Nature has inspired generations of people, offering a plethora of different materials for innovations. One such material is the molecule of the heritage, or DNA, thanks to its unique self-assembling properties. Researchers at the Nanoscience Center (NSC) of the University of Jyväskylä and BioMediTech (BMT) of the University of Tampere have now demonstrated a method to fabricate electronic devices by using DNA. The DNA itself has no part in the electrical function, but acts as a scaffold for forming a linear, pearl-necklace-like nanostructure consisting of three gold nanoparticles.
The research was funded by the Academy of Finland.
The nature of electrical conduction in nanoscale materials can differ vastly from regular, macroscale metallic structures, which have countless free electrons forming the current, thus making any effect by a single electron negligible. However, even the addition of a single electron into a nanoscale piece of metal can increase its energy enough to prevent conduction. This kind of addition of electrons usually happens via a quantum-mechanical effect called tunnelling, where electrons tunnel through an energy barrier. In this study, the electrons tunnelled from the electrode connected to a voltage source, to the first nanoparticle and onwards to the next particle and so on, through the gaps between them.
“Such single-electron devices have been fabricated within the scale of tens of nanometres by using conventional micro- and nanofabrication methods for more than two decades,” says Senior Lecturer Jussi Toppari from the NSC. Toppari has studied these structures already in his PhD work.
“The weakness of these structures has been the cryogenic temperatures needed for them to work. Usually, the operation temperature of these devices scales up as the size of the components decreases. Our ultimate aim is to have the devices working at room temperature, which is hardly possible for conventional nanofabrication methods – so new venues need to be found.”
Modern nanotechnology provides tools to fabricate metallic nanoparticles with the size of only a few nanometres. Single-electron devices fabricated from these metallic nanoparticles could function all the way up to room temperature. The NSC has long experience of fabricating such nanoparticles.
“After fabrication, the nanoparticles float in an aqueous solution and need to be organised into the desired form and connected to the auxiliary circuitry,” explains researcher Kosti Tapio. “DNA-based self-assembly together with its ability to be linked with nanoparticles offer a very suitable toolkit for this purpose.”
Gold nanoparticles are attached directly within the aqueous solution onto a DNA structure designed and previously tested by the involved groups. The whole process is based on DNA self-assembly, and yields countless of structures within a single patch. Ready structures are further trapped for measurements by electric fields.
“The superior self-assembly properties of the DNA, together with its mature fabrication and modification techniques, offer a vast variety of possibilities,” says Associate Professor Vesa Hytönen.
Electrical measurements carried out in this study demonstrated for the first time that these scalable fabrication methods based on DNA self-assembly can be efficiently utilised to fabricate single-electron devices that work at room temperature.
Experiments at CERN’s Large Hadron Collider generate 15 million gigabytes of data per year. That is a lot of digital data to inscribe on hard drives or beam up to the “cloud.”
Digital data storage degrades and can become obsolete and old-school books and paper require lots of space. Compared to digital and analog information storage, DNA is more compact and durable and never becomes obsolete. Readable DNA was extracted from the 600,000-year-old remains of a horse found in the Yukon.
Bachand was inspired by the recording of all of Shakespeare’s sonnets into 2.5 million base pairs of DNA — about half the genome of the tiny E. coli bacterium. Using this method, the group at the European Bioinformatics Institute could theoretically store 2.2 petabytes of information — 200 times the printed material in the Library of Congress — in one gram of DNA.
DNA may be the blueprint of life, but it’s also a molecule made from just a few simple chemical building blocks. Among its properties is the ability to conduct an electrical charge, fueling an engineering race to develop novel, low-cost nanoelectronic devices.
Now, a team led by ASU Biodesign Institute researcher Nongjian “N.J.” Tao and Duke theorist David Beratan has been able to understand and manipulate DNA to more finely tune the flow of electricity through it. The key findings, which can make DNA behave in different ways — cajoling electrons to smoothly flow like electricity through a metal wire, or hopping electrons about like the semiconductors materials that power our computers and cellphones — pave the way for an exciting new avenue of research advancements.
The results, published in the online edition of Nature Chemistry, may provide a framework for engineering more stable and efficient DNA nanowires, and for understanding how DNA conductivity might be used to identify gene damage.
Building on a series of recent works, the team has been able to better understand the physical forces behind DNA’s affinity for electrons.
“We’ve been able to show theoretically and experimentally that we can make DNA tunable by changing the sequence of the ‘A, T, C, or G’ chemical bases, by varying its length, by stacking them in different ways and directions, or by bathing it in different watery environments,” said Tao, who directs the Biodesign Center for Biolectronics and Biosensors and is a professor in the Ira A. Fulton Schools of Engineering.
Deep learning has already had a huge impact on computer vision and speech recognition, and it’s making inroads in areas as computer-unfriendly as cooking. Now a new startup led by University of Toronto professor Brendan Frey wants to cause similar reverberations in genomic medicine.
Deep Genomics plans to identify gene variants and mutations never before observed or studied and find how these link to various diseases. And through this work the company believes it can help usher in a new era of personalized medicine.
Genomic research is hard. Scientists still know relatively little about our genes and how they interrelate. But Frey and others in the field now know enough that they can equip machines to do the heavy lifting. And there’s an awful lot of this heavy lifting to do. “Genomics is no longer about small datasets,” Frey tells Gizmag. “It’s now about very, very large datasets.”
For context, the first effort to sequence a full human genome took 13 years – running from 1990 to 2003. There are now many companies working to sequence many genomes at a time. The largest of these is called Illumina. “Illumina,” Frey says, “expects to sequence one million genomes in the next year. Each genome contains three billion letters. That’s a lot of data.”
Researchers from the Lomonosov Moscow State University discovered a new mechanism of DNA repair, which will help to treat and to prevent diseases in the future
The DNA molecule is chemically unstable giving rise to DNA lesions of different nature. That is why DNA damage detection, signaling and repair, collectively known as the DNA damage response, are needed.
A group of researchers, lead by Vasily M. Studitsky, professor at the Lomonosov Moscow State University, discovered a new mechanism of DNA repair, which opens up new perspectives for the treatment and prevention of neurodegenerative diseases. The article describing their discovery is published in AAAS’ first open access online-only journal Science Advances.
“In higher organisms DNA is bound with proteins in complexes called the nucleosome. Every ~200 base pairs are organized in nucleosomes, consisting of eight histone proteins, which, like the thread on the bobbin, wound double helix of DNA, which is coiled into two supercoiled loops. Part of the surface of the DNA helix is hidden, because it interacts with histones. Our entire genome is packed this way, except for the areas, from which the information is being currently read”, — says Vasily M. Studitsky , who is the leading researcher and the head of the Laboratory of Regulation of Transcription and Replication at the Biological Faculty of the Lomonosov Moscow State University.
The dense packing allows DNA molecule with a length of about two meters to fit into a microscopic cell nucleus, but it makes significant surfaces of the DNA inaccessible for the repair enzymes — the proteins that manage the “repair” of damaged DNA regions. The damage of the DNA, if not repaired, leads to accumulation of mutations, cell death, and to the development of various diseases, including neurodegenerative, e.g. Alzheimer’s disease.
A group of researchers, lead by Vasily M. Studitsky, studied the mechanism of detection of single-stranded DNA breaks at which the connection is lost between nucleotides on one strand in the places where the DNA is associated with histones.
Scientists know quite a lot about the mechanism of the repair. It is known that for the synthesis of a protein, information written in the genetic code, which could be imagined as the manual for its assembly where triples of nucleotides match certain amino acids, should be taken out of the nucleus into the cytoplasm of the cell.
Thin and long strand of the DNA is packed in the nucleus and can tear at the exit to the outside. Moreover, it cannot be sacrificed as the cell’s nuclear DNA is is only present in two copies. Therefore, when it is necessary to synthesize specific protein, small region of DNA is unwound, the two strands are disconnected, and the information on the protein structure with one of the DNA strands is written in form of RNA, single-stranded molecule. The mRNA molecule, which serves as the template for making a protein, is synthesized by the principle of complementarity: each nucleotide pair corresponds to another one.
During the transcription of information (its rewriting into RNA) the RNA polymerase enzyme “rides” on the DNA chain, and stops when it finds the break. Like a proofreader of a text, RNA polymerase after it is stalled, triggers a cascade of reactions, resulting in the repair enzymes fixing the damaged area. At the same time, the RNA polymerase cannot detect discontinuities present in the other DNA strand.
A team of scientists from Arizona State University’s Biodesign Institute and IBM’s T.J. Watson Research Center have developed a prototype DNA reader that could make whole genome profiling an everyday practice in medicine.
“Our goal is to put cheap, simple and powerful DNA and protein diagnostic devices into every single doctor’s office,” said Stuart Lindsay, an ASU physics professor and director of Biodesign’s Center for Single Molecule Biophysics. Such technology could help usher in the age of personalized medicine, where information from an individual’s complete DNA and protein profiles could be used to design treatments specific to their individual makeup.
Such game-changing technology is needed to make genome sequencing a reality. The current hurdle is to do so for less than $1,000, an amount for which insurance companies are more likely to provide reimbursement.
In their latest research breakthrough, the team fashioned a tiny, DNA reading device a thousands of times smaller than width of a single human hair.
The device is sensitive enough to distinguish the individual chemical bases of DNA (known by their abbreviated letters of A, C, T or G) when they are pumped past the reading head.
Proof-of-concept was demonstrated, by using solutions of the individual DNA bases, which gave clear signals sensitive enough to detect tiny amounts of DNA (nanomolar concentrations), even better than today’s state-of-the-art, so called next-generation DNA sequencing technology.
Making the solid-state device is just like making a sandwich, just with ultra high-tech semiconductor tools used to slice and stack the atomic-sized layers of meats and cheeses like the butcher shop’s block. The secret is to make slice and stack the layers just so, to turn the chemical information of the DNA into a change in the electrical signal.
First, they made a “sandwich” composed of two metal electrodes separated by a two-nanometer thick insulating layer (a single nanometer is 10,000 times smaller than a human hair), made by using a semiconductor technology called atomic layer deposition.
Then a hole is cut through the sandwich: DNA bases inside the hole are read as they pass the gap between the metal layers.
“The technology we’ve developed might just be the first big step in building a single-molecule sequencing device based on ordinary computer chip technology,” said Lindsay.
There’s a good reason people over 60 are not donor candidates for bone marrow transplantation. The immune system ages and weakens with time, making the elderly prone to life-threatening infection and other maladies, and a UC San Francisco research team now has discovered a reason why.
“We have found the cellular mechanism responsible for the inability of blood-forming cells to maintain blood production over time in an old organism, and have identified molecular defects that could be restored for rejuvenation therapies,” said Emmanuelle Passegué, PhD, a professor of medicine and a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. Passegué, an expert on the stem cells that give rise to the blood and immune system, led a team that published the new findings online July 30, 2014 in the journal Nature.
Blood and immune cells are short-lived, and unlike most tissues, must be constantly replenished. The cells that must keep producing them throughout a lifetime are called “hematopoietic stem cells.” Through cycles of cell division these stem cells preserve their own numbers and generate the daughter cells that give rise to replacement blood and immune cells. But the hematopoietic stem cells falter with age, because they lose the ability to replicate their DNA accurately and efficiently during cell division, Passegué’s lab team determined.
Scientists at Cold Spring Harbor Laboratory (CSHL) and five other institutions have used an unconventional approach to cancer drug discovery to identify a new potential treatment for acute myeloid leukemia (AML).
As reported in Nature online on August 3, the scientists have pinpointed a protein called Brd4 as a novel drug target for AML, an aggressive blood cancer that is currently incurable in 70% of patients. Using a drug compound that inhibits the activity of Brd4, the scientists were able to suppress the disease in experimental models.
“The drug candidate not only displays remarkable anti-leukemia activity in aggressive disease models and against cells derived from patients with diverse, genetic subtypes of AML, but is also minimally toxic to non-cancerous cells,” says CSHL scientist Chris Vakoc, M.D., Ph.D., who led the team. “The drug is currently being developed for therapeutic use for cancer patients by Tensha Therapeutics and is expected to enter clinical trials within two years.”
The protein target identified in the RNAi screen described in the current study, Brd4 — which contains a distinct domain or region known as a bromodomain — is a member of the BET family of proteins, which help regulate gene expression. By “reading” certain epigenetic marks or chemical tags attached to chromatin — the combined package of DNA and proteins around which it is coiled within the cell’s nucleus — Brd4 helps control the pattern of which genes are switched on and how they work.
“Cancer is clearly a genetic disease, but we also appreciate that epigenetic changes in how genes are expressed contribute to the uncontrolled growth of cancer cells,” says Vakoc. Cancer cells exploit this altered epigenetic landscape to drive their cell-growth programs.
Vakoc and other scientists have seized on the idea of interfering with this epigenetic dependency to turn the tables on cancer. “Epigenetic alterations acquired during cancer progression are potentially reversible and therefore susceptible to drug intervention,” he explains. With this insight as the backbone of their strategy to find new therapies for cancer, “we began to systematically search for what the cancer needs to keep itself going, to find a way to shut down that cancer-fueling factor and develop a new therapy.”