By David N. Leff

Editor's note: Science Scan is a roundup of recently published, biotechnology-relevant research.

Chlorine is an element with a split poisonality - pun intended. On the one hand, chlorination purifies water supplies of bacterial pollution. On the other, widely used industrial solvents such as trichloroethylene (TCE) and tetrachloroethylene turn wells and water tables into hazardous waste sites. (See BioWorld Today, June 9, 1997, p. 1.)

Tetrachloroethylene is better known as perchloroethylene (PCE). "It's widely used as a degreaser," observed chemical engineer Thomas Wood, at the University of Connecticut in Storrs. "PCE is used a lot in military bases to clean aircraft engines. It's used in dry cleaning, and industrially to clean metal. It's been around since World War II." PCE also finds employment medically as a vermifuge - a deworming medicament.

PCE's resume is about on a par with TCE's. "They both have very similar properties," Wood pointed out, and are used to about the same extent. TCE is a little bit easier to degrade, because it has only three chlorine atoms compared to PCE's four. In general, the more chlorines there are in the molecule, the more difficult it is for natural bacteria to break it down."

He explained that bacteria existing in nature have a tough time degrading such manmade chemicals as PCE because they have never encountered such molecules, and don't have the enzymes to deal with them. Wood reports a happy and hopeful exception to this stand-off in the July 2000 issue of Nature Biotechnology. His paper is titled: "Aerobic degradation of tetrachloroethylene by toluene-o-xylene monooxygenase of Pseudomonas stutzeri OX1."

PCE pollution in the U.S. alone, Wood told BioWorld Today, "amounts to thousands of hazardous waste sites. Their danger to the public is poisoning of the drinking-water supply. Usually PCE spillages seep from the surface down to the underground aquifer. And because it's heavier than the water it will actually wind up at the bottom of that water table, from 5 to 100 feet underground, contaminating the aquifer itself on the way."

Lacking a friendly bacterium to chew up PCE, Wood said, "The traditional method would be to excavate the contaminated soil, strip out the chlorinated compound, adsorb it onto activated carbon, then incinerate the carbon, or try to recover the PCE.

"The bug we discovered, Pseudomonas stutzeri he continued, "was a natural bacterium taken from a municipal wastewater treatment plant in Italy. We were the first group to try to see if we could get it to degrade chlorinated compounds."

The secret of P. stutzeri's success, Wood and his co-authors determined, lay in its secretion of a chlorine-targeted enzyme called toluene-o-xylene monooxygenase - ToMO for short. "The bacterium grows on toluene and xylene," he continued. "That's why it got that name. The bug would prefer something like sugar, but if it doesn't have that then it can also grow on these two other compounds that have competitive advantage, and can outstrip other bacteria that lack this particular enzyme.

"That's why this work is so important," Wood pointed out, "because it's the first report of being able to do it aerobically - that is, a bacterium living and growing in the presence of oxygen. The anaerobic decay route," he explained, "removes only one chlorine at a time, so the tetrachloroethylene becomes trichloroethylene, which can become dichlorethylene. Then if you remove one more chlorine you have vinyl chloride. That's the big problem, because if you stop at vinyl chloride, it's much more toxic. Whereas PCE and TCE are suspected carcinogens, vinyl chloride is a known carcinogen."

Wood is now developing a method for hustling P. stutzeri down through the water table. "What we've done," he related, "is create a system where we take the bacteria and marry them to the roots of poplar trees - which grow about 10 feet a year, and put down a very extensive root structure. Wherever the root goes, the bacterium goes. So it cleans the soil and can go all the way down, cleaning the underground aquifer.

"It definitely works in the lab, and we're trying to set up field trials," Wood concluded. "Some Connecticut firms and international companies are interested."

Parkin, A Protein Expressed By parkin Gene, Linked To Ubiquitin's Degradation System

Between their late teens and 20s, numbers of young people in Japan have turned up with all the symptomatic hallmarks of Parkinson's disease (PD). At Keio University School of Medicine in Tokyo, two years ago, neurologists and neurogeneticists studied five such premature-PD patients. By positional cloning, they identified a gene on human chromosome 6, which they named parkin, and proposed that mutations in the gene's 465-amino-acid protein, Parkin, accounted for the young subjects' Parkinsonian symptoms.

But not all jerky, spasmodic movements, rigidity and other PD-like behavior necessarily diagnose PD itself, especially at such an early age of onset. The Japanese scientists dubbed it "autosomal recessive juvenile parkinsonianism" (AR-JP).

Now, in the July issue of Nature Genetics, the same Tokyo consortium reports that the "Familial Parkinson disease gene product, Parkin, is a ubiquitin-protein ligase." Their paper describes AR-JP as "one of the most common familial forms of Parkinson's disease."

In exploring the Parkin protein's function, as yet unknown, the co-authors implicate it in the activity of ubiquitin, a small polypeptide that occurs in virtually every cell of the mammalian body. It preps redundant or worn-out proteins for breakdown and recycling.

The article concludes: "Our findings should enhance the exploration of the molecular mechanisms of neurodegenerative diseases that are characterized by involvement of abnormal protein ubiquitination, including Alzheimer's disease, CAG triplet repeat disorders [notably, Huntington's disease] and amyotrophic lateral sclerosis."

DNA Crossover In Bloom's Syndrome Suggests Role For Mutant Gene In Tumor Suppression

Bloom's syndrome (BS) is a rare but horrendous autosomal recessive disorder marked by dwarfism, low fertility, and high risk of multiple cancers throughout life. British scientists at Oxford University's Radcliffe Hospital report in the Proceedings of the National Academy of Sciences (PNAS), released May 13, 2000, that "The Bloom's syndrome gene product promotes branch migration of Holliday junctions." (When two DNA double helices cross in a recombination event, the resulting structure is called a Holliday junction.) Their results suggest that the gene mutated in BS has implications in the suppression of tumorigenesis.