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Scientists Design Genome For Upgraded E. Coli

A team of Harvard Medical School scientists, which includes genetics professor George Church, have designed a bacterial genome that has been rewritten on a massive scale, with changes in more than 62,000 spots.

They haven’t used it to make living E. coli yet, but the findings, reported today in Science, mark progress towards genetically engineered bacteria that could make new materials without risk of exchanging genes with organisms in the wild.

“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,” Farren Isaacs of Yale University, who has worked with the team in the past, told Nature.

Exclusive: Controversial US scientist creates deadly new flu strain for pandemic research

The article overplays the alarmist tone a bit, but this is still an idiotic experiment.

If I understand correctly (the reporter didn’t explain it properly), he mutated the virus multiple times, until it no longer matches existing antibodies (i.e. somebody exposed would still become resistant — if they survived — and it is still possible to create new antiviral drugs that can target it); i.e. it is dangerous, but not invincible.

Given how long it takes to make new vaccinations for flue strains (and the cost of distributing them globally), this is still deeply irresponsible.


A controversial scientist who carried out provocative research on making influenza viruses more infectious has completed his most dangerous experiment to date by deliberately creating a pandemic strain of flu that can evade the human immune system.

Yoshihiro Kawaoka of the University of Wisconsin-Madison has genetically manipulated the 2009 strain of pandemic flu in order for it to “escape” the control of the immune system’s neutralising antibodies, effectively making the human population defenceless against its reemergence.

Most of the world today has developed some level of immunity to the 2009 pandemic flu virus, which means that it can now be treated as less dangerous “seasonal flu”. However, The Independent understands that Professor Kawaoka intentionally set out to see if it was possible to convert it to a pre-pandemic state in order to analyse the genetic changes involved.

Modifying a living genome with genetic equivalent of ‘search and replace’

Researchers including George Church have made further progress on the path to fully rewriting the genome of living bacteria. Such a recoded organism, once available, could feature functionality not seen in nature. It could also make the bacteria cultivated in pharmaceutical and other industries immune to viruses, saving billions of dollars of losses due to viral contamination. Finally, the altered genetic information in such an organism wouldn’t be able to contaminate natural cells because of the code’s limitations outside the lab, researchers say, so its creation could stop laboratory engineered organisms from genetically contaminating wildlife. In the DNA of living organisms, the same amino acid can be encoded by multiple codons — DNA “words” of three nucleotide letters. Here, building on previous work that demonstrated it was possible to use the genetic equivalent of “search and replace” in Escherichia coli to substitute a single codon with an alternative, Nili Ostrov, Church and colleagues explored the feasibility of replacing multiple codons, genome-wide. The researchers attempted to reduce the number of codons in the E. coli code from 64 to 57 by exploring how to eradicate more than 60,000 instances of seven different codons. They systematically replaced all 62,214 instances of these seven codons with alternatives. In the recoded E.coli segments that the researchers assembled and tested, 63% of all instances of the seven codons were replaced, the researchers say, and most of the genes impacted by underlying amino acid changes were expressed normally. Though they did not achieve a fully operational 57-codon E. coli, “a functionally altered genome of this scale has not yet been explored,” the authors write. Their results provide critical insights into the next step in the genome rewriting arena — creating a fully recoded organism.

Engineers program human cells to store complex histories in their DNA

Luv this.


MIT biological engineers have devised a way to record complex histories in the DNA of human cells, allowing them to retrieve “memories” of past events, such as inflammation, by sequencing the DNA.

This analog memory storage system—the first that can record the duration and/or intensity of events in human cells—could also help scientists study how cells differentiate into various tissues during embryonic development, how cells experience environmental conditions, and how they undergo genetic changes that lead to disease.

“To enable a deeper understanding of biology, we engineered human cells that are able to report on their own history based on genetically encoded recorders,” says Timothy Lu, an associate professor of electrical engineering and computer science, and of biological engineering. This technology should offer insights into how gene regulation and other events within cells contribute to disease and development, he adds.

From Sci Fi to reality: Unlocking the secret to growing new limbs

Many lower organisms retain the miraculous ability to regenerate form and function of almost any tissue after injury. Humans share many of our genes with these organisms, but our capacity for regeneration is limited. Scientists at the MDI Biological Laboratory in Bar Harbor, Maine, are studying the genetics of these organisms to find out how regenerative mechanisms might be activated in humans.

The ability of animals to regenerate body parts has fascinated scientists since the time of Aristotle. But until the advent of sophisticated tools for genetic and computational analysis, scientists had no way of studying the genetic machinery that enables regeneration. Using such tools, scientists at the MDI Biological Laboratory have identified genetic regulators governing regeneration that are common across species.

In a paper published in the journal PLOS ONE, MDI Biological Laboratory scientists Benjamin L. King, Ph.D., and Voot P. Yin, Ph.D., identified these common genetic regulators in three regenerative species: the zebrafish, a common aquarium fish originally from India; the axolotl, a salamander native to the lakes of Mexico; and the bichir, a ray-finned fish from Africa.

Normal radial migration and lamination are maintained in dyslexia-susceptibility candidate gene homolog Kiaa0319 knockout mice

Abstract.

Developmental dyslexia is a common disorder with a strong genetic component, but the underlying molecular mechanisms are still unknown. Several candidate dyslexia-susceptibility genes, including KIAA0319, DYX1C1, and DCDC2, have been identified in humans. RNA interference experiments targeting these genes in rat embryos have shown impairments in neuronal migration, suggesting that defects in radial cortical migration could be involved in the disease mechanism of dyslexia. Here we present the first characterisation of a Kiaa0319 knockout mouse line. Animals lacking KIAA0319 protein do not show anatomical abnormalities in any of the layered structures of the brain. Neurogenesis and radial migration of cortical projection neurons are not altered, and the intrinsic electrophysiological properties of Kiaa0319 -deficient neurons do not differ from those of wild-type neurons. Kiaa0319 overexpression in cortex delays radial migration, but does not affect final neuronal position. However, knockout animals show subtle differences suggesting possible alterations in anxiety-related behaviour and in sensorimotor gating. Our results do not reveal a migration disorder in the mouse model, adding to the body of evidence available for Dcdc2 and Dyx1c1 that, unlike in the rat in utero knockdown models, the dyslexia-susceptibility candidate mouse homolog genes do not play an evident role in neuronal migration. However, KIAA0319 protein expression seems to be restricted to the brain, not only in early developmental stages but also in adult mice, indicative of a role of this protein in brain function. The constitutive and conditional knockout lines reported here will be useful tools for further functional analyses of Kiaa0319.

Anti-inflammatory drug reverses memory loss in Alzheimer’s-disease-model mice

(credit: NIH National Institute on Aging)

Anti-inflammatory drug mefenamic acid completely reversed memory loss and brain inflammation in mice genetically engineered to develop symptoms of Alzheimer’s disease and amyloid beta-induced memory loss, a team led by David Brough, PhD, from the University of Manchester has discovered.

The non-steroidal anti-inflammatory drug (NSAID) drug targets an important inflammatory pathway called the NLRP3 inflammasome, which damages brain cells, according to Brough. This is the first time a drug has been shown to target this inflammatory pathway, highlighting its importance in the disease model, Brough said.

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