Lifeboat Foundation

The Aubrey de Grey and Matthew O’Connor SENS AMA on reddit Monday 12th 11am PST.

I am Dr. Aubrey De Grey, biologist, gerontologist PhD and author of the book Ending Aging and Chief Science Officer at the SENS Research Foundation. I am here with researcher Dr. Matthew O’Connor from the MitoSENS project who is an expert on “allotopic expression” of mitochondrial genes. His team has been working on engineering mitochondrial genes to be expressed from the nucleus and targeted to the mitochondia as part of the MitoSENS approach to one of the damages of aging.

Each cell in the body is dependent on the efficient generation of cellular energy by mitochondria to stay alive. Critical to this process are genes encoded within the mitochondrial genome. Over time however, mutations in these genes occur as a result of constant exposure to reactive oxygen species produced by oxidative phosphorylation, the mitochondrial energy generation process. Unlike genes within the nucleus, mitochondria lack an efficient system to repair damaged DNA. This leads to accumulated mutations, resulting in mitochondrial defects and an increase in oxidative stress throughout the body. Closely correlated with this is the observation that organisms which age more slowly also consistently display lower rates of mitochondrial free radical damage. Thus, reversing and/or preventing damage to mitochondrial DNA may be a key factor in slowing the aging process.

Continue reading “Aubrey de Grey & Matthew O’Connor AMA! • /r/Futurology” »

DNA, our genetic material, normally has the structure of a twisted rope ladder. Experts call this structure a double helix. Among other things, it is stabilized by stacking forces between base pairs. Scientists at the Technical University of Munich (TUM) have succeeded at measuring these forces for the very first time on the level of single base pairs. This new knowledge could help to construct precise molecular machines out of DNA. The researchers published their findings in the journal Science.

Over 60 years ago, the researchers Crick and Watson identified the structure of deoxyribonucleic acid, which is more commonly known as DNA. They compared the double helix to a rope ladder that had been twisted into a spiral. The rungs of this ladder consisted of guanine/cytosine and thymine/adenine base pairs. But what keeps the DNA strands in that spiral structure?

OAHU, HAWAI’I — As thousands of government representatives and conservationists convene in Oahu this week for the 2016 World Conservation Congress, international conservation and environmental leaders are raising awareness about the potentially dangerous use of gene drives — a controversial new synthetic biology technology intended to deliberately cause targeted species to become extinct.

Members of the International Union for the Conservation of Nature (IUCN), including NGOs, government representatives, and scientific and academic institutions, overwhelmingly voted to adopt a de facto moratorium on supporting or endorsing research into gene drives for conservation or other purposes until the IUCN has fully assessed their impacts. News of the August 26 digital vote comes as an important open letter to the group is being delivered.

Scientists and environmental experts and organizations from around the globe have advocated for a halt to proposals for the use of gene drive technologies in conservation. Announced today, a long list of environmental leaders, including Dr. Jane Goodall, DBE, genetics professor and broadcaster Dr. David Suzuki, Dr. Fritjof Capra, entomologist Dr. Angelika Hilbeck, Indian environmental activist Dr. Vandana Shiva and organic pioneer and biologist Nell Newman, have lent their support to the open letter: “A Call for Conservation with a Conscience: No Place for Gene Drives in Conservation.” The letter states, in part: “Gene drives, which have not been tested for unintended consequences, nor fully evaluated for ethical and social impacts, should not be promoted as conservation tools.”

Continue reading “Genetic ‘extinction’ technology rejected” »

NICE.

Scientists at the Swiss Nanoscience Institute, the University of Basel, and the University Hospital Basel have developed and have been testing a device that can screen people with malignant melanoma for a spcific genetic mutation. About half of malignant melanoma cases involve the BRAF gene that results in rapid cell division and drugs targeting this type of cancer are available. The problem is that without knowing if a patient exhibits the mutation, it is dangerous to prescribe the medications since they will not work and will only cause additional problems.

The new device was used to analyze malignant melanoma tissue samples and to find whether the relevant genetic sequence is present. It relies on microscopic cantilevers, some of which have a coating to which the particular genetic sequence sticks to. Other cantilevers have a coating without the sequence. RNA isolated from the biopsy samples was then introduced into the device and the molecules that stuck to the cantilevers made them bend. This bending can be detected, pointing to the presence of the searched for mutation.

Continue reading “Device Detects Malignant Melanoma Type to Prescribe Proper Medication” »

The SENS Research Foundation has finally published this anticipated and important paper on mitochondrial gene transfer which has ramifications for mitochondrial diseases and more importantly one of the processes of aging. It is great to see that finally after a decade of criticism Aubrey de Grey has proven his approach is viable.

We explore the possibility of re-engineering mitochondrial genes and expressing them from the nucleus as an approach to rescue defects arising from mitochondrial DNA mutations. We have used a patient cybrid cell line with a single point mutation in the overlap region of the ATP8 and ATP6 genes of the human mitochondrial genome. These cells are null for the ATP8 protein, have significantly lowered ATP6 protein levels and no Complex V function. Nuclear expression of only the ATP8 gene with the ATP5G1 mitochondrial targeting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities but, failed to restore ATP hydrolysis and was insensitive to various inhibitors of oxidative phosphorylation. Co-expressing both ATP8 and ATP6 genes under similar conditions resulted in stable protein expression leading to successful integration into Complex V of the oxidative phosphorylation machinery. Tests for ATP hydrolysis / synthesis, oxygen consumption, glycolytic metabolism and viability all indicate a significant functional rescue of the mutant phenotype (including re-assembly of Complex V) following stable co-expression of ATP8 and ATP6. Thus, we report the stable allotopic expression, import and function of two mitochondria encoded genes, ATP8 and ATP6, resulting in simultaneous rescue of the loss of both mitochondrial proteins.

Amazing research on how PTSD can be pass down to the survivor’s offspring due to trauma altering the traumatic victim’s DNA Sequence.

Philadelphia, PA, September 1, 2016 – The children of traumatized people have long been known to be at increased risk for posttraumatic stress disorder (PTSD), and mood and anxiety disorders. However, according to Rachel Yehuda from the James J. Peters Veterans Affairs Medical Center at the Icahn School of Medicine at Mount Sinai who led a new study in Biological Psychiatry, there are very few opportunities to examine biologic alterations in the context of a watershed trauma in exposed people and their adult children born after the event.

One of the most intensively studied groups in this regard are the children of survivors of the Nazi concentration camps. From the work of Yehuda and others, there has been growing evidence that concentration camp survivors and their children might show changes in the epigenetic regulation of genes.

Epigenetic processes alter the expression of a gene without producing changes in the DNA sequence. DNA methylation is one of these epigenetic modifications, which regulates genome function through processes that add or remove a methyl group to a specific site in DNA, potentially affecting gene transcription.

Continue reading “Trauma’s epigenetic fingerprint observed in children of Holocaust survivors” »

I remember 4 years ago at a CIO Life Sciences Conference in AZ when one of the leaders over a research lab mention the desire to finally enable patients to share their entire DNA sequence on a thumb drive with their doctor in order to be treated properly as well as have insights on the patient’s future risks. However, limitations such as HIPAA was brought up in the discussion. Personally, with how we’re advancing things like synthetic biology which includes DNA data storage, cell circuitry, electronic tattoos, etc. thumb drive maybe too outdated.

The circle that is personalized medicine consists of more than just doctor, patient, and patient data. Other elements are in the loop, such as EHR systems that incorporate gene-drug information and updated clinical guidelines.

Very interesting and extremely interesting as we do more work on synthetic DNA as well.

Epigenetics isn’t limited to studying marks on chromatin; it can also put chromatin on a hair trigger, bringing spring-loaded action to its bead-on-a-string structures, exposing disease processes to transcriptional crossfire.

Chromatin proteins have expanded the mammalian synthetic biology toolbox by enabling control of active and silenced states at endogenous genes. Others have reported synthetic proteins that bind DNA and regulate genes by altering chromatin marks, such as histone modifications. Previously we reported the first synthetic transcriptional activator, the “Polycomb-based transcription factor” (PcTF), that reads histone modifications through a protein-protein interaction between the PCD motif and trimethylated lysine 27 of histone H3 (H3K27me3). Here, we describe the genome-wide behavior of PcTF. Transcriptome and chromatin profiling revealed PcTF-sensitive promoter regions marked by proximal PcTF and distal H3K27me3 binding. These results illuminate a mechanism in which PcTF interactions bridge epigenetic marks with the transcription initiation complex. In three cancer-derived human cell lines tested here, many PcTF-sensitive genes encode developmental regulators and tumor suppressors. Thus, PcTF represents a powerful new fusion-protein-based method for cancer research and treatment where silencing marks are translated into direct gene activation.