Further, the researchers linked an additional enzyme—a uracil-DNA glycosylase inhibitor—to the Cas9-deaminase complex, increasing the efficiency of the complex in creating cytosine-to-thymine substitutions and minimizing the creation of inadvertent deletion mutations in mammaIian cell lines.
The modified gene-editing complex also worked well in mammalian cell lines and resulted in relatively few off-target mutations. In yeast, expression of either version of the DNA-editing complex resulted in better growth compared to cells that expressed the standard CRISPR/Cas9 system, suggesting that the new tool is also less toxic.
The so-called Target-AID complex had high specificity, modifying a cytosine within a three to five base pair window within the target gene, the team reported. “We were surprised that the mutation window was so very narrow,” said Nishida.
By comparison, Liu and his colleagues reported variants of their base-editing tool—using a deaminase derived from rats—with windows ranging between three and six nucleotides. “To be maximally useful, the base-editing window needs to be neither too wide nor too narrow so it is helpful that both of these approaches offer researchers more choices, increasing the chance that they can solve their base-editing need,”
archive.is
Science Updates August 2016
soon the bourgs will be immortal
so will we comrade, long live anarcho-tranhumanism!!
how? they will attempt to adopt it early with their massive money
I don't understand a drop of what's being said here. Somebody give it to me quick and dirty.
Scientists are getting better at creating zombie viruses.
I'm thinking bullets will still do the trick.
sadly, like most invention this will end up being used for military purpose.
i smell bio-ethnic weapon, able to target the specific DNA of the enemy.
the future seem to be getting darker, just pray to god this doesn't end up in the wrong hand while you're in the wrong ethnicity
Why not all ethnicities?
Each side tries to target a "race" and there being more than two sides several of them fail and their viruses begin targeting all humans. Finding vaccines for several different types of wildly infectious deadly viruses becomes impossible as they continue mutating.
one way or another, its highly likely that no human will be left alive after ww3
The machines will pick up the mantle.
Up.
I guarantee they're up to some shady shit with this. Potential planned mass depopulation of the proles incoming.
CRISPR has been giving me a raging stiffie since I heard of it.
I am perfectly fine with this.
As a transhumanist, why would you maintain a sexuality? You are intelligent enough to know you must breed and such things, without being distracted by it during research.
Because discarding asexual reproduction to "avoid distraction" is kind of stupid.
ILLOGICAL. DOES NOT COMPUTE.
That should be "discarding sexual reproduction".
Is that the argument because I refuted it before I finished writing my last post.
You are intelligent enough to bypass most instincts and desires and also to make yourself any goals you believe are favorable to your being. Sexuality that isn't for reproduction is largely an empty rush like going after sugars and fats.
It is not that you would be incapable of this type of reproduction but that you would not be overwhelmed by the attempts at it, most of which would fail.
Instead you would use all types of reproduction from asexual cloning to genetic engineering which includes old fashioned sexual mixture with unknown mates in the middle of the spectrum. So why waste your mind resources for a low success rate activity with a fleeting pleasure reward?
Mind you that since you have become transhumanist, increasing your mood levels is much more under your control. You have rewired your brain to be immune to addictions.
Because that would be losing the forest for the trees. Sex is a fun bonding experience. So is having drinking buddies. So is camping together. Elevating what humans can do doesn't mean losing touch with what it means to be human.
Your prewritten reply is insufficient as a rebuttal to my points.
Your desire for fruitless activities bars you from accomplishing fuck all.
How does I splice luciferin into my genome?
It'd probably be easiest to splice a bit of code into the genes activated in pigment cells that would translate into rna sequences that code for proteins needed to produce luceferin.
The real question is what would happen to your level of homeostasis if we did that.
Test it on rat, first.
That's usually what we do.
and this often delays research we know will work fine on humans because rats arent exactly humans
many effective medical techniques have been delayed by these red tape rules and only vindicated or made obsolete when tissue growth in the lab was used to test on human cells which gets better results
Grey-Death anyone?
Remember in the industrial age how steam engines would make us all unemployed and poor?
Well yes, but I wouldn't call making glow in the dark people high priority.
Then you don't know what you're talking about.
Making a tissue light up ONLY when a chemical is produced in it because of a different product that you aren't sure will be produced because of a gene you modified that you don't fully understand is a great investigative technique. Especially when you can measure the intensity of the glow and then do it for another chemical in a separate subject or in the same one.
MacArthur and colleagues pooled exome data contributed by researchers from more than two dozen disease-specific projects, creating a list of more than 7.4 million genetic variants from 60,706 individuals—10-fold larger than any prior exome database. The information took up almost a petabyte of storage (an aggregate of 4,000 laptops worth of raw data, according to MacArthur).
“Many of these projects were directly studying common human diseases but had variable success which points to the fact that data can have uses besides its intended purpose,” Shendure told The Scientist.
The team, led by Monkol Lek, a research fellow in the MacArthur lab, found variants spaced around every eight base pairs, on average, within regions of the genome that are particularly prone to variation. The researchers often captured the same variant over and over, suggesting that the dataset is large enough that variants within these regions were becoming saturated. While the dataset is not large enough to see every possible genetic variant, at these particular sites, the team was able to capture about 63 percent of all possible synonymous variants. “I find that exciting, as it previews what is in store in the long future trajectory of this field as we sequence millions of human genomes,” said Shendure.
The large number of exomes allowed the researchers to find that 183 of 192 allelic variants previously categorized as pathogenic (but found at a relatively high frequency in the ExAC database) are likely benign.
The team also identified 3,230 genes that are particularly intolerant to mutation even when the second copy of the gene is wild-type. Seventy-two percent of these genes have not been linked to any known disease, demonstrating the ability of data from apparently healthy individuals to reveal genes that—when mutated—may contribute to disease.
In both the lab and the lake, cyanobacteria's genetic makeup changed in response to increasing CO2 concentrations. 'It's a textbook example of natural selection', says lead author Giovanni Sandrini. 'Cyanobacteria absorb CO2 during photosynthesis to produce their biomass, and we observed that the strain best equipped to absorb dissolved CO2 eventually gains the upper hand.'
Some Microcystis strains have a slow but efficient carbon uptake system that enables them to squeeze out the last bit of CO2 from the water even at very low concentrations. Those strains become dominant in low CO2 conditions. By contrast, other strains have a fast uptake system that allows them to take up dissolved CO2 at very high rates when in high concentrations. 'We discovered that these high-speed strains enjoy a major selective advantage in CO2-rich water', Sandrini continues. 'Given the rising atmospheric CO2 values, these strains are poised to thrive.'
Bathing and drinking water
Cyanobacteria's adaptation to rising CO2 is cause for concern. That's because Microcystis can produce microcystin, a toxin that causes liver damage in birds and mammals. In high concentrations, cyanobacteria also disrupt freshwater ecosystems, killing fish and aquatic plants. In the Netherlands, blue-green algal blooms regularly put swimming areas off limits.
archive.is
Among the various microbial platforms, E. coli remains dominant. And E. coli protein expression in inclusion bodies (IBs) continues to dominate manufacturing, with about 85–90% capacity. More microbial users are seeking to avoid the refolding problems and lower purification yields associated with IBs, and are adopting newer E. coli soluble expression systems. Currently, soluble E. coli expression systems involve protein excretion into the cell cytoplasm. Likely, 10 years out, the vast majority of E. coli new processes will be secretory.
archive.is
The E. coli plasmid, called lncX4, which the researchers recovered from the patient was 99.9 percent similar in sequence to a Klebsiella pneumonia plasmid taken from a person in China and to an E. coli plasmid collected from a pig slurry in Estonia.
“What is surprising is the fact that the IncX4 plasmids bearing mcr-1 obtained from different bacterial species, belonging to different [sequence types], isolated in different clinical contexts and found in different continents are highly similar in the plasmid backbone sequences,” the authors wrote. “This strongly suggests that self-transmissible IncX4-type plasmids may represent promiscuous plasmids contributing to the intercontinental spread of the mcr-1 gene.”
archive.is
tl;dr ?
Something like this:
Translation: we accidentally bioweapons.
Translation: global warming is not happening because of blue algae, but your ponds will become a stinking mess.
Translation: Oh, shit. Old drugs may stop working soon.
“Going down from 64 to 57 codons is a dramatic departure from what exists in nature,” says Farren Isaacs, a synthetic biologist at Yale University in New Haven, Connecticut, who worked with Church on previous recoding studies but was not involved in this project. “It‘s an important step forward for demonstrating the malleability of the genetic code and how entirely new types of biological functions and properties can be extracted from organisms through genomes that have been recoded.”
Church’s lab and others have previously shown2 that it is possible to recode single amino acids in E. coli so that the bacterium can incorporate amino acids not found in nature. Such reprogrammed organisms are highly resistant to viral infection, because they no longer contain the genetic machinery common to all natural organisms that viruses exploit to survive. They can also be made entirely dependent on synthetic amino acids in their diets, to allay the fear that recoded bacteria could escape from a lab and wreak havoc in the wild.
As part of a large phylogenetic study, researchers at the US Department of Energy’s Joint Genome Institute (JGI) in Walnut Creek, California, and their colleagues studied the alignment of predicted proteins in 700 orthologous genes from 29 different yeasts in an effort to identify conserved amino acids and determine which codons they came from. “It’s sort of a footprint of what the organism is using that codon for,” study coauthor Robert Riley, a bioinformatician at the JGI, told The Scientist.
For most species studied, CUG coded for conserved leucine between 70 percent and 86 percent of the time, but for P. tannophilus the standard coding occurred only 7 percent of the time, instead aligning 25 percent with alanine, the researchers reported.
To determine which amino acid was actually present in the proteins, Riley and colleagues extracted peptides from P. tannophilus grown in culture and analyzed them using liquid chromatography mass spectrometry (LC-MS). They found 178 identifiable peptides that mapped to coding sequences containing CUGs; 90 percent of them had LC-MS peaks indicating alanine and only 9 percent of the spectrum implied leucine. When they transformed P. tannophilus with either a wild-type or CUG-replaced, hygromycin–resistance gene, only the yeasts with the altered selection gene grew on antibiotic plates.
Codon modification may be required for researchers using yeast to express novel proteins in P. tannophilus and other yeast species, such as the workhorse Saccharomyces cerevisiae, Riley noted.
Beyond its potential effects on this and other biotech applications, CUG alanine coding might change the way scientists consider codon and transfer RNA (tRNA) evolution.
archive.is
Soon to begin trialing a new CRISPR-based immunotherapy in 10 patients with non-small cell lung cancer that has metastasized and is not responding to treatment. They will remove T cells from patients’ blood, then use the CRISPR-Cas9 system to delete the PD-1 gene, eliminating the surface receptor that binds tumor-produced ligands and tells the immune cells not to fight the cancer. The edited T cells would then be expanded in culture and those that are missing only their PD-1 gene will be infused back into patients. The trial is slated to include a total of 10 patients, but the researchers plan to start with just one, and slowly increase to three different dosage regimens in the remaining patients.
“It’s an exciting step forward,” UPenn’s Carl June, an immunotherapy pioneer and a scientific adviser on the proposed US trial, told Nature. (The US trial would similarly knock out the PD-1 gene, but would also make two other genetic alterations in the cells before they are infused into the patients.)
archive.is
Injecting the bacteria expressing the immune-activating gene directly into the tumor was the most effective in deterring malignant growth in a colorectal cancer mouse model, the researchers found.
Next, Hasty and colleagues orally administered a mixture of all three bacterial strains to mice with colorectal tumor metastases, and simultaneously treated the animals with the chemotherapy drug 5-fluorouracil (5-FU). The team found that this combination increased overall survival of the mice compared to either chemotherapy or the bacterial strains alone.
The researchers found that the population of bacteria cycled within the mice for 18 days. While the orally injected bacteria are spread systemically, the anaerobic bacteria are likely able to infiltrate and grow within the anaerobic tumor where standard drug penetration is poor, according to Hasty.
One major question, according to Elowitz, is how to reliably get the synthetic bacteria to efficiently home to the diseased tissue or organ while not harming healthy tissue.
Hasty’s team is now working to develop a modified strain that, rather than cycling through growth and lysis phases on its own, can be killed and mopped by the delivery of a subsequent dose of the bacteria.
archive.is