Teach genetics first and then teaching evolution could be a breeze. Source: Shutterstock

Evolution is one of the trickiest subjects to teach and not just because some people find it controversial. The ideas are subtle, the language and concepts can be confusing how many of us have thought survival of the fittest was an encouragement to go to the gym. Many studies have sought to discover the reasons why evolution is so difficult for students to understand and accept, but few have attempted to find ways to improve the understanding of evolution in the classroom.

As there is such a direct connection between genetics and evolution, we thought perhaps if you teach genetics first, this might help students understand evolution better. Our large randomised control trial of UK secondary school students, published in PLOS Biology, showed this to be true to a surprising degree.

It seemed intuitive to us a good understanding of genetics should help theunderstanding of evolution DNA is the heritable material through which variation needed for evolution occurs. If you understand DNA, you can understand what mutations are. And if you understand what mutations are, you can understand they can change frequency in populations and bingo, evolution can happen.

In its simplest, evolution is no more than mutations changing frequency. The differences between species started out as new mutations that went from being rare within one species, but then became very common.

While this connection might seem self-evident, genetics and evolution are typically taught to 14 to 16-year-old secondary school students as separate topics with few links and in no particular order. Sometimes theres a large time span between the two. Our idea was simple teach genetics first and look at how that affects the understanding and acceptance of evolution.

Using questionnaires, we conducted a study of almost 2,000 students over three years. Importantly, all that was changed in our study was the order of the teaching material exactly what was to be taught was left to the teachers. This meant our study was a realistic mimic of what would happen should any switch be made. We tested students before and after the two subjects were taught and so could examine the extent to which students improved in their understanding.

Not your grandfathers great-grandfather. Source: Flickr/Afrika Force

Schools typically split students by their ability, into higher level and foundation level classes. Importantly, we found both ability groups did best when taught genetics first.

An understanding of evolution and acceptance of the idea of evolution are two different things. Acceptance is the belief the scientific view of evolution is the correct version you can understand evolution but not accept it and you can accept it but not understand it.

We found students typically accepted evolution to a greater degree after taking the evolution class. Both before and after testing, the students with a better understanding were those with higher levels of acceptance. However, these effects were not strong.

We also set up a series of focus groups to find out why the understanding and acceptance of evolution are not more strongly coupled. Evidence from these suggests what is more important for evolution acceptance is not what is taught, but who provides the endorsement. For some students, being told key authority figures such as parents or teachers approve of scientific evidence for evolution made a big difference to their ability to accept it.

Television documentaries were commonly given as a source of reassurance about evolution, and some students felt these, and their presenters, were important in helping them accept evolution. Perhaps more predictable, religious leaders, and their views on evolution, were also of key importance. For students from a Catholic background, being told the Pope approves of evolution was important in helping them to approach evolution as any other science.

Our study was not designed to investigate why teaching order has an effect. Ordering effects like the one we looked at have been seen before indeed, in the field of artificial intelligence, there are cases where ordering matters for computers to learn too. But why does the order matter? Our original idea was what psychologists called priming preloading with some facts to make it easier to take in other information.

But could it also be that teaching genetics first minimises the disruption to understanding that can happen when people think that their beliefs are being questioned or challenged? Many students told us that the perceived conflict between their religious views and the science made it hard for them to study evolution.

Perhaps helping them understand that mutations can change frequency under the banner of genetics enabled students to learn with less of a clash of ideas? We suggest a simple test: dont teach students material labelled as evolution, teach it as population genetics instead and then tell them after the fact that they have just learned about evolution.

Whatever the underlying cause, the data suggest a really simple, minimally disruptive and cost-free modification to teaching practice: teach genetics first. This will at least increase evolution understanding, if not acceptance. As with many emotive subjects, it takes more than teaching the facts to shift hearts as well as minds.

ByLaurence D. Hurst, Professor of Evolutionary Genetics at The Milner Centre for Evolution, University of Bath; Momna Hejmadi, Associate professor, University of Bath, and Rebecca Mead, Postdoctoral Researcher of Education, University of Bath

This article was originally published on The Conversation. Read the original article.

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Best way to get children to understand evolution? Teach genetics first - Study International News

By Natalie Grover and Bill Berkrot

Merck & Co's immunotherapy Keytruda chalked up another approval on Tuesday as the U.S. Food and Drug Administration said the cancer medicine can be used to treat children and adults who carry a specific genetic feature regardless of where the disease originated.

It is the first time the agency has approved a cancer treatment based solely on a genetic biomarker.

"Until now, the FDA has approved cancer treatments based on where in the body the cancer started - for example, lung or breast cancers," said Richard Pazdur, head of oncology products for the FDA's Center for Drug Evaluation and Research. "We have now approved a drug based on a tumor's biomarker without regard to the tumor's original location."

The accelerated approval was for solid tumor cancers not eligible for surgery or that have spread in patients identified as having a biomarker called microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR).

Tumors with those traits are most common in colorectal, endometrial and gastrointestinal cancers, but may also appear in cancers of the breast, prostate, bladder and thyroid gland.

The approval covers patients whose cancer has progressed despite prior treatment and those who have no satisfactory alternative treatment options. It also includes patients with colorectal cancer whose disease has advanced after chemotherapy.

The FDA grants accelerated approvals to drugs for serious conditions with unmet medical needs if the treatment appears to have certain effects deemed reasonably likely to predict a clinical benefit. Merck must still conduct studies to confirm the anticipated benefit.

Keytruda belongs to a new class of drugs called PD-1 or PD-L1 inhibitors that help the immune system fight cancer by blocking a mechanism tumors use to evade detection.

It was previously approved to treat advanced melanoma, advanced non-small cell lung cancer, head and neck cancers and classical Hodgkin lymphoma.

Merck shares rose 0.8 percent to $64.55.

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FDA Clears First Cancer Drug Based on Genetics of Disease, Not Tumor Location - Scientific American

May 25, 2017 A fruit fly wing, tagged with fluorescence to study gene development. Credit: McKay Lab (UNC-Chapel Hill)

Every animal starts as a clump of cells, which over time multiply and mature into many different types of cells, tissues, and organs. This is fundamental biology. Yet, the details of this process remain largely mysterious. Now, scientists at the University of North Carolina at Chapel Hill have begun to unravel an important part of that mystery.

Using the fruit fly Drosophila, a standard lab model for studying animal biology, the researchers discovered a cascade of molecular signals that program gene activity to drive the fly from one stage of maturation to the next, like a baby turning into an adult. Part of this programming, they found, involves alterations to the way DNA is packaged. Those alterations open up certain regions of DNA to allow gene activity and close off other regions to prevent gene activity. The scientists found evidence that these changes to DNA accessibility occur in sequence.

"We're finally getting at one of the core mechanisms in biology, which determine the timing and sequence of events in normal animal development at the level of our genes," said Daniel J. McKay, PhD, assistant professor of genetics at the UNC School of Medicine and biology at the UNC College of Arts and Sciences.

This basic biology finding could have significance for human health, too. The changes to cell reprogramming that the scientists observed in the young flies can occur inappropriately in adult human cells - spurring cancer, for example.

"We hope that this work will help us better understand what goes awry in cancer and other diseases," McKay said.

In the study, published in Genes & Development, McKay and colleagues began by examining the molecular impact of the fruit fly hormone ecdysone, which causes a young insect to shed its old form and adopt a new one as it moves toward maturity.

Scientists know that ecdysone binds to a receptor, EcR, in the nuclei of cells throughout the bodies of insects. EcR is a transcription factor, a genetic master switch. When bound by ecdysone, it turns on a particular set of genes. And those genes, in turn, are involved in the development of proteins - the machines of biology.

Analyzing Drosophila wing cells, McKay and colleagues found evidence that wing development occurs via a cascade of these changes in gene activity.

"We found first-tier genes that respond immediately to ecdysone, and then they - together with EcR - activate a second tier of genes, and then these two tiers of genes, operating in concert, act on a third tier," said McKay. "So we observed these waves of changes in gene expression that drive the development of wing tissue."

Using genome-wide sequencing technologies, McKay's team found that these changes in gene expression are associated with changes in the way DNA is "packaged."

DNA is looped around support proteins called histones, and this histone-DNA combination is called chromatin.

When chromatin is relatively loose and open, genes can become active. When chromatin is tight and closed, genes are mostly silenced. McKay and colleagues found that ecdysone activates some genes to produce special transcription factor proteins that open or close chromatin. This altering of chromatin represents a fundamental reprogramming of cells.

McKay and colleagues had shown in prior work that the pattern of chromatin accessibility in the fruit fly appears to change significantly over the course of development but can be very similar at any given time across fly tissues.

To the scientists, these findings collectively suggest that changes in chromatin leads to cascades of gene activity that drive fly development. That is, chromatin changes - over time - would help enforce the timing of the various processes underway during biological development. And these changes represent an important developmental mechanism, one that is likely at work in humans.

McKay and his team plan further research to study how these cascades of changing chromatin accessibility and gene activity differ from one part of the fly to another.

As McKay notes, this area of investigation could have relevance beyond developmental biology. The expression of growth and survival genes is normal during early biological development - when we're young. But cancerous cells, for example, use those genes to sustain runaway proliferation to cause disease.

Therefore, understanding the molecular factors that open or close chromatin - and allow or shut down the activity of these powerful genes - may give biologists a better picture of how cancers arise. Armed with that knowledge, scientists could try to create more precise weapons with which to fight cancer cells.

Explore further: Altered primary chromatin structures and their implications in cancer development

More information: Christopher M. Uyehara et al, Hormone-dependent control of developmental timing through regulation of chromatin accessibility, Genes & Development (2017). DOI: 10.1101/gad.298182.117

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Living cells must constantly process information to keep track of the changing world around them and arrive at an appropriate response.

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In fruit fly and human genetics, timing is everything - Phys.Org