Which technique is used to introduce genes into dicots? ?->(Show Answer!)

1. Which technique is used to introduce genes into dicots?

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MCQ->Which technique is used to introduce genes into dicots?....

MCQ-> Analyse the following passage and provide appropriate answers for questions that follow. Certain variants of key behavioural genes, “risk allele” make people more vulnerable to certain mood, psychiatric, or personality disorders. An allele is any of the variants of a gene that takes more than one form. A risk allele, then, is simply a gene variant that increases your likelihood of developing a problem. Researchers have identified a dozen - odd gene variants that can increase a person’s susceptibility to depression, anxiety and antisocial, sociopathic, or violent behaviours, and other problems - if, and only if, the person carrying the variant suffers a traumatic or stressful childhood or faces particularly trying experiences later in life. This hypothesis, often called the “stress diathesis” or “genetic vulnerability” model, has come to saturate psychiatry and behavioural science. Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. This new model suggests that it’s a mistake to understand these “risk” genes only as liabilities. According to this new thinking, these “bad genes” can create dysfunctions in unfavourable contexts - but they can also enhance function in favourable contexts. The genetic sensitivities to negative experience that the vulnerability hypothesis has identified, it follows, are just the downside of a bigger phenomenon: a heightened genetic sensitivity to all experience. This hypothesis has been anticipated by Swedish folk wisdom which has long spoken of “dandelion” children. These dandelion children - equivalent to our “normal” or “healthy” children, with “resilient” genes - do pretty well almost anywhere, whether raised in the equivalent of a sidewalk crack or well - tended garden. There are also “orchid” children, who will wilt if ignored or maltreated but bloom spectacularly with greenhouse care. According to this orchid hypothesis, risk becomes possibility; vulnerability becomes plasticity and responsiveness. Gene variants generally considered misfortunes can instead now be understood as highly leveraged evolutionary bets, with both high risks and high potential rewards. In this view, having both dandelion and orchid kids greatly raises a family’s (and a species’) chance of succeeding, over time and in any given environment. The behavioural diversity provided by these two different types of temperament also supplies precisely what a smart, strong species needs if it is to spread across and dominate a changing world. The many dandelions in a population provide an underlying stability. The less - numerous orchids, meanwhile, may falter in some environments but can excel in those that suit them. And even when they lead troubled early lives, some of the resulting heightened responses to adversity that can be problematic in everyday life - increased novelty - seeking, restlessness of attention, elevated risk - taking, or aggression - can prove advantageous in certain challenging situations: wars, social strife of many kinds, and migrations to new environments. Together, the steady dandelions and the mercurial orchids offer an adaptive flexibility that neither can provide alone. Together, they open a path to otherwise unreachable individual and collective achievements.The passage suggests ‘orchids’:
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MCQ-> Read the passage carefully and answer the questions givenGrove snails as a whole are distributed all over Europe, but a specific variety of the snail, with a distinctive white-lipped shell, is found exclusively in Ireland and in the Pyrenees mountains that lie on the border between France and Spain. The researchers sampled a total of 423 snail specimens from 36 sites distributed across Europe, with an emphasis on gathering large numbers of the white-lipped variety. When they sequenced genes from the mitochondrial DNA of each of these snails and used algorithms to analyze the genetic diversity between them, they found that. . . a distinct lineage (the snails with the white-lipped shells) was indeed endemic to the two very specific and distant places in question.Explaining this is tricky. Previously, some had speculated that the strange distributions of creatures such as the white-lipped grove snails could be explained by convergent evolution—in which two populations evolve the same trait by coincidence—but the underlying genetic similarities between the two groups rules that out. Alternately, some scientists had suggested that the white-lipped variety had simply spread over the whole continent, then been wiped out everywhere besides Ireland and the Pyrenees, but the researchers say their sampling and subsequent DNA analysis eliminate that possibility too. “If the snails naturally colonized Ireland, you would expect to find some of the same genetic type in other areas of Europe, especially Britain. We just don’t find them,” Davidson, the lead author, said in a press statement.Moreover, if they’d gradually spread across the continent, there would be some genetic variation within the white-lipped type, because evolution would introduce variety over the thousands of years it would have taken them to spread from the Pyrenees to Ireland. That variation doesn’t exist, at least in the genes sampled. This means that rather than the organism gradually expanding its range, large populations instead were somehow moved en mass to the other location within the space of a few dozen generations, ensuring a lack of genetic variety.“There is a very clear pattern, which is difficult to explain except by involving humans,” Davidson said. Humans, after all, colonized Ireland roughly 9,000 years ago, and the oldest fossil evidence of grove snails in Ireland dates to roughly the same era. Additionally, there is archaeological evidence of early sea trade between the ancient peoples of Spain and Ireland via the Atlantic and even evidence that humans routinely ate these types of snails before the advent of agriculture, as their burnt shells have been found in Stone Age trash heaps.The simplest explanation, then? Boats. These snails may have inadvertently traveled on the floor of the small, coast-hugging skiffs these early humans used for travel, or they may have been intentionally carried to Ireland by the seafarers as a food source. “The highways of the past were rivers and the ocean-as the river that flanks the Pyrenees was an ancient trade route to the Atlantic, what we’re actually seeing might be the long lasting legacy of snails that hitched a ride…as humans travelled from the South of France to Ireland 8,000 years ago,” Davidson said.The passage outlines several hypotheses and evidence related to white-lipped grove snails to arrive at the most convincing explanation for:
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MCQ-> Cells are the ultimate multi-taskers: they can switch on genes and carry out their orders, talk to each other, divide in two, and much more, all at the same time. But they couldn’t do any of these tricks without a power source to generate movement. The inside of a cell bustles with more traffic than Delhi roads, and, like all vehicles, the cell’s moving parts need engines. Physicists and biologists have looked ‘under the hood’ of the cell and laid out the nuts and bolts of molecular engines.The ability of such engines to convert chemical energy into motion is the envy nanotechnology researchers looking for ways to power molecule-sized devices. Medical researchers also want to understand how these engines work. Because these molecules are essential for cell division, scientists hope to shut down the rampant growth of cancer cells by deactivating certain motors. Improving motor-driven transport in nerve cells may also be helpful for treating diseases such as Alzheimer’s, Parkinson’s or ALS, also known as Lou Gehrig’s disease.We wouldn’t make it far in life without motor proteins. Our muscles wouldn’t contract. We couldn’t grow, because the growth process requires cells to duplicate their machinery and pull the copies apart. And our genes would be silent without the services of messenger RNA, which carries genetic instructions over to the cell’s protein-making factories. The movements that make these cellular activities possible occur along a complex network of threadlike fibers, or polymers, along which bundles of molecules travel like trams. The engines that power the cell’s freight are three families of proteins, called myosin, kinesin and dynein. For fuel, these proteins burn molecules of ATP, which cells make when they break down the carbohydrates and fats from the foods we eat. The energy from burning ATP causes changes in the proteins’ shape that allow them to heave themselves along the polymer track. The results are impressive: In one second, these molecules can travel between 50 and 100 times their own diameter. If a car with a five-foot-wide engine were as efficient, it would travel 170 to 340 kilometres per hour.Ronald Vale, a researcher at the Howard Hughes Medical Institute and the University of California at San Francisco, and Ronald Milligan of the Scripps Research Institute have realized a long-awaited goal by reconstructing the process by which myosin and kinesin move, almost down to the atom. The dynein motor, on the other hand, is still poorly understood. Myosin molecules, best known for their role in muscle contraction, form chains that lie between filaments of another protein called actin. Each myosin molecule has a tiny head that pokes out from the chain like oars from a canoe. Just as rowers propel their boat by stroking their oars through the water, the myosin molecules stick their heads into the actin and hoist themselves forward along the filament. While myosin moves along in short strokes, its cousin kinesin walks steadily along a different type of filament called a microtubule. Instead of using a projecting head as a lever, kinesin walks on two ‘legs’. Based on these differences, researchers used to think that myosin and kinesin were virtually unrelated. But newly discovered similarities in the motors’ ATP-processing machinery now suggest that they share a common ancestor — molecule. At this point, scientists can only speculate as to what type of primitive cell-like structure this ancestor occupied as it learned to burn ATP and use the energy to change shape. “We’ll never really know, because we can’t dig up the remains of ancient proteins, but that was probably a big evolutionary leap,” says Vale.On a slightly larger scale, loner cells like sperm or infectious bacteria are prime movers that resolutely push their way through to other cells. As L. Mahadevan and Paul Matsudaira of the Massachusetts Institute of Technology explain, the engines in this case are springs or ratchets that are clusters of molecules, rather than single proteins like myosin and kinesin. Researchers don’t yet fully understand these engines’ fueling process or the details of how they move, but the result is a force to be reckoned with. For example, one such engine is a spring-like stalk connecting a single-celled organism called a vorticellid to the leaf fragment it calls home. When exposed to calcium, the spring contracts, yanking the vorticellid down at speeds approaching three inches (eight centimetres) per second.Springs like this are coiled bundles of filaments that expand or contract in response to chemical cues. A wave of positively charged calcium ions, for example, neutralizes the negative charges that keep the filaments extended. Some sperm use spring-like engines made of actin filaments to shoot out a barb that penetrates the layers that surround an egg. And certain viruses use a similar apparatus to shoot their DNA into the host’s cell. Ratchets are also useful for moving whole cells, including some other sperm and pathogens. These engines are filaments that simply grow at one end, attracting chemical building blocks from nearby. Because the other end is anchored in place, the growing end pushes against any barrier that gets in its way.Both springs and ratchets are made up of small units that each move just slightly, but collectively produce a powerful movement. Ultimately, Mahadevan and Matsudaira hope to better understand just how these particles create an effect that seems to be so much more than the sum of its parts. Might such an understanding provide inspiration for ways to power artificial nano-sized devices in the future? “The short answer is absolutely,” says Mahadevan. “Biology has had a lot more time to evolve enormous richness in design for different organisms. Hopefully, studying these structures will not only improve our understanding of the biological world, it will also enable us to copy them, take apart their components and recreate them for other purpose.”According to the author, research on the power source of movement in cells can contribute to
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