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"CRACKING THE CODE"/"Cloning Paper Plasmid" activities can (1) serve as a review of the "genetic code" and the role it plays in our life; and, (2) to help students see how genes may be manipulated for genetic research, namely, gene cloning/genetic engineering. The laboratory time, the specialized equipment and expertise to carry out recombinant DNA experiments may be lacking in the high school. Activity 2 will help students conceptualize the mechanics involved in cutting and ligating DNAs into a plasmid vector with "sticky ends" of complementary DNA base pairs.

7:00 video: This film is the first of a two part series on the evolution of new genetic information. Here we focus on Point Mutations - the simplest natural mechanisms known to increase the genetic information of a population. Our second film of the series will focus on duplication events - natural mutations that increase the total amount of genetic information of an individual. This film was produced under the guidance of molecular biologist Dr. Nicholas Casewell. http://www.lstmed.ac.uk/about/people/... Point mutations are small, natural edits in the DNA code of an individual. These edits can be passed from parent to child. Because they are mere edits, point mutations usually do not increase the total amount of information in an individual. As new information is gained, old information is lost. Point mutations do, however, increase the total amount of information within a population. In this film you will see several examples of beneficial point mutations which have enhanced a creatures abilities or even given rise to entirely new abilities. The first two examples were directly observed in bacteria by scientists in the lab. The third is a case found in domestic dogs, the last example was discovered in several species of wild animal.

This directed case study follows the story of "Pauline," a 20-year-old college student who has just received results from a personal genetic testing kit she purchased online. The report shows a negative result for variants of the BRCA 1 and 2 genes, which are associated with a greater risk for breast cancer. Although Pauline has a family history of breast cancer, she concludes that she no longer needs to be concerned, or does she? As students work through the questions in this case study, they review the role of genes and how they code for proteins as well as the effects of proteins on health, especially on cellular growth regulation and cancer. They also learn about the process of genetic testing and consider the ramifications of positive and negative tests for diseases or health conditions, especially with respect to breast cancer. The case is designed for non-science majors in a scientific methods course and could also be used in an introductory biology course. The questions in the case could be adapted for an upper level genetics class.

In our first animation of this series we learned how point mutations can edit genetic information. Here we see how duplication events can dramatically lengthen the genetic code of an individual. As point mutations add up in the duplicated region across generations, entirely new genes with new functions can evolve. In the video we see three examples of gene duplications resulting in new traits for the creatures who inherit them: the evolution of a venom gene in snakes, the evolution of leaf digestion genes in monkeys, and the evolution of burrowing legs in hunting dogs.

Researchers led by Terra D. Barnes of Washington University discovered that their genetically-engineered mice stutter due to DNA defects in a humdrum "housekeeping" gene. This gene codes for a protein that simply places a "routing tag" on certain enzymes that shred cellular trash. The tag ensures that the shredding enzymes end up in chambers called lysosomes, basically the cell's garbage disposal. It's a mundane cellular activity, yet mutations in the same process in humans have also been linked to stuttering-a bizarrely specific condition for such a general gene. And, so far, scientists have no idea why the two are linked.

By early 2014, Flint, Kendler and a team of collaborators had analysed DNA sequences from 5,303 Chinese women with depression, and another 5,337 controls. As Flint expected, 85% of the depressed women had a severe form of the disorder called melancholia, which robs people of the ability to feel joy. "You can be a doting grandparent and your favourite grandchildren can show up at your door," says Douglas Levinson, a psychiatrist at Stanford University in California, "and you can't feel anything." The analysis yielded two genetic sequences that seemed to be linked to depression: one in a stretch of DNA that codes for an enzyme whose function is not fully understood, and the other next to the gene SIRT1, which is important for energy-producing cell structures called mitochondria. The correlations were confirmed in another set of more than 3,000 depressed men and women and over 3,000 controls.

Why does a snake have 25 or more rows of ribs, whereas a mouse has only 13? The answer, according to a new study, may lie in "junk DNA," large chunks of an animal's genome that were once thought to be useless. The findings could help explain how dramatic changes in body shape have occurred over evolutionary history. Scientists began discovering junk DNA sequences in the 1960s. These stretches of the genome-also known as noncoding DNA-contain the same genetic alphabet found in genes, but they don't code for the proteins that make us who we are. As a result, many researchers long believed this mysterious genetic material was simply DNA debris accumulated over the course of evolution. But over the past couple decades, geneticists have discovered that this so-called junk is anything but. It has important functions, such as switching genes on and off and setting the timing for changes in gene activity. 

Images collection for genetic topics from the Smithsonian Museum of Natural History

On June 14, 2013, the Smithsonian Institution in Washington, D.C. opened the high-tech, high-intensity exhibition Genome: Unlocking Life's Code to celebrate the 10th anniversary of researchers producing the first complete human genome sequence - the genetic blueprint of the human body - in April 2003. The exhibition is a collaboration between the Smithsonian's National Museum of Natural History (NMNH) and the National Human Genome Research Institute (NHGRI) of the National Institutes of Health.

Because the gene-enzyme system forms a closed loop, it presents us with a classic chicken or egg conundrum: Which came first, genes or the protein enzymes they code for? While the details are still not fully worked out, discoveries over the past few decades have lead researchers to a surprising possible solution: What really came first? Genes that act as enzymes! The RNA World Hypothesis is the idea that before living cells, the genetic code, and the gene/protein cycle ever existed, chains of a chemical called RNA were forming naturally. Once formed, some of these chains were able to function as enzymes, and were even able to evolve by making copies of themselves with slight, accidental modifications.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum - that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. "Genetic function somehow springs into existence," said David Begun, a biologist at the University of California, Davis.

Humans may in part owe their big brains to a DNA "typo" in their genetic code, research suggests. The mutation was also present in our evolutionary "cousins" - the Neanderthals and Denisovans. However, it is not found in humans' closest living relatives, the chimpanzees. As early humans evolved, they developed larger and more complex brains, which can process and store a lot of information. Last year, scientists pinpointed a human gene that they think was behind the expansion of a key brain region known as the neocortex.

Normally, male squirrel monkeys can't distinguish between red and green hues-they're what is called color-blind in humans. The South American Saimiri genus lacks a gene that allows color-sensitive cells in the eye, called cones, to differentiate red and green from gray. To these animals, other colors, such as blue, brown and orange, appear faded. But Sam was one of two males in the experimental group of a groundbreaking 2009 ophthalmological study conducted at the Washington National Primate Research Center in Seattle. Husband-and-wife vision researchers Jay and Maureen Neitz injected a viral vector behind the retinas, the part of the eye that responds to color, of Sam and his simian lab partner, Dalton. The virus contained the genetic code in human eyes for red pigment, giving the monkeys an extra class of cone photoreceptor.

This two-hour special, hosted by ABC "Nightline" correspondent Robert Krulwich, chronicles the fiercely competitive race to capture one of the biggest scientific prizes ever: the complete letter-by-letter sequence of genetic information that defines human life-the human genome. NOVA tells the story of the genome triumph and its profound implications for medicine and human health.

This directed case study examines the molecular basis of cystic fibrosis to emphasize the relationship between the genetic code stored in a DNA sequence and the encoded protein's structure and function. Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) protein that functions to help maintain salt and water balance along the surface of the lung and gastrointestinal tract. This case introduces students to "Maggie," who has just been diagnosed with cystic fibrosis. The students must identify the mutation causing Maggie's disease by transcribing and translating a portion of the wildtype and mutated CFTR gene. Students then compare the three-dimensional structures of the resulting proteins to better understand the effect a single amino acid mutation can have on the overall shape of a protein. Students also review the concepts of tonicity and osmosis to examine how the defective CFTR protein leads to an increase in the viscosity of mucus in cystic fibrosis patients. This case was developed for use in an introductory college-level biology course but could also be adapted for use in an upper-level cell or molecular biology course.

3:16 video

Origins of life with self-replicating molecules