Jennifer Doudna, one of CRISPR’s primary innovators, stays optimistic about how the gene-editing tool will continue to empower basic biological understanding.
Category: genetics – Page 449
Study finds specific mechanism that protects cells from natural DNA errors
What is less known is that a more problematic source of DNA damage is normal cellular processes such as DNA replication. These cannot be avoided because they are inevitably in action every time cells divide. The scale of this problem is best illustrated by realizing that our bodies are made up by successive divisions of trillions of cells, all originating from a single fertilized egg. Every day, a quarter of a trillion cells in the adult human body continue to divide to replenish old or damaged tissue. Amongst the multitude of DNA damage incurred during each such cell division process, the most dangerous are those that can be passed on from mother cells to newly born daughter cells. This inherited DNA damage is the true ‘enemy within’ that cannot be simply avoided by changing one’s lifestyle.
Researchers from the University of Copenhagen have identified a specific mechanism that protects our cells from natural DNA errors — an ‘enemy within’ — which could permanently damage our genetic code and lead to diseases such as cancer. The study has just been published in one of the most influential scientific journals, Nature Cell Biology.
Researchers from the University of Copenhagen have discovered a mechanism that gives human cells a chance to stop piling up mutations cells replicate and divide in the body. The discovery could prove to be very useful in the development of new treatments against diseases caused by changes in human DNA such as cancer.
To limit harmful changes in the genetic code that may lead to potential diseases, the cells in our body rely on a natural defense mechanism. The new study shows how specialized proteins engulf and protect the damaged DNA and ‘escort’ it until the damage can be repaired. The researchers discovered that this process relies on precise timing and meticulous control inside the cells.
Hachimoji DNA doubles the genetic code
Researchers in the US have built an “alien” DNA system from eight building block letters, so expanding the genetic code from four and doubling its information density. The new system meets all of the requirements for Darwinian evolution and can also be transcribed to RNA. It will be important for future synthetic biology applications and expands the scope of molecular structures that might be capable of supporting life, both here on Earth and more widely in the universe.
One of the main characteristics of life is that it can store and pass on genetic information. In modern-day organisms, this is done by DNA using just four building blocks: guanine, cytosine, adenine and thymine (G, A, C and T). Pairs of DNA strands form a double helix with A bonding to T and C bonding to G.
Four more building blocks .
Synthetic DNA demonstrates just how weird aliens might be
When astronomers search the skies for signs of alien life, they tend to focus on planets that are relatively similar to Earth. But while looking for the kinds of life we know exist is a good place to start, different conditions on different planets could have led life down paths that are completely … well, alien. To demonstrate, a NASA-funded study has successfully created a new synthetic genetic system that’s a viable alternative to DNA, made with twice as many “ingredients.”
Israeli team develops way to find genetic flaws in fetus at 11 weeks
Researchers at Tel Aviv University say they have developed a new, noninvasive method of discovering genetic disorders that can let parents find out the health of their fetus as early as 11 weeks into pregnancy.
A simple blood test lets doctors diagnose genetic disorders in fetuses early in pregnancy by sequencing small amounts of DNA in the mother’s and the father’s blood. A computer algorithm developed by the researchers analyzes the results of the sequencing and then produces a “map” of the fetal genome, predicting mutations with 99 percent or better accuracy, depending on the mutation type, the researchers said in a study published Wednesday in Genome Research.
The algorithm is able to distinguish between the genetic material of the parents and that of the fetus, said Prof. Noam Shomron of Tel Aviv University’s Sackler School of Medicine led the research, in a phone interview with The Times of Israel.
A CRISPR Gene Therapy for Hutchinson-Gilford Progeria
Researchers at the Salk Institute have moved a step closer to a possible therapy for Hutchinson-Gilford progeria syndrome, a rare genetic disorder that is often described as accelerated aging, as people with it appear to age far faster than normal. Using a new CRISPR/Cas9 gene therapy in a mouse model, they were able to slow down the pace of the condition, improve health, and increase lifespan.
What is Hutchinson-Gilford progeria?
Progeria is a degenerative disorder caused by a mutation in the LMNA gene. This disease has an early onset and progresses rapidly, and animals and humans with progeria show symptoms that are similar to regular aging, only on a much-accelerated timescale, giving them drastically shorter lifespans than normal. Humans with this condition rarely live very long, with the average being only 13 years old.
Single-dose CRISPR–Cas9 therapy extends lifespan of mice with Hutchinson–Gilford progeria syndrome
Hutchinson–Gilford progeria syndrome (HGPS) is a rare lethal genetic disorder characterized by symptoms reminiscent of accelerated aging. The major underlying genetic cause is a substitution mutation in the gene coding for lamin A, causing the production of a toxic isoform called progerin. Here we show that reduction of lamin A/progerin by a single-dose systemic administration of adeno-associated virus-delivered CRISPR–Cas9 components suppresses HGPS in a mouse model.
Slowing the Aging Process
It’s inevitable in life, but aging isn’t really something people look forward to. Researchers have been seeking ways to reduce the impact of aging, not only because of vanity but also because as we age, there is a greater risk of certain serious health conditions like cancer, heart disease and neurodegenerative conditions like Alzheimer’s disease. Salk Institute scientists have now used CRISPR/Cas9, the gene-editing tool, to slow down aging. The work, reported in Nature Medicine, showed accelerated aging can be slowed in mice modeling a rare genetic disorder called Hutchinson-Gilford progeria syndrome.
“Aging is a complex process in which cells start to lose their functionality, so it is critical for us to find effective ways to study the molecular drivers of aging,” said the senior author of the report Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory. “Progeria is an ideal aging model because it allows us to devise an intervention, refine it and test it again quickly.”