Engineers have long dreamed of using DNA as the backbone for the next generation of computer circuits. New research shows just how it might be done.
Instead of conventional circuits built of silicon that use electrical current, computer engineers could take advantage of the unique properties of DNA, the double-helix molecule that carries life’s information. “Conventional technology has reached its physical limits," said Chris Dwyer, assistant professor of electrical and computer engineering at Duke University's Pratt School of Engineering.
Dwyer recently demonstrated that by simply mixing customized snippets of DNA and other molecules, he could create billions of identical, tiny, waffle-looking structures.
These nanostructures can then be used as the building blocks for a variety of circuit-based applications, ranging from the biomedical to the computational. Key to the promise of these DNA nanostructures is an ability to rapidly "switch" between zeros or ones -- the basic on/off binary action that powers computation. Light can be used to stimulate similar binary responses from DNA-based switches, though at a much faster rate than in silicon.
“When light is shined on the chromophores" -- parts of DNA responsible for its color -- "they absorb it, exciting the electrons,” Dwyer said. “The energy released passes to a different type of chromophore nearby that absorbs the energy and then emits light of a different wavelength. That difference means this output light can be easily differentiated from the input light, using a detector.”
Dwyer added: "This is the first demonstration of such an active and rapid processing and sensing capacity at the molecular level."
Building computers with life's building blocks
Victorian stem cell scientists from Monash University have modified a human embryonic stem cell (hESC) line to glow red when the stem cells become red blood cells.
The modified hESC line, ErythRED, represents a major step forward to the eventual aim of generating mature, fully functional red blood cells from human embryonic stem cells.
The research, conducted by a team led by Professors Andrew Elefanty and Ed Stanley at the Monash Immunology and Stem Cell Laboratories that included scientists at the Murdoch Children's Research Institute, was published in today's issue of the prestigious journal, Nature Methods.
The work, funded by the Australian Stem Cell Centre (ASCC), will help scientists to track the differentiation of embryonic stem cells into red blood cells.
Stem cells have a unique ability: when they divide, they can either give rise to more stem cells, or to a variety of specialised cell types. In both mice and humans, a layer of cells at the base of the skin contains stem cells that can develop into the specialised cells in the layers above. Scientists at the European Molecular Biology Laboratory (EMBL) in Monterotondo, in collaboration with colleagues at the Centro de Investigaciones Energéticas, Medioambientales y Tecnologicas (CIEMAT) in Madrid, have discovered two proteins that control when and how these stem cells switch to being skin cells. The findings, published online today in Nature Cell Biology, shed light on the basic mechanisms involved not only in formation of skin, but also on skin cancer and other epithelial cancers
At some point in their lives, the stem cells at the base of the skin stop proliferating and start differentiating into the cells that form the skin itself. To do so, they must turn off the 'stem cell programme' in their genes and turn on the 'skin cell programme'. Researchers suspected that a family of proteins called C/EBPs might be involved in this process, as they were known to regulate it in other types of stem cell, but had so far failed to identify which C/EBP protein controlled the switch in skin. Claus Nerlov and his group at EMBL Monterotondo discovered it was not one protein, but two: C/EBPα and C/EBPβ
The EMBL researchers used genetic engineering techniques to delete the genes that encode C/EBPα and β specifically in the skin of mouse embryos, and found that without these proteins the skin of the mice did not form properly
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