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Wantable Inc. founder Jalem Getz has mostly Builder DNA. John Lauber, founder and president of LauberCFOs, has mostly Specialist DNA.

Author Joe Abraham

Both determined their Entrepreneurial DNA types through the BOSI DNA system developed by serial entrepreneur Joe Abraham.

BOSI stands for Abraham's four types of Entrepreneurial DNA: Builder, Opportunist, Specialist and Innovator.

JALEM GETZ DNA TYPE: BUILDER: Strategic, always looking for the upper hand TALENT: Creating scalable business ventures

In 2010, Abraham also started BOSI Global, an operating partner venture associated with the concept, which recently entered the Milwaukee market. It is based in Chicago, has offices in Sarasota, Fla., Houston, Singapore and Latvia, and employs about 20 seasoned entrepreneurs and executives.

TOM BENTLEY III DNA TYPE: OPPORTUNIST: Speculative, always in the right place at the right time TALENT: Making money fast

The original discovery happened quite by accident, he said. I was working with a group of companies, kind of helping them get to the next level, and was finding over and over again that the strategy that I was trying to provide them, one size wasn't fitting all.

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What's your Entrepreneurial DNA?

Scientists at the Scripps Research Institute (TSRI) in California have produced a living bacterium that has a strand of artificial DNA made with chemical letters not found in nature or any other organism.

Deoxyribonucleic acid (DNA) is the famous double helix discovered by Watson and Crick in the 1950s and commonly known as the carrier of the genetic code of life. Its found in all living things on Earth, from the smallest cells to the largest redwood trees, and in each and every one of these organisms the basic DNA structure is exactly the same.

Though the models of DNA that are on display in museums seem impossibly complex, it is actually a very simple molecule. Its twisty double backbone of phosphates and sugars carries branches that link the two spirals together like steps in a ladder. These steps consist of a surprisingly simple pairing of four nucleic acid bases: guanine (G), adenine (A), thymine (T), and cytosine (C). These bases pair up to one another like lock and key with guanine pairing with cytosine and adenine pairing with thymine.

This simple, predictable pairing allows life to happen. It provides a way to encode the genetic instructions needed to build and maintain cells. Under the influence of various enzymes, the DNA molecules unfasten and come apart like zippers, which provide the pattern for creating new strands of DNA.

This sort of base pairing is universal in all known life. If it has DNA, then it uses G-C and A-T pairs. The question is, is this pairing universal because of all life on Earth having a common ancestor, is it because of some fundamental law of chemistry, or both?

The result of years of research going back to the late 1990s, the TSRI teams project aimed to find molecules that would pair like those in DNA and would form stably on the helix backbone of the DNA molecule. They would also need to unzip like the known bases and transcribe onto the RNA molecules to create new DNA strands. In addition, they had to be able to survive the DNA repair mechanisms in the cell that might see the new bases as faulty strands and remove them.

In 2008, the team was able to create semi-artificial strands of DNA that would replicate in a test tube in the presence of the right enzymes and would transcribe onto RNA, but, according to the team, the big leap was to get the strands to work in a living cell. They did this by creating a plasmid, which is a circular strand of DNA, that was a mixture of natural and artificial DNA elements made of molecules known as d5SICS and dNaM, and then inserting it into escherichia coli bacteria.

Obviously, the result isn't artificial life, but it is, by any definition, a novelty. The bacteria carried in their nuclei DNA with bases not found in any other living organism. The pairs are able to duplicate so long as the chemical materials are available, and the duplication occurs with reasonable speed and accuracy, the repair mechanism didn't interfere, and the growth of the cells was not impaired.

However, the new bacteria are also no Frankensteins micro-monsters waiting to break out of the lab on an unsuspecting world. Since 5SICS and dNaM are not found in nature, the scientists have to supply them for the DNA strands to form and they need what are called triphosphate transporter molecules produced by a species of microalgae to move the molecules into the cells. What all that adds up to is that the artificial DNA wont work outside of the laboratory.

"When we stopped the flow of the unnatural triphosphate building blocks into the cells, the replacement of d5SICSdNaM with natural base pairs was very nicely correlated with the cell replication itself there didnt seem to be other factors excising the unnatural base pairs from the DNA, says team member Denis A. Malyshev. "An important thing to note is that these two breakthroughs also provide control over the system. Our new bases can only get into the cell if we turn on the base transporter protein. Without this transporter or when new bases are not provided, the cell will revert back to A, T, G, C, and the d5SICS and dNaM will disappear from the genome."

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Engineered bacterium is first living organism to use artificial DNA "letters"

St. Jude Children's Research Hospital scientists studying two rare, inherited childhood neurodegenerative disorders have identified a new, possibly common source of DNA damage that may play a role in other neurodegenerative diseases, cancer and aging. The findings appear in the current issue of the scientific journal Nature Neuroscience.

Researchers showed for the first time that an enzyme required for normal DNA functioning causes DNA damage in the developing brain. DNA is the molecule found in nearly every cell that carries the instructions needed to assemble and sustain life.

The enzyme is topoisomerase 1 (Top1). Normally, Top1 works by temporarily attaching to and forming a short-lived molecule called a Top1 cleavage complex (Top1cc). Top1ccs cause reversible breaks in one strand of the double-stranded DNA molecule. That prompts DNA to partially unwind, allowing cells to access the DNA molecule in preparation for cell division or to begin production of the proteins that do the work of cells.

Different factors, including the free radicals that are a byproduct of oxygen metabolism, result in Top1ccs becoming trapped on DNA and accumulating in cells. This study, however, is the first to link the buildup to disease. The results also broaden scientific understanding of the mechanisms that maintain brain health.

Investigators made the connection between DNA damage and accumulation of Top1cc while studying DNA repair problems in the rare neurodegenerative disorders ataxia telangiectasia (A-T) and spinocerebellar ataxia with axonal neuropathy 1(SCAN1). The diseases both involve progressive difficulty with walking and other movement. This study showed that A-T and SCAN1 also share the buildup of Top1ccs as a common mechanism of DNA damage. A-T is associated with a range of other health problems, including an increased risk of leukemia, lymphoma and other cancers.

"We are now working to understand how this newly recognized source of DNA damage might contribute to tumor development or the age-related DNA damage in the brain that is associated with neurodegenerative disorders like Alzheimer's disease," said co-corresponding author Peter McKinnon, Ph.D., a member of the St. Jude Department of Genetics. The co-corresponding author is Sachin Katyal, Ph.D., of the University of Manitoba Department of Pharmacology and Therapeutics and formerly of St. Jude.

A-T and SCAN1 are caused by mutations in different enzymes involved in DNA repair. Mutations in the ATM protein lead to A-T. Alterations in the Tdp1 protein cause SCAN1.

Working in nerve cells growing in the laboratory and in the nervous system of specially bred mice, researchers showed for the first time that ATM and Tdp1 work cooperatively to repair breaks in DNA. Scientists also demonstrated how the proteins accomplish the task.

The results revealed a new role for ATM in repairing single-strand DNA breaks. Until this study, ATM was linked to double-strand DNA repair. ATM was also known to work exclusively as a protein kinase. Kinases are enzymes that use chemicals called phosphate groups to regulate other proteins.

Scientists reported that when Top1ccs are trapped ATM functions as a protein kinase and alert cells to the DNA damage. But researchers found ATM also serves a more direct role by marking the trapped Top1ccs for degradation by the protein complex cells use to get rid of damaged or unnecessary proteins. ATM accomplishes that task by promoting the addition of certain proteins called ubiquitin and SUMO to the Top1cc surface.

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Rare, childhood neurodegenerative diseases linked to common problem in DNA repair