After eating up about one billion base pairs to fuel its synthetic biology and cell programming efforts, Ginkgo Bioworks is going back for seconds, with another large order from the DNA weaver Twis | After eating up about one billion base pairs to fuel its synthetic biology and cell programming efforts, Ginkgo Bioworks is going back for seconds, with another large order from the DNA weaver Twist Bioscience.
Scientists at The University of Texas at Austin have redesigned a key component of a widely used CRISPR-based gene-editing tool, called Cas9, to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version, making it potentially much safer.
Other labs have redesigned Cas9 to reduce off-target interactions, but so far, all these versions improve accuracy by sacrificing speed. SuperFi-Cas9, as this new version has been dubbed, is 4,000 times less likely to cut off-target sites but just as fast as naturally occurring Cas9. Bravo says you can think of the different lab-generated versions of Cas9 as different models of self-driving cars. Most models are really safe, but they have a top speed of 10 miles per hour.
“They’re safer than the naturally occurring Cas9, but it comes at a big cost: They’re going extremely slowly,” said Bravo. “SuperFi-Cas9 is like a self-driving car that has been engineered to be extremely safe, but it can still go at full speed.”
Innovations in computing tech have improved the accuracy of DNA synthesis and enabled synthetic biology to work in the real world.
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Scientists have created synthetic organisms that can self-replicate. Known as “Xenobots,” these tiny millimeter-wide biological machines now have the ability to reproduce — a striking leap forward in synthetic biology.
Published in the Proceedings of the National Academy of Sciences 0, a joint team from the University of Vermont, Tufts University, and Harvard University used Xenopus laevis frog embryonic cells to construct the Xenobots.
Their original work began in 2020 when the Xenobots were first “built.” The team designed an algorithm that assembled countless cells together to construct various biological machines, eventually settling on embryonic skin cells from frogs.
Engineers have discovered a way to more than double the lifespan of batteries used in smartphones and electric cars.
The battery breakthrough was successfully demonstrated by researchers at the University of Queensland in Australia, who increased the lifespan of a lithium-ion (li-ion) battery from several hundred charge/ discharge cycles, to more than 1,000.
“Our process will increase the lifespan of batteries in many things, from smartphones and laptops, to power tools and electric vehicles,” said Professor Lianzhou Wang from the Australian Institute for Bioengineering and Nanotechnology.
Despite a wealth of knowledge gained in the past three decades concerning the molecular underpinnings of Alzheimer’s disease (AD), progress towards obtaining effective, disease modifying therapies has proven to be challenging. In this manner, numerous clinical trials targeting the production, aggregation, and toxicity of beta-amyloid, have failed to meet efficacy standards. This puts into question the beta-amyloid hypothesis and suggests that additional treatment strategies should be explored. The recent emergence of CRISPR/Cas9 gene editing as a relatively straightforward, inexpensive, and precise system has led to an increased interest of applying this technique in AD. CRISPR/Cas9 gene editing can be used as a direct treatment approach or to help establish better animal models that more faithfully mimic human neurodegenerative diseases. In this manner, this technique has already shown promise in other neurological disorders, such as Huntington’s disease. The purpose of this review is to examine the potential utility of CRISPR/Cas9 as a treatment option for AD by targeting specific genes including those that cause early-onset AD, as well as those that are significant risk factors for late-onset AD such as the apolipoprotein E4 (APOE4) gene.
Keywords: Alzheimer’s disease, CRISPR/Cas9, Gene editing, Treatment, Huntington’s disease, iPSC neurons.
Alzheimer’s Disease (AD) is a progressive and fatal neurodegenerative disorder that primarily affects older adults and is the most common cause of dementia [1]. Currently it afflicts 5.5 million Americans and that number is expected to triple by 2050. At the present time, it is the third leading cause of death behind heart disease and cancer, with an estimated 700,000 Americans ages65 years will have AD when they die [2]. In addition, the cost of the disease is substantial with $259 billion health care dollars going to manage the disease currently, and by the middle of the century costs are predicted to soar over $1.2 trillion, which will completely bankrupt the healthcare system in the USA [3]. Worldwide, 47 million people live with dementia and that number is projected to increase to more than 131 million by 2050 with an estimated worldwide cost of US $818 billion [4].
The creation of new proteins and peptides for use with CRISPR represents the next stage in the evolution of this technology.
Janice Chen, Ph.D., one of Olympic gold medalist Nathan Chen’s siblings, is on a mission to build a $100 billion biotech company.
In 2018, she co-founded Mammoth Biosciences with Trevor Martin, Lucas Harrington and Jennifer Doudna 0, who won the Nobel Prize in Chemistry two years later for her pioneering work in CRISPR gene editing. Doudna also served as Chen’s mentor while she pursued her doctorate degree in molecular and cell biology at the University of California at Berkeley.
Mammoth is built on Chen’s work as a graduate student researcher in Doudna’s lab. Since the dawn of COVID-19 in 2020, the startup has seen accelerated growth as it snagged $100 million in multiple contracts and government grants.
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(Inside Science) — An enzyme in the bacterium E. coli made more errors copying synthetic DNA when exposed to zero gravity than the same enzyme did in normal gravity, a recent study finds.
The paper raises the possibility that some enzymes work differently in space compared to on Earth. “It gives us an idea that enzymes, like polymerases or others that are involved in maintaining the integrity of our DNA, may be influenced by spaceflight,” said Susan Bailey, a radiation cancer biologist at Colorado State University in Fort Collins who has studied DNA damage caused by space radiation and did not contribute to the new paper.
Aaron Rosenstein, lead author of the paper and a bioengineering graduate student at the University of Toronto, said the finding “warrants further investigation into other enzymes that are involved in crucial pathways that are inherent to life and survival.”
