant for leaves at the top of trees. This early giraffe had a relatively short neck, but during its life it spent so much time stretching to reach leaves that its neck lengthened slightly. The crucial point, said Lamarck, was that this slightly longer neck was somehow inherited by the giraffe’s offspring. These giraffes also stretched to reach high leaves during their lives, meaning their necks lengthened just a little bit more, and so on. Once Darwin’s ideas gained traction, Lamarck’s ideas became deeply unpopular. But the CRISPR immune system – in which specific lifetime experiences of the environment are passed on to the next generation – is one of a tiny handful of natural phenomena that arguably obeys Lamarckian principles.
“The realisation that Lamarckian type of evolution does occur and is common enough, was as startling to biologists as it seems to a layperson,” says Eugene Koonin at the National Institutes of Health in Bethesda, Maryland, who explored the idea with his colleagues in 2009, and does so again in a paper due to be published later this year. This isn’t to say that all of Lamarck’s thoughts on evolution are back in vogue. “Lamarck had additional ideas that were important to him, such as the inherent drive to perfection that to him was a key feature of evolution,” says Koonin. No modern evolutionary biologist goes along with that idea. But the discovery of the CRISPR system still implies that evolution isn’t purely the result of Darwinian random natural selection. It can sometimes involve elements of non-random Lamarckism too – a “continuum”, as Koonin puts it. In other words, the CRISPR story has had a profound scientific impact far beyond the doors of the genetic engineering lab. It truly was a transformative discovery.
Do the following statements agree with the information given in Reading Passage 1?
In boxes 1–5 on your answer sheet, write
TRUE – if the statement agrees with the information
FALSE – if the statement contradicts the information
NOT GIVEN – if there is no information on this
1. The research carried out at the Francis Crick Institute in London is likely to be controversial.
2. Gene editing, like the one in the upcoming research, can happen naturally in humans or other animals.
3. CRISPR-Cas is a gene editing technique.
4. CRISPR was noticed when the researchers saw some odd repetitive sequences at the ends of all bacterial genes.
5. A group of American researchers made an important revelation about the CRISPR.
Choose the correct letter, A, B, C or D.
Write the correct letter in boxes 6–9 on your answer sheet.
6. ‘Spacer’ sequences look odd because:
A. they are a bacterial immune system
B. they are DNA from viruses
C. they aren’t bacterial in origin
D. all of the above
7. The ones, who were excited about the CRISPR’s discovery, were:
D. A and B
8. Word “learns” in the line 44, 6th paragraph means:
B. gains awareness
9. What makes CRISPR better than even our adaptive immune system?
A. long history of existence
Complete the sentences below.
Write NO MORE THAN TWO WORDS from the passage for each answer.
Write your answers in boxes 10–16 on your answer sheet.
10. Vaccination is so effective, because it involves with a weakened version of……………………a pathogen.
11. CRISPR adaptive immune system works in a way that seems, at least superficially, superior to ours. But perhaps…………………………………our is the problem, according to Griffin.
12. Some microbes write their experience into the genome and pass the information to their………………………………..
13. Before Darwin, one of the most famous ideas was proposed by a……………………..scientist, Lamarck.
14. ……………………………..Are often used to demonstrate Lamarck’s hypothesis.
READING PASSAGE 2
You should spend about 20 minutes on Questions 15-27 which are based on Reading Passage 2 below.
The Disease Multiple Sclerosis
Multiple sclerosis (MS) is a disease in which the patient’s immune system attacks the central nervous system. This can lead to numerous physical and mental symptoms, as the disease affects the transmission of electrical signals between the body and the brain. However, the human body, being a flexible, adaptable system, can compensate for some level of damage, so a person with MS can look and feel fine even though the disease is present.
MS patients can have one of two main varieties of the disease: the relapsing form and the primary progressive form. In the relapsing form, the disease progresses in a series of jumps; at times it is in remission, which means that a person’s normal functions return for a period of time before the system goes into relapse and the disease again becomes more active. This is the most common form of MS; 80-90% of people have this form of the disease when they are first diagnosed. The relapse-remission cycle can continue for many years. Eventually, however, loss of physical and cognitive function starts to take place, and the remissions become less frequent.
In the primary progressive form of MS, there are no remissions, and a continual but steady loss of physical and cognitive functions takes place. This condition affects about 10-15% of sufferers at diagnosis.
The expected course of the disease, or prognosis, depends on many variables: the subtype of the disease, the patient’s individual characteristics and the initial symptoms. Life expectancy of patients, however, is often nearly the same as that of an unaffected person-provided that a reasonable standard of care is received. In some cases, a near-normal life span is possible.
The cause of the disease is unclear; it seems that some people have a genetic susceptibility, which is triggered by some unknown environmental factor. Onset of the disease usually occurs in young adults between the ages of 20 and 40. It is more common in women than men; however, it has also been diagnosed in young children and elderly people.
Hereditary factors have been seen to have some relevance. Studies of identical twins have shown that if one twin has the disease, then it is likely that the other twin will develop it. In addition, it is important to realize that close relatives of patients have a higher chance of developing the disease than people without a relative who has MS.
Where people live can be seen to have a clear effect, as MS does not occur as frequently in every country. It commonly affects Caucasian people, particularly in North America, Europe and Australia. It has been recognized that MS is more common the further the country is away from the equator, and the incidence of MS is generally much higher in northern countries with temperate climates than in warmer southern countries.
Three things, which do not normally occur in healthy people, happen to people who have MS. First, tiny patches of inflammation occur in the brain or spinal cord. Second, the protective coating around the axons, or nerve fibres, in the body start to deteriorate. Third, the axons themselves become damaged or destroyed. This can lead to a wide range of symptoms in the patient, depending on where the affected axons are located.
A common symptom of MS is blurred vision caused by inflammation of the optic nerve. Another sign is loss of muscle tone in arms and legs; this is when control of muscle movement, or strength in the arms or legs, can be lost. Sense of touch can be lost so that the body is unable to feel the heat or cold or the sufferer experiences temperature inappropriately; that is, feeling heat when it is cold and vice versa. Balance can also be affected; some people may eventually have to resort to a wheelchair, either on a permanent or temporary basis. The course of the disease varies from person to person.
A diagnosis of MS is often confirmed by the use of a magnetic resonance imaging (MRI) scan, which can show defects in the brain and spinal cord. Once diagnosed, MS is a lifelong disease; no cure exists, although a number of medical treatments have been shown to reduce relapses and slow the progression of the disease. It is important that patients with the disease are diagnosed early so that treatment, which can slow the disease, can be started early.
Reading Passage 2 has ten paragraphs labeled A-J.
Which paragraph contains the following information?
Write your answers in boxes 15-19 on your answer sheet
NB. You may use any letter more than once.
15. The main types of the disease
16. Loss of the sense of feeling
17. The progress of the disease
18. Treatments for the disease
19. The effects of geography
Complete this table below.
Choose NO MORE THAN TRE WORDS from the passage for each answer.
Write your answers in boxes 20-27 on your answer sheet.
Reading Passage 3
You should spend about 20 minutes on Questions 28 – 40 , which are based on Reading Passage 3 below.
‘Tiger of the skies’
A. As a result of being separated for tens of millions of years from other mainland ecosystems such as Australia or continental Asia, the biota of New Zealand evolved to include some of the most unique plants and animals on earth. Until the arrival of humans and their associated introduced species, such as rats and dogs, New Zealand was not home to a single ground mammal, and this encouraged bird-life to prevail. Another common feature of island ecosystems, whereby some species significantly outgrow their mainland relatives, also occurred in New Zealand. From these twin forces – the dominance of birds, and the tendency toward larger body sizes in island ecosystems – emerged one of the most formidable flying predators known on earth: the Haast’s eagle.
B. The largest known eagle ever documented, this fearsome creature weighed up to fifteen kilograms and sported wings spanning two to three metres in diameter. Although this wingspan is comparatively small (the Wandering Albatross and Andean Condor, for instance, each have wing spans in excess of three metres), the Haast’s eagle possessed a much larger body mass to wing ratio. While stubbier wings made the eagle ill-suited to prolonged flight, they did enable the Haast’s eagle to nimbly and swiftly manoeuvre its large frame around trees, which would have been vital for pursuing prey through New Zealand’s dense forest and scrubland.
C. The most impressive aspect of the bird’s anatomy, however, was its enormous talons. At almost 23 centimetres in length, these are comparable to those of some wild cats and have justifiably earned the Haast’s eagle the nickname ‘Tiger of the Skies’. With these talons the eagle would attack its prey in the only way it knew how – grasping the animal’s pelvis with one talon while crushing its skull with the other in a strike that, according to New Zealand researcher Richard Holdaway, is akin to that of a 15 kilogram concrete block dropping from an eight-storey building. This force was enough to bring down very large animals, and indeed the Haast’s eagle preyed primarily on the moa – a clumsy, flightless bird nearly fifteen times its size. Once immobilised, a large catch could feed the eagle over several days. With no other large predators, the Haast’s eagle could afford to take its time with the carcass of its prey until ready to return to the hunt.
D. This leads to an important question: How did such a ferocious predator fall from the top of the food chain and rapidly become extinct around AD 1500? The answer is that, like many other extinct animals, the Haast’s eagle could not diversify its behaviours and adapt to changing circumstances quickly enough to survive. Moa, an easy source of prey for the eagle, were likewise an easy source of food for Maori tribes people when they began to settle in New Zealand around AD 1200. These settlers quickly drove the moa to extinction, and with it went the primary food supply of the Haast’s eagle. This enormous predator then faced a scarcity of food. Undoubtedly, the horror stories of human encounters with the eagle in Maori legend are true to some extent; if the Haast’s eagle could take down a two hundred kilogram moa, some Maori tribesmen would have fallen prey to its massive claws at some point. The occasional human victim was insufficient to sustain the dietary requirements of a creature its size, however, and when the moa disappeared, the Haast’s eagle soon followed.
E. Mythology surrounding the existence of the Haast’s eagle has been passed down through Maori tradition for centuries, but due to a lack of physical evidence (only three full skeletons have ever been recovered), much about this bird remains a mystery. Artists have depicted the plumage of the Haast’s eagle in different ways;; for example, some see it as more of a muted brown, in line with other large forest eagles still in existence today, whereas others envision it displaying extravagant hues of green, red and purple. All of this is speculation, however; recovered bones and further DNA evidence can tell us about the genealogy of the Haast’s eagle and its size and skeletal structure, but the colour of its feathers, along with many other specifications, will forever be guesswork.
F. It is difficult to say whether the demise of the Haast’s eagle was tragic or fortuitous. No doubt the sight of this majestic bird swooping down swooping down from its perch at eighty kilometres per hour would have been an awe-inspiring sight, and it is easy to see why some early Maori settlers exalted the eagle in their imaginations as some kind of ‘Bird God’. If it were still around, however, there is no doubt that hiking, camping or even just taking a leisurely stroll through the woods in New Zealand would be a far more dangerous activity. With a force of impact powerful enough to knock an adult male unconscious, many people would never know what had hit them.
Reading Passage 2 has six paragraphs, A–F.
Which paragraph contains the following information?
Write the correct letter, A–F, in boxes 27 – 34 on your answer sheet.
28. A discussion about whether the Haast’s Eagle killed humans
29. An explanation of how the body proportions of the Haast’s eagle made it an efficient hunter
30. The mental image that the Maori people had of the Haast’s eagle
31. Facts about the early ecology of New Zealand
32. Conflicting views on the appearance of the Haast’s eagle
33. A comparison between the Haast’s eagle and other birds
34. An explanation of why the Haast’s eagle could eat its kills slowly
Choose TWO letters, A–E .
Write the correct letters in boxes 35 and 36 on your answer sheet.
Which TWO of the following are given as reasons why the Haast’s eagle originally evolved?
A. New Zealand has many unusual birds and plants.
B. New Zealand had no natural bird predators.
C. New Zealand has no native mammals.
D. New Zealand settlers brought other creatures with them.
E. New Zealand is an isolated island.
Choose the best answer.
Write the correct letter, A–D , in box 37 on your answer sheet.
Which of the following is NOT true?
A. The Haast’s eagle could only fly for short distances.
B. The Haast’s eagle was adapted to flying through forests.
C. The Haast’s eagle’s wings were shorter than other large birds.
D. The Haast’s eagle had small but very efficient claws.
Choose TWO letters, A–E.
Write the correct letters in boxes 38 and 39 on your answer sheet.
Which TWO of the following are given as reasons why the Haast’s eagle died out very quickly?
A. The first settlers ate all the moa.
B. The eagle was hunted by the first settlers.
C. The eagle could not survive by eating people.
D. The settlers destroyed the eagle’s habitat.
E. The eagle flew slowly and was easily caught.
Choose the best answer.
Write the correct letter, A–D , in box 40 on your answer sheet.
Which of the following is NOT the author’s opinion?
A. If the Haast’s eagle had not died out it would have attacked people.
B. It is sad that the Haast’s eagle died out because it was beautiful.
C. We can understand why the first settlers worshipped the Haast’s eagle.
D. The Maori people should have preserved the Haast’s eagle.
5. Not Given
11. Biological complexity
20. Multiple sclerosis/MS
21. Relapse form
23. Where people live
27. spinal cord
35. C and E or E and C
36. C and E or E and C
38. A and C or C and A
39. A and C or C and A