[onishadowolf]

I thought I would start this thread and sticky it here. Any one who comes across a fascinating read post it here. And if you can please site it.




Science Daily (May 31, 2009) — MIT and Boston University engineers have designed cells that can count and "remember" cellular events, using simple circuits in which a series of genes are activated in a specific order.
Integrated circuits.
Such circuits, which mimic those found on computer chips, could be used to count the number of times a cell divides, or to study a sequence of developmental stages. They could also serve as biosensors that count exposures to different toxins.
The team developed two types of cellular counters, both described in the May 29 issue of Science. Though the cellular circuits resemble computer circuits, the researchers are not trying to create tiny living computers.
"I don't think computational circuits in biology will ever match what we can do with a computer," said Timothy Lu, a graduate student in the Harvard-MIT Division of Health Sciences and Technology (HST) and one of two lead authors of the paper.
Performing very elaborate computing inside cells would be extremely difficult because living cells are much harder to control than silicon chips. Instead, the researchers are focusing on designing small circuit components to accomplish specific tasks.
"Our goal is to build simple design tools that perform some aspect of cellular function," said Lu.
Ari Friedland, a graduate student at Boston University, is also a lead author of the Science paper. Other authors are Xiao Wang, postdoctoral associate at BU; David Shi, BU undergraduate; George Church, faculty member at Harvard Medical School and HST; and James Collins, professor of biomedical engineering at BU.
Learning to count
To demonstrate their concept, the team built circuits that count up to three cellular events, but in theory, the counters could go much higher.
The first counter, dubbed the RTC (Riboregulated Transcriptional Cascade) Counter, consists of a series of genes, each of which produces a protein that activates the next gene in the sequence.
With the first stimulus — for example, an influx of sugar into the cell — the cell produces the first protein in the sequence, an RNA polymerase (an enzyme that controls transcription of another gene). During the second influx, the first RNA polymerase initiates production of the second protein, a different RNA polymerase.
The number of steps in the sequence is, in theory, limited only by the number of distinct bacterial RNA polymerases. "Our goal is to use a library of these genes to create larger and larger cascades," said Lu.
The counter's timescale is minutes or hours, making it suitable for keeping track of cell divisions. Such a counter would be potentially useful in studies of aging.
The RTC Counter can be "reset" to start counting the same series over again, but it has no way to "remember" what it has counted. The team's second counter, called the DIC (DNA Invertase Cascade) Counter, can encode digital memory, storing a series of "bits" of information.
The process relies on an enzyme known as invertase, which chops out a specific section of double-stranded DNA, flips it over and re-inserts it, altering the sequence in a predictable way.
The DIC Counter consists of a series of DNA sequences. Each sequence includes a gene for a different invertase enzyme. When the first activation occurs, the first invertase gene is transcribed and assembled. It then binds the DNA and flips it over, ending its own transcription and setting up the gene for the second invertase to be transcribed next.
When the second stimulus is received, the cycle repeats: The second invertase is produced, then flips the DNA, setting up the third invertase gene for transcription. The output of the system can be determined when an output gene, such as the gene for green fluorescent protein, is inserted into the cascade and is produced after a certain number of inputs or by sequencing the cell's DNA.
This circuit could in theory go up to 100 steps (the number of different invertases that have been identified). Because it tracks a specific sequence of stimuli, such a counter could be useful for studying the unfolding of events that occur during embryonic development, said Lu.
Other potential applications include programming cells to act as environmental sensors for pollutants such as arsenic. Engineers would also be able to specify the length of time an input needs to be present to be counted, and the length of time that can fall between two inputs so they are counted as two events instead of one.
They could also design the cells to die after a certain number of cell divisions or night-day cycles.
"There's a lot of concern about engineered organisms — if you put them in the environment, what will happen?" said Collins, who is also a Howard Hughes Medical Institute investigator. These counters "could serve as a programmed expiration date for engineered organisms."
The research was funded by the National Institute of Health Director's Pioneer Award Program, the National Science Foundation FIBR program, and the Howard Hughes Medical Institute.

[onishadowolf]

ScienceDaily (Aug. 14, 2007) — A major surprise emerging from genome sequencing projects is that humans have a comparable number of protein-coding genes as significantly less complex organisms such as the minute nematode worm Caenorhabditis elegans. Clearly something other than gene count is behind the genetic differences between simpler and more complex life forms.

Increased functional and cellular complexity can be explained, in large part, by how genes and the products of genes are regulated. A University of Toronto-led study published in the latest issue of Genome Biology reveals that a step in gene expression (referred to as alternative splicing) is more highly regulated in a cell and tissue-specific manner than previously appreciated and much of this additional regulation occurs in the nervous system. The alternative splicing step allows a single gene to specify multiple protein products by processing the RNA transcripts made from genes (which are translated to make protein).
"We are finding that a significant number of genes operating in the same biological processes and pathways are regulated by alternative splicing differently in nervous system tissues compared to other mammalian tissues," says lead investigator Professor Benjamin Blencowe of the Banting and Best Department of Medical Research and Centre for Cellular and Biomolecular Research (CCBR) at the University of Toronto.
According to Blencowe, it is particularly interesting that many of the genes have important and specific functions in the nervous system, including roles associated with memory and learning. However, in most cases the investigators working on these genes were not aware that their favorite genes are regulated at the level of splicing. Blencowe believes that the data his group has generated provides a valuable basis for understanding molecular mechanisms by which genes can function differently in different parts of the body.
Blencowe attributes these new findings in part to the power of a new tool that he, together with his colleagues including Profs. Brendan Frey (Department of Electrical and Computer Engineering) and Timothy Hughes (Banting and Best, CCBR), developed a few years ago. This tool, which comprises tailored designed microarrays or "gene chips" and computer algorithms, allows the simultaneous measurement of thousands of alternative splicing events in cells and tissues. "Until recently researchers studied splicing regulation on a gene by gene basis. Now we can obtain a picture of what is happening on a global scale, which provides a fascinating new perspective on how genes are regulated," Blencowe explains.
A challenge now is to figure out how the alternative splicing process is regulated in a cell and tissue-specific manner. In their new paper in Genome Biology, Dr. Yoseph Barash, a postdoctoral fellow working jointly with Blencowe and Frey, has provided what is likely part of the answer. By applying computational methods to the gene chip data generated by Matthew Fagnani (an MSc student) and other members of the Blencowe lab, Barash has uncovered what appears to be part of a "regulatory code" that controls alternative splicing patterns in the brain.
One outcome of these new studies is that the alternative splicing process appears to provide a largely separate layer of gene regulation that works in parallel with other important steps in gene regulation. "The number of genes and coordinated regulatory events involved in specifying cell and tissue type characteristics appear to be considerably more extensive than appreciated in previous studies," says Blencowe. "These findings also have implications for understanding human diseases such as cancers, since we can anticipate a more extensive role for altered regulation of splicing events that similarly went unnoticed due to the lack of the appropriate technology allowing their detection."
Blencowe's research is funded by grants from the Canadian Institutes of Health Research, the National Cancer Institute of Canada, and by Genome Canada through the Ontario Genomics Institute.
Co-authors of the study are: Matthew Fagnani, Yoseph Barash, Joanna Ip, Christine Misquitta, Qun Pan, Arneet Saltzman, Ofer Shai, Leo Lee, Aviad Rozenhek, Naveed Mohammad, Sandrine Willaime-Morawek, Tomas Babak, Wen Zhang, Timothy Hughes, Derek van der Kooy, Brendan Frey and Benjamin Blencowe.

[onishadowolf]

ScienceDaily (May 25, 2009) — Scientists at Oxford University have tamed a virus so that it attacks and destroys cancer cells but does not harm healthy cells.  They determined how to produce replication-competent viruses with key toxicities removed, providing a new platform for development of improved cancer treatments and better vaccines for a broad range of viral diseases.

Cellular microRNA molecules regulate the stability of mRNA in different cell types, and this newly-understood mechanism provides the possibility to engineer viruses for cell-specific inactivation. Cancer Research UK scientists at the University of Oxford, United Kingdom, with support from colleagues at Vrije Universiteit, Amsterdam, report that this approach can be used to regulate proliferation of adenovirus.
Adenovirus is a DNA virus widely used in cancer therapy but which causes hepatic disease in mice. Professor Len Seymour and colleagues found that introducing sites into the virus genome that are recognized by microRNA 122 leads to hepatic degradation of important viral mRNA, thereby diminishing the virus' ability to adversely affect the liver, while maintaining its ability to replicate in and kill tumor cells.
Tumor-killing replicating viruses are a hot topic in the biotherapeutics arena, with many clinical trials ongoing worldwide. That Professor Seymour's group set out to and has now defined a mechanism whereby wild type virus potency could be maintained in tumor cells but the virus could be 'turned off' in tissues vulnerable to pathology adds important information to the current base of knowledge.
"This approach is surprisingly effective and quite versatile. It could find a range of applications in controlling the activity of therapeutic viruses, both for cancer research and also to engineer a new generation of conditionally-replicating vaccines, where the vaccine pathogen is disabled in its primary sites of toxicity," Professor Seymour says.
The present study was intended mainly to explore and demonstrate the potential of this new mechanism to regulate virus activity. Although the current tumor-killing virus is useful in mice, transfer of the technology into the clinical setting will require re-engineering of the virus to overcome virus pathologies seen in humans, and it will be at least two years before this can be tested in the clinics.
Modified naturally-occurring viruses have already had important uses in medicine including their use as vaccines, notably for measles, mumps, polio, influenza, and chicken pox. They have already been developed as potential cancer-killing therapies, in an approach called virotherapy.
RC and FC are supported by Cancer Research UK; HC by a research studentship from the New Zealand Government, and MB by a Bellhouse Foundation Fellowship (Magdalen College, Oxford). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have declared that no competing interests exist.
Journal reference:
Ryan Cawood, Hannah H. Chen, Fionnadh Carroll, Miriam Bazan-Peregrino, Nico van Rooijen, Leonard W. Seymour. Use of Tissue-Specific MicroRNA to Control Pathology of Wild-Type Adenovirus without Attenuation of Its Ability to Kill Cancer Cells.







I'm going to have to find shorter summaries.

Makes it all sound so easy.
Ok this really is incredible stuff that they are doing, truly amazing!

I am astounded though that here we are engineering and training genes to disable specific cancer cells, yet at the same time we are failing as a species in the most simple areas of life, ie overpopulation and energy demands.

Can we have some scientists involved in social engineering and training please.

[Moloch]

Makes it all sound so easy.
Ok this really is incredible stuff that they are doing, truly amazing!

I am astounded though that here we are engineering and training genes to disable specific cancer cells, yet at the same time we are failing as a species in the most simple areas of life, ie overpopulation and energy demands.

Can we have some scientists involved in social engineering and training please.

First, that failure is more profound than you have stated, OB1. Here we are, striving to prolong the lives of individuals, when we already have nearly seven Billion of them, and more being born every day.

As for the folks to work on social engineering, we already have that. You can thank them for the current sorry state of affairs we're in now; where people fear death so much that they are willing to take a little bit more than they should - just to be able to keep going for a few more years.

[onishadowolf]

I found articles on that too. They are doing social experiments, and finding genes and RNA coders that cause certain social behavior. Just got to tired to post them.

And the last article about the manipulated  virus cancer killers; vaguely reminds me of the movie "I am legend".     

[Moloch]

That's also vaguely similar to the whole "T" cell stuff they used for an explanation in Resident Evil.

[onishadowolf]

You mean the T virus. The virus in Resident Evil series that reanimates dead cells. Yeah it does.

[onishadowolf]

ScienceDaily (June 9, 2009) — A synthetic DNA binding compound has proved surprisingly effective at binding to the DNA of bacteria and killing all the bacteria it touched within two minutes. The DNA binding properties of the compound were first discovered in the Department of Chemistry at the University of Warwick by Professor Mike Hannon and Professor Alison Rodger (Professor Mike Hannon is now at the University of Birmingham). However the strength of its antibiotic powers have now made it a compound of high interest for University of Warwick researchers working on the development of novel antibiotics.

Dr Adair Richards from the University of Warwick said: "This research will assist the design of new compounds that can attack bacteria in a highly effective way which gets around the methods bacteria have developed to resist our current antibacterial drugs. As this antibiotic compound operates by targeting DNA, it should avoid all current resistance mechanisms of multi-resistant bacteria such as MRSA."
The compound [Fe2L3]4+ is an iron triple helicate with three organic strands wrapped around two iron centres to give a helix which looks cylindrical in shape and neatly fits within the major groove of a DNA helix. It is about the same size as the parts of a protein that recognise and bind with particular sequences of DNA. The high positive charge of the compound enhances its ability to bind to DNA which is negatively charged.
When the iron-helicate binds to the major groove of DNA it coils the DNA so that it is no longer available to bind to anything else and is not able to drive biological or chemical processes. Initially the researchers focused on the application of this useful property for targeting the DNA of cancer cells as it could bind to, coil up and shut down the cancer cell's DNA either killing the cell or stopping it replicate. However the team quickly realised that it might also be a very clever way of targeting drug-resistant bacteria.
New research at the University of Warwick, led by Dr Adair Richards and Dr Albert Bolhuis, has now found that the [Fe2L3]4+ does indeed have a powerful effect on bacteria. When introduced to two test bacteria Bacillus subtilis and E. coli they found that it quickly bound to the bacteria's DNA and killed virtually every cell within two minutes of being introduced - though the concentration required for this is high.
Professor Alison Rodger, Professor of Biophysical Chemistry at the University of Warwick, said: "We were surprised at how quickly this compound killed bacteria and these results make this compound a key lead compound for researchers working on the development of novel antibiotics to target drug resistant bacteria."
The researchers will next try and understand how and why the compound can cross the bacteria cell wall and membranes. They plan to test a wide range of compounds to look for relatives of the iron helicate that have the same mechanism for action in collaboration with researchers around the world.
Journal reference:
Richards et al. Antimicrobial activity of an iron triple helicate. International Journal of Antimicrobial Agents, 2009; 33 (5): 469 DOI: 10.1016/j.ijantimicag.2008.10.031

[onishadowolf]

ScienceDaily (Nov. 6, 2008) — When a dividing cell duplicates its genetic material, a molecular machine called a sliding clamp travels along the DNA double helix, tethering the proteins that perform the replication. Researchers from the laboratory of Rockefeller University’s Michael O'Donnell, a Howard Hughes Medical Institute investigator, have discovered a small molecule that stops the sliding clamp in its tracks.

The finding will enable scientists to better study the proteins that duplicate DNA, and may ultimately provide a platform for developing improved antibiotics.
The process is akin to unzipping a zipper: The sliding clamp works its way along the DNA double helix while a network of proteins work together to unwind the two strands. Proteins known as polymerases then add, in assembly-line fashion, nucleotide bases — the building blocks that make up DNA — to convert the now-single-stranded templates into two new duplex DNA molecules. Bacteria have five known DNA
polymerases (higher organisms such as humans have more), only one of which, polymerase III (pol III) is responsible for replicating the chromosome, while the others appear to be involved in DNA repair.
To better understand the functions of the other polymerases, O’Donnell and colleagues at Rockefeller used a combination of biochemical techniques to identify a small molecule that would inhibit the binding of the polymerases to the beta sliding clamp. With the help of researchers in Rockefeller’s High Throughput Screening Resource Center, coauthors Roxana E. Georgescu and Olga Yurieva, research associates in O’Donnell’s lab, screened some 30,000 compounds using a technique called fluorescence anisotropy. Georgescu and Yurieva looked for compounds that would disrupt the interaction of a fluorophore-labeled peptide with the peptide-binding pocket of the sliding clamp. Because the peptide is small and the clamp is big, the signal generated by the fluorophore is very different.
Georgescu and Yurieva identified one compound, called RU7, that differentially inhibited polymerases II, III and IV. RU7 did not inhibit pol IV at all, while pol III was inhibited the most.
The researchers then used x-ray crystallography to compare how RU7 and polymerases II, III and IV bind to the clamp. They found that while all three polymerases and RU7 bind to the same peptide-binding site of the clamp, they do so in different ways. Polymerase IV, for example, forms additional contacts to the clamp outside of the peptide-binding site, which may account for its resistance to disruption by RU7.
“The role of polymerase III in replication has been very well studied, but the roles of the other polymerases are not well understood,” says O’Donnell. “RU7 may be an important tool as a chemical probe to better understand the functions of polymerases II and IV in normal cell growth and in response to DNA damage.”
Because RU7 halts the replication of bacterial DNA by disrupting polymerase III — but does not affect DNA replication in yeast, which uses the same molecular machinery as humans — O’Donnell’s research suggests that RU7 could provide a starting point for antibiotic drug design. Further tweaking, for example by adding atoms that enable the compound to fit into a second binding site, could even increase RU7’s potency.
Journal reference:
Georgescu et al. Structure of a small-molecule inhibitor of a DNA polymerase sliding clamp. Proceedings of the National Academy of Sciences, 2008; 105 (32): 11116 DOI: 10.1073/pnas.0804754105

[onishadowolf]

ScienceDaily (July 23, 2008) — For millennia, humans and viruses have been locked in an evolutionary back-and-forth -- one changes to outsmart the other, prompting the second to change and outsmart the first. With retroviruses, which work by inserting themselves into their host's DNA, the evidence remains in our genes.

Last year, researchers at Rockefeller University and the Aaron Diamond AIDS Research Center brought an ancient retrovirus back to life and showed it could reproduce and infect human cells. Now, the same scientists have looked at the human side of the story and found evidence that our ancestors fought back against that virus with a defense mechanism our bodies still use today.
"This is the first time that we've been able to take an ancient retrovirus and analyze how it interacts with host defense mechanisms in the laboratory in the present day," says Paul Bieniasz, who is an associate professor and head of the Laboratory of Retrovirology at Rockefeller and a scientist at the Aaron Diamond AIDS Research Center. Bieniasz and graduate student Youngnam Lee took their resurrected virus, called HERV-K, tested its strength against molecules involved in human antiviral defense.
Bieniasz, who also is an investigator at the Howard Hughes Medical Institute, and Lee found that, at least in the laboratory, human cells infected with HERV-K fought back with several antiviral proteins. One of those proteins, called APOBEC3G, leaves a tell-tale signature behind: It mutates virus DNA in a recognizable pattern and is one our cells use to attack modern retroviruses. "But this is the first time it's been shown for this ancient retrovirus," Bieniasz says.
Once the scientists found that modern human cells attacked HERV-K with this molecule, they went back to look at the "fossil evidence," remnants of the virus that still remain in our genes and that the researchers had previously used to reconstruct it. What emerged were two copies of HERV-K that had clearly been mutated, and thus inactivated, by the APOBEC3G protein. "We're looking at things that happened millions and millions of years ago," says Lee. "But these sorts of ancient interactions may have influenced how humans are able to combat these retroviruses today. These proteins help protect us against current retroviruses." Indeed, HERV-K may well have helped to shape the modern APOBEC3G defense.
The earlier study and this one provide two sides of the evolutionary coin: the infectious agent, and the host defense. "Retroviruses are able to infect us and leave remnants in our DNA, and our DNA also holds evidence of what we've done to them in return," Lee says. "It's an illustration of the fight between host and virus."
Journal reference:
Lee et al. Hypermutation of an ancient human retrovirus by APOBEC3G. Journal of Virology, 2008; DOI: 10.1128/JVI.00751-08

[onishadowolf]

ScienceDaily (June 2, 2009) — European researchers have developed a small robotic drone capable of helping save lives in emergency situations or preventing terrorist attacks in urban areas.

Drones, known as unmanned aerial vehicles (UAVs), have proven to be of great value in military operations, but so far, their advantages have not been fully exploited for civilian uses.
In civil life, drones are mainly used in the agriculture sector – for assessing how well crops are growing in a particular part of a field – or for meteorological measurements.
The main barrier to the wider use of drones is their large size and lack of manoeuvrability around obstacles. Most military drones are fixed-wing UAVs designed to operate at high altitudes and do not need a lot of manoeuvrability. In built up, highly populated areas such drones would pose a danger to people if they hit a tree or a building, or crashed due to the loss of its navigational signal.
Smaller, lighter and autonomous
Seeing a market opportunity, European researchers and companies that make up the EU-funded µDrone (Micro Drone Autonomous Navigation and Environment Sensing -- http://www.ist-microdrones.org/) project are developing a smaller, more manoeuvrable drone that is capable of sensing and avoiding objects in its flight path. The new drone would be capable of carrying out missions autonomously in places with obstacles, such as in an urban area or inside a building.
Such drones could be used to patrol sensitive areas to detect intruders, find the survivors of a disaster or detect chemical spills, among other operations, says project coordinator Christophe Leroux.
“The monitoring of public and private sites is becoming increasingly important in the field of security and surveillance,” says Leroux.  “Mobile multi-sensor surveillance systems, able to be deployed quickly to analyse a situation, will boost the efficiency of the security teams. By combining sensors and robots, we can develop applications to search and warn, and to detect hazardous materials.”
The project team is close to developing a prototype of a small-size UAV capable of vertical take off and landing and for autonomous inspection and survey operations in urban areas with moving obstacles.
The mini-UAV was developed by AirRobot, a Germany-based company which is part of the project consortium. The drone is about 50cm in diameter, weighs less than one kilogram and can carry about 200grams. It looks like a miniature helicopter with four propellers, allowing it to take off and land vertically. A protective band surrounds the machine, preventing harm to people and the machine if an accident occurs.
The team also developed the software and hardware so the drone can locate its position in the air, navigate autonomously, and respond to unexpected events, such as an obstacle. Mission planning, collision avoidance and trajectory determination have been built into the drone’s software and hardware. The software’s visual memory map allows it to return home along its previous flight path.
The drone can be controlled from the ground or it can fly on a mission autonomously following a predefined path. Manual control can be switched on and off depending on the mission. The software and interface allows an operator without any technical knowledge to control it easily in urban areas or inside a building, Leroux says.
Monitoring for safety and security
He believes the new drone will be useful for policing, for example to determine the extent of a riot and for deploying forces, or for support at a crime scene. A remotely operated micro-UAV could be used to explore a crime scene inside a building without endangering the lives of police officers.
It can also be used for security. If an intrusion is detected, a UAV should be able to move faster than any ground-based robot or a human guard. Public places, airports, oil production facilities, pipelines and nuclear sites could be monitored using the micro-UAV.
The consortium is now focusing on evaluating and testing the new drone with potential users, including fire services. A small-sized UAV could be used for reconnaissance of the fire scene, helping fire fighters better assess how the fire is developing and if lives need to be saved. The drone will be tested with a fire service in Greece in November 2009 to determine how it performs.
“There is a need in the market for such a drone,” Leroux says. “Many end-users have already expressed an interest.”
µDrone received funding from the Specific Targeted Research Projects (STREP) strand of the Sixth Framework Programme for research.
Adapted from materials provided by ICT Results.

[Moloch]

You mean the T virus. The virus in Resident Evil series that reanimates dead cells. Yeah it does.

Actually, they did state that the T virus was engineered from the original T cell in the human body. The T virus basically accelerates the body's own immune system to superhuman levels, which in some people actually makes them superhuman, while in most cases just causes outlandish mutations.

[onishadowolf]

That's right.

[onishadowolf]

Gene genesis
About a quarter of present-day life's DNA blueprint was sketched out by 2.8 billion years ago
By Tina Hesman Saey
Web edition : Tuesday, December 21st, 2010
font_down font_up Text Size

Using the genetic equivalent of the Hubble telescope, researchers have peered into the distant past and witnessed an explosion of new genes that happened more than 3 billion years ago.

About 27 percent of all gene families that exist today were born between 3.3 billion and 2.8 billion years ago, two researchers from MIT report online December 19 in Nature. The surge of gene births — which the scientists have dubbed the Archean expansion — predate some important changes in Earth’s early chemistry, including the appearance of large amounts of oxygen in the atmosphere, say evolutionary biologists Eric Alm and Lawrence David.

The study may show how early organisms responded to and helped alter the planet’s chemistry. Daniel Segrč, a computational biologist at Boston University, says that the work provides “insight into really ancient metabolic events.”

Fossils of organisms billions of years old are difficult to find; the earliest organisms might not have been preserved in stone at all. Most familiar fossils appeared in the Cambrian period more than 540 million years ago. Some stromatolites — fossils of cyanobacteria — are as much as 3.4 billion years old.

But the researchers have found a rich molecular fossil bed billions of years old in the genetic blueprints of living organisms.

“Imprinted in the DNA of modern organisms is the history of these Precambrian events,” says Alm.

To read that history, the researchers traced the evolution of 3,983 gene families in the genomes of 100 different living species. Gene families are groups of genes that share similar structures and functions. Analyzing that amount of data is a technical tour de force, says Jason Raymond of Arizona State University in Tempe. Most researchers painstakingly reconstruct the evolutionary history of one gene at a time, he says. By simultaneously examining how thousands of genes changed over time to produce the variation seen in organisms today, “they’ve leapfrogged other researchers,” he says. “If they’d have done this 10 years ago, I’d be out of a Ph.D.”

Genes for shuttling electrons burst onto the scene about 3.3 billion years ago, the researchers calculate. Those genes, known as electron transport genes, are important for such processes as photosynthesis and respiration. By increasing the energy efficiency of some early life forms, these genes may have enabled populations to thrive.

Genes for using oxygen appeared at the tail of the genetic expansion around 2.8 billion years ago, long before oxygen began accumulating in the atmosphere around 2.5 billion years ago. The team also found evidence for the birth of genes for processing nitrogen and for using iron, molybdenum, copper and other elements.

While the genetic predictions match geochemical data for many of the elements, a few appear to contradict ideas about Earth’s early history. For instance, the new data predict that genes for using nickel were increasing at a time when geochemists say nickel concentrations in the ocean were crashing.

“Somebody’s wrong, and that’s what’s really exciting to me,” says Timothy Lyons, a geochemist at the University of California, Riverside. While he doesn’t expect the genetic models to singlehandedly overturn geochemical models of the early ocean, the new study might help refine chemical predictions. The genetic data is “another control and constraint that can’t be ignored.”