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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.

"This modular case study tells the story of Dan and Annie, a married couple of Acadian ancestry who have a genetic form of deafblindness called Usher syndrome. They live in Southwest Louisiana, home of the largest population of DeafBlind citizens in the United States. Acadian Usher syndrome is caused by an allele of the USH1C gene that came to Louisiana with the first Acadian settlers from Canada who founded today's Cajun population. This allele's single nucleotide substitution creates an erroneous splice site that produces a defective cytoskeletal protein (harmonin) of the cochlear and vestibular hair cells and retinal photoreceptors. This splice site is the target of a promising gene therapy. The case study applies and connects Mendelian inheritance, chromosomes, cell division, vision and hearing, DNA sequences, gene expression, gene therapy and population genetics to a specific gene and its movement through generations of Dan and Annie's families.  After the introduction, each of the remaining sections can be used independently either for in-class team activities or out-of-class extensions or assignments over an entire year of introductory undergraduate biology. "

n this interrupted case study, students learn about the influence of early fetal nutritional conditions on the expression of genes related to metabolism and growth. Beginning with the true event of a food and fuel embargo that led to famine in the western Netherlands toward the end of World War II, students learn about the historical background of the Dutch Hunger Winter and its social impact. Using real data from the study conducted by Heijmans and coauthors (2008), students then compare the methylation level of a specific gene between individuals conceived during the famine and their unaffected siblings, and how changes in the expression of this metabolically important gene may impact the risk of developing type 2 diabetes. Supported by other studies on mice and in humans, students conclude that in utero events may impact the health of individuals later in life through epigenetic mechanisms. The case is ideally suited for a molecular or cell biology course, but is also appropriate for an introductory biology course in which students have an understanding of descriptive statistics, interpretation of statistical test results, eukaryotic gene structure, and regulation of gene expression.

At first, the researchers assumed that genes would shut down shortly after death, like the parts of a car that has run out of gas. What they found instead was that hundreds of genes ramped up. Although most of these genes upped their activity in the first 24 hours after the animals expired and then tapered off, in the fish some genes remained active 4 days after death.

The study is the first to examine all of the gene networks affected by fructose that result in changes to brain function and metabolism-more than 20,000 genes in total. Although the study was conducted using rats, the researchers report that the majority of the sequenced genes are comparable to those in humans, including more than 200 genes in the hippocampus, a brain area crucial to memory, and 700 in the hypothalamus, the seat of the brain's metabolic control center.

The activity of some of our genes varies with the seasons throughout the year. The discovery comes from an analysis of blood samples from more than 16,000 people in both hemispheres. The most striking pattern was that 147 genes involved in the immune system made it more reactive or "pro-inflammatory" during winter or rainy seasons, probably to battle the onslaught of cold and flu viruses

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. 

Explore gene regulation with the Amoeba Sisters, including the fascinating Lac Operon found in bacteria! Learn how genes can be turned "on" and "off" and why this is essential for cellular function.

In a study published Thursday in the journal Science, they report that they've pinpointed the bit of finch DNA behind the swift transition: a gene called HMGA2. In finches, HMGA2 seems to be the primary factor in beak size - like a really good group project leader, it orchestrates the expression of a number of other genes, each of which tweaks the size of the bird's beak. The same gene also appears in dogs, horses, even humans, holding sway over body size and stature.

Early-response genes, which are important for synaptic plasticity, are "switched off" under basal conditions by topological constraints. Neuronal activity triggers DNA breaks in a subset of early-response genes, which overrides these topological constraints, and "switches on" gene expression.

Sometimes, a genetic tweak can make a really big difference in an animal's appearance. That's what likely happened when the predecessors of modern snakes lost their legs, a process that started some 150 million years ago, two separate groups of scientists have discovered. Although the teams took very different approaches to solve the mystery of how those limbs vanished, both came up with similar results: Mutations in DNA located near a gene key to limb formation keep that gene from ever turning on, they report today.

Unprecedented multiple and extreme-level resistance is generated in mosquitoes found in the rice fields of Tiassalé in southern Côte d'Ivoire. A new study highlights the combination of stringently-replicated whole genome transcription profiling, in vivo transgenic gene expression and in vitro metabolism assays to identify and validate genes from the P450 detoxification enzyme superfamily which are highly expressed in the adult females from the area.

"Some of the most exciting things that we've seen from looking at gene expression in space is that we really see an explosion, like fireworks taking off, as soon as the human body gets into space," Twins Study principal investigator Chris Mason said in a statement.

Current CRISPR-based screens often mutate the beginning of a gene, which sometimes results in the expression of a functional protein variant. To circumvent this problem, researchers at Cold Spring Harbor Laboratory (CSHL) designed CRISPR guide RNAs that would mutate the portion of a gene encoding a domain on the surface of the protein where a small molecule could bind to alter the protein's function. The team had previously identified such a binding pocket on the protein BRD4, and a small molecule inhibitor that binds in the pocket is an effective leukemia treatment.

Research on a modified protein around which DNA is wrapped sheds light on how gene regulation is linked to aging and longevity in nematodes, fruit flies and possibly humans. The research has implications for how gene expression is regulated, and could offer a new drug target for age-related diseases.

Your ancestors' lousy childhoods or excellent adventures might change your personality, bequeathing anxiety or resilience by altering the epigenetic expressions of genes in the brain.

Almost every cell in your body has the same DNA sequence. So how come a heart cell is different from a brain cell? Cells use their DNA code in different ways, depending on their jobs. Just like orchestras can perform one piece of music in many different ways. A cell's combined set of changes in gene expression is called its epigenome. This week Nature publishes a slew of new data on the epigenomic landscape in lots of different cells. Learn how epigenomics works in this video. Read the latest research on epigenetics at http://www.nature.com/epigenomeroadmap

Even if you look like your mother, an innovative study suggests that not only humans but, in fact, all mammals are genetically more like Dad. We inherit equal amounts of genetic material from each parent, yet that coming from our father's side is more likely to take action, according to the study that was published in the journal Nature Genetics.

Through this method, the researchers were able to identify that the frizzled-6 gene was expressed around eight times more in tumor-forming cell lines. The specific cascade initiated by frizzled-6 and how it affects the development of cancerous cells has yet to be determined. The overexpression of frizzled-6 suggests that the protein either forms tumor cells directly or is an indirect result of other mutated pathways.

The behavior of a person's genes doesn't just depend on the genes' DNA sequence - it's also affected by so-called epigenetic factors. Changes in these factors can play a critical role in disease.