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The mouse is the leading organism for disease research. A rich resource of genetic variation occurs naturally in inbred and special strains owing to spontaneous mutations. However, one can also obtain desired gene mutations by using the following processes: targeted mutations that eliminate function in the whole organism or in a specific tissue; forward genetic screens using chemicals or transposons; or the introduction of exogenous transgenes as DNAs, bacterial artificial chromosomes (BACs) or reporter constructs. The mouse is the only mammal that provides such a rich resource of genetic diversity coupled with the potential for extensive genome manipulation, and is therefore a powerful application for modeling human disease.

This case study examines a variety of biological factors that may have been involved in the 2013 dolphin "unusual mortality event" (UME) on the East Coast of the United States. The story follows a news reporter and four different scientists who are preparing their notes for speaking at a public hearing about the dolphin die-off event. After reading the story, students assume the roles of these scientists and use the jigsaw method to gather, analyze, and share information.  Due to the interdisciplinary nature of environmental toxicology, this case study exposes students to four main topics: ecology of ecosystems, endocrine system/chemical messaging, immune system function, and virus biology.

Life sciences focus on all things living, exploring the patterns, processes and relationships of organisms. The goal of life sciences is to demonstrate how unifying principles can help us to make sense of the natural world and solve problems in the world we live in. High school life sciences extend student knowledge of topics such as organisms, ecosystems, heredity and evolution, integrating a long history of scientific research from multiple fields. In high school, students will build on their conceptual understanding of life sciences by investigating and witnessing the relationships among structure and function, matter and energy, ecosystems and natural selection. Students should be able to effectively communicate facts and findings, as supported in the science literacy skills covered in the Common Core State Standards.

Life on Earth is intimately connected to the natural cycles of light and dark that make up a 24-hour day. For plants, animals, and even bacteria, these circadian rhythms control many biological functions. Humans can overrule their body clocks, but at a price: People whose circadian rhythms are regularly disrupted-by frequent jet lag or shift work, for example-are more vulnerable to diabetes, obesity, cardiovascular disease, and cancer. There are various theories to explain these associations, and researchers now have a new player to consider: the bacteria that live in the digestive tract. According to a study in mice and a small group of human volunteers, the internal clocks of these gut microbes sync up with the clocks of their hosts. When our circadian rhythms get out of whack, so do those of our bacteria.

SciGuides are a collection of thematically aligned lesson plans, simulations, and web-based resources for teachers to use with their students centered on standards-aligned science concepts. Human modifications to communities of living organisms in an ecosystem can change the function and processes of that system. The flow of energy through an ecosystem depends upon the diversity of organisms within it; therefore, when this flow is altered, substantial biological and geological changes occur. It is important that our students not only realize that when a local ecosystem is destroyed or negatively affected by human transformations (building, agriculture, technology); the effect is eventually felt globally. We cannot ignore the fact that everything we do impacts our natural environment. The main question is, "How can we be better "keepers of the Earth"?

BodyMaps is an interactive visual search tool that allows users to explore the human body in 3-D. With easy-to-use navigation, users can search multiple layers of the human anatomy, view systems and organs down to their smallest parts, and understand in detail how the human body works. Using detailed 3-D models of body parts-including muscles, veins, bones, and organs-BodyMaps offers a new way to visualize and manage your health. See how the coronary artery delivers blood to the heart, and learn how plaque build-up on artery walls leads to heart disease. Locate the exact location of a pulled muscle or broken bone, and find information on how to prevent injuries. View a cross-section of the human brain, and learn which areas control certain emotions and body functions. By offering rich, detailed anatomical images alongside links to relevant and useful health information, BodyMaps allows you to leam about your body and your health in a personalized and revolutionary new way.

Where does bread get its fluffiness? Swiss cheese its holes? And what makes vinegar so sour? These foods may taste completely different, but all of these phenomena come from microorganisms chowing down on sugar and belching up some culinary byproducts. Erez Garty shows how your kitchen functions as a sort of biotechnology lab, manned by microorganisms that culture your cuisine.

Some thyroid 101 background: Your thyroid gland is the butterfly-shaped gland at the base of your neck that secretes two all-important hormones that control major bodily functions (including how you use energy, regulate body temperature, and digest food) and organs (including the heart, brain, liver, kidneys and skin). But with hypothyroidism, your body can have normal to low thyroxine hormone levels and elevated thyroid stimulating hormone (TSH) levels. These high TSH levels are a result of an overworked pituitary gland that is trying to elevate the hormone levels in an inadequately responsive thyroid.

A decade-old technique that allows researchers to control brain function in lab animals could partially restore sight to the blind. In a trial sponsored by RetroSense Therapeutics, a startup company in Ann Arbor, Michigan, doctors will inject a harmless virus loaded with DNA from photoreceptive algae into the eyes of 15 patients suffering from retinitis pigmentosa. The experimental procedure represents the first human test of optogenetics, which is a technique that genetically modifies neurons to make them responsive to light. Doctors from the Retina Foundation of the Southwest will perform the procedure, and attempt to transfer the job duties of photoreceptor cells to different cells in the eye to restore sight.

I learned that gene expression is the process by which the information of genes is used to direct the function of cells. Gene expression is regulated in all cells because not all genes are needed all the time or under all circumstances. For example, brain cells need to express certain genes that are not needed in muscle cells, and muscle cells need to express certain genes that are not needed in brain cells. Likewise, bacteria need to express different genes depending on the availability of food and other aspects of their surroundings.

The conclusion is that the high-fat diet triggered chronic inflammation, which in turn triggered an autoimmune response in the mice's central nervous systems. Normally this response protects the brain from invaders like bacteria, but a high-saturated fat diet knocks the process off track, resulting in damage to synapses in the brain - specifically in the hippocampus. Since the hippocampus is a brain area central to memory and learning, the eventual outcome is impaired brain function. In short, the high-fat diet caused brain damage.

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.

Bipolar disorder is a common, complex genetic disorder, but the mode of transmission remains to be discovered. Many researchers assume that common genomic variants carry some risk for manifesting the disease. The research community has celebrated the first genome-wide significant associations between common single nucleotide polymorphisms (SNPs) and bipolar disorder. Currently, attempts are under way to translate these findings into clinical practice, genetic counseling, and predictive testing. However, some experts remain cautious. After all, common variants explain only a very small percentage of the genetic risk, and functional consequences of the discovered SNPs are inconclusive. Furthermore, the associated SNPs are not disease specific, and the majority of individuals with a "risk" allele are healthy. On the other hand, population-based genome-wide studies in psychiatric disorders have rediscovered rare structural variants and mutations in genes, which were previously known to cause genetic syndromes and monogenic Mendelian disorders.

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. 

The DNA in just one of your cells gets damaged tens of thousands of times per day. Because DNA provides the blueprint for the proteins your cells need to function, this damage can cause serious issues-including cancer. Fortunately, your cells have ways of fixing most of these problems, most of the time. Monica Menesini details the processes of DNA damage and repair.

DNA is an interactive Web site where students can learn about DNA and its structure and function, the scientific history of its discovery and its development into a powerful tool in biology, technology, and medicine, and about the Human Genome Project, genetic engineering, and some of the implications and ethical issues surrounding genetic technology.

Panobinostat is a new type of drug that works by blocking an enzyme responsible for modifying DNA at the epigenetic level. Epigenetics refers to chemical marks on DNA itself or on the protein "spools" called histones that package DNA. These marks influence the activity of genes without changing the underlying sequence, essentially acting as volume knobs for genes. Earlier genomic studies showed that about 80 percent of DIPG tumors carry a mutation that alters a histone protein, resulting in changes to the way DNA is packaged and tagged with those chemical marks. This faulty epigenetic regulation results in activation of growth-promoting genes that should have been turned off, and shutdown of others that should have acted as brakes to cell multiplication. Cancer is the result. Panobinostat appears to work by restoring proper functioning of the cells' chemical tagging system.

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.

This flipped case study tells the story of Joyce, a biology student who notices the development of some unusual symptoms (foot slapping and slurred speech) in her mother. In an effort to understand the cause, Joyce views a documentary-style trigger video (created by the case author) that suggests to Joyce that her mom may in fact have amyotrophic lateral sclerosis or ALS. The rest of the case walks Joyce through understanding how normal neurons compare to neurons in ALS patients and how that might affect muscle function. The case explores the link between genes, particularly SOD-1, to the formation of malformed proteins and its potential role in the development of ALS. The case concludes with a discussion of drug development and highlights the timeline and costs associated with drug discovery as Joyce becomes concerned about the lack of drugs in the pipeline for ALS, which her mother is ultimately diagnosed with. The case is appropriate for a number of classes including general biology, biotechnology, anatomy and physiology, upper level-cell biology, or any human health and disease-related course.

She wanted to understand the effects of mutations that the gene for p53 is prone to. In dozens of simulations, she and her colleagues tracked how common p53 mutations further destabilize the already floppy protein, distorting it and preventing it from binding to DNA. Some simulations also revealed something else: a fingerhold for a potential drug. Once in a while, a small cleft forms in the mutated protein's core. When Amaro added virtual drug molecules into her models, the compounds lodged in that cleft, stabilizing p53 just enough to allow it to resume its normal functions.