By David N. Leff

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

In polite society, the judgmental adjective "promiscuous" means "indiscriminate, random, casual choice of sexual partners."

In agriculture, that word denotes transfer, by sexual reproduction, of the phenotype of one plant species to a different one. This implies not social but ecological public concern.

If a crop plant thus outcrosses its genes, which escape to a noxious weed, that pestiferous growth may generate resistance to the parent plant's natural herbicidal resistance to the weed. When farmers apply chemical herbicides, the weed responds by upping its resistance, while often the artificial weed-killer takes its toll on the crop plant it aims to protect.

To break this Catch-22, genetic engineers are inserting herbicidal transgenes into the chromosomes of marketable plants thus threatened. (See BioWorld Today, March 21, 1995, p. 1.)

One such gene is Csrl-1, which expresses acetolactate synthase, an intermediate in protein synthesis that targets the weedicide chlorsulfuron. This weed-control poison, with a trade name of Glean, is supplied worldwide by DuPont Agricultural Products, a subsidiary of Wilmington, Del.-based E.I. Du Pont de Nemours and Co.

At the University of Chicago, molecular ecologist Joy Bergelson wondered whether such transgenic plants might gain in promiscuity. "My motive," she told BioWorld Today, "was simply personal curiosity."

The field experiment that Bergelson mounted to answer this question appears as a one-page letter in the current issue of Nature, dated Sept. 3, 1998.

She and her co-authors inserted the Glean transgene into the all-purpose laboratory-model weed, Arabadopsis thaliana, which normally self-fertilizes. "At our field site in central Illinois," she recounted, "we set out 144 plantlet rosettes. One quarter of them were wild type; another quarter consisted of mutants carrying the natural herbicidal gene. The remaining half were transgenic plants, expressing the Csrl-1 Glean gene in a plasmid vector."

They grew this experimental crop free of herbicides and allowed it to be visited by pollinating syrphid flies, which look like bees and eat pollen.

At season's end, the group surveyed approximately 100,000 A. thaliana seeds, and found that the outcrossing rate per plant was 20 times higher in transgenic progenitors than in mutants.

They observed that although A. thaliana "is unlikely to become a pernicious weed, these results show that genetic engineering can substantially increase the probability of transgene escape." But they added, "Our results do not show that enhanced outcrossing is due to the transgene itself."

Bergelson concluded that her findings "are of broad relevance, because this Glean transgene has been introduced into over a dozen agricultural crops, including brassica and rice."

Milder Form Of Muscular Dystrophy Finds Chromosomes 4 and 10 Exchange Repeats

If a 7-year-old has difficulty whistling, the pediatrician may suspect a fairly benign inherited syndrome called fascioscapulohumeral muscular dystrophy (FSHD). Problems with closing eyes and lifting arms are other early symptoms of the disease. They result from weakness of facial and shoulder muscles, and often of the legs as well.

Unlike Duchenne's, the best-known muscular dystrophy, in which most patients die by age 20, children and teen-agers diagnosed with FSHD have normal life expectancy, complicated by muscle weakness and wasting, with relatively bearable disability.

But that diagnosis is itself problematic.

A paper in the August issue of the British journal Human Molecular Genetics bears the title "Inter- and intrachromosomal sub-telomeric rearrangements on [chromosome] 4q35: Implications for fascioscapulohumeral muscular dystrophy (FSHD) aetiology and diagnosis." Its authors are members of a mini-consortium in the Netherlands, Italy, and the U.K.

This group examined the genomes of 50 healthy unrelated males. Five of them showed tandem repeat sequences on the long arm of chromosome 4 showing up on one of their chromosomes 10. Another five subjects apparently had the reverse effect: chromosome 10 repeats on their chromosomes 4.

"Despite intensive efforts," the paper notes, "no transcribed sequences have been identified within this array." The authors suggest that "only the length of the repeat locus on chromosome 4, and not its intrinsic properties, is causally related to the disease." This finding supports their hypothesis that "FSHD is caused by a position effect in which the repeat structure influences the expression of genes nearby."

They explain why their finding "may complicate molecular diagnosis of FSHD," but conclude that "these sub-telomeric rearrangements may also occur without pathological consequences."

Ultraviolet-A Wavelength Proves To Be Pit Bull — Not Pussycat — For Skin, DNA

Ultimately, the source of all energy, and all life, on earth is a smallish star we know as the sun.

Although the sunbelt is the fastest-growing region in the U.S., sunshine is our foe as well as friend. Which is why suncreen creams are doing so well on the cosmetic market.

Besides warding off sunburn, these smoothed-on ultraviolet (UV) shields supposedly prevent the dark, sagging, leathery, prematurely wrinkled skin of chronic sun worshippers and their propensity to skin cancer.

Now comes the bad news:

Despite all the warnings from dermatologists to shun excess solar exposure, scientists still don't really understand how the sun damages human skin. They know a bit more now, thanks to a report in the current Proceedings of the National Academy of Sciences (PNAS), dated Sept. 1, 1998. The paper's title is "Epidermal trans-urocanic acid and the UV-A-induced photoaging of the skin."

Its authors are at two academic centers in the sunbelt, Duke University, in Durham, N.C., and the University of California at San Diego.

Their study focuses on the sun-sensitive molecule trans-urocanic acid (t-UA). This chromophore forms in the skin's epidermis. In the 1950s, dermatologists hailed t-UA as the body's own sunscreen, because it absorbs the B spectrum of UV light.

UV-B light causes the t-UA molecule to buckle in on itself and go from trans to cis structural form. But despite this defensive twist, the cis molecule still absorbed three times more solar energy than expected.

It turned out, as the paper reports, that light near the tail end of the UV-A range — thought harmless — actually zaps the molecule into creating harmful oxygen free radicals. Besides causing premature aging of skin, these rogue oxygen electrons damage DNA, suppress the immune system, and bring on breathing problems. *