Lifeboat Foundation

Based on marketing activation events the company ran over the summer in Seattle, Austin, and Palo Alto, the outlook for their first product looks pretty rosy. They gave away bags of salad (which were clearly labeled as being gene-edited) consisting of red-and green-leaf mustard greens, and asked people to complete a short survey about it. Adams estimated that more than 6,000 people tried the salads, and over 90 percent responded that they were “very motivated” or “somewhat motivated” to buy the product.

A New Green Revolution?

Continue reading “From Pitless Cherries to Softer Kale, This Startup Is Using CRISPR to Make Better Produce” »

Ribonucleic acid (RNA) is a polymeric molecule similar to DNA that is essential in various biological roles in coding, decoding, regulation and expression of genes. Both are nucleic acids, but unlike DNA, RNA is single-stranded. An RNA strand has a backbone made of alternating sugar (ribose) and phosphate groups. Attached to each sugar is one of four bases—adenine (A), uracil (U), cytosine ©, or guanine (G). Different types of RNA exist in the cell: messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA).” RNA is an important information transmitter in our cells and acts as a blueprint for protein production. When freshly formed RNA is processed, introns are removed to produce mature mRNA coding for protein. This cutting is known as “splicing,” and it is controlled by a complex known as the “spliceosome.”

“We found a gene in worms, called PUF60, that is involved in RNA splicing and regulates life span,” says Max Planck scientist Dr. Wenming Huang who made the discovery.

This gene’s mutations resulted in inaccurate splicing and the retention of introns within certain RNAs. As a result, less of the corresponding proteins were produced from this RNA. Surprisingly, worms with the PUF60 gene mutation survived significantly longer than normal worms.

In Switzerland, cancer is the second-leading cause of death. Non-small cell lung cancer (NSCLC) is the cancer form that kills the most people and is still mostly incurable. Unfortunately, only a small percentage of patients survive the metastatic stage for a long time, and even recently approved therapies can only prolong patients’ lives by a few months. As a result, researchers are looking for innovative cancer treatments. Researchers from the University of Bern and the Insel Hospital identified new targets for drug development for this cancer type in a recent study published in the journal Cell Genomics.

They searched for novel targets in the poorly understood class of genes known as “long noncoding RNAs (Ribonucleic acids)” (lncRNAs). LncRNAs are abundant in the “Dark Matter,” or non-protein-coding DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

Even more daring, biology’s “mirror dimension” may be a springboard to engineer synthetic life forms that exist outside of nature, but are literal reflections of ourselves. To rephrase: building a mirror-image version of biology means rewriting the fundamental operating system of life.

Sound a bit too sci-fi? Let me explain. Similar to how our left hand can’t wear a right-hand glove, the building blocks of life—DNA, RNA, and proteins—are etched into specific 3D structures. Flip them around, as if reflected by a mirror, and they can no longer function inside the body. Scientists aren’t yet sure why nature picked just one shape out of two potential mirror images. But they’re ready to test it out.

A new study in Science made strides by reworking parts of the body’s protein-making machine into its mirror image. At the center is a structure called the ribosome, which intakes genetic code and translates it into amino acids—the Lego blocks for all proteins. The ribosome is an iconic cellular architecture, fused from two main molecular components: RNA and proteins.

Summary: Mutations of the PTEN gene cause neurons to grow to twice the size and form four times the number of synaptic connections to other neurons as a normal neuron. Removing the RAPTOR gene, an essential gene in the mTORC1 signaling pathway, prevents the neuronal and synaptic overgrowth associated with PTEN mutations. Using Rapamycin to inhibit mTORC1 rescues all the changes in neuronal overgrowth.

Source: the geisel school of medicine at dartmouth.

Findings from a new study published in Cell Reports, involving a collaborative effort between researchers at the Luikart Laboratory at Dartmouth’s Geisel School of Medicine and the Weston Laboratory at the University of Vermont, are providing further insight into the neurobiological basis of autism spectrum disorders (ASD) and pointing to possible treatments.

In laboratory mice, pituitary dwarfism caused by genetic reduction or elimination of the activity of growth hormone (GH) significantly extends lifespan. The effects of congenital pituitary dwarfism on human longevity are not well documented. To analyse the effects of untreated pituitary dwarfism on human lifespan, the longevity of a diverse group of widely known little people, the 124 adults who played “Munchkins” in the 1939 movie The Wizard of Oz was investigated. Survival of “Munchkin” actors with those of controls defined as cast members of The Wizard of Oz and those of other contemporary Academy Award winning Hollywood movies was compared. According to the Kaplan–Meier survival curves, survival of female and male “Munchkin” actors was shorter than cast controls and Hollywood controls of respective sexes.

Turing’s machine should sound familiar for another reason. It’s similar to the way ribosomes read genetic code on ribbons of RNA to construct proteins.

Cellular factories are a kind of natural Turing machine. What Leigh’s team is after would work the same way but go beyond biochemistry. These microscopic Turing machines, or molecular computers, would allow engineers to write code for some physical output onto a synthetic molecular ribbon. Another molecule would travel along the ribbon, read (and one day write) the code, and output some specified action, like catalyzing a chemical reaction.

Now, Leigh’s team says they’ve built the first components of a molecular computer: A coded molecular ribbon and a mobile molecular reader of the code.

Scientists have discovered the cause of a rare condition within a part of the genome that has been largely unexplored in medical genetics. A team at the University of Exeter has found genetic changes in a region that controls the activity of the genome, turning on or off genes, and in doing so they have found a key that could unlock other causes of rare conditions.

The finding, published in Nature Genetics, is a very rare case of a cause of disease that only results from changes outside the exome, the region of the genome that codes for genes. It is also the first time that changes have been shown to affect a gene—known as HK1—that does not normally have a role in the relevant body tissue—in this case, the pancreas.

Until now, scientists have typically sequenced the part of the genome that describes the genetic code of all genes in individuals with a rare disease. They do this looking for variants in the DNA that affects a protein known to have an important role in the disease-relevant organ. A good example is observed in neonatal diabetes, where genetic variants disrupt the function of the pancreatic protein insulin, causing high blood sugar levels.

Klunk and colleagues identify signatures of natural selection imposed by Yersinia pestis and demonstrate their effect on genetic diversity and susceptibility to certain diseases in the present day.