Richard Casement Internship sample, The Economist
The central dogma of molecular biology, widely accepted as the foundation for modern genetics, amounts to so much rubbish. Or so asserts Barry Commoner, senior scientist at the Center for the Biology of Natural Systems at Queens College, City University of New York. Further, Dr Commoner believes that the continued (and, he claims, willful) ignorance of the falsity of this revered principle could have unintended and potentially disastrous health and environmental consequences.
To understand how the collapse of the central dogma might be troublesome as scientists forge ahead with transgenic genetic modification, one must understand the parsimony that it assumes. Essentially, the dogma endows the DNA molecule exclusive power over its own replication as well as the appearance of all inherited traits. It also asserts absolute unidirectionality: once a gene encodes a protein, the information that created the protein cannot get out again. Therefore, it might seem reasonable to expect a one-to-one ratio of genes to proteins. This logic was dismantled last February, when reports analyzing the Human Genome Project revealed that humans have an estimated 30,000 genes, a number far short of the 100,000 predicted by the number of proteins present in the human body. With humans possessing only about double the number of genes as a fruit fly, and obviously vastly different traits, Dr Commoner theorizes a far more complex process at work, and points to alternative splicing and the role of proteins in finishing up the job of inheritance.
Alternative splicing starts with the gene's original nucleotide sequence, and with the help of a specialized group of proteins and RNA molecules known as spliceosomes, breaks it apart and shuffles the sequence, recombining it to encode proteins. Studying this process, scientists have discovered that a gene known to encode a human inner-ear-cell protein also gives rise to 576 other proteins, all distinct in their amino acid sequences.
Proteins also aid in expressing the genome by improving DNA replication accuracy, cleaning up nucleotide errors and enabling newly made protein molecules to become biochemically active. This last role is critical, since, left alone, some proteins are likely to become misfolded (and so remain biochemically inactive) and only fold properly upon coming into contact with a special type of "chaperone" protein. Whereas this biochemical event is not possible under the central dogma's assumption that a protein's active structure is determined solely by its amino acid sequence, research on degenerative brain diseases suggests otherwise.
Dr Commoner cites the prion, an infectious and wholly nucleic-acid-free protein, as evidence that protein-to-protein information transmission can and does occur. In a scrapie-infected sheep, prions invade the brain, and though their amino acid sequence is the same as the normal brain protein, they behave differently, able to refold the normal protein into the prion's three-dimensional structure. A chain reaction occurs, with newly infectious proteins refolding their normal neighbors.
What this means for consumers of genetically modified products hinges on whether the transfer of a single alien gene into an organism will produce the single desired protein, or whether through alternative splicing, the gene will give rise to many unintended and potentially harmful variants. The biotechnology industry assumes the former, Dr Commoner the latter.
The evidence that Dr Commoner is right to be concerned is mounting. He cites Belgian research that recently discovered a genetically modified soybean plant with DNA scrambled enough to give it the potential to encode a new protein. Another recent study seeking to explain such phenomena suggests that the protein-based processes that correct replication errors may be rearranging the alien gene's nucleotide sequence. With billions of individual transgenic plants already being grown in the United States, and without any requirements to study successive generations of transgenic crops, it is difficult to know either the frequency or the severity of such events.
As the lengthy incubation period for mad cow disease suggests, evidence of a new, harmful protein entering the food supply may not turn up until it is too late. Given all that we do not understand about the processes that give rise to inherited traits, a modicum of caution is well advised.
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Hi. I'm Tiffany Hamburger. I'm a full-time freelance writer and editor based in Austin, Texas. I've written and edited professionally for a decade on a wide variety of subjects.
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